Sample records for aberrations sister chromatid

  1. Frequency of sister chromatid exchange and chromosomal aberrations in asbestos cement workers.

    PubMed

    Fatma, N; Jain, A K; Rahman, Q

    1991-02-01

    Exposure to asbestos minerals has been associated with a wide variety of adverse health effects including lung cancer, pleural mesothelioma, and cancer of other organs. It was shown previously that asbestos samples collected from a local asbestos factory enhanced sister chromatid exchanges (SCEs) and chromosomal aberrations in vitro using human lymphocytes. In the present study, 22 workers from the same factory and 12 controls were further investigated. Controls were matched for age, sex, and socioeconomic state. The peripheral blood lymphocytes were cultured and harvested at 48 hours for studies of chromosomal aberrations and at 72 hours for SCE frequency determinations. Asbestos workers had a raised mean SCE rate and increased numbers of chromosomal aberrations compared with a control population. Most of the chromosomal aberrations were chromatid gap and break types.

  2. Sister chromatid segregation in meiosis II

    PubMed Central

    Wassmann, Katja

    2013-01-01

    Meiotic divisions (meiosis I and II) are specialized cell divisions to generate haploid gametes. The first meiotic division with the separation of chromosomes is named reductional division. The second division, which takes place immediately after meiosis I without intervening S-phase, is equational, with the separation of sister chromatids, similar to mitosis. This meiotic segregation pattern requires the two-step removal of the cohesin complex holding sister chromatids together: cohesin is removed from chromosome arms that have been subjected to homologous recombination in meiosis I and from the centromere region in meiosis II. Cohesin in the centromere region is protected from removal in meiosis I, but this protection has to be removed—deprotected”—for sister chromatid segregation in meiosis II. Whereas the mechanisms of cohesin protection are quite well understood, the mechanisms of deprotection have been largely unknown until recently. In this review I summarize our current knowledge on cohesin deprotection. PMID:23574717

  3. Induction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.

    PubMed

    Latt, S A; Stetten, G; Juergens, L A; Buchanan, G R; Gerald, P S

    1975-10-01

    Sister chromatid exchanges, which may reflect chromosome repair in response to certain types of DNA damage, provide a means of investigating the increased chromosome fragility characteristic of Fanconi's anemia. By a recently developed technique using 33258 Hoechst and 5-bromodeoxyuridine, it was observed that the baseline frequency of sister chromatid exchanges in phytohemagglutinin-stimulated lymphocytes from four males with Fanconi's anemia differed little from that of normal lymphocytes. However, addition of the bifunctional alkylating agent mitomycin C (0.01 or 0.03 mug/ml) to the Fanconi's anemia cells during culture induces less than half of the increase in exchanges found in identically treated normal lymphocytes. This reduced increment in exchanges in accompanied by a partial suppression of mitosis and a marked increase in chromatid breaks and rearrangements. Many of these events occur at sites of incomplete chromatid interchange. The increase in sister chromatid exchanges induced in Fanconi's anemia lymphocytes by the monofunctional alkylating agent ethylmethane sulfonate (0.25 mg/ml) was slightly less than that in normal cells. Lymphocytes from two sets of parents of the patients with Fanconi's anemia exhibited a normal response to alkylating agents, while dermal fibroblasts from two different patients with Fanconi's anemia reacted to mitomycin C with an increase in chromatid breaks, but a nearly normal increment of sister chromatid exchanges. The results suggest that chromosomal breaks and rearrangements in Fanconi's anemia lymphocytes may result from a defect in a form of repair of DNA damage.

  4. Mechanics of Sister Chromatids studied with a Polymer Model English</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Zhang, Yang; Isbaner, Sebastian; Heermann, Dieter</p> <p>2013-10-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion denotes the phenomenon that <span class="hlt">sister</span> <span class="hlt">chromatids</span> are initially attached to each other in mitosis to guarantee the error-free distribution into the daughter cells. Cohesion is mediated by binding proteins and only resolved after mitotic chromosome condensation is completed. However, the amount of attachement points required to maintain <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion while still allowing proper chromosome condensation is not known yet. Additionally the impact of cohesion on the mechanical properties of chromosomes also poses an interesting problem. In this work we study the conformational and mechanical properties of <span class="hlt">sister</span> <span class="hlt">chromatids</span> by means of computer simulations. We model both protein-mediated cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> and chromosome condensation with a dynamic binding mechanisms. We show in a phase diagram that only specific link concentrations lead to connected and fully condensed <span class="hlt">chromatids</span> that do not intermingle with each other nor separate due to entropic forces. Furthermore we show that dynamic bonding between <span class="hlt">chromatids</span> decrease the Young's modulus compared to non-bonded <span class="hlt">chromatids</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1205336','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1205336"><span>Replication-Dependent <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Recombination in Rad1 Mutants of Saccharomyces Cerevisiae</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kadyk, L. C.; Hartwell, L. H.</p> <p>1993-01-01</p> <p>Homolog recombination and unequal <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination were monitored in rad1-1/rad1-1 diploid yeast cells deficient for excision repair, and in control cells, RAD1/rad1-1, after exposure to UV irradiation. In a rad1-1/rad1-1 diploid, UV irradiation stimulated much more <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination relative to homolog recombination when cells were irradiated in the G(1) or the G(2) phases of the cell cycle than was observed in RAD1/rad1-1 cells. Since <span class="hlt">sister</span> <span class="hlt">chromatids</span> are not present during G(1), this result suggested that unexcised lesions can stimulate <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination events during or subsequent to DNA replication. The results of mating rescue experiments suggest that unexcised UV dimers do not stimulate <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination during the G(2) phase, but only when they are present during DNA replication. We propose that there are two types of <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination in yeast. In the first type, unexcised UV dimers and other bulky lesions induce <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination during DNA replication as a mechanism to bypass lesions obstructing the passage of DNA polymerase, and this type is analogous to the type of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange commonly observed cytologically in mammalian cells. In the second type, strand scissions created by X-irradiation or the excision of damaged bases create recombinogenic sites that result in <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination directly in G(2). Further support for the existence of two types of <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination is the fact that events induced in rad1-1/rad1-1 were due almost entirely to gene conversion, whereas those in RAD1/rad1-1 cells were due to a mixture of gene conversion and reciprocal recombination. PMID:8454200</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11444040','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11444040"><span>Splitting the chromosome: cutting the ties that bind <span class="hlt">sister</span> <span class="hlt">chromatids</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nasmyth, K; Peters, J M; Uhlmann, F</p> <p>2001-01-01</p> <p>In eukaryotic cells, replicated DNA molecules remain physically connected from their synthesis in S phase until they are separated during anaphase. This phenomenon, called <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, is essential for the temporal separation of DNA replication and mitosis and for the equal separation of the duplicated genome. Recent work has identified a number of chromosomal proteins required for cohesion. In this review we discuss how these proteins may connect <span class="hlt">sister</span> <span class="hlt">chromatids</span> and how they are removed from chromosomes to allow <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation at the onset of anaphase.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=recombination&pg=4&id=EJ384605','ERIC'); return false;" href="https://eric.ed.gov/?q=recombination&pg=4&id=EJ384605"><span>How-to-Do-It: Demonstrating <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchanges.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Dye, Frank J.</p> <p>1988-01-01</p> <p>Outlines procedures for demonstrating and preparing a permanent slide of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and recombination events between the two <span class="hlt">chromatids</span> of a single chromosome. Provides the name of an additional resource for making preparations of exchanges. (RT)</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19002846','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19002846"><span>The effects of boric acid on <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and chromosome <span class="hlt">aberrations</span> in cultured human lymphocytes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Arslan, Mehmet; Topaktas, Mehmet; Rencuzogullari, Eyyüp</p> <p>2008-02-01</p> <p>The aim of this study was to determine the possible genotoxic effects of boric acid (BA) (E284), which is used as an antimicrobial agent in food, by using <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCEs) and chromosome <span class="hlt">aberration</span> (CAs) tests in human peripheral lymphocytes. The human lymphocytes were treated with 400, 600, 800, and 1000 mug/mL concentrations of BA dissolved in dimethyl sulfoxide (DMSO), for 24 h and 48 h treatment periods. BA did not increase the SCEs for all the concentrations and treatment periods when compared to control and solvent control (DMSO). BA induced structural and total CAs at all the tested concentrations for 24 and 48 h treatment periods. The induction of the total CAs was dose dependent for the 24 h treatment period. However, BA did not cause numerical CAs. BA showed a cytotoxic effect by decreasing the replication index (RI) and mitotic index (MI). BA decreased the MI in a dose-dependent manner for the 24 h treatment period.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8632802','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8632802"><span>Cut2 proteolysis required for <span class="hlt">sister-chromatid</span> seperation in fission yeast.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Funabiki, H; Yamano, H; Kumada, K; Nagao, K; Hunt, T; Yanagida, M</p> <p>1996-05-30</p> <p>Although mitotic cyclins are well-known substrates for ubiquitin-mediated proteolysis at the metaphase-anaphase transition, their degradation is not essential for separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span>; several lines of evidence suggest that proteolysis of other protein(s) is required, however. Here we report the anaphase-specific proteolysis of the Schizosaccharomyces pombe Cut2 protein, which is essential for <span class="hlt">sister-chromatid</span> separation. Cut2 is located in the nucleus, where it is concentrated along the short metaphase spindle. The rapid degradation of Cut2 at anaphase requires its amino-terminal region and the activity of Cut9 (ref. 14), a component of the 20S cyclosome/anaphase-promoting complex (APC), which is necessary for cyclin destruction. Expression of non-degradable Cut2 blocks <span class="hlt">sister-chromatid</span> separation but not cell-cycle progression. This defect can be overcome by grafting the N terminus of cyclin B onto the truncated Cut2, demonstrating that the regulated proteolysis of Cut2 is essential for <span class="hlt">sister-chromatid</span> separation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/1585081','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/1585081"><span>Effect of chloramphenicol on <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in bovine fibroblasts.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Arruga, M V; Catalan, J; Moreno, C</p> <p>1992-03-01</p> <p>The genotoxic potential of different chloramphenicol concentrations (5, 20, 40 and 60 micrograms ml-1) was investigated in bovine fibroblast primary lines by <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay. Chloramphenicol acted for long enough to ensure similar effects to persistent storage in the kidney. In this experiment 10 micrograms ml-1 of 5-bromodeoxyuridine was added for 60 hours for all doses of chloramphenicol and to the control. When the tissue culture cells were exposed to increasing doses, increased numbers of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges developed. Differences were significantly different to the control.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2567865','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2567865"><span>Shugoshin1 May Play Important Roles in Separation of Homologous Chromosomes and <span class="hlt">Sister</span> <span class="hlt">Chromatids</span> during Mouse Oocyte Meiosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Yin, Shen; Ai, Jun-Shu; Shi, Li-Hong; Wei, Liang; Yuan, Ju; Ouyang, Ying-Chun; Hou, Yi; Chen, Da-Yuan; Schatten, Heide; Sun, Qing-Yuan</p> <p>2008-01-01</p> <p>Background Homologous chromosomes separate in meiosis I and <span class="hlt">sister</span> <span class="hlt">chromatids</span> separate in meiosis II, generating haploid gametes. To address the question why <span class="hlt">sister</span> <span class="hlt">chromatids</span> do not separate in meiosis I, we explored the roles of Shogoshin1 (Sgo1) in chromosome separation during oocyte meiosis. Methodology/Principal Findings Sgo1 function was evaluated by exogenous overexpression to enhance its roles and RNAi to suppress its roles during two meioses of mouse oocytes. Immunocytochemistry and chromosome spread were used to evaluate phenotypes. The exogenous Sgo1 overexpression kept homologous chromosomes and <span class="hlt">sister</span> <span class="hlt">chromatids</span> not to separate in meiosis I and meiosis II, respectively, while the Sgo1 RNAi promoted premature separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Conclusions Our results reveal that prevention of premature separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> in meiosis I requires the retention of centromeric Sgo1, while normal separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> in meiosis II requires loss of centromeric Sgo1. PMID:18949044</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11862455','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11862455"><span>Colchicine promotes a change in chromosome structure without loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion in prometaphase I-arrested bivalents.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Rodríguez, E M; Parra, M T; Rufas, J S; Suja, J A</p> <p>2001-12-01</p> <p>In somatic cells colchicine promotes the arrest of cell division at prometaphase, and chromosomes show a sequential loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> arm and centromere cohesion. In this study we used colchicine to analyse possible changes in chromosome structure and <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion in prometaphase I-arrested bivalents of the katydid Pycnogaster cucullata. After silver staining we observed that in colchicine-arrested prometaphase I bivalents, and in contrast to what was found in control bivalents, <span class="hlt">sister</span> kinetochores appeared individualised and <span class="hlt">sister</span> <span class="hlt">chromatid</span> axes were completely separated all along their length. However, this change in chromosome structure occurred without loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> arm cohesion. We also employed the MPM-2 monoclonal antibody against mitotic phosphoproteins on control and colchicine-treated spermatocytes. In control metaphase I bivalents this antibody labelled the tightly associated <span class="hlt">sister</span> kinetochores and the interchromatid domain. By contrast, in colchicine-treated prometaphase I bivalents individualised <span class="hlt">sister</span> kinetochores appeared labelled, but the interchromatid domain did not show labelling. These results support the notion that MPM-2 phosphoproteins, probably DNA topoisomerase IIalpha, located in the interchromatid domain act as "chromosomal staples" associating <span class="hlt">sister</span> <span class="hlt">chromatid</span> axes in metaphase I bivalents. The disappearance of these chromosomal staples would induce a change in chromosome structure, as reflected by the separation of <span class="hlt">sister</span> kinetochores and <span class="hlt">sister</span> axes, but without a concomitant loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5060660-sister-chromatid-exchanges-induced-inhaled-anesthetics','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5060660-sister-chromatid-exchanges-induced-inhaled-anesthetics"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchanges induced by inhaled anesthetics</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>White,A.E.; Takehisa, S.; Eger II, E.I.</p> <p>1970-05-01</p> <p>There is sufficient evidence that anesthetics may cause cancer to justify a test of their carcinogenic potential. Baden et al., using the Ames test, a rapid and inexpensive genetic indicator of carcinogenicity, have shown that among currently used anesthetics fluorxene alone caused bacterial mutations. The authors used the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) technique, another rapid assay of mutagenic-carcinogenic potential. The frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in Chinese hamster ovary cells increases when the cell cultures are exposed to mutagen-carcinogens, particulary in the presence of a metabolic activating system. With this test system a one-hour exposure to 1 MAC nitrous oxide,more » diethyl ether, trichloroethylene, halothane, enflurane, isoflurane, methoxyflurane, or chloroform did not increase SCE values. Divinyl ether, fluroxene and ethyl vinyl ether increased SCE values in the same circumstances. Results of this study of mammalian cells suggest that no currently used anesthetic is a mutagen-carcinogen. The results also suggest that anesthetics containing a vinyl moiety may be mutagen-carcinogens.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/10827941','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/10827941"><span>Splitting the chromosome: cutting the ties that bind <span class="hlt">sister</span> <span class="hlt">chromatids</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nasmyth, K; Peters, J M; Uhlmann, F</p> <p>2000-05-26</p> <p>In eukaryotic cells, <span class="hlt">sister</span> DNA molecules remain physically connected from their production at S phase until their separation during anaphase. This cohesion is essential for the separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> to opposite poles of the cell at mitosis. It also permits chromosome segregation to take place long after duplication has been completed. Recent work has identified a multisubunit complex called cohesin that is essential for connecting <span class="hlt">sisters</span>. Proteolytic cleavage of one of cohesin's subunits may trigger <span class="hlt">sister</span> separation at the onset of anaphase.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2776007','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2776007"><span>Effect of borax on immune cell proliferation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in human chromosomes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Pongsavee, Malinee</p> <p>2009-01-01</p> <p>Background Borax is used as a food additive. It becomes toxic when accumulated in the body. It causes vomiting, fatigue and renal failure. Methods The heparinized blood samples from 40 healthy men were studied for the impact of borax toxicity on immune cell proliferation (lymphocyte proliferation) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in human chromosomes. The MTT assay and <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange (SCE) technic were used in this experiment with the borax concentrations of 0.1, 0.15, 0.2, 0.3 and 0.6 mg/ml. Results It showed that the immune cell proliferation (lymphocyte proliferation) was decreased when the concentrations of borax increased. The borax concentration of 0.6 mg/ml had the most effectiveness to the lymphocyte proliferation and had the highest cytotoxicity index (CI). The borax concentrations of 0.15, 0.2, 0.3 and 0.6 mg/ml significantly induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in human chromosomes (P < 0.05). Conclusion Borax had effects on immune cell proliferation (lymphocyte proliferation) and induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in human chromosomes. Toxicity of borax may lead to cellular toxicity and genetic defect in human. PMID:19878537</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=86942','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=86942"><span>Saccharomyces cerevisiae CTF18 and CTF4 Are Required for <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Cohesion</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hanna, Joseph S.; Kroll, Evgueny S.; Lundblad, Victoria; Spencer, Forrest A.</p> <p>2001-01-01</p> <p>CTF4 and CTF18 are required for high-fidelity chromosome segregation. Both exhibit genetic and physical ties to replication fork constituents. We find that absence of either CTF4 or CTF18 causes <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint. The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. We find that Ctf18p, an RFC1-like protein, directly interacts with Rfc2p, Rfc3p, Rfc4p, and Rfc5p. However, Ctf18p is not a component of biochemically purified proliferating cell nuclear antigen loading RF-C, suggesting the presence of a discrete complex containing Ctf18p, Rfc2p, Rfc3p, Rfc4p, and Rfc5p. Recent identification and characterization of the budding yeast polymerase κ, encoded by TRF4, strongly supports a hypothesis that the DNA replication machinery is required for proper <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. Analogous to the polymerase switching role of the bacterial and human RF-C complexes, we propose that budding yeast RF-CCTF18 may be involved in a polymerase switch event that facilities <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. The requirement for CTF4 and CTF18 in robust cohesion identifies novel roles for replication accessory proteins in this process. PMID:11287619</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25194916','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25194916"><span>"Breaking up is hard to do": the formation and resolution of <span class="hlt">sister</span> <span class="hlt">chromatid</span> intertwines.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Baxter, Jonathan</p> <p>2015-02-13</p> <p>The absolute necessity to resolve every intertwine between the two strands of the DNA double helix provides a massive challenge to the cellular processes that duplicate and segregate chromosomes. Although the overwhelming majority of intertwines between the parental DNA strands are resolved during DNA replication, there are numerous chromosomal contexts where some intertwining is maintained into mitosis. These mitotic <span class="hlt">sister</span> <span class="hlt">chromatid</span> intertwines (SCIs) can be found as; short regions of unreplicated DNA, fully replicated and intertwined <span class="hlt">sister</span> <span class="hlt">chromatids</span>--commonly referred to as DNA catenation--and as <span class="hlt">sister</span> <span class="hlt">chromatid</span> linkages generated by homologous recombination-associated processes. Several overlapping mechanisms, including intra-chromosomal compaction, topoisomerase action and Holliday junction resolvases, ensure that all SCIs are removed before they can prevent normal chromosome segregation. Here, I discuss why some DNA intertwines persist into mitosis and review our current knowledge of the SCI resolution mechanisms that are employed in both prokaryotes and eukaryotes, including how deregulating SCI formation during DNA replication or disrupting the resolution processes may contribute to aneuploidy in cancer. Copyright © 2014 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=43487&Lab=ORD&keyword=bone&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=43487&Lab=ORD&keyword=bone&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span>EVIDENCE FOR THE CHROMOSOMAL REPLICONS AS UNITS OF <span class="hlt">SISTER</span> <span class="hlt">CHROMATID</span> EXCHANGES</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>Current hypotheses of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) formation postulate that sites of SCE induction are associated with active replicons or replicon clusters. We have applied the FCC-SCD technique to in vivo studies of mouse bone marrow cells that have been treated with cycloph...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6842348-ultraviolet-induced-sister-chromatid-exchanges-cells-normal-brdurd-substituted-dna-influence-intercalating-substances-cysteine','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6842348-ultraviolet-induced-sister-chromatid-exchanges-cells-normal-brdurd-substituted-dna-influence-intercalating-substances-cysteine"><span>Ultraviolet-induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in V-79 cells with normal and BrdUrd-substituted DNA and the influence of intercalating substances and cysteine</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Speit, G.; Mehnert, K.; Wolf, M.</p> <p>1982-06-01</p> <p>The influence of intercalating substances (proflavine, ethidium bromide) and of an SH compound (L-cysteine) on uv-induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) was investigated in V-79 cells with normal and BrdUrd-substituted DNA. The results are discussed in relation to the primary damages leading to SCE induction produced by uv irradiation. The data indicate that neither the pyrimidine dimers nor DNA single-strand breaks are the primary cause of SCE induction, and that the damages leading to SCEs by uv irradiation differ from those which cause chromosome <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16309949','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16309949"><span>Evaluation of genotoxic effects of Apitol (cymiazole hydrochloride) in vitro by measurement of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stanimirovic, Zoran; Stevanovic, Jevrosima; Jovanovic, Slobodan; Andjelkovic, Marko</p> <p>2005-12-30</p> <p>Apitol, with cymiazole hydrochloride as the active ingredient, is used in bee-keeping against the ectoparasitic mite Varroa destructor. The preparation was evaluated for genotoxicity in cultured human peripheral blood lymphocytes. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange, the mitotic index and the cell proliferation index were determined for three experimental concentrations of Apitol (0.001, 0.01 and 0.1 mg/ml). All concentrations significantly (p < 0.001) increased the mitotic index (MI = 7.35+/-0.18%, 8.31+/-0.20% and 12.33+/-0.25%, respectively), the proliferative index (PI = 1.83+/-0.01, 1.84+/-0.01 and 1.88+/-0.02, respectively) and the frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE = 8.19+/-1.81, 8.78+/-1.80 and 13.46+/-1.88, respectively), suggesting that cymiazole hydrochloride has genotoxic potential.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li class="active"><span>1</span></li> <li><a href="#" onclick='return showDiv("page_2");'>2</a></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_1 --> <div id="page_2" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_1");'>1</a></li> <li class="active"><span>2</span></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="21"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27889450','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27889450"><span>RPA Mediates Recruitment of MRX to Forks and Double-Strand Breaks to Hold <span class="hlt">Sister</span> <span class="hlt">Chromatids</span> Together.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Seeber, Andrew; Hegnauer, Anna Maria; Hustedt, Nicole; Deshpande, Ishan; Poli, Jérôme; Eglinger, Jan; Pasero, Philippe; Gut, Heinz; Shinohara, Miki; Hopfner, Karl-Peter; Shimada, Kenji; Gasser, Susan M</p> <p>2016-12-01</p> <p>The Mre11-Rad50-Xrs2 (MRX) complex is related to SMC complexes that form rings capable of holding two distinct DNA strands together. MRX functions at stalled replication forks and double-strand breaks (DSBs). A mutation in the N-terminal OB fold of the 70 kDa subunit of yeast replication protein A, rfa1-t11, abrogates MRX recruitment to both types of DNA damage. The rfa1 mutation is functionally epistatic with loss of any of the MRX subunits for survival of replication fork stress or DSB recovery, although it does not compromise end-resection. High-resolution imaging shows that either the rfa1-t11 or the rad50Δ mutation lets stalled replication forks collapse and allows the separation not only of opposing ends but of <span class="hlt">sister</span> <span class="hlt">chromatids</span> at breaks. Given that cohesin loss does not provoke visible <span class="hlt">sister</span> separation as long as the RPA-MRX contacts are intact, we conclude that MRX also serves as a structural linchpin holding <span class="hlt">sister</span> <span class="hlt">chromatids</span> together at breaks. Copyright © 2016 Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=317234','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=317234"><span>Faithful anaphase is ensured by Mis4, a <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion molecule required in S phase and not destroyed in G1 phase</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Furuya, Kanji; Takahashi, Kohta; Yanagida, Mitsuhiro</p> <p>1998-01-01</p> <p>The loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion triggers anaphase spindle movement. The budding yeast Mcd1/Scc1 protein, called cohesin, is required for associating <span class="hlt">chromatids</span>, and proteins homologous to it exist in a variety of eukaryotes. Mcd1/Scc1 is removed from chromosomes in anaphase and degrades in G1. We show that the fission yeast protein, Mis4, which is required for equal <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation in anaphase is a different <span class="hlt">chromatid</span> cohesion molecule that behaves independent of cohesin and is conserved from yeast to human. Its inactivation in G1 results in cell lethality in S phase and subsequent premature <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation. Inactivation in G2 leads to cell death in subsequent metaphase–anaphase progression but missegregation occurs only in the next round of mitosis. Mis4 is not essential for condensation, nor does it degrade in G1. Rather, it associates with chromosomes in a punctate fashion throughout the cell cycle. mis4 mutants are hypersensitive to hydroxyurea (HU) and UV irradiation but retain the ability to restrain cell cycle progression when damaged or sustaining a block to replication. The mis4 mutation results in synthetic lethality with a DNA ligase mutant. Mis4 may form a stable link between <span class="hlt">chromatids</span> in S phase that is split rather than removed in anaphase. PMID:9808627</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/391300-induction-sister-chromatid-exchange-presence-gadolinium-dtpa-its-reduction-dimethyl-sulfoxide','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/391300-induction-sister-chromatid-exchange-presence-gadolinium-dtpa-its-reduction-dimethyl-sulfoxide"><span>Induction of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in the presence of gadolinium-DTPA and its reduction by dimethyl sulfoxide</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Yamazaki, Etsuo; Fukuda, Hozumi; Shibuya, Hitoshi</p> <p></p> <p>The authors investigate the frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) after the addition of gadolinium (Gd)-DTPA to venous blood samples. Venous blood was obtained from nonsmokers. Samples were incubated with Gd-DTPA alone or in combination with mitomycin C, cytarabine, and dimethyl sulfoxide (DMSO), and then evaluated for SCEs. The frequency of SCE increased with the concentration of Gd-DTPA and as each chemotherapeutic agent was added. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange frequencies were lower when the blood was treated with a combination of Gd-DTPA and DMSO compared with Gd-DTPA alone. The increase in frequency of SCE seen after the addition of Gd-DTPA wasmore » decreased by the addition of DMSO, indicating the production of hydroxyl radicals. The effect likely is dissociation-related. 14 refs., 6 tabs.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/6488477','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/6488477"><span>Increased incidence of chromosomal <span class="hlt">aberrations</span> in peripheral lymphocytes of retired nickel workers.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Waksvik, H; Boysen, M; Høgetveit, A C</p> <p>1984-11-01</p> <p>Chromosomal <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges were analysed in the peripheral lymphocytes of nine retired nickel refinery workers 4-15 years after the retirement and compared with 11 matched non-nickel exposed controls. None of the controls had previous occupations with known relation to induction of chromosomal <span class="hlt">aberrations</span> nor <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges. The groups were equal as to socioeconomic status and environmental factors other than the occupational ones, which could influence the chromosome parameters, were to the largest possible extent excluded. The nickel workers' previous occupational employment involved exposure to inhalation of furnace dust of Ni3S2 and NiO or aerosols of NiCl2 and NiSO4. The concentration of nickel in the working atmospheres has been higher than 1.0 mg/m3 air and the exposure time more than 25 years. The retired nickel workers showed an increased incidence of breaks (p less than 0.001) and gaps (p less than 0.05) but no difference in the incidence of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges when compared with the controls.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23681662','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23681662"><span>A CO-FISH assay to assess <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation patterns in mitosis of mouse embryonic stem cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sauer, Stephan; Burkett, Sandra S; Lewandoski, Mark; Klar, Amar J S</p> <p>2013-05-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatids</span> contain identical DNA sequence but are chiral with respect to both their helical handedness and their replication history. Emerging evidence from various model organisms suggests that certain stem cells segregate <span class="hlt">sister</span> <span class="hlt">chromatids</span> nonrandomly to either maintain genome integrity or to bias cellular differentiation in asymmetric cell divisions. Conventional methods for tracing of old vs. newly synthesized DNA strands generally lack resolution for individual chromosomes and employ halogenated thymidine analogs with profound cytotoxic effects on rapidly dividing cells. Here, we present a modified chromosome orientation fluorescence in situ hybridization (CO-FISH) assay, where identification of individual chromosomes and their replication history is achieved in subsequent hybridization steps with chromosome-specific DNA probes and PNA telomere probes. Importantly, we tackle the issue of BrdU cytotoxicity and show that our method is compatible with normal mouse ES cell biology, unlike a recently published related protocol. Results from our CO-FISH assay show that mitotic segregation of mouse chromosome 7 is random in ES cells, which contrasts previously published results from our laboratory and settles a controversy. Our straightforward protocol represents a useful resource for future studies on <span class="hlt">chromatid</span> segregation patterns of in vitro-cultured cells from distinct model organisms.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23417411','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23417411"><span>Histone hyperacetylation during meiosis interferes with large-scale chromatin remodeling, axial <span class="hlt">chromatid</span> condensation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation in the mammalian oocyte.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yang, Feikun; Baumann, Claudia; Viveiros, Maria M; De La Fuente, Rabindranath</p> <p>2012-01-01</p> <p>Histone acetylation regulates higher-order chromatin structure and function and is critical for the control of gene expression. Histone deacetylase inhibitors (HDACi) are currently under investigation as novel cancer therapeutic drugs. Here, we show that female germ cells are extremely susceptible to chromatin changes induced by HDACi. Our results indicate that exposure to trichostatin A (TSA) at nanomolar levels interferes with major chromatin remodeling events in the mammalian oocyte leading to chromosome instability. High resolution analysis of chromatin structure and live-cell imaging revealed a striking euchromatin decondensation associated with histone H4 hyperacetylation following exposure to 15 nM TSA in >90% of pre-ovulatory oocytes. Dynamic changes in large-scale chromatin structure were detected after 2 h of exposure and result in the formation of misaligned chromosomes in >75% (P<0.05) of in vitro matured oocytes showing chromosome lagging as well as abnormal <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation at anaphase I. Abnormal axial <span class="hlt">chromatid</span> condensation during meiosis results in the formation of elongated chromosomes exhibiting hyperacetylation of histone H4 at lysine 5 and lysine 16 at interstitial chromosome segments, but not pericentric heterochromatin, while highly decondensed bivalents exhibit prominent histone H3 phosphorylation at centromeric domains. Notably, no changes were observed in the chromosomal localization of the condensin protein SMC4. These results indicate that HDAC activity is required for proper chromosome condensation in the mammalian oocyte and that HDACi may induce abnormal chromosome segregation by interfering with both chromosome-microtubule interactions, as well as <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation. Thus, HDACi, proposed for cancer therapy, may disrupt the epigenetic status of female germ cells, predisposing oocytes to aneuploidy at previously unrecognized low doses.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11748978','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11748978"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange rate and alkaline comet assay scores in patients with ovarian cancer.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Baltaci, Volkan; Kayikçioğlu, Fulya; Alpas, Idil; Zeyneloğlu, Hulusi; Haberal, Ali</p> <p>2002-01-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange (SCE) frequencies were studied in patients with different types of ovarian malignancies and in healthy volunteers. The level of DNA damage in patients with ovarian malignancy and control subjects has also been studied by alkaline single cell gel electrophoresis (SCGE), also known as the comet assay. Peripheral blood was collected from 30 patients after histological confirmation of malignancy and 20 healthy female volunteers. The cells were evaluated according to their grade of damage. We found that the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange frequencies of cancer cases were significantly greater than that of controls (P < 0.001). The frequency of exchange in chromosomal groups A, B, and C, which include chromosomes 1-12, was higher than that of the other chromosomal groups in both groups. Comparison of the results of the alkaline comet assay in patient and control subjects showed a significant difference in the number of damaged cells. The frequency of limited migrated and extensive migrated cells in the women with ovarian malignancies was higher than that of control women (P < 0.001). SCE and SCGE can be used successfully to monitor DNA damage in women with ovarian cancer.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3078076','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3078076"><span>Mitotic centromeric targeting of HP1 and its binding to Sgo1 are dispensable for <span class="hlt">sister-chromatid</span> cohesion in human cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kang, Jungseog; Chaudhary, Jaideep; Dong, Hui; Kim, Soonjoung; Brautigam, Chad A.; Yu, Hongtao</p> <p>2011-01-01</p> <p>Human Shugoshin 1 (Sgo1) protects centromeric <span class="hlt">sister-chromatid</span> cohesion during prophase and prevents premature <span class="hlt">sister-chromatid</span> separation. Heterochromatin protein 1 (HP1) has been proposed to protect centromeric <span class="hlt">sister-chromatid</span> cohesion by directly targeting Sgo1 to centromeres in mitosis. Here we show that HP1α is targeted to mitotic centromeres by INCENP, a subunit of the chromosome passenger complex (CPC). Biochemical and structural studies show that both HP1–INCENP and HP1–Sgo1 interactions require the binding of the HP1 chromo shadow domain to PXVXL/I motifs in INCENP or Sgo1, suggesting that the INCENP-bound, centromeric HP1α is incapable of recruiting Sgo1. Consistently, a Sgo1 mutant deficient in HP1 binding is functional in centromeric cohesion protection and localizes normally to centromeres in mitosis. By contrast, INCENP or Sgo1 mutants deficient in HP1 binding fail to localize to centromeres in interphase. Therefore, our results suggest that HP1 binding by INCENP or Sgo1 is dispensable for centromeric cohesion protection during mitosis of human cells, but might regulate yet uncharacterized interphase functions of CPC or Sgo1 at the centromeres. PMID:21346195</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20630917','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20630917"><span>Genotoxic assessment in peripheral blood lymphocytes of post-polio individuals using <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange analysis and micronucleus assay.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bhattacharya, Saurabh Kumar; Saraswathy, Radha; Sivakumar, E</p> <p>2011-07-01</p> <p>Environmental pollution is a complex issue because of the diversity of anthropogenic agents, both chemical and physical, that have been detected and catalogued. The consequences to biota from exposure to genotoxic agents present an additional problem because of the potential for these agents to produce adverse change at the cellular and organism levels. Past studies in virus have focused on structural damage to the DNA of environmental species that may occur after exposure to genotoxic agents and the use of this information to document exposure and to monitor remediation. In an effort to predict effects at the population, community and ecosystem levels, in the present study, we attempt to characterize damage occurring through genotoxic agents like 5-bromo-2-deoxyuridine, BrdU, using <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange technique and the formation of micronuclei (MN) in the peripheral lymphocytes of the post-polio syndrome sequelae affected by poliovirus. Analysis of structural chromosomal <span class="hlt">aberrations</span> (CAs) and involvement of the specific chromosome break were pursued in this study. They revealed a significantly higher incidence of CAs (<span class="hlt">chromatid</span> and chromosome breaks) in patients compared with controls, where the specific chromosome break has emerged as specific. Also, the maximum numbers of breaks were found to be in chromosome 1 at the position 1p36.1. The results also suggest a correlation between CAs and content of MN.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4199498','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4199498"><span>The Chromosomal Association of the Smc5/6 Complex Depends on Cohesion and Predicts the Level of <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Entanglement</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Jeppsson, Kristian; Carlborg, Kristian K.; Nakato, Ryuichiro; Berta, Davide G.; Lilienthal, Ingrid; Kanno, Takaharu; Lindqvist, Arne; Brink, Maartje C.; Dantuma, Nico P.; Katou, Yuki; Shirahige, Katsuhiko; Sjögren, Camilla</p> <p>2014-01-01</p> <p>The cohesin complex, which is essential for <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion and chromosome segregation, also inhibits resolution of <span class="hlt">sister</span> <span class="hlt">chromatid</span> intertwinings (SCIs) by the topoisomerase Top2. The cohesin-related Smc5/6 complex (Smc5/6) instead accumulates on chromosomes after Top2 inactivation, known to lead to a buildup of unresolved SCIs. This suggests that cohesin can influence the chromosomal association of Smc5/6 via its role in SCI protection. Using high-resolution ChIP-sequencing, we show that the localization of budding yeast Smc5/6 to duplicated chromosomes indeed depends on <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion in wild-type and top2-4 cells. Smc5/6 is found to be enriched at cohesin binding sites in the centromere-proximal regions in both cell types, but also along chromosome arms when replication has occurred under Top2-inhibiting conditions. Reactivation of Top2 after replication causes Smc5/6 to dissociate from chromosome arms, supporting the assumption that Smc5/6 associates with a Top2 substrate. It is also demonstrated that the amount of Smc5/6 on chromosomes positively correlates with the level of missegregation in top2-4, and that Smc5/6 promotes segregation of short chromosomes in the mutant. Altogether, this shows that the chromosomal localization of Smc5/6 predicts the presence of the <span class="hlt">chromatid</span> segregation-inhibiting entities which accumulate in top2-4 mutated cells. These are most likely SCIs, and our results thus indicate that, at least when Top2 is inhibited, Smc5/6 facilitates their resolution. PMID:25329383</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1783675','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1783675"><span>Roles of the <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion apparatus in gene expression, development, and human syndromes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Dorsett, Dale</p> <p>2006-01-01</p> <p>The <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion apparatus mediates physical pairing of duplicated chromosomes. This pairing is essential for appropriate distribution of chromosomes into the daughter cells upon cell division. Recent evidence shows that the cohesion apparatus, which is a significant structural component of chromosomes during interphase, also affects gene expression and development. The Cornelia de Lange (CdLS) and Roberts/SC phocomelia (RBS/SC) genetic syndromes in humans are caused by mutations affecting components of the cohesion apparatus. Studies in Drosophila suggest that effects on gene expression are most likely responsible for developmental alterations in CdLS. Effects on <span class="hlt">chromatid</span> cohesion are apparent in RBS/SC syndrome, but data from yeast and Drosophila point to the likelihood that changes in expression of genes located in heterochromatin could contribute to the developmental deficits. PMID:16819604</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16131840','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16131840"><span>Telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in telomerase deficient murine cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wang, Yisong; Giannone, Richard J; Liu, Yie</p> <p>2005-10-01</p> <p>We have recently demonstrated that several types of genomic rearrangements (i.e., telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (T-SCE), genomic-SCE, or end-to-end fusions) were more often detected in long-term cultured murine telomerase deficient embryonic stem (ES) cells than in freshly prepared murine splenocytes, even through they possessed similar frequencies of critically short telomeres. The high rate of genomic rearrangements in telomerase deficient ES cells, when compared to murine splenocytes, may reflect the cultured cells' gained ability to protect chromosome ends with eroded telomeres allowing them to escape "end crisis". However, the possibility that ES cells were more permissive to genomic rearrangements than other cell types or that differences in the microenvironment or genetic background of the animals might consequentially determine the rate of T-SCEs or other genomic rearrangements at critically short telomeres could not be ruled out.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7688857','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7688857"><span><span class="hlt">Sister-chromatid</span> exchanges and cell-cycle kinetics in the lymphocytes of workers occupationally exposed to a chemical mixture in the tyre industry.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sasiadek, M</p> <p>1993-08-01</p> <p>Cytogenetic studies of clinically healthy workers employed in the rubber industry showed an increase in chromosome <span class="hlt">aberrations</span> (CAs), <span class="hlt">sister-chromatid</span> exchanges (SCEs) and a decrease in proliferation indices (PIs). The aim of the present study was to establish, using the SCE and PI tests, genotoxic effects of hazardous chemicals in the rubber industry. An increase in mean SCEs in the lymphocytes of vulcanizers as compared to controls was observed. Since the PI in the exposed group was insignificantly decreased as compared to the controls, it could be concluded that the SCE test is the most sensitive cytogenetic test for the detection of a genotoxic effect of chemicals in the rubber industry. There was no evidence in the present study that the genotoxic effect of chemicals in the rubber industry was enhanced by cigarette smoking.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5738888-enhanced-response-induction-sister-chromatid-exchange-gamma-radiation-neurofibromatosis','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5738888-enhanced-response-induction-sister-chromatid-exchange-gamma-radiation-neurofibromatosis"><span>Enhanced response to the induction of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange by gamma radiation in neurofibromatosis</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Hafez, M.; Abd el-Nabi, S.M.; el-Wehedi, G.</p> <p></p> <p>The study included 8 unrelated patients with neurofibromatosis, and 10 unrelated normal and healthy persons as controls. Whole blood samples were divided into plastic T flasks and exposed at room temperature to gamma rays. The radiation dose was 36 rad/minute, and the doses delivered were 0, 75, 150 and 300 rad. The lymphocytes were cultured in (RPMI) 1640 tissue culture medium and autologous serum (20%). Phytohemagglutinin and bromodeoxyuridine (Brdu) (10 microM) were added at initiation of culture and harvesting was done 64 to 68 hours after culture initiation. Slides were coded, differential staining was done, and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs)more » and <span class="hlt">aberrations</span> (gaps, breaks, dicentrics, fragments and minutes) were counted. In the controls no significant increase in frequency of SCE has been found (P greater than 0.5). In the patients, the frequencies significantly increased with the increase of dose of irradiation (P less than 0.001). Furthermore, after irradiation, the incidence of gaps, breaks, and dicentrics were significantly increased in patients compared with controls. Moreover, the incidence increased with the increase in the dose of radiation. The results are discussed with a conclusion that the results add to the indication of a genetic predisposition to develop cancer in neurofibromatosis patients.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/978252-telomere-sister-chromatid-exchange-telomerase-deficient-murine-cells','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/978252-telomere-sister-chromatid-exchange-telomerase-deficient-murine-cells"><span>Telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in telomerase deficient murine cells</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Wang, Yisong; Giannone, Richard J; Liu, Yie</p> <p>2005-01-01</p> <p>We have recently demonstrated that several types of genomic rearrangements (i.e., telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (T-SCE), genomic-SCE, or end-to-end fusions) were more often detected in long-term cultured murine telomerase deficient embryonic stem (ES) cells than in freshly prepared murine splenocytes, even through they possessed similar frequencies of critically short telomeres. The high rate of genomic rearrangements in telomerase deficient ES cells, when compared to murine splenocytes, may reflect the cultured cells' gained ability to protect chromosome ends with eroded telomeres allowing them to escape 'end crisis'. However, the possibility that ES cells were more permissive to genomic rearrangements than othermore » cell types or that differences in the microenvironment or genetic background of the animals might consequentially determine the rate of T-SCEs or other genomic rearrangements at critically short telomeres could not be ruled out.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=39928&Lab=ORD&keyword=infusion&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=39928&Lab=ORD&keyword=infusion&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span>INDUCTION, ACCUMULATION, AND PERSISTENCE OF <span class="hlt">SISTER</span> <span class="hlt">CHROMATID</span> EXCHANGES IN WOMEN WITH BREAST CANCER RECEIVING CYCLOPHOSPHAMIDE, ANDRIAMYCIN, AND 5-FLUOROACIL CHEMOTHERAPY</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>The induction, stimulation, and persistence of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE's) and high SCE frequency cells (HFC's) was measured in peripheral lymphocytes of women with breast cancer before chemotherapy and on multiple occasions during and after therapy. Chemotherapy consisted...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1216365','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1216365"><span>Lack of Spontaneous <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchanges in Somatic Cells of DROSOPHILA MELANOGASTER</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Gatti, M.; Santini, G.; Pimpinelli, S.; Olivieri, G.</p> <p>1979-01-01</p> <p>Neural ganglia of wild type third-instar larvae of Drosophila melanogaster were incubated for 13 hours at various concentrations of BUdR (1, 3, 9, 27 µg/ml). Metaphases were collected with colchicine, stained with Hoechst 33258, and scored under a fluorescence microscope. Metaphases in which the <span class="hlt">sister</span> <span class="hlt">chromatids</span> were clearly differentiated were scored for the presence of <span class="hlt">sister-chromatid</span> exchanges (SCEs). At the lowest concentration of BUdR (1 µg/ml), no SCEs were observed in either male or female neuroblasts. The SCEs were found at the higher concentrations of BUdR (3, 9 and 27 µg/ml) and with a greater frequency in females than in males. Therefore SCEs are not a spontaneous phenomenon in D. melanogaster, but are induced by BUdR incorporated in the DNA. A striking nonrandomness was found in the distribution of SCEs along the chromosomes. More than a third of the SCEs were clustered in the junctions between euchromatin and heterochromatin. The remaining SCEs were preferentially localized within the heterochromatic regions of the X chromosome and the autosomes and primarily on the entirely heterochromatic Y chromosome.—In order to find an alternative way of measuring the frequency of SCEs in Drosophila neuroblasts, the occurrence of double dicentric rings was studied in two stocks carrying monocentric ring-X chromosomes. One ring chromosome, C(1)TR 94–2, shows a rate of dicentric ring formation corresponding to the frequency of SCEs observed in the BUdR-labelled rod chromosomes. The other ring studied, R(1)2, exhibits a frequency of SCEs higher than that observed with both C(1)TR 94–2 and rod chromosomes. PMID:109350</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4214429','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4214429"><span>Alternative meiotic <span class="hlt">chromatid</span> segregation in the holocentric plant Luzula elegans</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Heckmann, Stefan; Jankowska, Maja; Schubert, Veit; Kumke, Katrin; Ma, Wei; Houben, Andreas</p> <p>2014-01-01</p> <p>Holocentric chromosomes occur in a number of independent eukaryotic lineages. They form holokinetic kinetochores along the entire poleward <span class="hlt">chromatid</span> surfaces, and owing to this alternative chromosome structure, species with holocentric chromosomes cannot use the two-step loss of cohesion during meiosis typical for monocentric chromosomes. Here we show that the plant Luzula elegans maintains a holocentric chromosome architecture and behaviour throughout meiosis, and in contrast to monopolar <span class="hlt">sister</span> centromere orientation, the unfused holokinetic <span class="hlt">sister</span> centromeres behave as two distinct functional units during meiosis I, resulting in <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation. Homologous non-<span class="hlt">sister</span> <span class="hlt">chromatids</span> remain terminally linked after metaphase I, by satellite DNA-enriched chromatin threads, until metaphase II. They then separate at anaphase II. Thus, an inverted sequence of meiotic <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation occurs. This alternative meiotic process is most likely one possible adaptation to handle a holocentric chromosome architecture and behaviour during meiosis. PMID:25296379</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1128680','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1128680"><span>DNA single strand breakage, DNA adducts, and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in lymphocytes and phenanthrene and pyrene metabolites in urine of coke oven workers.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Popp, W; Vahrenholz, C; Schell, C; Grimmer, G; Dettbarn, G; Kraus, R; Brauksiepe, A; Schmeling, B; Gutzeit, T; von Bülow, J; Norpoth, K</p> <p>1997-01-01</p> <p>OBJECTIVES: To investigate the specificity of biological monitoring variables (excretion of phenanthrene and pyrene metabolites in urine) and the usefulness of some biomarkers of effect (alkaline filter elution, 32P postlabelling assay, measurement of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange) in workers exposed to polycyclic aromatic hydrocarbons (PAHs). METHODS: 29 coke oven workers and a standardised control group were investigated for frequencies of DNA single strand breakage, DNA protein cross links (alkaline filter elution assay), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, and DNA adducts (32P postlabelling assay) in lymphocytes. Phenanthrene and pyrene metabolites were measured in 24 hour urine samples. 19 different PAHs (including benzo(a)pyrene, pyrene, and phenanthrene) were measured at the workplace by personal air monitoring. The GSTT1 activity in erythrocytes and lymphocyte subpopulations in blood was also measured. RESULTS: Concentrations of phenanthrene, pyrene, and benzo(a)pyrene in air correlated well with the concentration of total PAHs in air; they could be used for comparisons of different workplaces if the emission compositions were known. The measurement of phenanthrene metabolites in urine proved to be a better biological monitoring variable than the measurement of 1-hydroxypyrene. Significantly more DNA strand breaks in lymphocytes of coke oven workers were found (alkaline filter elution assay); the DNA adduct rate was not significantly increased in workers, but correlated with exposure to PAHs in a semiquantitative manner. The number of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges was lower in coke oven workers but this was not significant; thus counting <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges was not a good variable for biomonitoring of coke oven workers. Also, indications for immunotoxic influences (changes in lymphocyte subpopulations) were found. CONCLUSIONS: The measurement of phenanthrene metabolites in urine seems to be a better biological monitoring variable for exposure to PAHs than</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/2009589','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/2009589"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange in children of Seventh-Day Adventists and matched controls.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hermansen, R; Waksvik, H; Fønnebø, V</p> <p>1991-03-01</p> <p>The low risk of cancer in Seventh-Day Adventists (SDAs) has been suggested to be due to genetic selection. To investigate this claim we examined the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) frequency in peripheral blood lymphocytes in 16 SDA children in Tromsø, all aged 0.5-8 years and 16 controls matched for sex and age. In 12 of 16 pairs, the SDA children had a lower SCE frequency than the controls. The mean difference was 4.06 (95% confidence interval -17.02-8.89, P = 0.51). There was no sex difference, and no correlation between age and SCE frequency. The genetic starting point with regard to SCE frequency seems to be the same for SDA children and controls.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_1");'>1</a></li> <li class="active"><span>2</span></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_2 --> <div id="page_3" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_1");'>1</a></li> <li><a href="#" onclick='return showDiv("page_2");'>2</a></li> <li class="active"><span>3</span></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="41"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7527908','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7527908"><span>Analysis of chromosomal <span class="hlt">aberrations</span>, <span class="hlt">sister-chromatid</span> exchanges and micronuclei in peripheral lymphocytes of pharmacists before and after working with cytostatic drugs.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Roth, S; Norppa, H; Järventaus, H; Kyyrönen, P; Ahonen, M; Lehtomäki, J; Sainio, H; Sorsa, M</p> <p>1994-12-01</p> <p>The frequencies of chromosome <span class="hlt">aberrations</span>, SCEs and micronuclei (cytokinesis-block method) in blood lymphocytes were compared among six nonsmoking female pharmacists before and after 1 year of working with cytostatic drugs. All possible precautions were taken to avoid exposure to cytostatics, including proper protective clothing and a monitored, negative-pressured working environment with vertical laminar flow cabinet. As referents, an age-matched group of six nonsmoking female hospital workers not dealing with cytostatics was simultaneously sampled twice with the same time interval. The pharmacists showed a marginally higher mean frequency of SCEs/cell (6.3; P = 0.049) after the working period than 1 year earlier (5.8). On the other hand, the referents, with no obvious exposure, had a higher mean number of cells with <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span>, gaps excluded, in the second sampling (2.0%; P = 0.048) than in the first one (0.5%). In addition, a slight (P = 0.055) trend towards a higher frequency of micronucleated binucleate cells was observed in the second sampling for both the exposed and control subjects. As such findings suggest technical variation in the cytogenetic parameters, the small difference observed in SCEs for the pharmacists between the two samplings was probably not related to the cytostatics exposure. No statistically significant differences were observed for any of the cytogenetic parameters in comparisons between the pharmacists and the referents. The findings suggest that caution should be exercised in comparing results obtained from two different samplings in prospective cytogenetic studies.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/3442830','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/3442830"><span>Indirect intergenic suppression of a radiosensitive mutant of Sordaria macrospora defective in <span class="hlt">sister-chromatid</span> cohesiveness.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Huynh, A D; Leblon, G; Zickler, D</p> <p>1986-01-01</p> <p>Six ultra violet (UV) mutageneses were performed on the spo76 UV-sensitive mutant of Sordaria macrospora. Spo76 shows an early centromere cleavage associated with an arrest at the first meiotic division and therefore does not form ascospores. Moreover, it exhibits altered pairing structure (synaptonemal complex), revealing a defect in the <span class="hlt">sister-chromatid</span> cohesiveness. From 37 revertants which partially restored sporulation, 34 extragenic suppressors of spo76 were isolated. All suppressors are altered in chromosomal pairing but, unlike spo76, show a wild type centromere cleavage. The 34 suppressors were assigned to six different genes and mapped. Only one of the suppressor genes is involved in repair functions.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/978251-increase-telomere-sister-chromatid-exchange-murine-embryonic-stem-cells-possessing-critically-shortened-telomeres','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/978251-increase-telomere-sister-chromatid-exchange-murine-embryonic-stem-cells-possessing-critically-shortened-telomeres"><span>An increase in telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in murine embryonic stem cells possessing critically shortened telomeres</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Wang, Yisong; Giannone, Richard J; Wu, Jun</p> <p></p> <p>Telomerase deficiency leads to a progressive loss of telomeric DNA that eventually triggers cell apoptosis in human primary cells during prolonged growth in culture. Rare survivors can maintain telomere length through either activation of telomerase or recombination-based telomere lengthening, and thus proliferate indefinitely. We have explored the possibility that telomeres may be maintained through telomere <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (T-SCE) in murine telomere reverse transcriptase-deficient (mTert -/-) splenocytes and ES cells. Because telomerase deficiency leads to gradual loss of telomeric DNA in mTert -/- splenocytes and ES cells and eventually to chromosomes with telomere signal-free ends (SFEs), we examined these cellmore » types for evidence of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange at telomeres, and observed an increase in T-SCEs only in a subset of mTert -/- splenocytes or ES cells that possessed multiple SFEs. Furthermore, T-SCEs were more often detected in ES cells than in splenocytes that harbored a similar frequency of SFEs. In mTert heterozygous (mTert +/-) ES cells or splenocytes, which are known to exhibit a decrease in average telomere length but no SFEs, no increase in T-SCE was observed. In addition to T-SCE, other genomic rearrangements (i.e., SCE) were also significantly increased in mTert -/- ES cells possessing critically short telomeres, but not in splenocytes. Our results suggest that animals and cell culture differ in their ability to carry out genomic rearrangements as a means of maintaining telomere integrity when telomeres become critically shortened.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4199692','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4199692"><span>Regulation of Centromere Localization of the Drosophila Shugoshin MEI-S332 and <span class="hlt">Sister-Chromatid</span> Cohesion in Meiosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Nogueira, Cristina; Kashevsky, Helena; Pinto, Belinda; Clarke, Astrid; Orr-Weaver, Terry L.</p> <p>2014-01-01</p> <p>The Shugoshin (Sgo) protein family helps to ensure proper chromosome segregation by protecting cohesion at the centromere by preventing cleavage of the cohesin complex. Some Sgo proteins also influence other aspects of kinetochore-microtubule attachments. Although many Sgo members require Aurora B kinase to localize to the centromere, factors controlling delocalization are poorly understood and diverse. Moreover, it is not clear how Sgo function is inactivated and whether this is distinct from delocalization. We investigated these questions in Drosophila melanogaster, an organism with superb chromosome cytology to monitor Sgo localization and quantitative assays to test its function in <span class="hlt">sister-chromatid</span> segregation in meiosis. Previous research showed that in mitosis in cell culture, phosphorylation of the Drosophila Sgo, MEI-S332, by Aurora B promotes centromere localization, whereas Polo phosphorylation promotes delocalization. These studies also suggested that MEI-S332 can be inactivated independently of delocalization, a conclusion supported here by localization and function studies in meiosis. Phosphoresistant and phosphomimetic mutants for the Aurora B and Polo phosphorylation sites were examined for effects on MEI-S332 localization and chromosome segregation in meiosis. Strikingly, MEI-S332 with a phosphomimetic mutation in the Aurora B phosphorylation site prematurely dissociates from the centromeres in meiosis I. Despite the absence of MEI-S332 on meiosis II centromeres in male meiosis, <span class="hlt">sister</span> <span class="hlt">chromatids</span> segregate normally, demonstrating that detectable levels of this Sgo are not essential for chromosome congression, kinetochore biorientation, or spindle assembly. PMID:25081981</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12787819','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12787819"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchanges and micronuclei analysis in lymphocytes of men exposed to simazine through drinking water.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Suárez, Susanna; Rubio, Arantxa; Sueiro, Rosa Ana; Garrido, Joaquín</p> <p>2003-06-06</p> <p>In some cities of the autonomous community of Extremadura (south-west of Spain), levels of simazine from 10 to 30 ppm were detected in tap water. To analyse the possible effect of this herbicide, two biomarkers, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) and micronuclei (MN), were used in peripheral blood lymphocytes from males exposed to simazine through drinking water. SCE and MN analysis failed to detect any statistically significant increase in the people exposed to simazine when compared with the controls. With respect to high frequency cells (HFC), a statistically significant difference was detected between exposed and control groups.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25213378','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25213378"><span><span class="hlt">Sister</span> kinetochores are mechanically fused during meiosis I in yeast.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sarangapani, Krishna K; Duro, Eris; Deng, Yi; Alves, Flavia de Lima; Ye, Qiaozhen; Opoku, Kwaku N; Ceto, Steven; Rappsilber, Juri; Corbett, Kevin D; Biggins, Sue; Marston, Adèle L; Asbury, Charles L</p> <p>2014-10-10</p> <p>Production of healthy gametes requires a reductional meiosis I division in which replicated <span class="hlt">sister</span> <span class="hlt">chromatids</span> comigrate, rather than separate as in mitosis or meiosis II. Fusion of <span class="hlt">sister</span> kinetochores during meiosis I may underlie <span class="hlt">sister</span> <span class="hlt">chromatid</span> comigration in diverse organisms, but direct evidence for such fusion has been lacking. We used laser trapping and quantitative fluorescence microscopy to study native kinetochore particles isolated from yeast. Meiosis I kinetochores formed stronger attachments and carried more microtubule-binding elements than kinetochores isolated from cells in mitosis or meiosis II. The meiosis I-specific monopolin complex was both necessary and sufficient to drive these modifications. Thus, kinetochore fusion directs <span class="hlt">sister</span> <span class="hlt">chromatid</span> comigration, a conserved feature of meiosis that is fundamental to Mendelian inheritance. Copyright © 2014, American Association for the Advancement of Science.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/6865499','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/6865499"><span>Cyclophosphamide-induced in vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in Mus Musculus. II: Effect of age and genotype on <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, micronuclei and metaphase index.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Reimer, D L; Singh, S M</p> <p>1983-01-01</p> <p>In vivo cyclophosphamide-induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) micronuclei, and metaphase indices were assessed in two age groups (10.8 +/- 0.9 weeks' an 33.1 +/- 1.3 weeks' old) of female mice from three genetic strains (C3H/S, C57BL/6J, and Balb/c). In general, older animals showed diminished SCE induction over their younger counterparts. The relative difference between individuals of the two ages is strain-dependent. Unlike C57BL/6J and Balb/c, strain C3H/S showed significantly lower SCE values in the older animals at every cyclophosphamide treatment. It may reflect on the possible involvement of genetic determinant(s) for the component(s) of SCE formation during aging. Frequencies of micronuclei, however, were consistently higher in older animals than in their younger counterparts. Furthermore, cytotoxicity of cyclophosphamide, as reflected in metaphase indices, was also higher in older animals. Lower metaphase indices associated with higher micronuclei levels in older individuals may suggest a decline in the rate of cellular replication in these animals. Furthermore, the lower metaphase indices associated with lower SCE values, and increasing micronuclei levels accompanied by decreasing SCE frequencies in older animals, may reflect reduced DNA repair ability during aging. These results support the hypothesis of genotype-dependent decline in the rate of DNA repair and replication during aging, particularly under stressed conditions.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26207596','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26207596"><span>Baseline frequency of chromosomal <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in peripheral blood lymphocytes of healthy individuals living in Turin (North-Western Italy): assessment of the effects of age, sex and GSTs gene polymorphisms on the levels of genomic damage.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Santovito, Alfredo; Cervella, Piero; Delpero, Massimiliano</p> <p>2016-05-01</p> <p>The increased exposure to environmental pollutants has led to the awareness of the necessity for constant monitoring of human populations, especially those living in urban areas. This study evaluated the background levels of genomic damage in a sample of healthy subjects living in the urban area of Turin (Italy). The association between DNA damage with age, sex and GSTs polymorphisms was assessed. One hundred and one individuals were randomly sampled. <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchanges (SCEs) and Chromosomal <span class="hlt">Aberrations</span> (CAs) assays, as well as genotyping of GSTT1 and GSTM1 genes, were performed. Mean values of SCEs and CAs were 5.137 ± 0.166 and 0.018 ± 0.002, respectively. Results showed age and gender associated with higher frequencies of these two cytogenetic markers. The eldest subjects (51-65 years) showed significantly higher levels of genomic damage than younger individuals. GSTs polymorphisms did not appear to significantly influence the frequencies of either markers. The CAs background frequency observed in this study is one of the highest reported among European populations. Turin is one of the most polluted cities in Europe in terms of air fine PM10 and ozone and the clastogenic potential of these pollutants may explain the high frequencies of chromosomal rearrangements reported here.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/3724775','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/3724775"><span>Very low <span class="hlt">sister-chromatid</span> exchange rate in Seventh-Day Adventists.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wulf, H C; Iversen, A S; Husum, B; Niebuhr, E</p> <p>1986-08-01</p> <p>42 Seventh-Day Adventists (SDAs) and 42 controls matched for sex, age and occupation had their <span class="hlt">sister-chromatid</span> exchange (SCE) examined in peripheral blood lymphocytes. This was done to examine if the SCE frequency was lower in this group of people, who are known to have a decreased cancer risk compared to the general population. The average SCE/cell in 30 cells from each person was 5.54 +/- 0.07 (mean +/- standard error of the mean) for the SDAs and 8.00 +/- 0.15 for the controls, the difference being statistically significant (p less than 0.00001). No difference in SCE frequency was found between SDAs eating only an ovo-lacto-vegetarian diet and those eating some fish or meat. The mitotic index (MI) was significantly higher and the replication index (RI) was significantly lower in SDAs than in controls. No correlation was found between gamma (a statistical transformation of SCEs/cell) and MI or RI within the groups of SDAs or controls. In the pooled data there was a negative correlation of gamma and MI and a positive correlation of gamma and RI. Of the interpersonal variation in gamma 8% and 14% could be explained by MI and RI. The finding of a lower SCE frequency in a group of SDAs who have a low risk of cancer might indirectly indicate a relation between SCE and cancer and encourages further studies of SCE and diet.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=61071&keyword=SCG&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=61071&keyword=SCG&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span>INVESTIGATION OF DNA REPAIR BY <span class="hlt">SISTER</span> <span class="hlt">CHROMATID</span> EXCHANGE (SCE) ANALYSIS AND THE ALKALINE SINGLE CELL GEL ASSAY (SCG) IN MAMMALIAN GO-LYMPHOCYTES AFTER IN VITRO EXPOSURE TO ETHYLENE OXIDE (EO)</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>Investigation ofDNA Repair by <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange (SCE) Analysis and the Alkaline Single Cell Gel Assay (SCG) in Mammalian Go-Lymphocytes after In Vitro Exposure to Ethylene Oxide (EO). <br><br>EO is a large volume chemical used primarily as an intermediate in manufacturing...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7300853','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7300853"><span><span class="hlt">Sister-chromatid</span> exchanges in lymphocytes in women with cancer of the breast.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Husum, B; Wulf, H C; Niebuhr, E</p> <p>1981-10-01</p> <p>Examination of <span class="hlt">sister-chromatid</span> exchanges (SCE) in lymphocytes may be useful for the evaluation of exposure to mutagens/carcinogens. Information of a possible association between SCE and cancer is scarce. We therefore examined SCE in peripheral lymphocytes in 131 women, aged 17-90 years (median 51.8 years), coming to operation because of a tumor of the breast. Venous blood samples were cultivated during PHA stimulation in the presence of BrdU. After treatment with colcemid (R), fixation, treatment with bisbenzimide and staining with Giemsa, 30 metaphases were scored in each specimen. 52 patients with peroperatively demonstrated carcinoma of the breast had 9.39 +/- 0.17 SCE/cell and the remaining 79 women with non-malignant fibroadenomatosis had 9.88 +/- 0.18 SCE/cell. By multiple regression analysis it appeared that the character of the tumor, the patient's age, hormone treatment and preoperative examination by mammography all were without significant influence on the SCE rate. A statistically significant correlation was found between SCE and cigarette smoking. THe 45 cigarette-smoking patients had 10.49 +/- 0.23 SCE/cell compared with 9.26 +/- 0.13 SCE/cell in the 86 non-smokers. It was concluded that spontaneous SCE in lymphocytes is not an indicator of carcinoma of the breast.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25553380','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25553380"><span>Selective <span class="hlt">chromatid</span> segregation mechanism for Bruchus wings piebald color.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Klar, Amar J S</p> <p>2015-01-01</p> <p>The mechanisms of asymmetric organ development have been under intensive investigation for years, yet the proposed mechanisms remain controversial (1-3). The female Bruchus quadrimaculatus beetle insect develops two black-colored spots bilaterally located on each upper elytra wing by an unknown mechanism. Fifty percent of the P (for piebald, two colors) gene homozygous mutant insects, described in 1925, had a normal left elytrum (with two black spots) and an abnormal right elytrum (with two red spots) and the balance supported the converse lateralized pigment arrangement (4). Rather than supporting the conventional morphogen model for the wings pigmentation development, their biological origin is explained here with the somatic strand-specific epigenetic imprinting and selective <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation (SSIS) mechanism (5). We propose that the P gene product performs the selective <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation function to produce symmetric cell division of a specific cell during embryogenesis to result in the bilateral symmetric development of elytra black color spots and that the altered <span class="hlt">chromatid</span> segregation pattern of the mutant causes asymmetric cell division to confer the piebald phenotype. </p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19345191','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19345191"><span>Separase is recruited to mitotic chromosomes to dissolve <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion in a DNA-dependent manner.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sun, Yuxiao; Kucej, Martin; Fan, Heng-Yu; Yu, Hong; Sun, Qing-Yuan; Zou, Hui</p> <p>2009-04-03</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> separation is triggered by the separase-catalyzed cleavage of cohesin. This process is temporally controlled by cell-cycle-dependent factors, but its biochemical mechanism and spatial regulation remain poorly understood. We report that cohesin cleavage by human separase requires DNA in a sequence-nonspecific manner. Separase binds to DNA in vitro, but its proteolytic activity, measured by its autocleavage, is not stimulated by DNA. Instead, biochemical characterizations suggest that DNA mediates cohesin cleavage by bridging the interaction between separase and cohesin. In human cells, a fraction of separase localizes to the mitotic chromosome. The importance of the chromosomal DNA in cohesin cleavage is further demonstrated by the observation that the cleavage of the chromosome-associated cohesins is sensitive to nuclease treatment. Our observations explain why chromosome-associated cohesins are specifically cleaved by separase and the soluble cohesins are left intact in anaphase.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28781233','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28781233"><span>Phospho-H1 Decorates the Inter-<span class="hlt">chromatid</span> Axis and Is Evicted along with Shugoshin by SET during Mitosis.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Krishnan, Swathi; Smits, Arne H; Vermeulen, Michiel; Reinberg, Danny</p> <p>2017-08-17</p> <p>Precise control of <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation during mitosis is pivotal to maintaining genomic integrity. Yet, the regulatory mechanisms involved are not well understood. Remarkably, we discovered that linker histone H1 phosphorylated at S/T18 decorated the inter-<span class="hlt">chromatid</span> axial DNA on mitotic chromosomes. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> resolution during mitosis required the eviction of such H1S/T18ph by the chaperone SET, with this process being independent of and most likely downstream of arm-cohesin dissociation. SET also directed the disassembly of Shugoshins in a polo-like kinase 1-augmented manner, aiding centromere resolution. SET ablation compromised mitotic fidelity as evidenced by unresolved <span class="hlt">sister</span> <span class="hlt">chromatids</span> with marked accumulation of H1S/T18ph and centromeric Shugoshin. Thus, chaperone-assisted eviction of linker histones and Shugoshins is a fundamental step in mammalian mitotic progression. Our findings also elucidate the functional implications of the decades-old observation of mitotic linker histone phosphorylation, serving as a paradigm to explore the role of linker histones in bio-signaling processes. Copyright © 2017 Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/3365681','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/3365681"><span>Effect of betel chewing on the frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in pregnant women and women using oral contraceptives.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ghosh, P K; Ghosh, R</p> <p>1988-06-01</p> <p>The incidence of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) was investigated in the lymphocyte chromosomes of betel chewing and non-chewing normal women, pregnant women, and women using oral contraceptives. The frequency of SCE was found to be 7.82 +/- 0.24 and 8.27 +/- 0.27 in non-chewing pregnant women and women using oral contraceptives respectively, which were significantly higher than the mean value of 5.21 +/- 0.18 observed in non-chewing normal women. Betel chewing induced higher SCE in pregnant women and women using oral contraceptives, the frequencies being 11.79 +/- 0.38 and 12.51 +/- 0.44, respectively, which were significantly higher than the SCE frequency of 6.28 +/- 0.21 found in normal betel chewing females.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26122845','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26122845"><span>Defects in the Fanconi Anemia Pathway and <span class="hlt">Chromatid</span> Cohesion in Head and Neck Cancer.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stoepker, Chantal; Ameziane, Najim; van der Lelij, Petra; Kooi, Irsan E; Oostra, Anneke B; Rooimans, Martin A; van Mil, Saskia E; Brink, Arjen; Dietrich, Ralf; Balk, Jesper A; Ylstra, Bauke; Joenje, Hans; Feller, Stephan M; Brakenhoff, Ruud H</p> <p>2015-09-01</p> <p>Failure to repair DNA damage or defective <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, a process essential for correct chromosome segregation, can be causative of chromosomal instability (CIN), which is a hallmark of many types of cancers. We investigated how frequent this occurs in head and neck squamous cell carcinoma (HNSCC) and whether specific mechanisms or genes could be linked to these phenotypes. The genomic instability syndrome Fanconi anemia is caused by mutations in any of at least 16 genes regulating DNA interstrand crosslink (ICL) repair. Since patients with Fanconi anemia have a high risk to develop HNSCC, we investigated whether and to which extent Fanconi anemia pathway inactivation underlies CIN in HNSCC of non-Fanconi anemia individuals. We observed ICL-induced chromosomal breakage in 9 of 17 (53%) HNSCC cell lines derived from patients without Fanconi anemia. In addition, defective <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion was observed in five HNSCC cell lines. Inactivation of FANCM was responsible for chromosomal breakage in one cell line, whereas in two other cell lines, somatic mutations in PDS5A or STAG2 resulted in inadequate <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. In addition, FANCF methylation was found in one cell line by screening an additional panel of 39 HNSCC cell lines. Our data demonstrate that CIN in terms of ICL-induced chromosomal breakage and defective <span class="hlt">chromatid</span> cohesion is frequently observed in HNSCC. Inactivation of known Fanconi anemia and <span class="hlt">chromatid</span> cohesion genes does explain CIN in the minority of cases. These findings point to phenotypes that may be highly relevant in treatment response of HNSCC. ©2015 American Association for Cancer Research.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/17451994','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/17451994"><span>Vicia root-mirconucleus and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assays on the genotoxicity of selenium compounds.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yi, Huilan; Si, Liangyan</p> <p>2007-06-15</p> <p>Selenium (Se) is an important metalloid with industrial, environmental, biological and toxicological significance. Excessive selenium in soil and water may contribute to environmental selenium pollution, and affect plant growth and human health. By using Vicia faba micronucleus (MN) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) tests, possible genotoxicity of sodium selenite and sodium biselenite was evaluated in this study. The results showed that sodium selenite, at concentrations from 0.01 to 10.0mg/L, induced a 1.9-3.9-fold increase in MN frequency and a 1.5-1.6-fold increase in SCE frequency, with a statistically significantly difference from the control (P<0.05 and 0.01, respectively). Sodium selenite also caused mitotic delay and a 15-80% decrease in mitotic indices (MI), but at the lowest concentration (0.005mg/L), it slightly stimulated mitotic activity. Similarly, the frequencies of MN and SCE also increased significantly in sodium biselenite treated samples, with MI decline only at relatively higher effective concentrations. Results of the present study suggest that selenite is genotoxic to V. faba root cells and may be a genotoxic risk to human health.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/6872102','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/6872102"><span>Alkaline DNA fragmentation, DNA disentanglement evaluated viscosimetrically and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, after treatment in vivo with nitrofurantoin.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Parodi, S; Pala, M; Russo, P; Balbi, C; Abelmoschi, M L; Taningher, M; Zunino, A; Ottaggio, L; de Ferrari, M; Carbone, A; Santi, L</p> <p>1983-07-01</p> <p>Nitrofurantoin was not positive as a carcinogen in long term assays. In vitro it was positive in some short term tests and negative in others. We have examined Nitrofurantoin for its capability of inducing DNA damage in vivo. With the alkaline elution technique, Nitrofurantoin appeared clearly positive in all the tissues examined (liver, kidney, lung, spleen and bone marrow). In the liver we also observed some cross-linking effect. In bone marrow cells Nitrofurantoin was also clearly positive in terms of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) induction. DNA damage in vivo was also examined with a viscosimetric method, more sensitive than alkaline elution. With this method the results were essentially negative, suggesting that the two methods detect different types of damage. In view of its positivity in many organs and in two short term tests in vivo, the carcinogenic potential of Nitrofurantoin should be reconsidered.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28590163','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28590163"><span>Merotelic kinetochore attachment in oocyte meiosis II causes <span class="hlt">sister</span> <span class="hlt">chromatids</span> segregation errors in aged mice.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cheng, Jin-Mei; Li, Jian; Tang, Ji-Xin; Hao, Xiao-Xia; Wang, Zhi-Peng; Sun, Tie-Cheng; Wang, Xiu-Xia; Zhang, Yan; Chen, Su-Ren; Liu, Yi-Xun</p> <p>2017-08-03</p> <p>Mammalian oocyte chromosomes undergo 2 meiotic divisions to generate haploid gametes. The frequency of chromosome segregation errors during meiosis I increase with age. However, little attention has been paid to the question of how aging affects <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation during oocyte meiosis II. More importantly, how aneuploid metaphase II (MII) oocytes from aged mice evade the spindle assembly checkpoint (SAC) mechanism to complete later meiosis II to form aneuploid embryos remains unknown. Here, we report that MII oocytes from naturally aged mice exhibited substantial errors in chromosome arrangement and configuration compared with young MII oocytes. Interestingly, these errors in aged oocytes had no impact on anaphase II onset and completion as well as 2-cell formation after parthenogenetic activation. Further study found that merotelic kinetochore attachment occurred more frequently and could stabilize the kinetochore-microtubule interaction to ensure SAC inactivation and anaphase II onset in aged MII oocytes. This orientation could persist largely during anaphase II in aged oocytes, leading to severe chromosome lagging and trailing as well as delay of anaphase II completion. Therefore, merotelic kinetochore attachment in oocyte meiosis II exacerbates age-related genetic instability and is a key source of age-dependent embryo aneuploidy and dysplasia.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5587752','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5587752"><span>FANCJ helicase controls the balance between short- and long-tract gene conversions between <span class="hlt">sister</span> <span class="hlt">chromatids</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Nath, Sarmi; Somyajit, Kumar; Mishra, Anup; Scully, Ralph</p> <p>2017-01-01</p> <p>Abstract The FANCJ DNA helicase is linked to hereditary breast and ovarian cancers as well as bone marrow failure disorder Fanconi anemia (FA). Although FANCJ has been implicated in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR), the molecular mechanism underlying the tumor suppressor functions of FANCJ remains obscure. Here, we demonstrate that FANCJ deficient human and hamster cells exhibit reduction in the overall gene conversions in response to a site-specific chromosomal DSB induced by I-SceI endonuclease. Strikingly, the gene conversion events were biased in favour of long-tract gene conversions in FANCJ depleted cells. The fine regulation of short- (STGC) and long-tract gene conversions (LTGC) by FANCJ was dependent on its interaction with BRCA1 tumor suppressor. Notably, helicase activity of FANCJ was essential for controlling the overall HR and in terminating the extended repair synthesis during <span class="hlt">sister</span> <span class="hlt">chromatid</span> recombination (SCR). Moreover, cells expressing FANCJ pathological mutants exhibited defective SCR with an increased frequency of LTGC. These data unravel the novel function of FANCJ helicase in regulating SCR and SCR associated gene amplification/duplications and imply that these functions of FANCJ are crucial for the genome maintenance and tumor suppression. PMID:28911102</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_1");'>1</a></li> <li><a href="#" onclick='return showDiv("page_2");'>2</a></li> <li class="active"><span>3</span></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_3 --> <div id="page_4" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_2");'>2</a></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li class="active"><span>4</span></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="61"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3514784','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3514784"><span>Cell elongation is an adaptive response for clearing long <span class="hlt">chromatid</span> arms from the cleavage plane</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kotadia, Shaila; Montembault, Emilie; Sullivan, William</p> <p>2012-01-01</p> <p>Chromosome segregation must be coordinated with cell cleavage to ensure correct transmission of the genome to daughter cells. Here we identify a novel mechanism by which Drosophila melanogaster neuronal stem cells coordinate <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation with cleavage furrow ingression. Cells adapted to a dramatic increase in <span class="hlt">chromatid</span> arm length by transiently elongating during anaphase/telophase. The degree of cell elongation correlated with the length of the trailing <span class="hlt">chromatid</span> arms and was concomitant with a slight increase in spindle length and an enlargement of the zone of cortical myosin distribution. Rho guanine-nucleotide exchange factor (Pebble)–depleted cells failed to elongate during segregation of long <span class="hlt">chromatids</span>. As a result, Pebble-depleted adult flies exhibited morphological defects likely caused by cell death during development. These studies reveal a novel pathway linking trailing <span class="hlt">chromatid</span> arms and cortical myosin that ensures the clearance of <span class="hlt">chromatids</span> from the cleavage plane at the appropriate time during cytokinesis, thus preserving genome integrity. PMID:23185030</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25420521','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25420521"><span>Isolation and evaluation of cytogenetic effect of Brahmi saponins on cultured human lymphocytes exposed in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kalachaveedu, Mangathayaru; Papacchan, Sunu; Sanyal, Sudip; Koshy, Teena; Telapolu, Srivani</p> <p>2015-01-01</p> <p>Major saponins of Brahmi (Bacopa monniera, Fam: Scrophulariaceae) - bacosides A and B - were isolated from the total methanol extract and characterised based on melting point, TLC, IR, (1)H NMR and (13)C NMR. They were evaluated for their in vitro cytogenetic effects on human peripheral blood lymphocytes by chromosomal <span class="hlt">aberration</span> (CA) assay and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) assay. The frequency of <span class="hlt">chromatid</span> type <span class="hlt">aberrations</span> and reciprocal interchanges between <span class="hlt">sister</span> <span class="hlt">chromatids</span> in the treated cells was scored in comparison to the untreated control. At 30 μg/mL dose, bacoside A showed a statistically significant increase in the frequency of both CA and SCE and bacoside B showed an increase only in SCE. Our report of the genotoxicity of the saponins is significant in view of the reports of anticancer activity of Brahmi extracts.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20730658','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20730658"><span>Increased frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and decrease in cell viability and proliferation kinetics in human peripheral blood lymphocytes after in vitro exposure to whole bee venom.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Gajski, Goran; Garaj-Vrhovac, Vera</p> <p>2010-10-01</p> <p>The present study was aimed to investigate the impact of bee venom on frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) and viability in human peripheral blood lymphocytes in vitro. In addition, the proportion of lymphocytes that undergo one, two or three cell divisions as well as proliferative rate index (PRI) have been determined. Aqueous solution of whole bee venom was added to whole blood samples in concentrations ranging from 0.1 microg/mL to 20 microg/mL in different lengths of time. Results showed that whole bee venom inhibited cell viability, resulting in a 22.86 +/- 1.14% and 51.21 +/- 0.58% reduction of viable cells at 1 hour and 6 hours, respectively. The mean SCE per cell in all the exposed samples was significantly higher than in the corresponding controls. In addition, the percentage of high frequency cells (HFC) for each sample was estimated using the pooled distribution of all SCE measurements. This parameter was also significantly higher compared to the control. Inhibition of proliferation was statistically significant for both exposure times and concentrations and was time and dose dependent. These data indicate that whole bee venom inhibited cell proliferation, resulting in a 36.87 +/- 5.89% and 38.43 +/- 1.96% reduction of proliferation at 1 hour and 6 hours, respectively. In conclusion, this report demonstrated that whole bee venom is capable of inducing DNA alterations by virtue of increasing <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in addition to the cell viability decrease and inhibition of proliferation kinetics in human peripheral blood lymphocytes in vitro.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24852491','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24852491"><span>Health assessment of gasoline and fuel oxygenate vapors: micronucleus and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange evaluations.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schreiner, Ceinwen A; Hoffman, Gary M; Gudi, Ramadevi; Clark, Charles R</p> <p>2014-11-01</p> <p>Micronucleus and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) tests were performed for vapor condensate of baseline gasoline (BGVC), or gasoline with oxygenates, methyl tert-butyl ether (G/MTBE), ethyl tert butyl ether (G/ETBE), t-amyl methyl ether (G/TAME), diisopropyl ether (G/DIPE), t-butyl alcohol (TBA), or ethanol (G/EtOH). Sprague Dawley rats (the same 5/sex/group for both endpoints) were exposed to 0, 2000, 10,000, or 20,000mg/m(3) of each condensate, 6h/day, 5days/week over 4weeks. Positive controls (5/sex/test) were given cyclophosphamide IP, 24h prior to sacrifice at 5mg/kg (SCE test) and 40mg/kg (micronucleus test). Blood was collected from the abdominal aorta for the SCE test and femurs removed for the micronucleus test. Blood cell cultures were treated with 5μg/ml bromodeoxyuridine (BrdU) for SCE evaluation. No significant increases in micronucleated immature erythrocytes were observed for any test material. Statistically significant increases in SCE were observed in rats given BGVC alone or in female rats given G/MTBE. G/TAME induced increased SCE in both sexes at the highest dose only. Although DNA perturbation was observed for several samples, DNA damage was not expressed as increased micronuclei in bone marrow cells. Inclusion of oxygenates in gasoline did not increase the effects of gasoline alone or produce a cytogenetic hazard. Copyright © 2014 Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11287300','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11287300"><span>Frequency of <span class="hlt">sister-chromatid</span> exchange among greenhouse farmers exposed to pesticides.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Shaham, J; Kaufman, Z; Gurvich, R; Levi, Z</p> <p>2001-04-05</p> <p><span class="hlt">Sister-chromatid</span> exchange (SCE) was measured in peripheral lymphocytes of 104 greenhouse farmers exposed to pesticides and 44 unexposed workers. The results of SCEs are expressed in two variables: (a) mean number of SCEs per chromosome and, (b) proportion of high frequency cells (cells with more than eight SCEs). A high correlation was found between these two variables. The adjusted means of both SCEs variables were significantly higher among the farmers compared with the unexposed group (P < 0.01). Adjustment was made for smoking, age, education, and origin. The adjusted means of both SCE variables, were significantly elevated (P < 0.05) among the farmers who prepared and applied more than 70% of the pesticides by themselves compared with those who prepared and applied less than 70% of the pesticides by themselves. Both SCEs variables were also significantly elevated (P < 0.05) among farmers who were involved in more than 7.4 sprays per year compared with those with 7.4 or less sprays per year (P < 0.05). We found a tendency towards elevation of the two variables of SCEs among those who did not use protective measures while preparing the pesticides. Evaluation of the influence of years of exposure on the frequency of SCEs showed that the two variables of SCEs were higher among those farmers who were exposed to pesticides for more than 21 years than among those with less than 21 years of exposure. The variables that had the most influence on the elevation of SCEs were self-preparation of the pesticide mixtures and the number of sprayings per year. Because the farmers used a mixture of almost 24 different chemical classes it was impossible to attribute exposure to a specific pesticide or group of pesticides to single farmers. Our finding of a significant increase of SCEs frequency in peripheral lymphocytes in greenhouse farmers indicates a potential cytogenetic hazard due to pesticides exposure.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19066927','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19066927"><span>Influence of the bystander phenomenon on the chromosome <span class="hlt">aberration</span> pattern in human lymphocytes induced by in vitro alpha-particle exposure.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schmid, Ernst; Roos, H</p> <p>2009-04-01</p> <p>A recent publication on both chromosome-type and <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> in lymphocytes of patients during treatment with radium-224 for ankylosing spondilitis has revived the question of whether the <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> may be the consequence of factors released by irradiated cells. Therefore, the aim of the present study was to investigate the influence of such a bystander phenomenon on the chromosome <span class="hlt">aberration</span> pattern of lymphocytes. Monolayers of human lymphocytes were irradiated with 1 Gy of alpha-particles from an americium-241 source in the absence or presence of whole blood, autologous plasma or culture medium. In the presence of any liquid covering the monolayer during irradiation, the <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> were, contrary to expectation, elevated. Whereas the intercellular distribution of dicentrics was significantly overdispersed, the <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> showed a regular dispersion. It can be concluded that the enhanced frequency of <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> is the result of a damage signal or a bystander phenomenon released by irradiated cells.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/7050066-vitro-effect-fenthion-human-lymphocytes','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/7050066-vitro-effect-fenthion-human-lymphocytes"><span>In vitro effect of fenthion on human lymphocytes</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Rani, M.V.U.; Rao, M.S.</p> <p>1991-08-01</p> <p>Fenthion is an organophosphorus insecticide which is extensively used in control of leaf hoppers, cutworms, mites on vegetable crops. It has been reported that organophosphorus pesticides cause a significant increase in <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in mammalian cell lines. A significant increase of chromosomal <span class="hlt">aberrations</span> has been reported in rural population exposed to pesticides. Organosphosphorus pesticides malathion, diazinon, dimethoate, phosdrin and dursban induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in human lymphoid cells. Exchange type of <span class="hlt">aberration</span> has been reported in fluoriculturist who were exposed to organophosphorus, organochlorine pesticides. In the present investigation an attempt has been made to evaluate the cytogenetic effect ofmore » fenthion in human lymphocyte cultures in vitro.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4224182','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4224182"><span><span class="hlt">Sisters</span> Unbound Is Required for Meiotic Centromeric Cohesion in Drosophila melanogaster</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Krishnan, Badri; Thomas, Sharon E.; Yan, Rihui; Yamada, Hirotsugu; Zhulin, Igor B.; McKee, Bruce D.</p> <p>2014-01-01</p> <p>Regular meiotic chromosome segregation requires <span class="hlt">sister</span> centromeres to mono-orient (orient to the same pole) during the first meiotic division (meiosis I) when homologous chromosomes segregate, and to bi-orient (orient to opposite poles) during the second meiotic division (meiosis II) when <span class="hlt">sister</span> <span class="hlt">chromatids</span> segregate. Both orientation patterns require cohesion between <span class="hlt">sister</span> centromeres, which is established during meiotic DNA replication and persists until anaphase of meiosis II. Meiotic cohesion is mediated by a conserved four-protein complex called cohesin that includes two structural maintenance of chromosomes (SMC) subunits (SMC1 and SMC3) and two non-SMC subunits. In Drosophila melanogaster, however, the meiotic cohesion apparatus has not been fully characterized and the non-SMC subunits have not been identified. We have identified a novel Drosophila gene called <span class="hlt">sisters</span> unbound (sunn), which is required for stable <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion throughout meiosis. sunn mutations disrupt centromere cohesion during prophase I and cause high frequencies of non-disjunction (NDJ) at both meiotic divisions in both sexes. SUNN co-localizes at centromeres with the cohesion proteins SMC1 and SOLO in both sexes and is necessary for the recruitment of both proteins to centromeres. Although SUNN lacks sequence homology to cohesins, bioinformatic analysis indicates that SUNN may be a structural homolog of the non-SMC cohesin subunit stromalin (SA), suggesting that SUNN may serve as a meiosis-specific cohesin subunit. In conclusion, our data show that SUNN is an essential meiosis-specific Drosophila cohesion protein. PMID:25194162</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2715236','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2715236"><span>The Walker B motif in avian FANCM is required to limit <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges but is dispensable for DNA crosslink repair</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Rosado, Ivan V.; Niedzwiedz, Wojciech; Alpi, Arno F.; Patel, Ketan J.</p> <p>2009-01-01</p> <p>FANCM, the most highly conserved component of the Fanconi Anaemia (FA) pathway can resolve recombination intermediates and remodel synthetic replication forks. However, it is not known if these activities are relevant to how this conserved protein activates the FA pathway and promotes DNA crosslink repair. Here we use chicken DT40 cells to systematically dissect the function of the helicase and nuclease domains of FANCM. Our studies reveal that these domains contribute distinct roles in the tolerance of crosslinker, UV light and camptothecin-induced DNA damage. Although the complete helicase domain is critical for crosslink repair, a predicted inactivating mutation of the Walker B box domain has no impact on FA pathway associated functions. However, this mutation does result in elevated <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE). Furthermore, our genetic dissection indicates that FANCM functions with the Blm helicase to suppress spontaneous SCE events. Overall our results lead us to reappraise the role of helicase domain associated activities of FANCM with respect to the activation of the FA pathway, crosslink repair and in the resolution of recombination intermediates. PMID:19465393</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21743463','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21743463"><span>Cleavage of cohesin rings coordinates the separation of centrioles and <span class="hlt">chromatids</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schöckel, Laura; Möckel, Martin; Mayer, Bernd; Boos, Dominik; Stemmann, Olaf</p> <p>2011-07-10</p> <p>Cohesin pairs <span class="hlt">sister</span> <span class="hlt">chromatids</span> by forming a tripartite Scc1-Smc1-Smc3 ring around them. In mitosis, cohesin is removed from chromosome arms by the phosphorylation-dependent prophase pathway. Centromeric cohesin is protected by shugoshin 1 and protein phosphatase 2A (Sgo1-PP2A) and opened only in anaphase by separase-dependent cleavage of Scc1 (refs 4-6). Following chromosome segregation, centrioles loosen their tight orthogonal arrangement, which licenses later centrosome duplication in S phase. Although a role of separase in centriole disengagement has been reported, the molecular details of this process remain enigmatic. Here, we identify cohesin as a centriole-engagement factor. Both premature <span class="hlt">sister-chromatid</span> separation and centriole disengagement are induced by ectopic activation of separase or depletion of Sgo1. These unscheduled events are suppressed by expression of non-cleavable Scc1 or inhibition of the prophase pathway. When endogenous Scc1 is replaced by artificially cleavable Scc1, the corresponding site-specific protease triggers centriole disengagement. Separation of centrioles can alternatively be induced by ectopic cleavage of an engineered Smc3. Thus, the chromosome and centrosome cycles exhibit extensive parallels and are coordinated with each other by dual use of the cohesin ring complex.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29410075','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29410075"><span>The small molecule CS1 inhibits mitosis and <span class="hlt">sister</span> <span class="hlt">chromatid</span> resolution in HeLa cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wu, Xingkang; Li, Zhenyu; Shen, Yuemao</p> <p>2018-05-01</p> <p>Mitosis, the most dramatic event in the cell cycle, involves the reorganization of virtually all cellular components. Antimitotic agents are useful for dissecting the mechanism of this reorganization. Previously, we found that the small molecule CS1 accumulates cells in G2/M phase [1], but the mechanism of its action remains unknown. Cell cycle analysis, live cell imaging and nuclear staining were used. Chromosomal morphology was detected by chromosome spreading. The effects of CS1 on microtubules were confirmed by tubulin polymerization, colchicine tubulin-binding, cellular tubulin polymerization and immunofluorescence assays and by analysis of microtubule dynamics and molecular modeling. Histone phosphoproteomics was performed using mass spectrometry. Cell signaling cascades were analyzed using immunofluorescence, immunoprecipitation, immunoblotting, siRNA knockdown and chemical inhibition of specific proteins. The small molecule CS1 was shown to be an antimitotic agent. CS1 potently inhibited microtubule polymerization via interaction with the colchicine-binding pocket of tubulin in vitro and inhibited the formation of the spindle apparatus by reducing the bulk of growing microtubules in HeLa cells, which led to activation of the spindle assembly checkpoint (SAC) and mitotic arrest of HeLa cells. Compared with colchicine, CS1 impaired the progression of <span class="hlt">sister</span> <span class="hlt">chromatid</span> resolution independent of cohesin dissociation, and this was reversed by the removal of CS1. Additionally, CS1 induced unique histone phosphorylation patterns distinct from those induced by colchicine. CS1 is a unique antimitotic small molecule and a powerful tool with unprecedented value over colchicine that makes it possible to specifically and conditionally perturb mitotic progression. Copyright © 2018 Elsevier B.V. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24444548','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24444548"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange, (SCE), High-Frequency Cells (HFCs) and SCE distribution patterns in peripheral blood lymphocytes of Spanish adult smokers compared to non-smokers.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sebastià, Natividad; Hervás, David; Almonacid, Miguel; Villaescusa, Juan Ignacio; Soriano, José Miguel; Sahuquillo, Vicenta; Esteban, Valentín; Barquinero, Joan Francesc; Verdú, Gumersindo; Cervera, José; Such, Esperanza; Montoro, Alegría</p> <p>2014-04-01</p> <p>According to the International Agency for Research on Cancer, smoking tobacco is a major cause of cancer in humans. It causes about half of all male cancer deaths and an ever increasing number of cancer deaths in females. The aim of this study was to establish whether cigarette smoking increases <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) in peripheral blood lymphocytes in two Spanish population groups; light and heavy smokers. The mean number of High-Frequency Cells (HFCs) was determined and, the SCE distribution pattern among the chromosomes was analysed represented by a ratio described below. A local sample of 101 adult smokers (n=48) and non-smokers (n=53), aged from 18 to 49 years, was studied using SCE levels in peripheral lymphocytes. Heavy smoking (≥ 10 cigarettes per day) increased significantly the SCE frequency and the HFC parameters. Neither age nor sex significantly influenced the frequencies in the groups studied. Crown Copyright © 2014. Published by Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8248278','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8248278"><span>Enhancement of antineoplastic effect and attenuation of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges by prostaglandin E2 in Ehrlich ascites tumour cells treated with cyclophosphamide in vivo.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mourelatos, D; Kritsi, Z; Mioglou, E; Dozi-Vassiliades, J</p> <p>1993-09-01</p> <p>Reduced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) frequency in response to cyclophosphamide (CP) was observed when Ehrlich ascites tumour (EAT) cells were exposed in vivo to 2 micrograms/g body weight of prostaglandin E2 (PGE2). 1 h before i.p. injection of 5-bromodeoxyuridine (BrdUrd) adsorbed to activated charcoal, EAT-bearing mice treated i.p. with CP appeared to have increased SCE rates and cell division delays. PGE2 had no effect on survival and in inhibiting tumour growth. CP had only a slight non-significant effect on survival and in inhibiting tumour growth. In mice treated with the combined CP (5 micrograms/g bd wt) plus PGE2 (2 micrograms/g bd wt) a significant enhancement (P < 0.01) of survival time was accompanied by inhibition of tumour growth (P < 0.01) in comparison with the untreated controls. These data imply that SCEs might result from errors in a repair process which might involve a PGE2 sensitive step.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12132876','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12132876"><span>Comparative study of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange induction and antitumor effects by homo-aza-steroidal esters of [p-[bis(2-chloroethyl)amino]phenyl]butyric acid.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Camoutsis, C; Catsoulacos, D; Karayiann, V; Papageorgiou, A; Mourelatos, D; Mioglou, E; Kritsi, Z; Nikolaropoulos, S</p> <p>2001-01-01</p> <p>The present work was undertaken in order to test the hypothesis that the <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange (SCE) assay in vitro can be used for the prediction of in vivo tumor response to newly synthesized potential chemotherapeutics. The effect of three homo-aza-steroidal esters containing the -CONH- in the steroidal nucleus, 1, 2, and 3 on SCE rates and on cell kinetics in cultured human lymphocytes was studied. The antitumor activity of these compounds was tested on leukemia P388- and leukemia L1210-bearing mice. The three substances induced statistically significant enhancement of SCEs and of cell division delays. Compounds 1 and 3 were identified, on a molar basis, as more effective inducers of SCEs and of cell division delays compared with compound 2. Compounds 1 and 3 had upon both experimental tumors better therapeutic effects compared with compound 2 at equitoxic doses. Therefore, the order of the antitumor effectiveness of the three compounds coincided with the order of the cytogenetic effects they induced.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3003188','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3003188"><span><span class="hlt">Sister</span> acts: coordinating DNA replication and cohesion establishment</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Sherwood, Rebecca; Takahashi, Tatsuro S.; Jallepalli, Prasad V.</p> <p>2010-01-01</p> <p>The ring-shaped cohesin complex links <span class="hlt">sister</span> <span class="hlt">chromatids</span> and plays crucial roles in homologous recombination and mitotic chromosome segregation. In cycling cells, cohesin's ability to generate cohesive linkages is restricted to S phase and depends on loading and establishment factors that are intimately connected to DNA replication. Here we review how cohesin is regulated by the replication machinery, as well as recent evidence that cohesin itself influences how chromosomes are replicated. PMID:21159813</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/10189155','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/10189155"><span><span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange analysis in workers exposed to noise and vibration.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Silva, M J; Carothers, A; Castelo Branco, N A; Dias, A; Boavida, M G</p> <p>1999-03-01</p> <p>There has been a growing interest in the combined effects of noise and vibration. In a population of aeronautical workers diagnosed with vibroacoustic disease (VAD), a large incidence of malignancy was detected. These workers were exposed to large pressure amplitude (LPA) (> or = 90 dB SPL) noise, with energy content concentrated within the low frequency (LF) bands (< or = 500 Hz) and whole-body vibration (WBV). To our knowledge, there are no studies conducted in humans or animals that address the issue of the potential genotoxic effects of vibration combined with noise. In the present study, the levels of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) and of cells with high frequencies of SCE (HFC) were analyzed in peripheral blood lymphocytes of workers employed in various occupations within the aeronautical industry. SCE and HFC were analyzed in lymphocytes of 50 workers occupationally exposed to noise and vibration and of 34 office-worker controls (G0). The exposed group included: 10 hand-vibrating tool operators (G1), 15 engine test cell technicians (G2), 12 aircraft run-up technicians (G3) and 13 Portuguese Air Force helicopter pilots (G4). Groups 2-4 were exposed to WBV and LPALF noise; group 1 was exposed to LPA high frequency noise and local vibration. Statistical analysis of the mean SCE count per cell was carried out by multiple regression analysis comparing various predictor variables: type of exposure, duration of exposure, age, and cigarette consumption. Only cigarette consumption and type of exposure were found to be significantly correlated with the mean SCE frequency. After allowing for the effects of smoking, the analysis indicates that: 1) there was no significant difference between G1 and G0 (p > 0.05); 2) the differences between G2 and G0, G3 and G0, G4 and G0 were all highly significant (p < 0.001); 3) there was no significant difference between G2 and G3 (p > 0.05), nor between G2 and G3 combined and G4 (p > 0.05); and 4) G2 and G4 combined had a</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11948630','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11948630"><span>Low frequency noise and whole-body vibration cause increased levels of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in splenocytes of exposed mice.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Silva, M J; Dias, A; Barreta, A; Nogueira, P J; Castelo-Branco, N A A; Boavida, M G</p> <p>2002-01-01</p> <p>Chronic exposure to low frequency (LF) noise and whole-body vibration (WBV) induces both physiological and psychological alterations in man. Recently, we have shown that long-term occupational exposure to LF noise and WBV produces genotoxic effects in man expressed as an increase in <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) levels in lymphocytes. The objectives of the present study were to investigate whether the observed effect could be reproduced in a murine model and, if so, which of the agents, LF noise alone or in combination with WBV, would be instrumental in the SCE induction. SCEs were analyzed in spleen lymphocytes of mice exposed to LF noise alone and in combination with WBV for 300 and 600 hr. An effect at the cell cycle kinetics level was also investigated. The results revealed significant increases in the mean SCE number per cell and in the proportion of cells with high frequency of SCEs (HFCs) in lymphocytes of mice submitted to combined noise and WBV over controls. No significant differences were found between single noise-exposed and control mice. A cell cycle delay was observed exclusively in the noise and WBV exposure groups. In conclusion, we demonstrated that, as in exposed workers, prolonged exposure to the combination of LF noise and WBV determines an increase in SCE level in mice while LF noise alone is not effective in SCE induction. Copyright 2002 Wiley-Liss, Inc.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11406183','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11406183"><span>Differences in sensitivity of murine spermatogonia and somatic cells in vivo to <span class="hlt">sister-chromatid</span> exchange induction by nitrosoureas.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Morales-Ramírez, P; Cruz-Vallejo, V; Rodríguez-Reyes, R</p> <p>2001-07-01</p> <p>Previously published data indicate that spermatogonia (SPG) are less sensitive to a <span class="hlt">sister-chromatid</span> exchange (SCE) induction for different mutagens. In an earlier study, we have observed that bromodeoxyuridine (BrdU) substituted murine SPG are less sensitive to SCE induction by gamma ray in cells, than bone marrow (BM) and salivary gland (SG) cells in vivo. This was interpreted to mean that SPG are more efficient in DNA repair or are less prone to SCE induction. That the lower induction of SCE could be due to a reduced accessibility of mutagens to the SPG by virtue of a physiological barrier, was discarded by using gamma radiation. The aim of the present study was to establish whether or not there are differences in SCE induction by nitrosoureas among SPG, SG and BM cells with BrdU substituted or unsubstituted DNA. It was observed that SCE induction by methylnitrosourea (MNU) or by ethylnitrosourea (ENU) in SPG was, respectively, five and two times lower than in SG, and ten and three times lower than in BM. In SPG after BrdU incorporation, there was no increase in efficiency of SCE induction; in fact, there was even a slight decrease by exposure to MNU or ENU. BM and SG cells showed an increased efficiency in SCE induction after BrdU incorporation. This implies that SPG are also less sensitive to SCE induction by nitrosoureas, which cause a different kind of damage from previously assayed mutagens.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19500270','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19500270"><span>Micronuclear and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange analyses in peripheral lymphocytes of patients with oral lichen planus--a pilot study.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ergun, S; Warnakulasuriya, S; Duman, N; Saruhanoğlu, A; Sevinç, B; Oztürk, S; Ozel, S; Cefle, K; Palanduz, S; Tanyeri, H</p> <p>2009-10-01</p> <p>The purpose of this study was to determine the genetic instability of peripheral blood lymphocytes from patients diagnosed with oral lichen planus (OLP) by investigation of frequencies of micronuclei (MN) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE). A total of 22 newly diagnosed and untreated patients with OLP of same severity scores and twenty healthy controls participated in this study. They were all non-smokers with no previous history or family history of cancer. The periodontal status, flow rate and buffering capacity of whole mouth saliva were recorded. SCE and MN analyses were performed on peripheral blood lymphocytes of OLP patients and healthy controls. The frequencies of MN (50.00 +/- 22.36) and SCE (6.89 +/- 1.48) in OLP patients were found to be significantly elevated compared with that in normal individuals (25.20 +/- 9.52 and 5.93 +/- 1.31; z = 3.946, P = 0.0001; z = 2.346, P = 0.019). There were no significant differences in the MN frequency and SCE between the two subgroups with reticular or erosive types of OLP. These pilot data indicate an increased genomic instability in peripheral blood lymphocytes of a cohort of Turkish patients diagnosed with oral lichen planus as compared with that of healthy individuals. As patients with OLP may have an increased or potential risk for oral malignancy, these assays could be used in translational research to monitor beneficial effects of interventions and long-term prognosis.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12678382','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12678382"><span>Chromosome <span class="hlt">aberration</span> analysis in peripheral lymphocytes of Gulf War and Balkans War veterans.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schröder, H; Heimers, A; Frentzel-Beyme, R; Schott, A; Hoffmann, W</p> <p>2003-01-01</p> <p>Chromosome <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) were determined in standard peripheral lymphocyte metaphase preparations of 13 British Gulf War veterans, two veterans of the recent war in the Balkans and one veteran of both wars. All 16 volunteers suspect exposures to depleted uranium (DU) while deployed at the two different theatres of war in 1990 and later on. The Bremen laboratory control served as a reference in this study. Compared with this control there was a statistically significant increase in the frequency of dicentric chromosomes (dic) and centric ring chromosomes (cR) in the veterans' group. indicating a previous exposure to ionising radiation. The statistically significant overdispersion of die and cR indicates non-uniform irradiation as would be expected after non-uniform exposure and/or exposure to radiation with a high linear energy transfer (LET). The frequency of SCEs was decreased when compared with the laboratory control.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_2");'>2</a></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li class="active"><span>4</span></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_4 --> <div id="page_5" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li class="active"><span>5</span></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="81"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8175058','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8175058"><span>[Cytogenetic examinations in biomonitoring residents residing closest to the area near the Sendzimir metallurgy plant in Krakow exposed to environmental pollution].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kubiak, R; Rudek, Z; Cieszkowski, J; Garlicki, S</p> <p>1993-01-01</p> <p>There are many studies done to identify the genetic hazard from occupational exposure of workers, but rather little is known about genetic effects in inhabitants of polluted areas. The aim of the study was to examine chromosome <span class="hlt">aberrations</span>, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and number of micronuclei in lymphocytes of persons living in the close vicinity of a large metallurgical plant. The results were compared with those obtained for the inhabitants of a village located 40 km from the city of Cracow and from the plant. An increased incidence of chromosome <span class="hlt">aberrations</span> (0.66-4.66%, control 0.78%), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (mean 9.73, control: 6.0) was found in the group living near the steel foundry. The paper also includes some data on measurements of the air pollution in the Nowa Huta region as well as on the amounts of heavy metals in vegetables in this region. Environmental pollution is worsening.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27120695','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27120695"><span>Separase Is Required for Homolog and <span class="hlt">Sister</span> Disjunction during Drosophila melanogaster Male Meiosis, but Not for Biorientation of <span class="hlt">Sister</span> Centromeres.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Blattner, Ariane C; Chaurasia, Soumya; McKee, Bruce D; Lehner, Christian F</p> <p>2016-04-01</p> <p>Spatially controlled release of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion during progression through the meiotic divisions is of paramount importance for error-free chromosome segregation during meiosis. Cohesion is mediated by the cohesin protein complex and cleavage of one of its subunits by the endoprotease separase removes cohesin first from chromosome arms during exit from meiosis I and later from the pericentromeric region during exit from meiosis II. At the onset of the meiotic divisions, cohesin has also been proposed to be present within the centromeric region for the unification of <span class="hlt">sister</span> centromeres into a single functional entity, allowing bipolar orientation of paired homologs within the meiosis I spindle. Separase-mediated removal of centromeric cohesin during exit from meiosis I might explain <span class="hlt">sister</span> centromere individualization which is essential for subsequent biorientation of <span class="hlt">sister</span> centromeres during meiosis II. To characterize a potential involvement of separase in <span class="hlt">sister</span> centromere individualization before meiosis II, we have studied meiosis in Drosophila melanogaster males where homologs are not paired in the canonical manner. Meiosis does not include meiotic recombination and synaptonemal complex formation in these males. Instead, an alternative homolog conjunction system keeps homologous chromosomes in pairs. Using independent strategies for spermatocyte-specific depletion of separase complex subunits in combination with time-lapse imaging, we demonstrate that separase is required for the inactivation of this alternative conjunction at anaphase I onset. Mutations that abolish alternative homolog conjunction therefore result in random segregation of univalents during meiosis I also after separase depletion. Interestingly, these univalents become bioriented during meiosis II, suggesting that <span class="hlt">sister</span> centromere individualization before meiosis II does not require separase.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=38455&Lab=NHEERL&keyword=bone&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=38455&Lab=NHEERL&keyword=bone&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span>CYTOGENETIC ANALYSES OF MICE EXPOSED TO DICHLOROMETHANE</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>Chromosome damage was studied in female B6C3F1 mice exposed to dichloromethane (DCM) by subcutaneous or inhalation treatments. o increase in either the frequencies of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) or chromosome <span class="hlt">aberrations</span> (CAs) in bone marrow cells was observed after a singl...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040112536&hterms=Furusawa&qs=N%3D0%26Ntk%3DAuthor-Name%26Ntx%3Dmode%2Bmatchall%26Ntt%3DFurusawa%252C%2BM','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040112536&hterms=Furusawa&qs=N%3D0%26Ntk%3DAuthor-Name%26Ntx%3Dmode%2Bmatchall%26Ntt%3DFurusawa%252C%2BM"><span>Dose--response of initial G2-<span class="hlt">chromatid</span> breaks induced in normal human fibroblasts by heavy ions</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Kawata, T.; Durante, M.; Furusawa, Y.; George, K.; Takai, N.; Wu, H.; Cucinotta, F. A.; Dicello, J. F. (Principal Investigator)</p> <p>2001-01-01</p> <p>PURPOSE: To investigate initial <span class="hlt">chromatid</span> breaks in prematurely condensed G2 chromosomes following exposure to heavy ions of different LET. MATERIAL AND METHODS: Exponentially growing human fibroblast cells AG1522 were irradiated with gamma-rays, energetic carbon (13 keV/ microm, 80 keV/microm), silicon (55 keV/microm) and iron (140 keV/microm, 185keV/microm, 440keV/microm) ions. Chromosomes were prematurely condensed using calyculin-A. Initial <span class="hlt">chromatid</span>-type and isochromatid breaks in G2 cells were scored. RESULTS: The dose response curves for total <span class="hlt">chromatid</span> breaks were linear regardless of radiation type. The relative biological effectiveness (RBE) showed a LET-dependent increase, peaking around 2.7 at 55-80keV/microm and decreasing at higher LET. The dose response curves for isochromatid-type breaks were linear for high-LET radiations, but linear-quadratic for gamma-rays and 13 keV/microm carbon ions. The RBE for the induction of isochromatid breaks obtained from linear components increased rapidly between 13keV/microm (about 7) and 80keV/microm carbon (about 71), and decreased gradually until 440 keV/microm iron ions (about 66). CONCLUSIONS: High-LET radiations are more effective at inducing isochromatid breaks, while low-LET radiations are more effective at inducing <span class="hlt">chromatid</span>-type breaks. The densely ionizing track structures of heavy ions and the proximity of <span class="hlt">sister</span> <span class="hlt">chromatids</span> in G2 cells result in an increase in isochromatid breaks.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7168826','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7168826"><span>Cyclophosphamide induced in vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) in Mus musculus. I: Strain differences and empirical association with relative chromosome size.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Reimer, D L; Singh, S M</p> <p>1982-01-01</p> <p>The inducibility of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) by cyclophosphamide (CP) in bone marrow cells was evaluated in vivo in the three genetic strains of mice (C3H/s, C57BL/6J, and Balb/c). Female mice (10 to 12 wks old, mean = 22.9g, SD = 3.2g) were administered with nine hourly injections of 214.19 mg/kg 5-Bromo-2' deoxyuridine (BrdU) followed by 0, 0.048, 0.449, 4.585 or 46.93 mg/kg CP and 4 mg/kg colcemid. SCEs were evaluated following differential staining procedures of Perry and Wolff (1974). The base-line SCEs were similar in all strains with about ten SCEs/cell. Increasing CP concentrations yielded an increased level of SCEs. Most cells showed extensive damage in CP doses exceeding 4.55 mg/kg. No SCE evaluation was possible beyond this concentration. Strain differences were evident at every dose of CP, and Balb/c was the least susceptible strain to SCE induction. F1 hybrids involving C3H/s female and Balb/c male showed SCE values closer to Balb/c. Data on the association between chromosome length and frequency of SCEs are provided. They empirically establish a positive correlation (r = 0.90) between the two features. Most induced SCEs were interstitially located rather than terminally positioned on the chromosome.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2224871','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2224871"><span>The Rejoining Time of <span class="hlt">Chromatid</span> Breaks Induced by Gamma Radiation in Vicia faba Root Tips at 3 °C</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Savage, J. R. K.; Neary, G. J.; Evans, H. J.</p> <p>1960-01-01</p> <p>The observation was made previously that the reduction in radiosensitivity in Vicia faba (as measured by postirradiation root growth) by prolonging the exposure time from about 10 minutes to 24 hours is much less marked at 3°C. than at 19°C. If chromosome damage is mainly responsible for the reduced root growth, this observation might be explained by a smaller drop in the "two-hit" <span class="hlt">aberration</span> component, resulting from an increased time for which breaks are available for rejoining at 3°C. This hypothesis was tested by comparing <span class="hlt">chromatid</span> <span class="hlt">aberration</span> frequencies in root meristem cells produced by 105 rads of 60Co γ rays, given at dose rates of 19.4 and 0.073 rads per minute. Beans were maintained in aerated water at 2°C. prior to and during irradiation, and at this temperature the rate of development of cells was such that the two different exposure times both occupied a period during which the cell sensitivity was approximately constant. Immediately subsequent to irradiation, the roots were returned to 19°C. and examined cytologically. All <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> were less frequent after low dose rate treatment, but only the <span class="hlt">chromatid</span> interchange reduction was significant. The average time for which breaks are available for reunion, calculated from Lea's G function, was found to be 12 hours (95 per cent C.L. 6 to 24 hours). PMID:14442001</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4847790','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4847790"><span>Separase Is Required for Homolog and <span class="hlt">Sister</span> Disjunction during Drosophila melanogaster Male Meiosis, but Not for Biorientation of <span class="hlt">Sister</span> Centromeres</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Blattner, Ariane C.; McKee, Bruce D.; Lehner, Christian F.</p> <p>2016-01-01</p> <p>Spatially controlled release of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion during progression through the meiotic divisions is of paramount importance for error-free chromosome segregation during meiosis. Cohesion is mediated by the cohesin protein complex and cleavage of one of its subunits by the endoprotease separase removes cohesin first from chromosome arms during exit from meiosis I and later from the pericentromeric region during exit from meiosis II. At the onset of the meiotic divisions, cohesin has also been proposed to be present within the centromeric region for the unification of <span class="hlt">sister</span> centromeres into a single functional entity, allowing bipolar orientation of paired homologs within the meiosis I spindle. Separase-mediated removal of centromeric cohesin during exit from meiosis I might explain <span class="hlt">sister</span> centromere individualization which is essential for subsequent biorientation of <span class="hlt">sister</span> centromeres during meiosis II. To characterize a potential involvement of separase in <span class="hlt">sister</span> centromere individualization before meiosis II, we have studied meiosis in Drosophila melanogaster males where homologs are not paired in the canonical manner. Meiosis does not include meiotic recombination and synaptonemal complex formation in these males. Instead, an alternative homolog conjunction system keeps homologous chromosomes in pairs. Using independent strategies for spermatocyte-specific depletion of separase complex subunits in combination with time-lapse imaging, we demonstrate that separase is required for the inactivation of this alternative conjunction at anaphase I onset. Mutations that abolish alternative homolog conjunction therefore result in random segregation of univalents during meiosis I also after separase depletion. Interestingly, these univalents become bioriented during meiosis II, suggesting that <span class="hlt">sister</span> centromere individualization before meiosis II does not require separase. PMID:27120695</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5120376-induction-sister-chromatid-exchange-preimplantation-mouse-embryos-vitro-sup-thymidine-ultraviolet-light-combination-caffeine','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5120376-induction-sister-chromatid-exchange-preimplantation-mouse-embryos-vitro-sup-thymidine-ultraviolet-light-combination-caffeine"><span>Induction of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in preimplantation mouse embryos in vitro by /sup 3/H-thymidine or ultraviolet light in combination with caffeine</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Mueller, W.U.S.; Spindle, A.</p> <p>1986-01-01</p> <p>Preimplantation mouse embryos were exposed in vitro to /sup 3/H-thymidine (25, 100, or 250 Bq/ml) or ultraviolet (UV) light (1.35 or 4.05 J/m2), either alone or in combination with caffeine (1 mM with /sup 3/H-thymidine and 0.5 mM with UV light). Exposure to /sup 3/H-thymidine lasted for 2 days, from the two-cell stage to the late morula/early blastocyst stage, and UV radiation was applied acutely at the late morula/early blastocyst stage. The effects were quantified by the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) assay. All three agents induced SCEs when used singly. /sup 3/H-thymidine was effective in inducing SCEs only at 250more » Bq/ml, whereas UV light was effective at both fluences. Although caffeine did not induce SCEs when it was added before exposure to bromodeoxyuridine (BrdUrd), which is used to visualize SCEs, it did induce SCEs when present during the entire culture period (/sup 3/H-thymidine experiments) or during incubation in BrdUrd (UV experiments). Caffeine markedly enhanced the SCE-inducing effect of UV light but did not influence the effect of /sup 3/H-thymidine.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.dtic.mil/docs/citations/ADA202780','DTIC-ST'); return false;" href="http://www.dtic.mil/docs/citations/ADA202780"><span>Effects of Simultaneous Radiofrequency Radiation and Chemical Exposure of Mammalian Cells. Volume 2</span></a></p> <p><a target="_blank" href="http://www.dtic.mil/">DTIC Science & Technology</a></p> <p></p> <p>1988-07-01</p> <p>chromosome - - - - - - -I <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE). Yao (1982) exposed rat kangaroo RH5 and RH1l6 cells to 2.45 GHz radiation, and...control was reported in chromosome <span class="hlt">aberrations</span>. Yac (1982) investigated the cytogenetic consequences of chronic microwave exposure on rat kangaroo RH5...was said to be 280C. The cells were exposed both as conidia, which are "rather inactive metabolically ," and also after DNA replication had been</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11287309','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11287309"><span>Genotoxic effects of styrene-7,8-oxide in human white blood cells: comet assay in relation to the induction of <span class="hlt">sister-chromatid</span> exchanges and micronuclei.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Laffon, B; Pásaro, E; Méndez, J</p> <p>2001-04-05</p> <p>Styrene is used in the production of plastics, resins and rubber. The highest human exposures to styrene take place by inhalation during the production of fiberglass reinforced plastics. Styrene is metabolized mainly in the liver to styrene-7,8-oxide (SO), its principal in vivo mutagenic metabolite. In this study, human peripheral white blood cells were exposed to several SO concentrations (10-200 microM) in order to evaluate its genotoxic properties by means of comet assay, <span class="hlt">sister-chromatid</span> exchanges (SCE) and cytokinesis-blocked micronucleus (MN) test, in addition to determine its clastogenic or aneugenic properties by combining MN with fluorescence in situ hybridization (FISH) procedures. Our results show that SO induces DNA damage, SCE and MN in human leukocytes in vitro at concentrations above 50 microM, and that there is a strong relationship between DNA damage, as measured by the comet assay, and cytogenetic damage induced by SO at the doses employed. SO shows preferentially a clastogenic activity and produces a cytostatic effect at high doses, reflected by the significant decrease of the calculated proliferation indices. A good dose-effect relationship is obtained in the three tests performed at the concentration range assayed.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2811031','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2811031"><span>Yeast cohesin complex embraces 2 micron plasmid <span class="hlt">sisters</span> in a tri-linked catenane complex</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ghosh, Santanu K.; Huang, Chu-Chun; Hajra, Sujata; Jayaram, Makkuni</p> <p>2010-01-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion, crucial for faithful segregation of replicated chromosomes in eukaryotes, is mediated by the multi-subunit protein complex cohesin. The Saccharomyces cerevisiae plasmid 2 micron circle mimics chromosomes in assembling cohesin at its partitioning locus. The plasmid is a multi-copy selfish DNA element that resides in the nucleus and propagates itself stably, presumably with assistance from cohesin. In metaphase cell lysates, or fractions enriched for their cohesed state by sedimentation, plasmid molecules are trapped topologically by the protein ring formed by cohesin. They can be released from cohesin’s embrace either by linearizing the DNA or by cleaving a cohesin subunit. Assays using two distinctly tagged cohesin molecules argue against the hand-cuff (an associated pair of monomeric cohesin rings) or the bracelet (a dimeric cohesin ring) model as responsible for establishing plasmid cohesion. Our cumulative results most easily fit a model in which a single monomeric cohesin ring, rather than a series of such rings, conjoins a pair of <span class="hlt">sister</span> plasmids. These features of plasmid cohesion account for its <span class="hlt">sister-to-sister</span> mode of segregation by cohesin disassembly during anaphase. The mechanistic similarities of cohesion between mini-chromosome <span class="hlt">sisters</span> and 2 micron plasmid <span class="hlt">sisters</span> suggest a potential kinship between the plasmid partitioning locus and centromeres. PMID:19920123</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=134466','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=134466"><span><span class="hlt">Aberrant</span> meiotic behavior in Agave tequilana Weber var. azul</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ruvalcaba-Ruiz, Domingo; Rodríguez-Garay, Benjamin</p> <p>2002-01-01</p> <p>Background Agave tequilana Weber var. azul, is the only one variety permitted by federal law in México to be used for tequila production which is the most popular contemporary alcoholic beverage made from agave and recognized worldwide. Despite the economic, genetic, and ornamental value of the plant, it has not been subjected to detailed cytogenetic research, which could lead to a better understanding of its reproduction for future genetic improvement. The objective of this work was to study the meiotic behavior in pollen mother cells and its implications on the pollen viability in Agave tequilana Weber var. azul. Results The analysis of Pollen Mother Cells in anaphase I (A-I) showed 82.56% of cells with a normal anaphase and, 17.44% with an irregular anaphase. In which 5.28% corresponded to cells with side arm bridges (SAB); 3.68% cells with one bridge and one fragment; 2.58% of irregular anaphase showed cells with one or two lagging chromosomes and 2.95% showed one acentric fragment; cells with two bridges and cells with two bridges and one acentric fragment were observed in frequencies of 1.60% and 1.35% respectively. In anaphase II some cells showed bridges and fragments too. <span class="hlt">Aberrant</span> A-I cells had many shrunken or empty pollen grains (42.00%) and 58.00 % viable pollen. Conclusion The observed meiotic irregularities suggest that structural chromosome <span class="hlt">aberrations</span> have occurred, such as heterozygous inversions, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, deletions and duplications which in turn are reflected in a low pollen viability. PMID:12396234</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12396234','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12396234"><span><span class="hlt">Aberrant</span> meiotic behavior in Agave tequilana Weber var. azul.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ruvalcaba-Ruiz, Domingo; Rodríguez-Garay, Benjamin</p> <p>2002-10-23</p> <p>Agave tequilana Weber var. azul, is the only one variety permitted by federal law in México to be used for tequila production which is the most popular contemporary alcoholic beverage made from agave and recognized worldwide. Despite the economic, genetic, and ornamental value of the plant, it has not been subjected to detailed cytogenetic research, which could lead to a better understanding of its reproduction for future genetic improvement. The objective of this work was to study the meiotic behavior in pollen mother cells and its implications on the pollen viability in Agave tequilana Weber var. azul. The analysis of Pollen Mother Cells in anaphase I (A-I) showed 82.56% of cells with a normal anaphase and, 17.44% with an irregular anaphase. In which 5.28% corresponded to cells with side arm bridges (SAB); 3.68% cells with one bridge and one fragment; 2.58% of irregular anaphase showed cells with one or two lagging chromosomes and 2.95% showed one acentric fragment; cells with two bridges and cells with two bridges and one acentric fragment were observed in frequencies of 1.60% and 1.35% respectively. In anaphase II some cells showed bridges and fragments too. <span class="hlt">Aberrant</span> A-I cells had many shrunken or empty pollen grains (42.00%) and 58.00 % viable pollen. The observed meiotic irregularities suggest that structural chromosome <span class="hlt">aberrations</span> have occurred, such as heterozygous inversions, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, deletions and duplications which in turn are reflected in a low pollen viability.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4183305','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4183305"><span>Absence of SUN-domain protein Slp1 blocks karyogamy and switches meiotic recombination and synapsis from homologs to <span class="hlt">sister</span> <span class="hlt">chromatids</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Vasnier, Christelle; de Muyt, Arnaud; Zhang, Liangran; Tessé, Sophie; Kleckner, Nancy E.; Zickler, Denise; Espagne, Eric</p> <p>2014-01-01</p> <p>Karyogamy, the process of nuclear fusion is required for two haploid gamete nuclei to form a zygote. Also, in haplobiontic organisms, karyogamy is required to produce the diploid nucleus/cell that then enters meiosis. We identify sun like protein 1 (Slp1), member of the mid–Sad1p, UNC-84–domain ubiquitous family, as essential for karyogamy in the filamentous fungus Sordaria macrospora, thus uncovering a new function for this protein family. Slp1 is required at the last step, nuclear fusion, not for earlier events including nuclear movements, recognition, and juxtaposition. Correspondingly, like other family members, Slp1 localizes to the endoplasmic reticulum and also to its extensions comprising the nuclear envelope. Remarkably, despite the absence of nuclear fusion in the slp1 null mutant, meiosis proceeds efficiently in the two haploid “twin” nuclei, by the same program and timing as in diploid nuclei with a single dramatic exception: the normal prophase program of recombination and synapsis between homologous chromosomes, including loading of recombination and synaptonemal complex proteins, occurs instead between <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Moreover, the numbers of recombination-initiating double-strand breaks (DSBs) and ensuing recombinational interactions, including foci of the essential crossover factor Homo sapiens enhancer of invasion 10 (Hei10), occur at half the diploid level in each haploid nucleus, implying per-chromosome specification of DSB formation. Further, the distribution of Hei10 foci shows interference like in diploid meiosis. Centromere and spindle dynamics, however, still occur in the diploid mode during the two meiotic divisions. These observations imply that the prophase program senses absence of karyogamy and/or absence of a homolog partner and adjusts the interchromosomal interaction program accordingly. PMID:25210014</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4041417','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4041417"><span>Histone H3 K79 methylation states play distinct roles in UV-induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and cell cycle checkpoint arrest in Saccharomyces cerevisiae</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Rossodivita, Alyssa A.; Boudoures, Anna L.; Mecoli, Jonathan P.; Steenkiste, Elizabeth M.; Karl, Andrea L.; Vines, Eudora M.; Cole, Arron M.; Ansbro, Megan R.; Thompson, Jeffrey S.</p> <p>2014-01-01</p> <p>Histone post-translational modifications have been shown to contribute to DNA damage repair. Prior studies have suggested that specific H3K79 methylation states play distinct roles in the response to UV-induced DNA damage. To evaluate these observations, we examined the effect of altered H3K79 methylation patterns on UV-induced G1/S checkpoint response and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE). We found that the di- and trimethylated states both contribute to activation of the G1/S checkpoint to varying degrees, depending on the synchronization method, although methylation is not required for checkpoint in response to high levels of UV damage. In contrast, UV-induced SCE is largely a product of the trimethylated state, which influences the usage of gene conversion versus popout mechanisms. Regulation of H3K79 methylation by H2BK123 ubiquitylation is important for both checkpoint function and SCE. H3K79 methylation is not required for the repair of double-stranded breaks caused by transient HO endonuclease expression, but does play a modest role in survival from continuous exposure. The overall results provide evidence for the participation of H3K79 methylation in UV-induced recombination repair and checkpoint activation, and further indicate that the di- and trimethylation states play distinct roles in these DNA damage response pathways. PMID:24748660</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/2687630','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/2687630"><span>Induction of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and cell division delays in human lymphocytes by the anti-tumour agent homo-aza-steroidal ester of p-bis(2-chloroethyl)aminophenoxy acetic acid.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Tselepi, M R; Demopoulos, N A; Catsoulacos, P</p> <p>1989-09-01</p> <p>3 beta-Hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstan-17-oic-13,17-lactam-p-bis(2-chloroethyl) aminophenoxyacetate (NSC 294859) is a new modified steroidal alkylating agent. This compound was given by i.p. administration to mice bearing different types of tumour. It was found to exhibit good activity in L1210 and P388 leukaemias with maintenance of activity against advanced tumours. The treatment of colon 26 tumour and B16 melanoma resulted in positive antineoplastic activity. The drug was not shown to be active in a melphalan-resistant P388 line. In this study, NSC 294859 was found to be effective in causing statistically significant increases in <span class="hlt">sister-chromatid</span> exchange (SCE) rates and cell division delays. The alkylating agent component, p-bis-(2-chloroethyl)aminophenoxy acetic acid, was shown to be less effective than the parent compound, while the modified steroid component, 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstan-17-oic-13,17-lactam, showed no effect. There were no statistically significant differences among donors regarding the induction of SCEs and replication indices (RIs) for the compounds tested.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20120016379','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20120016379"><span>Detection of chromosomal inversions using non-repetitive nucleic acid probes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Bedford, Joel S. (Inventor); Cornforth, Michael N. (Inventor); Bailey, Susan M. (Inventor); Ray, F. Andrew (Inventor); Goodwin, Edwin H. (Inventor)</p> <p>2012-01-01</p> <p>A method for the identification of chromosomal inversions is described. Single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span> are generated, for example by CO-FISH. A plurality of non-repetitive, labeled probes of relatively small size are hybridized to portions of only one of a pair of single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span>. If no inversion exists, all of the probes will hybridize to a first <span class="hlt">chromatid</span>. If an inversion has occurred, these marker probes will be detected on the <span class="hlt">sister</span> <span class="hlt">chromatid</span> at the same location as the inversion on the first <span class="hlt">chromatid</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20150003185','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20150003185"><span>Detection of Chromosomal Inversions Using Non-Repetitive Nucleic Acid Probes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ray, F. Andrew (Inventor); Goodwin, Edwin H. (Inventor); Bedford, Joel S. (Inventor); Cornforth, Michael N. (Inventor); Bailey, Susan M. (Inventor)</p> <p>2014-01-01</p> <p>A method and a kit for the identification of chromosomal inversions are described. Single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span> are generated, for example by CO-FISH. A plurality of non-repetitive, labeled probes of relatively small size are hybridized to portions of only one of a pair of single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span>. If no inversion exists, all of the probes will hybridize to a first <span class="hlt">chromatid</span>. If an inversion has occurred, these marker probes will be detected on the <span class="hlt">sister</span> <span class="hlt">chromatid</span> at the same location as the inversion on the first <span class="hlt">chromatid</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23970416','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23970416"><span>DNA asymmetry in stem cells - immortal or mortal?</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yadlapalli, Swathi; Yamashita, Yukiko M</p> <p>2013-09-15</p> <p>The immortal strand hypothesis proposes that stem cells retain a template copy of genomic DNA (i.e. an 'immortal strand') to avoid replication-induced mutations. An alternative hypothesis suggests that certain cells segregate <span class="hlt">sister</span> <span class="hlt">chromatids</span> non-randomly to transmit distinct epigenetic information. However, this area of research has been highly controversial, with conflicting data even from the same cell types. Moreover, historically, the same term of 'non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation' or 'biased <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation' has been used to indicate distinct biological processes, generating a confusion in the biological significance and potential mechanism of each phenomenon. Here, we discuss the models of non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation, and we explore the strengths and limitations of the various techniques and experimental model systems used to study this question. We also describe our recent study on Drosophila male germline stem cells, where <span class="hlt">sister</span> <span class="hlt">chromatids</span> of X and Y chromosomes are segregated non-randomly during cell division. We aim to integrate the existing evidence to speculate on the underlying mechanisms and biological relevance of this long-standing observation on non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15162016','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15162016"><span>Progress towards understanding the nature of <span class="hlt">chromatid</span> breakage.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bryant, P E; Gray, L J; Peresse, N</p> <p>2004-01-01</p> <p>The wide range of sensitivities of stimulated T-cells from different individuals to radiation-induced <span class="hlt">chromatid</span> breakage indicates the involvement of several low penetrance genes that appear to link elevated <span class="hlt">chromatid</span> breakage to cancer susceptibility. The mechanisms of <span class="hlt">chromatid</span> breakage are not yet fully understood. However, evidence is accumulating that suggests <span class="hlt">chromatid</span> breaks are not simply expanded DNA double-strand breaks (DSB). Three models of <span class="hlt">chromatid</span> breakage are considered. The classical breakage-first and the Revell "exchange" models do not accord with current evidence. Therefore a derivative of Revell's model has been proposed whereby both spontaneous and radiation-induced <span class="hlt">chromatid</span> breaks result from DSB signaling and rearrangement processes from within large looped chromatin domains. Examples of such rearrangements can be observed by harlequin staining whereby an exchange of strands occurs immediately adjacent to the break site. However, these interchromatid rearrangements comprise less than 20% of the total breaks. The rest are thought to result from intrachromatid rearrangements, including a very small proportion involving complete excision of a looped domain. Work is in progress with the aim of revealing these rearrangements, which may involve the formation of inversions adjacent to the break sites. It is postulated that the disappearance of <span class="hlt">chromatid</span> breaks with time results from the completion of such rearrangements, rather than from the rejoining of DSB. Elevated frequencies of <span class="hlt">chromatid</span> breaks occur in irradiated cells with defects in both nonhomologous end-joining (NHEJ) and homologous recombination (HR) pathways, however there is little evidence of a correlation between reduced DSB rejoining and disappearance of <span class="hlt">chromatid</span> breaks. Moreover, at least one treatment which abrogates the disappearance of <span class="hlt">chromatid</span> breaks with time leaves DSB rejoining unaffected. The I-SceI DSB system holds considerable promise for the elucidation of these</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_3");'>3</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li class="active"><span>5</span></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_5 --> <div id="page_6" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li class="active"><span>6</span></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="101"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21543101','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21543101"><span>Influence of GSTM1 and GSTT1 genotypes and confounding factors on the frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and micronucleus among road construction workers.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kumar, Anil; Yadav, Anita; Giri, Shiv Kumar; Dev, Kapil; Gautam, Sanjeev Kumar; Gupta, Ranjan; Aggarwal, Neeraj</p> <p>2011-07-01</p> <p>In the present study, we have investigated the influence of polymorphism of GSTM1 and GSTT1 genes and confounding factors such as age, sex, exposure duration and consumption habits on cytogenetic biomarkers. Frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs), high frequency cell (HFC) and cytokinesis blocked micronuclei (CBMN) were evaluated in peripheral blood lymphocytes of 115 occupationally exposed road construction workers and 105 unexposed individuals. The distribution of null and positive genotypes of glutathione-S transferase gene was evaluated by multiplex PCR among control and exposed subjects. An increased frequency of CBMN (7.03±2.08); SCE (6.95±1.76) and HFC (6.28±1.69) were found in exposed subjects when compared to referent (CBMN - 3.35±1.10; SCE - 4.13±1.30 and HFC - 3.98±1.56). These results were found statistically significant at p<0.05. When the effect of confounding factors on the frequency of studied biomarkers was evaluated, a strong positive interaction was found. The individuals having GSTM1 and GSTT1 null genotypes had higher frequency of CBMN, SCE and HFC. The association between GSTM1 and GSTT1 genotypes and studied biomarkers was found statistically significant at p<0.05. Our findings suggest that individuals having null type of GST are more susceptible to cytogenetic damage by occupational exposure regardless of confounding factors. There is a significant effect of polymorphism of these genes on cytogenetic biomarkers which are considered as early effects of genotoxic carcinogens. Copyright © 2011 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/1427859-structural-evidence-scc4-dependent-localization-cohesin-loading','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/1427859-structural-evidence-scc4-dependent-localization-cohesin-loading"><span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Hinshaw, Stephen M.; Makrantoni, Vasso; Kerr, Alastair</p> <p></p> <p>The cohesin ring holds newly replicated <span class="hlt">sister</span> <span class="hlt">chromatids</span> together until their separation at anaphase. Initiation of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion depends on a separate complex, Scc2NIPBL/Scc4Mau2 (Scc2/4), which loads cohesin onto DNA and determines its localization across the genome. Proper cohesin loading is essential for cell division, and partial defects cause chromosome missegregation and <span class="hlt">aberrant</span> transcriptional regulation, leading to severe developmental defects in multicellular organisms. We present here a crystal structure showing the interaction between Scc2 and Scc4. Scc4 is a TPR array that envelops an extended Scc2 peptide. Using budding yeast, we demonstrate that a conserved patch on the surfacemore » of Scc4 is required to recruit Scc2/4 to centromeres and to build pericentromeric cohesion. These findings reveal the role of Scc4 in determining the localization of cohesin loading and establish a molecular basis for Scc2/4 recruitment to centromeres.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2013AdSpR..51..450H','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2013AdSpR..51..450H"><span>No significant level of inheritable interchromosomal <span class="hlt">aberrations</span> in the progeny of bystander primary human fibroblasts after alpha particle irradiation</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Hu, Burong; Zhu, Jiayun; Zhou, Hongning; Hei, Tom K.</p> <p>2013-02-01</p> <p>A major concern for bystander effects is the probability that normal healthy cells adjacent to the irradiated cells become genomically unstable and undergo further carcinogenesis after therapeutic irradiation or space mission where astronauts are exposed to low dose of heavy ions. Genomic instability is a hallmark of cancer cells. In the present study, two irradiation protocols were performed in order to ensure pure populations of bystander cells and the genomic instability in their progeny were investigated. After irradiation, chromosomal <span class="hlt">aberrations</span> of cells were analyzed at designated time points using G2 phase premature chromosome condensation (G2-PCC) coupled with Giemsa staining and with multiplex fluorescent in situ hybridization (mFISH). Our Giemsa staining assay demonstrated that elevated yields of <span class="hlt">chromatid</span> breaks were induced in the progeny of pure bystander primary fibroblasts up to 20 days after irradiation. mFISH assay showed no significant level of inheritable interchromosomal <span class="hlt">aberrations</span> were induced in the progeny of the bystander cell groups, while the fractions of gross <span class="hlt">aberrations</span> (<span class="hlt">chromatid</span> breaks or chromosomal breaks) significantly increased in some bystander cell groups. These results suggest that genomic instability occurred in the progeny of the irradiation associated bystander normal fibroblasts exclude the inheritable interchromosomal <span class="hlt">aberration</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23503090','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23503090"><span>No significant level of inheritable interchromosomal <span class="hlt">aberrations</span> in the progeny of bystander primary human fibroblast after alpha particle irradiation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hu, Burong; Zhu, Jiayun; Zhou, Hongning; Hei, Tom K</p> <p>2013-02-01</p> <p>A major concern for bystander effects is the probability that normal healthy cells adjacent to the irradiated cells become genomically unstable and undergo further carcinogenesis after therapeutic irradiation or space mission where astronauts are exposed to low dose of heavy ions. Genomic instability is a hallmark of cancer cells. In the present study, two irradiation protocols were performed in order to ensure pure populations of bystander cells and the genomic instability in their progeny were investigated. After irradiation, chromosomal <span class="hlt">aberrations</span> of cells were analyzed at designated time points using G 2 phase premature chromosome condensation (G 2 -PCC) coupled with Giemsa staining and with multiplex fluorescent in situ hybridization (mFISH). Our Giemsa staining assay demonstrated that elevated yields of <span class="hlt">chromatid</span> breaks were induced in the progeny of pure bystander primary fibroblasts up to 20 days after irradiation. MFISH assay showed no significant level of inheritable interchromosomal <span class="hlt">aberrations</span> were induced in the progeny of the bystander cell groups, while the fractions of gross <span class="hlt">aberrations</span> (<span class="hlt">chromatid</span> breaks or chromosomal breaks) significantly increased in some bystander cell groups. These results suggest that genomic instability occurred in the progeny of the irradiation associated bystander normal fibroblasts exclude the inheritable interchromosomal <span class="hlt">aberration</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3772383','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3772383"><span>DNA asymmetry in stem cells – immortal or mortal?</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Yadlapalli, Swathi; Yamashita, Yukiko M.</p> <p>2013-01-01</p> <p>Summary The immortal strand hypothesis proposes that stem cells retain a template copy of genomic DNA (i.e. an ‘immortal strand’) to avoid replication-induced mutations. An alternative hypothesis suggests that certain cells segregate <span class="hlt">sister</span> <span class="hlt">chromatids</span> non-randomly to transmit distinct epigenetic information. However, this area of research has been highly controversial, with conflicting data even from the same cell types. Moreover, historically, the same term of ‘non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation’ or ‘biased <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation’ has been used to indicate distinct biological processes, generating a confusion in the biological significance and potential mechanism of each phenomenon. Here, we discuss the models of non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation, and we explore the strengths and limitations of the various techniques and experimental model systems used to study this question. We also describe our recent study on Drosophila male germline stem cells, where <span class="hlt">sister</span> <span class="hlt">chromatids</span> of X and Y chromosomes are segregated non-randomly during cell division. We aim to integrate the existing evidence to speculate on the underlying mechanisms and biological relevance of this long-standing observation on non-random <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation. PMID:23970416</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20150014994','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20150014994"><span>Characterization of Chromosomal Inversions Using Anti-Parallel Probes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ray, F. Andrew (Inventor)</p> <p>2015-01-01</p> <p>A method for the characterization of chromosomal inversions using anti-parallel probes is described. Reporter species are attached to oligonucleotide strands designed such that they may hybridize to portions of only one of a pair of single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span> which may be prepared by the CO-FISH procedure. If an inversion has occurred, these marker probes will be detected on the second <span class="hlt">sister</span> <span class="hlt">chromatid</span> at the same location as the inversion on the first <span class="hlt">chromatid</span>. Further, one or more reporter species are replaced with anti-parallel probes that hybridize at known locations along the second <span class="hlt">sister</span> <span class="hlt">chromatid</span> such that the position and size of the inversion may be identified/estimated.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3469440','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3469440"><span>Meiosis in male Drosophila</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>McKee, Bruce D.; Yan, Rihui; Tsai, Jui-He</p> <p>2012-01-01</p> <p>Meiosis entails sorting and separating both homologous and <span class="hlt">sister</span> <span class="hlt">chromatids</span>. The mechanisms for connecting <span class="hlt">sister</span> <span class="hlt">chromatids</span> and homologs during meiosis are highly conserved and include specialized forms of the cohesin complex and a tightly regulated homolog synapsis/recombination pathway designed to yield regular crossovers between homologous <span class="hlt">chromatids</span>. Drosophila male meiosis is of special interest because it dispenses with large segments of the standard meiotic script, particularly recombination, synapsis and the associated structures. Instead, Drosophila relies on a unique protein complex composed of at least two novel proteins, SNM and MNM, to provide stable connections between homologs during meiosis I. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion in Drosophila is mediated by cohesins, ring-shaped complexes that entrap <span class="hlt">sister</span> <span class="hlt">chromatids</span>. However, unlike other eukaryotes Drosophila does not rely on the highly conserved Rec8 cohesin in meiosis, but instead utilizes two novel cohesion proteins, ORD and SOLO, which interact with the SMC1/3 cohesin components in providing meiotic cohesion. PMID:23087836</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20142422','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20142422"><span>SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yan, Rihui; Thomas, Sharon E; Tsai, Jui-He; Yamada, Yukihiro; McKee, Bruce D</p> <p>2010-02-08</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion is essential to maintain stable connections between homologues and <span class="hlt">sister</span> <span class="hlt">chromatids</span> during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, <span class="hlt">sisters</span> on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, <span class="hlt">sister</span> centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion in Drosophila meiosis.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28060322','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28060322"><span>Analysis of the Ambient Particulate Matter-induced Chromosomal <span class="hlt">Aberrations</span> Using an In Vitro System.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Miousse, Isabelle R; Koturbash, Igor; Chalbot, Marie-Cécile; Hauer-Jensen, Martin; Kavouras, Ilias; Pathak, Rupak</p> <p>2016-12-21</p> <p>Exposure to particulate matter (PM) is a major world health concern, which may damage various cellular components, including the nuclear genetic material. To assess the impact of PM on nuclear genetic integrity, structural chromosomal <span class="hlt">aberrations</span> are scored in the metaphase spreads of mouse RAW264.7 macrophage cells. PM is collected from ambient air with a high volume total suspended particles sampler. The collected material is solubilized and filtered to retain the water-soluble, fine portion. The particles are characterized for chemical composition by nuclear magnetic resonance (NMR) spectroscopy. Different concentrations of particle suspension are added onto an in vitro culture of RAW264.7 mouse macrophages for a total exposure time of 72 hr, along with untreated control cells. At the end of exposure, the culture is treated with colcemid to arrest cells in metaphase. Cells are then harvested, treated with hypotonic solution, fixed in acetomethanol, dropped onto glass slides and finally stained with Giemsa solution. Slides are examined to assess the structural chromosomal <span class="hlt">aberrations</span> (CAs) in metaphase spreads at 1,000X magnification using a bright-field microscope. 50 to 100 metaphase spread are scored for each treatment group. This technique is adapted for the detection of structural chromosomal <span class="hlt">aberrations</span> (CAs), such as <span class="hlt">chromatid</span>-type breaks, <span class="hlt">chromatid</span>-type exchanges, acentric fragments, dicentric and ring chromosomes, double minutes, endoreduplication, and Robertsonian translocations in vitro after exposure to PM. It is a powerful method to associate a well-established cytogenetic endpoint to epigenetic alterations.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23924178','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23924178"><span><span class="hlt">Sister-sister</span> incest: data from an anonymous computerized survey.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stroebel, Sandra S; O'Keefe, Stephen L; Griffee, Karen; Kuo, Shih-Ya; Beard, Keith W; Kommor, Martin J</p> <p>2013-01-01</p> <p>Retrospective data were entered anonymously by 1,521 adult women using a computer-assisted self-interview. Thirty-one participants were victims of <span class="hlt">sister-sister</span> incest, 40 were victims of brother-<span class="hlt">sister</span> incest, 19 were victims of father-daughter incest, 8 were victims of sexual abuse by an adult female (including one mother), and 232 were victims of sexual abuse by an adult male other than their father before reaching 18 years of age. The rest (1,203) served as controls. The victims of <span class="hlt">sister-sister</span> incest had significantly more problematic outcomes than controls on many measures as adults. Victims of <span class="hlt">sister-sister</span> incest were more depressed and more likely than controls to be distant from the perpetrator-<span class="hlt">sister</span> and to have traded sex for money, experienced an unplanned pregnancy, engaged in four different types of masturbation, and engaged in 13 different same-sex behaviors. Our findings were consistent with other reports of early eroticization and persistent hypereroticization of incest victims.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/10390512','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/10390512"><span>Induction and prevention of micronuclei and chromosomal <span class="hlt">aberrations</span> in cultured human lymphocytes exposed to the light of halogen tungsten lamps.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>D'Agostini, F; Caimo, A; De Filippi, S; De Flora, S</p> <p>1999-07-01</p> <p>Previous studies have shown that the light emitted by halogen tungsten lamps contains UV radiation in the UV-A, UV-B and UV-C regions, induces mutations and irreparable DNA damage in bacteria, enhances the frequency of micronuclei in cultured human lymphocytes and is potently carcinogenic to the skin of hairless mice. The present study showed that the light emitted by an uncovered, traditional halogen lamp induces a significant, dose-related and time-related increase not only in micronuclei but also in chromosome-type <span class="hlt">aberrations</span>, such as breaks, and even more in <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span>, such as isochromatid breaks, exchanges and isochromatid/<span class="hlt">chromatid</span> interchanges, all including gaps or not, in cultured human lymphocytes. All these genotoxic effects were completely prevented by shielding the same lamp with a silica glass cover, blocking UV radiation. A new model of halogen lamp, having the quartz bulb treated in order to reduce the output of UV radiation, was considerably less genotoxic than the uncovered halogen lamp, yet induction of chromosomal alterations was observed at high illuminance levels.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2734174','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2734174"><span>The Cellular Phenotype of Roberts Syndrome Fibroblasts as Revealed by Ectopic Expression of ESCO2</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>van der Lelij, Petra; van Gosliga, Djoke; Oostra, Anneke B.; Steltenpool, Jûrgen; de Groot, Jan; Scheper, Rik J.; Wolthuis, Rob M.; Waisfisz, Quinten; Darroudi, Firouz; Joenje, Hans; de Winter, Johan P.</p> <p>2009-01-01</p> <p>Cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> is essential for faithful chromosome segregation. In budding yeast, the acetyltransferase Eco1/Ctf7 establishes cohesion during DNA replication in S phase and in response to DNA double strand breaks in G2/M phase. In humans two Eco1 orthologs exist: ESCO1 and ESCO2. Both proteins are required for proper <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, but their exact function is unclear at present. Since ESCO2 has been identified as the gene defective in the rare autosomal recessive cohesinopathy Roberts syndrome (RBS), cells from RBS patients can be used to elucidate the role of ESCO2. We investigated for the first time RBS cells in comparison to isogenic controls that stably express V5- or GFP-tagged ESCO2. We show that the <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion defect in the transfected cell lines is rescued and suggest that ESCO2 is regulated by proteasomal degradation in a cell cycle-dependent manner. In comparison to the corrected cells RBS cells were hypersensitive to the DNA-damaging agents mitomycin C, camptothecin and etoposide, while no particular sensitivity to UV, ionizing radiation, hydroxyurea or aphidicolin was found. The cohesion defect of RBS cells and their hypersensitivity to DNA-damaging agents were not corrected by a patient-derived ESCO2 acetyltransferase mutant (W539G), indicating that the acetyltransferase activity of ESCO2 is essential for its function. In contrast to a previous study on cells from patients with Cornelia de Lange syndrome, another cohesinopathy, RBS cells failed to exhibit excessive chromosome <span class="hlt">aberrations</span> after irradiation in G2 phase of the cell cycle. Our results point at an S phase-specific role for ESCO2 in the maintenance of genome stability. PMID:19738907</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4190664','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4190664"><span>Chiasmatic and achiasmatic inverted meiosis of plants with holocentric chromosomes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Cabral, Gabriela; Marques, André; Schubert, Veit; Pedrosa-Harand, Andrea; Schlögelhofer, Peter</p> <p>2014-01-01</p> <p>Meiosis is a specialized cell division in sexually reproducing organisms before gamete formation. Following DNA replication, the canonical sequence in species with monocentric chromosomes is characterized by reductional segregation of homologous chromosomes during the first and equational segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> during the second meiotic division. Species with holocentric chromosomes employ specific adaptations to ensure regular disjunction during meiosis. Here we present the analysis of two closely related plant species with holocentric chromosomes that display an inversion of the canonical meiotic sequence, with the equational division preceding the reductional. In-depth analysis of the meiotic divisions of Rhynchospora pubera and R. tenuis reveals that during meiosis I <span class="hlt">sister</span> <span class="hlt">chromatids</span> are bi-oriented, display amphitelic attachment to the spindle and are subsequently separated. During prophase II, <span class="hlt">chromatids</span> are connected by thin chromatin threads that appear instrumental for the regular disjunction of homologous non-<span class="hlt">sister</span> <span class="hlt">chromatids</span> in meiosis II. PMID:25295686</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1469616','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1469616"><span>Cytogenetic Monitoring of Farmers exposed to pesticides in Colombia.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hoyos, L S; Carvajal, S; Solano, L; Rodriguez, J; Orozco, L; López, Y; Au, W W</p> <p>1996-01-01</p> <p>We have monitored 30 pesticide-exposed workers and 30 matched controls for expression of chromosome <span class="hlt">aberrations</span> (CA) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) in their lymphocytes. Peripheral blood cultures were set up within 3 hr after the collection of samples, and four cultures were set up from each donor. For CA analysis, 100 complete metaphase cells from each donor were evaluated. For the SCE assay, 50 complete metaphase cells from each donor were analyzed. The CA and SCE data were analyzed for differences between the two groups using the chi 2 and the Student's t-test, respectively. From the CA analysis it was obvious that the overwhelming majority of <span class="hlt">aberrations</span> were <span class="hlt">chromatid</span> breaks and isochromatid breaks; therefore, only these data are presented and used for statistical analysis. Isochromatid breaks were counted as two breaks each and <span class="hlt">chromatid</span> breaks as one in calculating the total <span class="hlt">chromatid</span> break frequencies. Statistical evaluation of the data indicates that there is no significant difference (p > 0.05; chi 2 test) between the exposed and the nonexposed groups based on <span class="hlt">chromatid</span> breaks per 100 cells (1.2 +/- 0.3 and 1.5 +/- 0.2, respectively) and total <span class="hlt">chromatid</span> breaks per 100 cells (1.7 +/- 0.3 and 2.1 +/- 0.2, respectively). No significantly difference between the two groups (p > 0.05, Student's t-test) was observed with SCE frequencies (5.0 +/- 1.1 and 4.8 +/- 0.9, respectively). Linear regression analysis indicates that the data were not influenced by age, cigarette smoking, or alcohol consumption. It is assuring that the exposure conditions among these Indian farmers have not caused detectable increases of chromosome damage using standard assays; this suggests the lack of serious long-term health problems. However, periodic monitoring of such exposed populations should be conducted using the same or other more sensitive assays. In addition, other populations with exposure to different types of pesticides in Colombia should also be investigated. PMID</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3791154','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3791154"><span>Strand-seq: a unifying tool for studies of chromosome segregation</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Falconer, Ester; Lansdorp, Peter M.</p> <p>2013-01-01</p> <p>Non random segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> has been implicated to help specify daughter cell fate (the Silent <span class="hlt">Sister</span> Hypothesis [1]) or to protect the genome of long-lived stem cells (the Immortal Strand Hypothesis [2]). The idea that <span class="hlt">sister</span> <span class="hlt">chromatids</span> are non-randomly segregated into specific daughter cells is only marginally supported by data in sporadic and often contradictory studies. As a result, the field has moved forward rather slowly. The advent of being able to directly label and differentiate <span class="hlt">sister</span> <span class="hlt">chromatids</span> in vivo using fluorescence in situ hybridization [3] was a significant advance for such studies. However, this approach is limited by the need for large tracks of unidirectional repeats on chromosomes and the reliance on quantitative imaging of fluorescent probes and rigorous statistical analysis to discern between the two competing hypotheses. A novel method called Strand-seq which uses next-generation sequencing to assay <span class="hlt">sister</span> <span class="hlt">chromatid</span> inheritance patterns independently for each chromosome [4] offers a comprehensive approach to test for non-random segregation. In addition Strand-seq enables studies on the deposition of chromatin marks in relation to DNA replication. This method is expected to help unify the field by testing previous claims of non-random segregation in an unbiased way in many model systems in vitro and in vivo. PMID:23665005</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20551608','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20551608"><span>Behavior of centromeres in univalents and centric misdivision in wheat.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lukaszewski, A J</p> <p>2010-07-01</p> <p>Centromeres are responsible for the proper behavior of chromosomes in cell divisions. In meiosis the process is more complicated than in mitosis, as each chromosome in a bivalent has 2 <span class="hlt">sister</span> centromeres and their behavior has to be strictly coordinated. Here, the behavior of <span class="hlt">sister</span> centromeres in univalents in wheat is examined, showing that by metaphase I they often lose their coordination. This loss accelerates with the progression of anaphase I, leading to stable bipolar attachment and frequent separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> or to misdivision. Depending on the orientation of a univalent and its <span class="hlt">sister</span> centromeres, misdivision may occur across the centromere region or across the pericentric chromatin. Chromosome fragments consisting of only the centromere region did not survive to the next generation. Midget chromosomes composed of the centromeres and parts of the pericentric chromatin did survive, but their transmission rates were low and appeared related to the amount of pericentric chromatin, probably because only the pericentric chromatin provides <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. As the cohesion of <span class="hlt">sister</span> <span class="hlt">chromatids</span> appears to be a function of the proximity to the kinetochore region, the definition of the centromere need not include pericentric regions. Copyright 2010 S. Karger AG, Basel.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19545645','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19545645"><span>Chromosomal <span class="hlt">aberrations</span> in a fish, Channa punctata after in vivo exposure to three heavy metals.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yadav, Kamlesh K; Trivedi, Sunil P</p> <p>2009-08-01</p> <p>The studies were designed to assess the extent of chromosomal <span class="hlt">aberrations</span> (CA) under the exposure of three common heavy metalic compounds, viz. mercuric chloride, arsenic trioxide and copper sulphate pentahydrate, in vivo using fish, Channa punctata (2n=32), as a test model. Prior acclimatized fishes were divided into five groups. Group I and II served as negative and positive control, respectively. An intramuscular injection of Mitomycin-C (@ 1mg/kg body wt.) was administered to group II only. Fishes of groups III, IV and V were subjected to sublethal concentrations (10% of 96h LC(50)), of HgCl(2) (0.081mg/L), As(2)O(3) (6.936mg/L) and CuSO(4)x5H(2)O (0.407mg/L). Fishes of all the groups were exposed uninterrupted for 24, 48, 72, 96 and 168h. Observations of kidney cells of exposed fishes revealed <span class="hlt">chromatid</span> and chromosome breaks, <span class="hlt">chromatid</span> and chromosome gaps along with ring and di-centric chromosomes. A significant increase over negative control in the frequency of chromosomal <span class="hlt">aberrations</span> (CA) was observed in fish exposed to Mitomycin-C, Hg(II), As(III) and Cu(II). As the average + or - SE total number of CA, average number of CA per metaphase and %incidence of <span class="hlt">aberrant</span> cells in Hg(II) was 104.40 + or - 8.189, 0.347 + or - 0.027 and 10.220 + or - 0.842, respectively; in As(III) 109.20 + or - 8.309, 0.363 + or - 0.027 and 10.820 + or - 2.347, respectively and in Cu(II) 89.00 + or - 19.066, 0.297 + or - 0.028 and 8.900 + or - 0.853, respectively. Hence, it reveals that the order of induction of frequency of CA was Cu<Hg<As. The findings depict genotoxic potential of these metals even in sublethal concentrations.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23665005','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23665005"><span>Strand-seq: a unifying tool for studies of chromosome segregation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Falconer, Ester; Lansdorp, Peter M</p> <p>2013-01-01</p> <p>Non random segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> has been implicated to help specify daughter cell fate (the Silent <span class="hlt">Sister</span> Hypothesis [1]) or to protect the genome of long-lived stem cells (the Immortal Strand Hypothesis [2]). The idea that <span class="hlt">sister</span> <span class="hlt">chromatids</span> are non-randomly segregated into specific daughter cells is only marginally supported by data in sporadic and often contradictory studies. As a result, the field has moved forward rather slowly. The advent of being able to directly label and differentiate <span class="hlt">sister</span> <span class="hlt">chromatids</span> in vivo using fluorescence in situ hybridization [3] was a significant advance for such studies. However, this approach is limited by the need for large tracks of unidirectional repeats on chromosomes and the reliance on quantitative imaging of fluorescent probes and rigorous statistical analysis to discern between the two competing hypotheses. A novel method called Strand-seq which uses next-generation sequencing to assay <span class="hlt">sister</span> <span class="hlt">chromatid</span> inheritance patterns independently for each chromosome [4] offers a comprehensive approach to test for non-random segregation. In addition Strand-seq enables studies on the deposition of chromatin marks in relation to DNA replication. This method is expected to help unify the field by testing previous claims of non-random segregation in an unbiased way in many model systems in vitro and in vivo. Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=132653&Lab=OEI&keyword=weinberg&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=132653&Lab=OEI&keyword=weinberg&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span><span class="hlt">SISTER</span> STUDY</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>The <span class="hlt">Sister</span> Study will investigate the role of genetic, environmental, and lifestyle factors on the risk of breast cancer and other diseases in <span class="hlt">sisters</span> of women with breast cancer. This research study will enroll 50,000 women who live in the United States and who are the cancer-fr...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23700831','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23700831"><span>[Comparative analysis of cytogenetic examination of control groups of subjects carried out in different Russian laboratories].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sevan'kaev, A V; Khvostunov, I K; Snigireva, G P; Novitskaia, N N; Antoshchina, M M; Fesenko, E V; Vorobtsova, I E; Neronova, E G; Domracheva, E V; Nugis, V Iu; Govorun, R D; Handogina, E K</p> <p>2013-01-01</p> <p>The incidence of unstable chromosome <span class="hlt">aberrations</span> in peripheral blood lymphocytes from unirradiated control subjects was analyzed using cytogenetic data obtained from 9 cytogenetic laboratories located in Moscow, St.-Petersburg, Obninsk, and Dubna (Russia). The objective of this study was to estimate the level and spectrum of spontaneous chromosome <span class="hlt">aberrations</span> in human lymphocytes. 1140 blood samples were taken from 1112 subjects (594 men and 546 women) aged 1 to 72. The total metaphase number was 466795. The uniform Giemsa method for peripheral blood lymphocyte cultures was used. After counting 466795 metaphases, 4288 chromosomal <span class="hlt">aberrations</span> of various types were classified. The most frequent types of <span class="hlt">aberrations</span> were acentrics and <span class="hlt">chromatid</span> deletions. They made up 90% of the total number of <span class="hlt">aberrations</span>. The remaining 10% were exchange <span class="hlt">aberrations</span>. The number of chromosome exchanges (dicentrics and centric rings) was twice the number of <span class="hlt">chromatid</span> exchanges. Overall, the portion ofcells with chromosomal or (and) <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> was 0.89 +/- 0.01%; the frequency of acentrics was 0.29 +/- 0.01; the frequency of dicentrics was 0.046 +/- 0.003; the frequency of unstable chromosome <span class="hlt">aberrations</span> was 0.35 +/- 0.01; and the frequency of <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> was 0.57 +/- 0.01 per 100 cells.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_4");'>4</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li class="active"><span>6</span></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_6 --> <div id="page_7" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li class="active"><span>7</span></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="121"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20170009516','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20170009516"><span>Kits for Characterization of Chromosomal Inversions Using Probes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ray, F. Andrew (Inventor)</p> <p>2017-01-01</p> <p>A kit for the characterization of chromosomal inversions using single-stranded probes that are either all identical or all complementary to a single-stranded <span class="hlt">chromatid</span> is described. Reporter species are attached to oligonucleotide strands designed such that they may hybridize to portions of only one of a pair of single-stranded <span class="hlt">sister</span> <span class="hlt">chromatids</span> which may be prepared by the CO-FISH procedure. If an inversion has occurred, these marker probes will be detected on the second <span class="hlt">sister</span> <span class="hlt">chromatid</span> at the same location as the inversion on the first <span class="hlt">chromatid</span>. The kit includes non-repetitive probes that are either all identical or all complementary to at least a portion of a target DNA sequence of only one DNA strand of only one <span class="hlt">chromatid</span> and may in some embodiments include reagents suitable for performing CO-FISH and/or reagents for hybridizing the probes to the target DNA sequence.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7935987','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7935987"><span>Evaluation of chemopreventive effects of betel leaf on the genotoxicity of pan masala.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Trivedi, A H; Patel, R K; Rawal, U M; Adhvaryu, S G; Balar, D B</p> <p>1994-01-01</p> <p>The antigenotoxic effect of the aqueous extract of betel leaf (BL-ext.) against the pan masala was tested with the help of cytogenetic endpoints like chromosome <span class="hlt">aberration</span> (CA) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) utilizing Chinese hamster ovary (CHO) cells. Compared to the cultures treated with aqueous extract of pan masala alone, a reduction in CA and SCE frequencies in CHO cells was observed following a combined treatment with pan masala (with or without tobacco) extract and BL-ext. The protective effect of BL-ext. against the genomic damage caused by pan masala was statistically significant only after treating the cells for a longer period.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25961503','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25961503"><span>Condensin confers the longitudinal rigidity of chromosomes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Houlard, Martin; Godwin, Jonathan; Metson, Jean; Lee, Jibak; Hirano, Tatsuya; Nasmyth, Kim</p> <p>2015-06-01</p> <p>In addition to inter-<span class="hlt">chromatid</span> cohesion, mitotic and meiotic <span class="hlt">chromatids</span> must have three physical properties: compaction into 'threads' roughly co-linear with their DNA sequence, intra-<span class="hlt">chromatid</span> cohesion determining their rigidity, and a mechanism to promote <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement. A fundamental issue in chromosome biology is whether a single molecular process accounts for all three features. There is universal agreement that a pair of Smc-kleisin complexes called condensin I and II facilitate <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement, but whether they also confer thread formation or longitudinal rigidity is either controversial or has never been directly addressed respectively. We show here that condensin II (beta-kleisin) has an essential role in all three processes during meiosis I in mouse oocytes and that its function overlaps with that of condensin I (gamma-kleisin), which is otherwise redundant. Pre-assembled meiotic bivalents unravel when condensin is inactivated by TEV cleavage, proving that it actually holds chromatin fibres together.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16828123','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16828123"><span><span class="hlt">Aberrant</span> and multiaberrant (rogue) cells in peripheral lymphocytes of Hodgkin's lymphoma patients after chemotherapy.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ryabchenko, Nikolay I; Nasonova, Valentina A; Fesenko, Eleonora V; Kondrashova, Tatiana V; Antoschina, Margarita M; Pavlov, Vyacheslav V; Ryabikina, Natalya V</p> <p>2006-10-10</p> <p>We analyzed spontaneous chromosome lesions in peripheral lymphocytes cultured from Hodgkin's lymphoma (HL) patients before and after cytostatic chemotherapy. The mean <span class="hlt">aberration</span> frequency was significantly higher in HL patients after chemotherapy (7.20+/-0.58 per 100 metaphases) than in non-treated HL patients (4.80+/-0.54), and in non-treated patients than in healthy subjects (2.12+/-0.13). In lymphocytes of HL patients, who received chemotherapy, we found, in addition to ordinary <span class="hlt">aberrant</span> cells, a large number of multiaberrant (or rogue) cells, i.e. metaphases carrying multiple (at least four) chromosome-type exchange <span class="hlt">aberrations</span>. Rogue cells were found in 15 out of 18 chemotherapeutically treated HL patients (in total, 60 rogue cells per 5,568 scored cells), whereas in 30 non-treated patients only 1 rogue cell was found (per 4,988 scored cells). No correlation was found between the yield of rogue cells and the <span class="hlt">aberration</span> frequency in ordinary <span class="hlt">aberrant</span> cells. <span class="hlt">Aberration</span> spectra (ratios of <span class="hlt">chromatid</span>- to chromosome-type <span class="hlt">aberrations</span> and of breaks to exchanges) were essentially different in ordinary <span class="hlt">aberrant</span> and multiaberrant cells. These data, as well as analysis of cellular distributions of <span class="hlt">aberrations</span>, implied independent induction of chromosome damage in ordinary <span class="hlt">aberrant</span> and rogue cells. Analysis of <span class="hlt">aberration</span> patterns in diploid and polyploid rogue metaphases belonging to the first, second, and third in vitro division indicated that rogue cells could be formed both in vivo and in vitro, and could survive at least two rounds of in vitro replication, given blocked chromosome segregation. These results suggested that formation of rogue cells, unlike ordinary <span class="hlt">aberrant</span> cells, was triggered by events other than direct DNA and/or chromosome lesions. A hypothesis regarding disrupted apoptosis as a candidate mechanism for rogue cell formation seems to be most suitable for interpretation of our data. Cultured lymphocytes of chemotherapeutically treated HL patients may</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11531014','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11531014"><span>A comparative study on cytogenetic and antineoplastic effects induced by two modified steroidal alkylating agents.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Papageorgiou, A; Tsavdaridis, D; Geromichalos, G D; Camoutsis, C; Karaberis, E; Mourelatos, D; Chrysogelou, E; Houvartas, S; Kotsis, A</p> <p>2001-01-01</p> <p>We investigated the effects of two newly synthesized steroidal derivatives of nitrogen mustard on <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange rates and on human lymphocyte proliferation kinetics. The compound 33-hydroxy-5alpha,22alpha-spirostan- 12-one-p-(N,N-bis(2-chloroethyl)amino)phenylacetate(1) was, on a molar basis, less effective in inducing <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and suppressing cell proliferation rate indices than compound 3beta-hydroxy-12alpha-aza-C-homo-5alpha,22alpha-spirostan-12-one-p-(N,N-bis(2-chloroethyl)amino)phenylacetate(2). A correlation was observed between the magnitude of the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange response and the depression of cell proliferation index. We also studied the effects of the aforementioned compounds on Lewis lung carcinoma. The order of the percent inhibition of tumor growth achieved by the compounds coincides with the order of the cytogenetic effects they induce.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15162039','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15162039"><span>Complex <span class="hlt">chromatid</span>-isochromatid exchanges following irradiation with heavy ions?</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Loucas, B D; Eberle, R L; Durante, M; Cornforth, M N</p> <p>2004-01-01</p> <p>We describe a peculiar and relatively rare type of chromosomal rearrangement induced in human peripheral lymphocytes that were ostensibly irradiated in G(0) phase of the cell cycle by accelerated heavy ions, and which, to the best of our knowledge, have not been previously described. The novel rearrangements which were detected using mFISH following exposure to 500 MeV/nucleon and 5 GeV/n 56Fe particles, but were not induced by either 137Cs gamma rays or 238Pu alpha particles, can alternatively be described as either complex <span class="hlt">chromatid</span>-isochromatid or complex <span class="hlt">chromatid</span>-chromosome exchanges. Different mechanisms potentially responsible for their formation are discussed. Copyright 2003 S. Karger AG, Basel</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2969851','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2969851"><span>BubR1- and Polo-Coated DNA Tethers Facilitate Poleward Segregation of Acentric <span class="hlt">Chromatids</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Royou, Anne; Gagou, Mary E.; Karess, Roger; Sullivan, William</p> <p>2010-01-01</p> <p>Summary The mechanisms that safeguard cells against chromosomal instability (CIN) are of great interest, as CIN contributes to tumorigenesis. To gain insight into these mechanisms, we studied the behavior of cells entering mitosis with damaged chromosomes. We used the endonuclease I-CreI to generate acentric chromosomes in Drosophila larvae. While I-CreI expression produces acentric chromosomes in the majority of neuronal stem cells, remarkably, it has no effect on adult survival. Our live studies reveal that acentric <span class="hlt">chromatids</span> segregate efficiently to opposite poles. The acentric <span class="hlt">chromatid</span> poleward movement is mediated through DNA tethers decorated with BubR1, Polo, INCENP, and Aurora-B. Reduced BubR1 or Polo function results in abnormal segregation of acentric <span class="hlt">chromatids</span>, a decrease in acentric chromosome tethering, and a great reduction in adult survival. We propose that BubR1 and Polo facilitate the accurate segregation of acentric <span class="hlt">chromatids</span> by maintaining the integrity of the tethers that connect acentric chromosomes to their centric partners. PMID:20141837</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5732777','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5732777"><span>PARP inhibition causes premature loss of cohesion in cancer cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kukolj, Eva; Kaufmann, Tanja; Dick, Amalie E.; Zeillinger, Robert; Gerlich, Daniel W.; Slade, Dea</p> <p>2017-01-01</p> <p>Poly(ADP-ribose) polymerases (PARPs) regulate various aspects of cellular function including mitotic progression. Although PARP inhibitors have been undergoing various clinical trials and the PARP1/2 inhibitor olaparib was approved as monotherapy for BRCA-mutated ovarian cancer, their mode of action in killing tumour cells is not fully understood. We investigated the effect of PARP inhibition on mitosis in cancerous (cervical, ovary, breast and osteosarcoma) and non-cancerous cells by live-cell imaging. The clinically relevant inhibitor olaparib induced strong perturbations in mitosis, including problems with chromosome alignment at the metaphase plate, anaphase delay, and premature loss of cohesion (cohesion fatigue) after a prolonged metaphase arrest, resulting in <span class="hlt">sister</span> <span class="hlt">chromatid</span> scattering. PARP1 and PARP2 depletion suppressed the phenotype while PARP2 overexpression enhanced it, suggesting that olaparib-bound PARP1 and PARP2 rather than the lack of catalytic activity causes this phenotype. Olaparib-induced mitotic <span class="hlt">chromatid</span> scattering was observed in various cancer cell lines with increased protein levels of PARP1 and PARP2, but not in non-cancer or cancer cell lines that expressed lower levels of PARP1 or PARP2. Interestingly, the <span class="hlt">sister</span> <span class="hlt">chromatid</span> scattering phenotype occurred only when olaparib was added during the S-phase preceding mitosis, suggesting that PARP1 and PARP2 entrapment at replication forks impairs <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. Clinically relevant DNA-damaging agents that impair replication progression such as topoisomerase inhibitors and cisplatin were also found to induce <span class="hlt">sister</span> <span class="hlt">chromatid</span> scattering and metaphase plate alignment problems, suggesting that these mitotic phenotypes are a common outcome of replication perturbation. PMID:29262611</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040088536&hterms=incubation&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D60%26Ntt%3Dincubation','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040088536&hterms=incubation&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D60%26Ntt%3Dincubation"><span>Kinetics of <span class="hlt">chromatid</span> break repair in G2-human fibroblasts exposed to low- and high-LET radiations</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Kawata, T.; Durante, M.; George, K.; Furusawa, Y.; Gotoh, E.; Takai, N.; Wu, H.; Cucinotta, F. A.</p> <p>2001-01-01</p> <p>The purpose of this study is to determine the kinetics of <span class="hlt">chromatid</span> break rejoining following exposure to radiations of different quality. Exponentially growing human fibroblast cells AG1522 were irradiated with gamma-rays, energetic carbon (290 MeV/u), silicon (490 MeV/u) and iron (200 MeV/u, 600 MeV/u). Chromosomes were prematurely condensed using calyculin A. Prematurely condensed chromosomes were collected after several post-irradiation incubation times, ranging from 5 to 600 minutes, and the number of <span class="hlt">chromatid</span> breaks and exchanges in G2 cells were scored. The relative biological effectiveness (RBE) for initial <span class="hlt">chromatid</span> breaks per unit dose showed LET dependency having a peak at 55 keV/micrometers silicon (2.4) or 80 keV/micrometers carbon particles (2.4) and then decreased with increasing LET. The kinetics of <span class="hlt">chromatid</span> break rejoining following low- or high-LET irradiation consisted of two exponential components. <span class="hlt">Chromatid</span> breaks decreased rapidly after exposure, and then continued to decrease at a slower rate. The rejoining kinetics was similar for exposure to each type of radiation, although the rate of unrejoined breaks was higher for high-LET radiation. <span class="hlt">Chromatid</span> exchanges were also formed quickly.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5998375-chromosomal-aberrations-delays-cell-progression-induced-rays-tradescantia-clone-meristems','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5998375-chromosomal-aberrations-delays-cell-progression-induced-rays-tradescantia-clone-meristems"><span>Chromosomal <span class="hlt">aberrations</span> and delays in cell progression induced by x-rays in Tradescantia clone 02 meristems</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Geard, C.R.</p> <p>1983-01-01</p> <p>In root meristems of Tradescantia clone 02 (developed by Sparrow and his colleagues for mutation studies), X-rays interfere with the progression of cells through the cell cycle and induce chromosomal <span class="hlt">aberrations</span> in a dose-dependent manner consistent with linear-quadratic kinetics. Sequential mitotic cell accumulations after irradiation indicate that sensitivity to <span class="hlt">aberration</span> induction is probably greatest in cells from late S to early G2, with <span class="hlt">chromatid</span> interchanges the most frequent <span class="hlt">aberration</span> type and all <span class="hlt">aberrations</span> consistent with initiation from the interaction between two lesions. The ratio of the coefficients in the linear (..cap alpha..) and the quadratic (..beta..) terms (..cap alpha../..beta..) ismore » equal to the dose average of specific energy produced by individual particles in the site where interaction takes place. The ratio ..cap alpha../..beta.. for chromosomal <span class="hlt">aberrations</span> is similar to that previously found for X-ray-induced mutation in Tradescantia stamen hairs, supporting the proposal that radiation-induced mutational events are due to chromosomal <span class="hlt">aberrations</span> with interaction distances of about 1..mu..m. Abrahamson and co-workers have noted that both ..cap alpha../..beta.. ratios appear to be related to nuclear target size and are similar for chromosomal and mutational endpoints in the same organism. These findings support this concept; however, it is apparent that any situation which diminishes yield at high doses (e.g., mitotic delay) will probably affect the ..beta.. component. 23 references, 5 figures, 2 tables.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11287294','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11287294"><span>Cytogenetic analysis of children under long-term antibacterial therapy with nitroheterocyclic compound furagin.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Slapsyte, G; Jankauskiene, A; Mierauskiene, J; Lazutka, J R</p> <p>2001-04-05</p> <p>Cytogenetic analysis of chromosome <span class="hlt">aberrations</span> (CAs) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) was performed in 109 blood samples from 95 pediatric patients with urinary tract infections (UTIs). Children were exposed to diagnostic levels of X-rays during voiding cystourethrography and subsequently treated for one to 12 months with low doses of furagin - N-(5-nitro-2-furyl)-allylidene-1-aminohydantoin. Furagin is 2-substituted 5-nitrofuran, chemically and structurally similar to well-known antibacterial compound nitrofurantoin. Increased frequencies of CAs were found in children undergoing voiding cystourethrography as compared with the unexposed, acentric fragments being the most frequent alteration (2.03 versus 0.88 per 100 cells, P=0.006). However, a significant decrease in the frequency of acentric fragments was determined with the time elapsed since X-ray examination was performed. A time-independent increase in SCE frequency was found in lymphocytes of children treated with furagin. Total CA frequency did not differ significantly between groups of children with various duration of furagin treatment. However, frequency of <span class="hlt">chromatid</span> exchanges (triradials and quadriradials) increased significantly with duration of treatment.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/17630407','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/17630407"><span>A comparison of G2 phase radiation-induced <span class="hlt">chromatid</span> break kinetics using calyculin-PCC with those obtained using colcemid block.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bryant, Peter E; Mozdarani, Hossein</p> <p>2007-09-01</p> <p>To study the possible influence of cell-cycle delay on cells reaching mitosis during conventional radiation-induced <span class="hlt">chromatid</span> break experiments using colcemid as a blocking agent, we have compared the <span class="hlt">chromatid</span> break kinetics following a single dose of gamma rays (0.75 Gy) in metaphase CHO cells using calyculin-induced premature chromosome condensation (PCC), with those using colcemid block. Calyculin-induced PCC causes very rapid condensation of G2 cell chromosomes without the need for a cell to progress to mitosis, hence eliminating any effect of cell-cycle checkpoint on <span class="hlt">chromatid</span> break frequency. We found that the kinetics of the exponential first-order decrease in <span class="hlt">chromatid</span> breaks with time after irradiation was similar (not significantly different) between the two methods of chromosome condensation. However, use of the calyculin-PCC technique resulted in a slightly increased rate of disappearance of <span class="hlt">chromatid</span> breaks and thus higher frequencies of breaks at 1.5 and 2.5 h following irradiation. We also report on the effect of the nucleoside analogue ara A on <span class="hlt">chromatid</span> break kinetics using the two chromosome condensation techniques. Ara A treatment of cells abrogated the decrease in <span class="hlt">chromatid</span> breaks with time, both using the calyculin-PCC and colcemid methods. We conclude that cell-cycle delay may be a factor determining the absolute frequency of <span class="hlt">chromatid</span> breaks at various times following irradiation of cells in G2 phase but that the first-order disappearance of <span class="hlt">chromatid</span> breaks with time and its abrogation by ara A are not significantly influenced by the G2 checkpoint.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5272283-chromosomal-aberrations-delays-cell-progression-induced-rays-tradescantia-clone-meristems','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5272283-chromosomal-aberrations-delays-cell-progression-induced-rays-tradescantia-clone-meristems"><span>Chromosomal <span class="hlt">aberrations</span> and delays in cell progression induced by x-rays in Tradescantia clone 02 meristems</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Geard, C.R.</p> <p>1983-01-01</p> <p>In root meristems of Tradescantia clone 02 (developed by Sparrow and his colleagues for mutation studies), X-rays interfere with the progression of cells through the cell cycle and induce chromosomal <span class="hlt">aberrations</span> in a dose-dependent manner consistent with linear-quadratic kinetics. Sequential mitotic cell accumulations after irradiation indicate that sensitivity to aberrration induction is probably greatest in cells from late S to early G2, with <span class="hlt">chromatid</span> interchanges the most frequent <span class="hlt">aberration</span> type and all <span class="hlt">aberrations</span> consistent with intiation from the interaction between two lesions. The ratio of the coefficients in the linear (..cap alpha..) and the quadratic (..beta..) terms (..cap alpha../..beta..) ismore » equal to the dose average of specific energy produced by individual particles in the site where interaction takes place. The ratio ..cap alpha../..beta.. for chromosomal <span class="hlt">aberrations</span> is similar to that previously found for X-ray-induced mutation in Tradescantia stamen hairs, supporting the proposal that radiation-induced mutational events are due to chromosomal <span class="hlt">aberrations</span> with interaction distances of about 1 ..mu..m. Abrahmson and co-workers have noted that both ..cap alpha../..beta.. ratios appear to be related to nuclear target size and are similar for chromosomal and mutational endpoints in the same organism. These findings support this concept; however, it is apparent that any situation which diminishes yield at high doses (e.g., mitotic delay) will primarily affect the ..beta.. component, resulting in low assessments of interaction site diameters.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1009291','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1009291"><span>Chromosome analysis from peripheral blood lymphocytes of workers after an acute exposure to benzene.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Clare, M G; Yardley-Jones, A; Maclean, A C; Dean, B J</p> <p>1984-01-01</p> <p>A spillage of about 1200 gallons of benzene occurred during the loading of a ship, and 10 workers on a single shift were exposed to benzene. Shortly afterwards, an assay of the urine of these individuals showed that substantial amounts of phenol were being excreted. About three months after the incident samples of venous blood were taken from 10 individuals exposed to benzene and 11 men on a comparable shift who acted as controls. The lymphocytes were stimulated to divide in short term cultures. For each subject, 200 cells at metaphase were examined for chromosome damage using 48 h cultures, and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) were analysed from about 30 cells in their second division, using 72 h cultures. The most frequent types of <span class="hlt">aberrations</span> in all the individuals were <span class="hlt">chromatid</span> gaps, with occasional breaks of <span class="hlt">chromatids</span> and chromosomes. There were few exchanges within or between the arms of <span class="hlt">chromatids</span> or chromosomes. More cells in the control than in the exposed group showed damage, an effect that was especially noticeable for <span class="hlt">chromatid</span> gaps. All values, however, were considered to be within a normal range. There were slightly more SCE in some of the exposed individuals than in the controls and there was a trend towards a positive association between the frequency of SCE recorded for each individual and the maximum value for the excretion of phenol in the urine on the day after the incident. There is no evidence to indicate that benzene induced any type of lasting chromosome damage in the lymphocytes of the 10 exposed workers when cells were examined about three months after the incident. PMID:6722051</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3442196','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3442196"><span>Perturbation of Incenp function impedes anaphase <span class="hlt">chromatid</span> movements and chromosomal passenger protein flux at centromeres</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ahonen, Leena J.; Kukkonen, Anu M.; Pouwels, Jeroen; Bolton, Margaret A.; Jingle, Christopher D.; Stukenberg, P. Todd; Kallio, Marko J.</p> <p>2012-01-01</p> <p>Incenp is an essential mitotic protein that, together with Aurora B, Survivin, and Borealin, forms the core of the chromosomal passenger protein complex (CPC). The CPC regulates various mitotic processes and functions to maintain genomic stability. The proper subcellular localization of the CPC and its full catalytic activity require the presence of each core subunit in the complex. We have investigated the mitotic tasks of the CPC using a function blocking antibody against Incenp microinjected into cells at different mitotic phases. This method allowed temporal analysis of CPC functions without perturbation of complex assembly or activity prior to injection. We have also studied the dynamic properties of Incenp and Aurora B using fusion protein photobleaching. We found that in early mitotic cells, Incenp and Aurora B exhibit dynamic turnover at centromeres, which is prevented by the anti-Incenp antibody. In these cells, the loss of centromeric CPC turnover is accompanied by forced mitotic exit without the execution of cytokinesis. Introduction of anti-Incenp antibody into early anaphase cells causes abnormalities in <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation through defects in anaphase spindle functions. In summary, our data uncovers new mitotic roles for the CPC in anaphase and proposes that CPC turnover at centromeres modulates spindle assembly checkpoint signaling. PMID:18784935</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/18784935','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/18784935"><span>Perturbation of Incenp function impedes anaphase <span class="hlt">chromatid</span> movements and chromosomal passenger protein flux at centromeres.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ahonen, Leena J; Kukkonen, Anu M; Pouwels, Jeroen; Bolton, Margaret A; Jingle, Christopher D; Stukenberg, P Todd; Kallio, Marko J</p> <p>2009-02-01</p> <p>Incenp is an essential mitotic protein that, together with Aurora B, Survivin, and Borealin, forms the core of the chromosomal passenger protein complex (CPC). The CPC regulates various mitotic processes and functions to maintain genomic stability. The proper subcellular localization of the CPC and its full catalytic activity require the presence of each core subunit in the complex. We have investigated the mitotic tasks of the CPC using a function blocking antibody against Incenp microinjected into cells at different mitotic phases. This method allowed temporal analysis of CPC functions without perturbation of complex assembly or activity prior to injection. We have also studied the dynamic properties of Incenp and Aurora B using fusion protein photobleaching. We found that in early mitotic cells, Incenp and Aurora B exhibit dynamic turnover at centromeres, which is prevented by the anti-Incenp antibody. In these cells, the loss of centromeric CPC turnover is accompanied by forced mitotic exit without the execution of cytokinesis. Introduction of anti-Incenp antibody into early anaphase cells causes abnormalities in <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation through defects in anaphase spindle functions. In summary, our data uncovers new mitotic roles for the CPC in anaphase and proposes that CPC turnover at centromeres modulates spindle assembly checkpoint signaling.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29368476','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29368476"><span>[Inverted meiosis and its place in the evolution of sexual reproduction pathways].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bogdanov, Yu F</p> <p>2016-05-01</p> <p>Inverted meiosis is observed in plants (Cyperaceae and Juncaceae) and insects (Coccoidea, Aphididae) with holocentric chromosomes, the centromeres of which occupy from 70 to 90% of the metaphase chromosome length. In the first meiotic division (meiosis I), chiasmata are formed and rodlike bivalents orient equationally, and in anaphase I, <span class="hlt">sister</span> <span class="hlt">chromatids</span> segregate to the poles; the diploid chromosome number is maintained. Non-<span class="hlt">sister</span> <span class="hlt">chromatids</span> of homologous chromosomes remain in contact during interkinesis and prophase II and segregate in anaphase II, forming haploid chromosome sets. The segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> in meiosis I was demonstrated by example of three plant species that were heterozygous for chromosomal rearrangements. In these species, <span class="hlt">sister</span> <span class="hlt">chromatids</span>, marked with rearrangement, segregated in anaphase I. Using fluorescent antibodies, it was demonstrated that meiotic recombination enzymes Spo11 and Rad5l, typical of canonical meiosis, functioned at the meiotic prophase I of pollen mother cells of Luzula elegance and Rhynchospora pubera. Moreover, antibodies to synaptonemal complexes proteins ASY1 and ZYP1 were visualized as filamentous structures, pointing to probable formation of synaptonemal complexes. In L. elegance, chiasmata are formed by means of chromatin threads containing satellite DNA. According to the hypothesis of the author of this review, equational division of <span class="hlt">sister</span> <span class="hlt">chromatids</span> at meiosis I in the organisms with inverted meiosis can be explained by the absence of specific meiotic proteins (shugoshins). These proteins are able to protect cohesins of holocentric centromeres from hydrolysis by separases at meiosis I, as occurs in the organisms with monocentric chromosomes and canonical meiosis. The basic type of inverted meiosis was described in Coccoidea and Aphididae males. In their females, the variants of parthenogenesis were also observed. Until now, the methods of molecular cytogenetics were not applied for the analysis of</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21894441','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21894441"><span>Chromosome <span class="hlt">aberrations</span> in peripheral blood lymphocytes of individuals living in high background radiation areas of Ramsar, Iran.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zakeri, F; Rajabpour, M R; Haeri, S A; Kanda, R; Hayata, I; Nakamura, S; Sugahara, T; Ahmadpour, M J</p> <p>2011-11-01</p> <p>In order to investigate the biological effects of exposure to low-dose radiation and to assess the dose-effect relationship in residents of high background radiation areas (HBRAs) of Ramsar, cytogenetic investigation of unstable-type <span class="hlt">aberrations</span> was performed in 15 healthy elderly women in a HBRA of Ramsar, Talesh mahalle, and in 10 elderly women living in a nearby control area with normal background radiation. In total, 77,714 cells were analyzed; 48,819 cells in HBRA residents and 28,895 cells in controls. On average, 3,108 cells per subject were analyzed (range 1,475-5,007 cells). Significant differences were found in the frequency of dicentric plus centric rings in 100 cells (0.207 ± 0.103 vs. 0.047 ± 0.027, p < 0.0005), total chromosome-type <span class="hlt">aberrations</span> per 100 cells (0.86 ± 0.44 vs. 0.23 ± 0.17, p < 0.0005), and <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> per 100 cells (3.31 ± 2.01 vs. 1.66 ± 0.63, p = 0.01) by the Mann-Whitney U test between HBRA and the control, respectively. Using chromosomal <span class="hlt">aberrations</span> as the main endpoint to assess the dose-effect relationship in residents of HBRAs in Ramsar, no positive correlation was found between the frequency of dicentric plus centric ring <span class="hlt">aberrations</span> and the cumulative dose of the inhabitants estimated by direct individual dosimetry; however, obvious trends of increase with age appeared in the control group. Based on these results, individuals residing in HBRAs of Ramsar have an increased frequency of detectable abnormalities in unstable <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/servlets/purl/6440856','SCIGOV-STC'); return false;" href="https://www.osti.gov/servlets/purl/6440856"><span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Harrison, F.L.; Rice, D.W. Jr., Moore, D.H.</p> <p></p> <p>Traditional bioassays are unsuitable for assessing sublethal effects from ocean disposal of low-level radioactive waste because mortality and phenotypic responses are not anticipated. We compared the usefulness of chromosomal <span class="hlt">aberration</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) induction as measures of low-level radiation effects in a sediment-dwelling marine worm, Neanthes arenaceodentata. The SCEs, in contrast to chromosomal <span class="hlt">aberrations</span>, do not alter the overall chromosome morphology and in mammalian cells appear to be a more sensitive indicator of DNA alterations caused by environmental mutagens. Newly hatched larvae were exposed to two radiation-exposure regimes of either x rays at a high dose rate ofmore » 0.7 Gy (70 rad)/min for as long as 5.5 min or to /sup 60/Co gamma rays at a low dose rate of from 4.8 x 10/sup -5/ to 1.2 x 10/sup -1/ Gy (0.0048 to 12 rad)/h for 24 h. After irradiation, the larvae were exposed to 3 x 10/sup -5/M bromodeoxyuridine (BrdUrd) for 28 h (x-ray-irradiated larvae) or for 54 h (/sup 60/Co-irradiated larvae). Larval cells were examined for the proportion of cells in first, second, and third or greater division. Frequencies of chromosomal <span class="hlt">aberrations</span> and SCEs were determined in first and second division cells, respectively. Results from x-ray irradiation indicated that dose-related increases occur in chromosome and <span class="hlt">chromatid</span> deletions, but a dose of equal or greater 2 Gy (equal to or greater than 200 rad) was required to observe a significant increase. Worm larvae receiving /sup 60/Co irradiation showed elevated SCE frequencies with a significant increase of 0.6 Gy (60 rad). We suggest that both SCEs and chromosomal <span class="hlt">aberrations</span> may be useful for measuring effects on genetic material induced by radiation. 56 references, 7 figures, 9 tables.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/9113588','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/9113588"><span>Pregnant and parenting adolescents and their younger <span class="hlt">sisters</span>: the influence of relationship qualities for younger <span class="hlt">sister</span> outcomes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>East, P L; Shi, C R</p> <p>1997-04-01</p> <p>On the basis of social modeling theory and a sibling interaction hypothesis, it was hypothesized that specific relationship qualities between a pregnant or parenting teen and her younger <span class="hlt">sister</span> would be associated with permissive younger <span class="hlt">sister</span> outcomes, such as permissive childbearing attitudes and permissive sexual behavior. Results indicated that negative relationship qualities, such as rivalry, competition, and conflict, were more closely related to younger <span class="hlt">sisters</span> engaging in problem delinquent-like behavior and sexual behavior than were positive relationship qualities, such as warmth and closeness. Additionally, a shared friendship network with the older <span class="hlt">sister</span> was found to be associated with extensive younger <span class="hlt">sister</span> problem behavior and sexual behavior. Three potential explanatory processes are discussed.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_5");'>5</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li class="active"><span>7</span></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_7 --> <div id="page_8" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li class="active"><span>8</span></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="141"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/18820001','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/18820001"><span>A proteomic approach to identifying new drug targets (potentiating topoisomerase II poisons).</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Jenkins, J R</p> <p>2008-10-01</p> <p>Topoisomerase II poisons are an established part of best clinical practice for the treatment of a number of solid tumours and haematological malignancies. However, toxicity and resistance to chemotherapeutic drugs often complicate the treatment. Furthermore, topoisomerase II poisons can also induce <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, chromosomal recombination and chromosome <span class="hlt">aberrations</span> and are associated with a significant risk of secondary leukaemia. It would therefore be of great clinical benefit if the efficacy of topoisomerase II inhibitors could be enhanced without the increased toxic side effects. It is proposed that clinical agents targeting topoisomerase II can be enhanced by inhibiting proteins that modulate topoisomerase II. The aim is to identify proteins, that by the nature of their interaction with topoisomerase II, represent putative drug targets.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6485860-induction-chromosome-aberrations-mitotic-arrest-cytomegalovirus-human-cells','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6485860-induction-chromosome-aberrations-mitotic-arrest-cytomegalovirus-human-cells"><span>Induction of chromosome <span class="hlt">aberrations</span> and mitotic arrest by cytomegalovirus in human cells</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>AbuBakar, S.; Au, W.W.; Legator, M.S.</p> <p>1988-01-01</p> <p>Human cytomegalovirus (CMV) is potentially an effective but often overlooked genotoxic agent in humans. We report here evidence that indicates that infection by CMV can induce chromosome alterations and mitotic inhibition. The frequency of chromosome <span class="hlt">aberrations</span> induced was dependent on the input multiplicity of infection (m.o.i.) for human lung fibroblasts (LU), but not for human peripheral blood lymphocytes (PBLs) when both cell types were infected at the GO phase of the cell cycle. The <span class="hlt">aberrations</span> induced by CMV were mostly <span class="hlt">chromatid</span> breaks and chromosome pulverizations that resembled prematurely condensed S-phase chromatin. Pulverized chromosomes were not observed in LU cells infectedmore » with virus stocks that had been rendered nonlytic by UV-irradiation at 24,000 ergs/mm2 or from infection of human lymphocytes. In LU cells infected with UV-irradiated CMV, the frequency of <span class="hlt">aberrations</span> induced was inversely dependent on the extent of the exposure of the CMV stock to the UV-light. In permissive CMV infection of proliferating LU cells at 24 hr after subculture, a high percentage (greater than 40%) of the metaphase cells were arrested at their first metaphase and displayed severely condensed chromosomes when harvested 48 hr later. A significant increase (p less than 0.05) in the chromosome <span class="hlt">aberration</span> frequency was also observed. Our study shows that CMV infection is genotoxic to host cells. The types and extent of damage are dependent on the viral genome expression and on the cell cycle stage of the cells at the time of infection. The possible mechanisms for induction of chromosome damage by CMV are discussed.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3715423','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3715423"><span>The Cohesion Protein SOLO Associates with SMC1 and Is Required for Synapsis, Recombination, Homolog Bias and Cohesion and Pairing of Centromeres in Drosophila Meiosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Yan, Rihui; McKee, Bruce D.</p> <p>2013-01-01</p> <p>Cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> is mediated by cohesin and is essential for proper meiotic segregation of both <span class="hlt">sister</span> <span class="hlt">chromatids</span> and homologs. solo encodes a Drosophila meiosis-specific cohesion protein with no apparent sequence homology to cohesins that is required in male meiosis for centromere cohesion, proper orientation of <span class="hlt">sister</span> centromeres and centromere enrichment of the cohesin subunit SMC1. In this study, we show that solo is involved in multiple aspects of meiosis in female Drosophila. Null mutations in solo caused the following phenotypes: 1) high frequencies of homolog and <span class="hlt">sister</span> <span class="hlt">chromatid</span> nondisjunction (NDJ) and sharply reduced frequencies of homolog exchange; 2) reduced transmission of a ring-X chromosome, an indicator of elevated frequencies of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE); 3) premature loss of centromere pairing and cohesion during prophase I, as indicated by elevated foci counts of the centromere protein CID; 4) instability of the lateral elements (LE)s and central regions of synaptonemal complexes (SCs), as indicated by fragmented and spotty staining of the chromosome core/LE component SMC1 and the transverse filament protein C(3)G, respectively, at all stages of pachytene. SOLO and SMC1 are both enriched on centromeres throughout prophase I, co-align along the lateral elements of SCs and reciprocally co-immunoprecipitate from ovarian protein extracts. Our studies demonstrate that SOLO is closely associated with meiotic cohesin and required both for enrichment of cohesin on centromeres and stable assembly of cohesin into chromosome cores. These events underlie and are required for stable cohesion of centromeres, synapsis of homologous chromosomes, and a recombination mechanism that suppresses SCE to preferentially generate homolog crossovers (homolog bias). We propose that SOLO is a subunit of a specialized meiotic cohesin complex that mediates both centromeric and axial arm cohesion and promotes homolog bias as a component of chromosome</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23874232','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23874232"><span>The cohesion protein SOLO associates with SMC1 and is required for synapsis, recombination, homolog bias and cohesion and pairing of centromeres in Drosophila Meiosis.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yan, Rihui; McKee, Bruce D</p> <p>2013-01-01</p> <p>Cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> is mediated by cohesin and is essential for proper meiotic segregation of both <span class="hlt">sister</span> <span class="hlt">chromatids</span> and homologs. solo encodes a Drosophila meiosis-specific cohesion protein with no apparent sequence homology to cohesins that is required in male meiosis for centromere cohesion, proper orientation of <span class="hlt">sister</span> centromeres and centromere enrichment of the cohesin subunit SMC1. In this study, we show that solo is involved in multiple aspects of meiosis in female Drosophila. Null mutations in solo caused the following phenotypes: 1) high frequencies of homolog and <span class="hlt">sister</span> <span class="hlt">chromatid</span> nondisjunction (NDJ) and sharply reduced frequencies of homolog exchange; 2) reduced transmission of a ring-X chromosome, an indicator of elevated frequencies of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE); 3) premature loss of centromere pairing and cohesion during prophase I, as indicated by elevated foci counts of the centromere protein CID; 4) instability of the lateral elements (LE)s and central regions of synaptonemal complexes (SCs), as indicated by fragmented and spotty staining of the chromosome core/LE component SMC1 and the transverse filament protein C(3)G, respectively, at all stages of pachytene. SOLO and SMC1 are both enriched on centromeres throughout prophase I, co-align along the lateral elements of SCs and reciprocally co-immunoprecipitate from ovarian protein extracts. Our studies demonstrate that SOLO is closely associated with meiotic cohesin and required both for enrichment of cohesin on centromeres and stable assembly of cohesin into chromosome cores. These events underlie and are required for stable cohesion of centromeres, synapsis of homologous chromosomes, and a recombination mechanism that suppresses SCE to preferentially generate homolog crossovers (homolog bias). We propose that SOLO is a subunit of a specialized meiotic cohesin complex that mediates both centromeric and axial arm cohesion and promotes homolog bias as a component of chromosome</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25975148','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25975148"><span>[Structural and functional organization of centromeres in plant chromosomes].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Silkova, O G; Loginova, D B</p> <p>2014-12-01</p> <p>The centromere is a specific chromosomal locus that forms the protein complex and kinetochore, maintains <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, controls chromosome attachment to the spindle, and coordinates chromosome movement during mitosis and meiosis. Defective centromere assembly or its dysfunction causes cell cycle arrest, structural abnormalities of the chromosomes, and aneuploidy. This review collects the data on the structure, functions, and epigenetic modification of centromeric chromatin, the structure and functions of the kinetochore, and <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. Taken together, these data provide insight into the specific architecture and functioning of the centromere during chromosome division and segregation in plants.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://pubs.er.usgs.gov/publication/70013469','USGSPUBS'); return false;" href="https://pubs.er.usgs.gov/publication/70013469"><span>THREE <span class="hlt">SISTERS</span> WILDERNESS, OREGON.</span></a></p> <p><a target="_blank" href="http://pubs.er.usgs.gov/pubs/index.jsp?view=adv">USGS Publications Warehouse</a></p> <p>MacLeod, Norman S.; Causey, J. Douglas</p> <p>1984-01-01</p> <p>A mineral survey of the Three <span class="hlt">Sisters</span> Wilderness, Oregon indicated little promise for the occcurrence of metallic mineral resources. Block pumice suitable for commercial uses occurs at an undeveloped claim at Rock Mesa in the wilderness, but numerous other sources occur outside the wilderness closer to markets. A broad area centered around South <span class="hlt">Sister</span> volcano is among the most favorable targets for geothermal resources in the Oregon Cascade Range, based on the very young age and large volume of silicic volcanic rocks that occur in this area. Deep exploration holes could be drilled in areas outside the wilderness south of South <span class="hlt">Sister</span> to provide data on the subsurface thermal and hydrologic regimes in the southern part of the area most likely to contain geothermal resources.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/4069583','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/4069583"><span>Abnormal centromere-<span class="hlt">chromatid</span> apposition (ACCA) and Peters' anomaly.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wertelecki, W; Dev, V G; Superneau, D W</p> <p>1985-08-01</p> <p>Abnormal centromere-<span class="hlt">chromatid</span> apposition (ACCA) was noted in a patient with Peters' anomaly. Previous reports of ACCA emphasized its association with tetraphocomelia and other congenital malformations (Roberts, SC Phocomelia, Pseudothalidomide Syndromes). This report expands the array of congenital malformations associated with ACCA and emphasizes the diagnostic importance of ocular defects for the ascertainment of additional cases of ACCA and its possible relationship with abnormal cell division.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3113765','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3113765"><span>Scc2 regulates gene expression by recruiting cohesin to the chromosome as a transcriptional activator during yeast meiosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Lin, Weiqiang; Jin, Hui; Liu, Xiuwen; Hampton, Kristin; Yu, Hong-Guo</p> <p>2011-01-01</p> <p>To tether <span class="hlt">sister</span> <span class="hlt">chromatids</span>, a protein-loading complex, including Scc2, recruits cohesin to the chromosome at discrete loci. Cohesin facilitates the formation of a higher-order chromosome structure that could also influence gene expression. How cohesin directly regulates transcription remains to be further elucidated. We report that in budding yeast Scc2 is required for <span class="hlt">sister-chromatid</span> cohesion during meiosis for two reasons. First, Scc2 is required for activating the expression of REC8, which encodes a meiosis-specific cohesin subunit; second, Scc2 is necessary for recruiting meiotic cohesin to the chromosome to generate <span class="hlt">sister-chromatid</span> cohesion. Using a heterologous reporter assay, we have found that Scc2 increases the activity of its target promoters by recruiting cohesin to establish an upstream cohesin-associated region in a position-dependent manner. Rec8-associated meiotic cohesin is required for the full activation of the REC8 promoter, revealing that cohesin has a positive feedback on transcriptional regulation. Finally, we provide evidence that chromosomal binding of cohesin is sufficient for target-gene activation during meiosis. Our data support a noncanonical role for cohesin as a transcriptional activator during cell differentiation. PMID:21508318</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27225972','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27225972"><span>Teenage pregnancy: the impact of maternal adolescent childbearing and older <span class="hlt">sister</span>'s teenage pregnancy on a younger <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wall-Wieler, Elizabeth; Roos, Leslie L; Nickel, Nathan C</p> <p>2016-05-25</p> <p>Risk factors for teenage pregnancy are linked to many factors, including a family history of teenage pregnancy. This research examines whether a mother's teenage childbearing or an older <span class="hlt">sister</span>'s teenage pregnancy more strongly predicts teenage pregnancy. This study used linkable administrative databases housed at the Manitoba Centre for Health Policy (MCHP). The original cohort consisted of 17,115 women born in Manitoba between April 1, 1979 and March 31, 1994, who stayed in the province until at least their 20(th) birthday, had at least one older <span class="hlt">sister</span>, and had no missing values on key variables. Propensity score matching (1:2) was used to create balanced cohorts for two conditional logistic regression models; one examining the impact of an older <span class="hlt">sister</span>'s teenage pregnancy and the other analyzing the effect of the mother's teenage childbearing. The adjusted odds of becoming pregnant between ages 14 and 19 for teens with at least one older <span class="hlt">sister</span> having a teenage pregnancy were 3.38 (99 % CI 2.77-4.13) times higher than for women whose older <span class="hlt">sister(s</span>) did not have a teenage pregnancy. Teenage daughters of mothers who had their first child before age 20 had 1.57 (99 % CI 1.30-1.89) times higher odds of pregnancy than those whose mothers had their first child after age 19. Educational achievement was adjusted for in a sub-population examining the odds of pregnancy between ages 16 and 19. After this adjustment, the odds of teenage pregnancy for teens with at least one older <span class="hlt">sister</span> who had a teenage pregnancy were reduced to 2.48 (99 % CI 2.01-3.06) and the odds of pregnancy for teen daughters of teenage mothers were reduced to 1.39 (99 % CI 1.15-1.68). Although both were significant, the relationship between an older <span class="hlt">sister</span>'s teenage pregnancy and a younger <span class="hlt">sister</span>'s teenage pregnancy is much stronger than that between a mother's teenage childbearing and a younger daughter's teenage pregnancy. This study contributes to understanding of the broader topic "who is</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=leadership%2bpoverty&pg=4&id=EJ1009515','ERIC'); return false;" href="https://eric.ed.gov/?q=leadership%2bpoverty&pg=4&id=EJ1009515"><span><span class="hlt">Sister</span> R. Leadership: Doing the Seemingly Impossible</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Sena, Rachel; Schoorman, Dilys; Bogotch, Ira</p> <p>2013-01-01</p> <p><span class="hlt">Sister</span> R., the first author, is a Dominican <span class="hlt">Sister</span> of Peace. Until recently, <span class="hlt">Sister</span> R. had been the director of the Maya Ministry Family Literacy Program, working with the Maya Community in Lake Worth, Palm Beach County, Florida. She described her work with these indigenous, preliterate, hardworking peoples as "a university of the poor"…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/EJ1081574.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/EJ1081574.pdf"><span>A Brief Analysis of <span class="hlt">Sister</span> Carrie's Character</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Yu, Hanying</p> <p>2010-01-01</p> <p>Carrie is always dreaming while the rocking chair is rocking again and again, this is the deep impression on us after we read "<span class="hlt">Sister</span> Carrie" which is the first novel of Theodore Dreiser. In this novel the protagonist <span class="hlt">Sister</span> Carrie is a controversial person. This paper tries to analyze the character of <span class="hlt">Sister</span> Carrie in order to find out…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20060003825&hterms=ito&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D40%26Ntt%3Dito','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20060003825&hterms=ito&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D40%26Ntt%3Dito"><span>G2 <span class="hlt">Chromatid</span> Damage and Repair Kinetics in Normal Human Fibroblast Cells Exposed to Low-or High-LET Radiation</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Kawata, T.; Ito, H.; Uno, T.; Saito, M.; Yamamoto, S.; Furusawa, Y.; Durante, M.; George, K.; Wu, H.; Cucinotta, F. A.</p> <p>2004-01-01</p> <p>Radiation-induced chromosome damage can be measured in interphase using the Premature Chromosome Condensation (PCC) technique. With the introduction of a new PCC technique using the potent phosphatase inhibitor calyculin-A, chromosomes can be condensed within five minutes, and it is now possible to examine the early damage induced by radiation. Using this method, it has been shown that high-LET radiation induces a higher frequency of <span class="hlt">chromatid</span> breaks and a much higher frequency of isochromatid breaks than low-LET radiation. The kinetics of <span class="hlt">chromatid</span> break rejoining consists of two exponential components representing a rapid and a slow time constant, which appears to be similar for low- and high- LET radiations. However, after high-LET radiation exposures, the rejoining process for isochromatid breaks influences the repair kinetics of <span class="hlt">chromatid</span>-type breaks, and this plays an important role in the assessment of <span class="hlt">chromatid</span> break rejoining in the G2 phase of the cell cycle.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/2434036','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/2434036"><span>Somatomedin C deficiency in Asian <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>McGraw, M E; Price, D A; Hill, D J</p> <p>1986-12-01</p> <p>Two <span class="hlt">sisters</span> of Asian origin showed typical clinical and biochemical features of primary somatomedin C (SM-C) deficiency (Laron dwarfism). Abnormalities of SM-C binding proteins were observed, one <span class="hlt">sister</span> lacking the high molecular weight (150 Kd) protein.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1778201','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1778201"><span>Somatomedin C deficiency in Asian <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>McGraw, M E; Price, D A; Hill, D J</p> <p>1986-01-01</p> <p>Two <span class="hlt">sisters</span> of Asian origin showed typical clinical and biochemical features of primary somatomedin C (SM-C) deficiency (Laron dwarfism). Abnormalities of SM-C binding proteins were observed, one <span class="hlt">sister</span> lacking the high molecular weight (150 Kd) protein. Images Figure PMID:2434036</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2013-title40-vol17/pdf/CFR-2013-title40-vol17-sec79-53.pdf','CFR2013'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2013-title40-vol17/pdf/CFR-2013-title40-vol17-sec79-53.pdf"><span>40 CFR 79.53 - Tier 2.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2013&page.go=Go">Code of Federal Regulations, 2013 CFR</a></p> <p></p> <p>2013-07-01</p> <p>..., Salmonella typhimurium Reverse Mutation Assay). (b) Manufacturer determination. Manufacturers shall determine... <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange Assay, and § 79.68 Salmonella typhimurium Reverse Mutation Assay. Teratogenic...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2012-title40-vol17/pdf/CFR-2012-title40-vol17-sec79-53.pdf','CFR2012'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2012-title40-vol17/pdf/CFR-2012-title40-vol17-sec79-53.pdf"><span>40 CFR 79.53 - Tier 2.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2012&page.go=Go">Code of Federal Regulations, 2012 CFR</a></p> <p></p> <p>2012-07-01</p> <p>..., Salmonella typhimurium Reverse Mutation Assay). (b) Manufacturer Determination. Manufacturers shall determine... <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange Assay, and § 79.68 Salmonella typhimurium Reverse Mutation Assay. Teratogenic...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title40-vol16/pdf/CFR-2011-title40-vol16-sec79-53.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title40-vol16/pdf/CFR-2011-title40-vol16-sec79-53.pdf"><span>40 CFR 79.53 - Tier 2.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-07-01</p> <p>..., Salmonella typhimurium Reverse Mutation Assay). (b) Manufacturer Determination. Manufacturers shall determine... <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange Assay, and § 79.68 Salmonella typhimurium Reverse Mutation Assay. Teratogenic...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol17/pdf/CFR-2014-title40-vol17-sec79-53.pdf','CFR2014'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol17/pdf/CFR-2014-title40-vol17-sec79-53.pdf"><span>40 CFR 79.53 - Tier 2.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2014&page.go=Go">Code of Federal Regulations, 2014 CFR</a></p> <p></p> <p>2014-07-01</p> <p>..., Salmonella typhimurium Reverse Mutation Assay). (b) Manufacturer Determination. Manufacturers shall determine... <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange Assay, and § 79.68 Salmonella typhimurium Reverse Mutation Assay. Teratogenic...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol16/pdf/CFR-2010-title40-vol16-sec79-53.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol16/pdf/CFR-2010-title40-vol16-sec79-53.pdf"><span>40 CFR 79.53 - Tier 2.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-07-01</p> <p>..., Salmonella typhimurium Reverse Mutation Assay). (b) Manufacturer Determination. Manufacturers shall determine... <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Exchange Assay, and § 79.68 Salmonella typhimurium Reverse Mutation Assay. Teratogenic...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://pubs.er.usgs.gov/publication/70035238','USGSPUBS'); return false;" href="https://pubs.er.usgs.gov/publication/70035238"><span>Eruptive history of South <span class="hlt">Sister</span>, Oregon Cascades</span></a></p> <p><a target="_blank" href="http://pubs.er.usgs.gov/pubs/index.jsp?view=adv">USGS Publications Warehouse</a></p> <p>Fierstein, J.; Hildreth, W.; Calvert, A.T.</p> <p>2011-01-01</p> <p>South <span class="hlt">Sister</span> is southernmost and highest of the Three <span class="hlt">Sisters</span>, three geologically dissimilar stratovolcanoes that together form a spectacular 20km reach along the Cascade crest in Oregon. North <span class="hlt">Sister</span> is a monotonously mafic edifice as old as middle Pleistocene, Middle <span class="hlt">Sister</span> a basalt-andesite-dacite cone built between 48 and 14ka, and South <span class="hlt">Sister</span> is a basalt-free edifice that alternated rhyolitic and intermediate modes from 50ka to 2ka (largely contemporaneous with Middle <span class="hlt">Sister</span>). Detailed mapping, 330 chemical analyses, and 42 radioisotopic ages show that the oldest exposed South <span class="hlt">Sister</span> lavas were initially rhyolitic ~50ka. By ~37ka, rhyolitic lava flows and domes (72-74% SiO2) began alternating with radially emplaced dacite (63-68% SiO2) and andesite (59-63% SiO2) lava flows. Construction of a broad cone of silicic andesite-dacite (61-64% SiO2) culminated ~30ka in a dominantly explosive sequence that began with crater-forming andesitic eruptions that left fragmental deposits at least 200m thick. This was followed at ~27ka by growth of a steeply dipping summit cone of agglutinate-dominated andesite (56-60.5% SiO2) and formation of a summit crater ~800m wide. This crater was soon filled and overtopped by a thick dacite lava flow and then by >150m of dacitic pyroclastic ejecta. Small-volume dacite lavas (63-67% SiO2) locally cap the pyroclastic pile. A final sheet of mafic agglutinate (54-56% SiO2) - the most mafic product of South <span class="hlt">Sister</span> - erupted from and drapes the small (300-m-wide) present-day summit crater, ending a summit-building sequence that lasted until ~22ka. A 20kyr-long-hiatus was broken by rhyolite eruptions that produced (1) the Rock Mesa coulee, tephra, and satellite domelets (73.5% SiO2) and (2) the Devils Chain of ~20 domes and short coulees (72.3-72.8% SiO2) from N-S vent alignments on South <span class="hlt">Sister</span>'s flanks. The compositional reversal from mafic summit agglutinate to recent rhyolites epitomizes the frequently changing compositional modes of the</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_6");'>6</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li class="active"><span>8</span></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_8 --> <div id="page_9" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li class="active"><span>9</span></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="161"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2011JVGR..207..145F','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2011JVGR..207..145F"><span>Eruptive history of South <span class="hlt">Sister</span>, Oregon Cascades</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Fierstein, Judy; Hildreth, Wes; Calvert, Andrew T.</p> <p>2011-10-01</p> <p>South <span class="hlt">Sister</span> is southernmost and highest of the Three <span class="hlt">Sisters</span>, three geologically dissimilar stratovolcanoes that together form a spectacular 20 km reach along the Cascade crest in Oregon. North <span class="hlt">Sister</span> is a monotonously mafic edifice as old as middle Pleistocene, Middle <span class="hlt">Sister</span> a basalt-andesite-dacite cone built between 48 and 14 ka, and South <span class="hlt">Sister</span> is a basalt-free edifice that alternated rhyolitic and intermediate modes from 50 ka to 2 ka (largely contemporaneous with Middle <span class="hlt">Sister</span>). Detailed mapping, 330 chemical analyses, and 42 radioisotopic ages show that the oldest exposed South <span class="hlt">Sister</span> lavas were initially rhyolitic ~ 50 ka. By ~ 37 ka, rhyolitic lava flows and domes (72-74% SiO 2) began alternating with radially emplaced dacite (63-68% SiO 2) and andesite (59-63% SiO 2) lava flows. Construction of a broad cone of silicic andesite-dacite (61-64% SiO 2) culminated ~ 30 ka in a dominantly explosive sequence that began with crater-forming andesitic eruptions that left fragmental deposits at least 200 m thick. This was followed at ~ 27 ka by growth of a steeply dipping summit cone of agglutinate-dominated andesite (56-60.5% SiO 2) and formation of a summit crater ~ 800 m wide. This crater was soon filled and overtopped by a thick dacite lava flow and then by > 150 m of dacitic pyroclastic ejecta. Small-volume dacite lavas (63-67% SiO 2) locally cap the pyroclastic pile. A final sheet of mafic agglutinate (54-56% SiO 2) - the most mafic product of South <span class="hlt">Sister</span> - erupted from and drapes the small (300-m-wide) present-day summit crater, ending a summit-building sequence that lasted until ~ 22 ka. A 20 kyr-long-hiatus was broken by rhyolite eruptions that produced (1) the Rock Mesa coulee, tephra, and satellite domelets (73.5% SiO 2) and (2) the Devils Chain of ~ 20 domes and short coulees (72.3-72.8% SiO 2) from N-S vent alignments on South <span class="hlt">Sister</span>'s flanks. The compositional reversal from mafic summit agglutinate to recent rhyolites epitomizes the frequently</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29186203','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29186203"><span>Chl1 DNA helicase and Scc2 function in chromosome condensation through cohesin deposition.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Shen, Donglai; Skibbens, Robert V</p> <p>2017-01-01</p> <p>Chl1 DNA helicase promotes <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion and associates with both the cohesion establishment acetyltransferase Eco1/Ctf7 and the DNA polymerase processivity factor PCNA that supports Eco1/Ctf7 function. Mutation in CHL1 results in precocious <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation and cell aneuploidy, defects that arise through reduced levels of chromatin-bound cohesins which normally tether together <span class="hlt">sister</span> <span class="hlt">chromatids</span> (trans tethering). Mutation of Chl1 family members (BACH1/BRIP/FANCJ and DDX11/ChlR1) also exhibit genotoxic sensitivities, consistent with a role for Chl1 in trans tethering which is required for efficient DNA repair. Chl1 promotes the recruitment of Scc2 to DNA which is required for cohesin deposition onto DNA. There is limited evidence, however, that Scc2 also directs the deposition onto DNA of condensins which promote tethering in cis (intramolecular DNA links). Here, we test the ability of Chl1 to promote cis tethering and the role of both Chl1 and Scc2 to promote condensin recruitment to DNA. The results reveal that chl1 mutant cells exhibit significant condensation defects both within the rDNA locus and genome-wide. Importantly, chl1 mutant cell condensation defects do not result from reduced chromatin binding of condensin, but instead through reduced chromatin binding of cohesin. We tested scc2-4 mutant cells and similarly found no evidence of reduced condensin recruitment to chromatin. Consistent with a role for Scc2 specifically in cohesin deposition, scc2-4 mutant cell condensation defects are irreversible. We thus term Chl1 a novel regulator of both chromatin condensation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion through cohesin-based mechanisms. These results reveal an exciting interface between DNA structure and the highly conserved cohesin complex.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5706694','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5706694"><span>Chl1 DNA helicase and Scc2 function in chromosome condensation through cohesin deposition</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Shen, Donglai</p> <p>2017-01-01</p> <p>Chl1 DNA helicase promotes <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion and associates with both the cohesion establishment acetyltransferase Eco1/Ctf7 and the DNA polymerase processivity factor PCNA that supports Eco1/Ctf7 function. Mutation in CHL1 results in precocious <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation and cell aneuploidy, defects that arise through reduced levels of chromatin-bound cohesins which normally tether together <span class="hlt">sister</span> <span class="hlt">chromatids</span> (trans tethering). Mutation of Chl1 family members (BACH1/BRIP/FANCJ and DDX11/ChlR1) also exhibit genotoxic sensitivities, consistent with a role for Chl1 in trans tethering which is required for efficient DNA repair. Chl1 promotes the recruitment of Scc2 to DNA which is required for cohesin deposition onto DNA. There is limited evidence, however, that Scc2 also directs the deposition onto DNA of condensins which promote tethering in cis (intramolecular DNA links). Here, we test the ability of Chl1 to promote cis tethering and the role of both Chl1 and Scc2 to promote condensin recruitment to DNA. The results reveal that chl1 mutant cells exhibit significant condensation defects both within the rDNA locus and genome-wide. Importantly, chl1 mutant cell condensation defects do not result from reduced chromatin binding of condensin, but instead through reduced chromatin binding of cohesin. We tested scc2-4 mutant cells and similarly found no evidence of reduced condensin recruitment to chromatin. Consistent with a role for Scc2 specifically in cohesin deposition, scc2-4 mutant cell condensation defects are irreversible. We thus term Chl1 a novel regulator of both chromatin condensation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion through cohesin-based mechanisms. These results reveal an exciting interface between DNA structure and the highly conserved cohesin complex. PMID:29186203</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27527863','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27527863"><span>Radiation induces premature <span class="hlt">chromatid</span> separation via the miR-142-3p/Bod1 pathway in carcinoma cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Pan, Dong; Du, Yarong; Ren, Zhenxin; Chen, Yaxiong; Li, Xiaoman; Wang, Jufang; Hu, Burong</p> <p>2016-09-13</p> <p>Radiation-induced genomic instability plays a vital role in carcinogenesis. Bod1 is required for proper chromosome biorientation, and Bod1 depletion increases premature <span class="hlt">chromatid</span> separation. MiR-142-3p influences cell cycle progression and inhibits proliferation and invasion in cervical carcinoma cells. We found that radiation induced premature <span class="hlt">chromatid</span> separation and altered miR-142-3p and Bod1 expression in 786-O and A549 cells. Overexpression of miR-142-3p increased premature <span class="hlt">chromatid</span> separation and G2/M cell cycle arrest in 786-O cells by suppressing Bod1 expression. We also found that either overexpression of miR-142-3p or knockdown of Bod1 sensitized 786-O and A549 cells to X-ray radiation. Overexpression of Bod1 inhibited radiation- and miR-142-3p-induced premature <span class="hlt">chromatid</span> separation and increased resistance to radiation in 786-O and A549 cells. Taken together, these results suggest that radiation alters miR-142-3p and Bod1 expression in carcinoma cells, and thus contributes to early stages of radiation-induced genomic instability. Combining ionizing radiation with epigenetic regulation may help improve cancer therapies.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29760389','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29760389"><span>Aurora A-dependent CENP-A phosphorylation at inner centromeres protects bioriented chromosomes against cohesion fatigue.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Eot-Houllier, Grégory; Magnaghi-Jaulin, Laura; Fulcrand, Géraldine; Moyroud, François-Xavier; Monier, Solange; Jaulin, Christian</p> <p>2018-05-14</p> <p>Sustained spindle tension applied to <span class="hlt">sister</span> centromeres during mitosis eventually leads to uncoordinated loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, a phenomenon known as "cohesion fatigue." We report that Aurora A-dependent phosphorylation of serine 7 of the centromere histone variant CENP-A (p-CENP-AS7) protects bioriented chromosomes against cohesion fatigue. Expression of a non-phosphorylatable version of CENP-A (CENP-AS7A) weakens <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion only when <span class="hlt">sister</span> centromeres are under tension, providing the first evidence of a regulated mechanism involved in protection against passive cohesion loss. Consistent with this observation, p-CENP-AS7 is detected at the inner centromere where it forms a discrete domain. The depletion or inhibition of Aurora A phenocopies the expression of CENP-AS7A and we show that Aurora A is recruited to centromeres in a Bub1-dependent manner. We propose that Aurora A-dependent phosphorylation of CENP-A at the inner centromere protects chromosomes against tension-induced cohesion fatigue until the last kinetochore is attached to spindle microtubules.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1202954','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1202954"><span>One-Step and Stepwise Magnification of a BOBBED LETHAL Chromosome in DROSOPHILA MELANOGASTER</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Endow, Sharyn A.; Komma, Donald J.</p> <p>1986-01-01</p> <p>Bobbed lethal (bbl) chromosomes carry too few ribosomal genes for homozygous flies to be viable. Reversion of bbl chromosomes to bb or nearly bb + occurs under magnifying conditions at a low frequency in a single generation. These reversions occur too rapidly to be accounted for by single unequal <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and seem unlikely to be due to multiple <span class="hlt">sister</span> strand exchanges within a given cell lineage. Analysis of several one-step revertants indicates that they are X-Y recombinant chromosomes which probably arise from X-Y recombination at bb. The addition of ribosomal genes from the Y chromosome to the bbl chromosome explains the more rapid reversion of the bbl chromosome than is permitted by single events of unequal <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange. Analysis of stepwise bbl magnified chromosomes, which were selected over a period of 4–9 magnifying generations, shows ribosomal gene patterns that are closely similar to each other. Similarity in rDNA pattern among stepwise magnified products of the same parental chromosome is consistent with reversion by a mechanism of unequal <span class="hlt">sister</span> strand exchange. PMID:3095184</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=nun+AND+study&pg=2&id=EJ656516','ERIC'); return false;" href="https://eric.ed.gov/?q=nun+AND+study&pg=2&id=EJ656516"><span>The Lay <span class="hlt">Sister</span> in Educational History and Memory.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Jack, Christine Trimingham</p> <p>2000-01-01</p> <p>Focuses on the construction of lay <span class="hlt">sisters</span> in a religious order and school setting using a poststructuralist orientation. Explains that in the study documents were examined and interviews were conducted with ex-students, choir nuns, and a lay <span class="hlt">sister</span> at a small Catholic girls-preparatory boarding school. Explores the narrative of one lay <span class="hlt">sister</span>.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12020436','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12020436"><span>Induction and disappearance of G2 <span class="hlt">chromatid</span> breaks in lymphocytes after low doses of low-LET gamma-rays and high-LET fast neutrons.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Vral, A; Thierens, H; Baeyens, A; De Ridder, L</p> <p>2002-04-01</p> <p>To determine by means of the G2 assay the number of <span class="hlt">chromatid</span> breaks induced by low-LET gamma-rays and high-LET neutrons, and to compare the kinetics of <span class="hlt">chromatid</span> break rejoining for radiations of different quality. The G2 assay was performed on blood samples of four healthy donors who were irradiated with low-LET gamma-rays and high-LET neutrons. In a first set of experiments a dose-response curve for the formation of <span class="hlt">chromatid</span> breaks was carried out for gamma-rays and neutrons with doses ranging between 0.1 and 0.5 Gy. In a second set of experiments, the kinetics of <span class="hlt">chromatid</span> break formation and disappearance were investigated after a dose of 0.5 Gy using post-irradiation times ranging between 0.5 and 3.5 h. For the highest dose of 0.5 Gy, the number of isochromatid breaks was also scored. No significant differences in the number of <span class="hlt">chromatid</span> breaks were observed between low-LET gamma-rays and high-LET neutrons for the four donors at any of the doses given. The dose-response curves for the formation of <span class="hlt">chromatid</span> breaks are linear for both radiation qualities and RBEs = 1 were obtained. Scoring of isochromatid breaks at the highest dose of 0.5 Gy revealed that high-LET neutrons were, however, more effective at inducing isochromatid breaks (RBE = 6.2). The rejoining experiments further showed that the kinetics of disappearance of <span class="hlt">chromatid</span> breaks following irradiation with low-LET gamma-rays or high-LET neutrons were not significantly different. Half-times of 0.92 h for gamma-rays and 0.84 h for neutrons were obtained. Applying the G2 assay, the results demonstrate that at low doses of irradiation, the induction as well as the disappearance of <span class="hlt">chromatid</span> breaks is independent of the LET of the radiation qualities used (0.24 keV x microm(-1) 60Co gamma-rays and 20 keV x microm(-1) fast neutrons). As these radiation qualities produce the same initial number of double-strand breaks, the results support the signal model that proposes that <span class="hlt">chromatid</span> breaks are the result</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5545718-studies-dna-chromosome-damage-skin-fibroblasts-blood-lymphocytes-from-psoriasis-patients-treated-methoxypsoralen-uva-irradiation','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5545718-studies-dna-chromosome-damage-skin-fibroblasts-blood-lymphocytes-from-psoriasis-patients-treated-methoxypsoralen-uva-irradiation"><span>Studies of DNA and chromosome damage in skin fibroblasts and blood lymphocytes from psoriasis patients treated with 8-methoxypsoralen and UVA irradiation</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Bredberg, A.; Lambert, B.; Lindblad, A.</p> <p>1983-08-01</p> <p>Exposure of human lymphocytes and skin fibroblasts in vitro to a single, clinically used dose of PUVA, i.e., 0.1 micrograms/ml of 8-methoxypsoralen (8-MOP) plus 0.9-4 J/cm2 of longwave ultraviolet radiation (UVA), lead to the formation of DNA damage as determined by alkaline elution, and to chromosome <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE). When lymphocyte-enriched plasma was obtained from psoriasis patients 2 h after oral intake of 8-MOP and then UVA irradiated (1.8-3.6 J/cm2) in vitro, an increased frequency of chromosome <span class="hlt">aberrations</span> and SCE was observed. Normal levels of chromosome <span class="hlt">aberrations</span> and SCE were found in lymphocytes of psoriasis patients aftermore » 3-30 weeks of PUVA treatment in vivo. A small but statistically significant increase in the SCE frequency was observed in the lymphocytes of psoriasis patients treated for 1-6 years with PUVA (mean 18.0 SCE/cell) as compared with before PUVA (mean 15.8, p less than 0.05). Skin fibroblasts of psoriasis patients analyzed 5 years after the start of PUVA treatment showed a normal number of SCE but a high fraction of filter-retained DNA in the alkaline elution assay, suggesting the presence of cross-linked DNA.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4081007','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4081007"><span>Meiosis-Specific Cohesin Component, Stag3 Is Essential for Maintaining Centromere <span class="hlt">Chromatid</span> Cohesion, and Required for DNA Repair and Synapsis between Homologous Chromosomes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hopkins, Jessica; Bedigian, Rick; Oka, Kazuhiro; Overbeek, Paul; Murray, Steve; Jordan, Philip W.</p> <p>2014-01-01</p> <p>Cohesins are important for chromosome structure and chromosome segregation during mitosis and meiosis. Cohesins are composed of two structural maintenance of chromosomes (SMC1-SMC3) proteins that form a V-shaped heterodimer structure, which is bridged by a α-kleisin protein and a stromal antigen (STAG) protein. Previous studies in mouse have shown that there is one SMC1 protein (SMC1β), two α-kleisins (RAD21L and REC8) and one STAG protein (STAG3) that are meiosis-specific. During meiosis, homologous chromosomes must recombine with one another in the context of a tripartite structure known as the synaptonemal complex (SC). From interaction studies, it has been shown that there are at least four meiosis-specific forms of cohesin, which together with the mitotic cohesin complex, are lateral components of the SC. STAG3 is the only meiosis-specific subunit that is represented within all four meiosis-specific cohesin complexes. In Stag3 mutant germ cells, the protein level of other meiosis-specific cohesin subunits (SMC1β, RAD21L and REC8) is reduced, and their localization to chromosome axes is disrupted. In contrast, the mitotic cohesin complex remains intact and localizes robustly to the meiotic chromosome axes. The instability of meiosis-specific cohesins observed in Stag3 mutants results in <span class="hlt">aberrant</span> DNA repair processes, and disruption of synapsis between homologous chromosomes. Furthermore, mutation of Stag3 results in perturbation of pericentromeric heterochromatin clustering, and disruption of centromere cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> during meiotic prophase. These defects result in early prophase I arrest and apoptosis in both male and female germ cells. The meiotic defects observed in Stag3 mutants are more severe when compared to single mutants for Smc1β, Rec8 and Rad21l, however they are not as severe as the Rec8, Rad21l double mutants. Taken together, our study demonstrates that STAG3 is required for the stability of all meiosis-specific cohesin</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24992337','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24992337"><span>Meiosis-specific cohesin component, Stag3 is essential for maintaining centromere <span class="hlt">chromatid</span> cohesion, and required for DNA repair and synapsis between homologous chromosomes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hopkins, Jessica; Hwang, Grace; Jacob, Justin; Sapp, Nicklas; Bedigian, Rick; Oka, Kazuhiro; Overbeek, Paul; Murray, Steve; Jordan, Philip W</p> <p>2014-07-01</p> <p>Cohesins are important for chromosome structure and chromosome segregation during mitosis and meiosis. Cohesins are composed of two structural maintenance of chromosomes (SMC1-SMC3) proteins that form a V-shaped heterodimer structure, which is bridged by a α-kleisin protein and a stromal antigen (STAG) protein. Previous studies in mouse have shown that there is one SMC1 protein (SMC1β), two α-kleisins (RAD21L and REC8) and one STAG protein (STAG3) that are meiosis-specific. During meiosis, homologous chromosomes must recombine with one another in the context of a tripartite structure known as the synaptonemal complex (SC). From interaction studies, it has been shown that there are at least four meiosis-specific forms of cohesin, which together with the mitotic cohesin complex, are lateral components of the SC. STAG3 is the only meiosis-specific subunit that is represented within all four meiosis-specific cohesin complexes. In Stag3 mutant germ cells, the protein level of other meiosis-specific cohesin subunits (SMC1β, RAD21L and REC8) is reduced, and their localization to chromosome axes is disrupted. In contrast, the mitotic cohesin complex remains intact and localizes robustly to the meiotic chromosome axes. The instability of meiosis-specific cohesins observed in Stag3 mutants results in <span class="hlt">aberrant</span> DNA repair processes, and disruption of synapsis between homologous chromosomes. Furthermore, mutation of Stag3 results in perturbation of pericentromeric heterochromatin clustering, and disruption of centromere cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span> during meiotic prophase. These defects result in early prophase I arrest and apoptosis in both male and female germ cells. The meiotic defects observed in Stag3 mutants are more severe when compared to single mutants for Smc1β, Rec8 and Rad21l, however they are not as severe as the Rec8, Rad21l double mutants. Taken together, our study demonstrates that STAG3 is required for the stability of all meiosis-specific cohesin</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6396241-vitro-genotoxicity-chlorinated-drinking-water-processed-from-humus-rich-surface-water','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6396241-vitro-genotoxicity-chlorinated-drinking-water-processed-from-humus-rich-surface-water"><span>In vitro genotoxicity of chlorinated drinking water processed from humus-rich surface water</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Liimatainen, A.; Grummt, T.</p> <p></p> <p>Chlorination by-products of drinking waters are capable of inducing <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) and chromosome <span class="hlt">aberrations</span> (CA) in vitro, in addition to their mutagenic activity in the Ames test. Finnish drinking waters, processed from humus-rich surface water using chlorine disinfection, have been found to be highly mutagenic in the Ames' test. The highest activities have been found in the acidic, non-volatile fraction of the water concentrates using tester strain TA100 without metabolic activation by S9mix. The mutagenicities have varied between 500 and 14,000 induced revertants per liter. These figures are one to two magnitudes higher than those reported elsewhere. Themore » authors studied five Finnish drinking water samples for their potency to exert genotoxic effects, SCEs and CAs, in mammalian cells in vitro (human peripheral lymphocytes and Chinese hamster lung fibroblasts).« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20136045','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20136045"><span>Modulatory effects of garlic extract against the cyclophosphamide induced genotoxicity in human lymphocytes in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sowjanya, B Lakshmi; Devi, K Rudrama; Madhavi, D</p> <p>2009-09-01</p> <p>Cyclophosphamide (CP) is a commonly used chemotherapeutic and immunosuppressive agent which is used in the treatment of wide range of cancers and autoimmune diseases. Besides that it is a well known carcinogen. In this study by using chromosomal <span class="hlt">aberrations</span> (CA) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) assays method, the modulatory effects exerted by the extract of garlic against the CP induced genotoxicity in the human lymphocyte cultures in vitro were tested. Three different doses of garlic extract were tested for their modulatory capacity on the mutagenecity exerted by 100 microg ml(-1) of CR The results indicate a significant decrease in the frequency of CA and SCE suggesting that the garlic extract modulates the CP induced genotoxicity in a dose dependent manner. These findings provide the future directions for the research on design and development of possible modulatory drugs containing garlic extract.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=jealousy&pg=7&id=EJ537653','ERIC'); return false;" href="https://eric.ed.gov/?q=jealousy&pg=7&id=EJ537653"><span>Crocodile Talk: Attributions of Incestuously Abused and Nonabused <span class="hlt">Sisters</span>.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Monahan, Kathleen</p> <p>1997-01-01</p> <p>This qualitative study analyzed the retrospective attributions of adult <span class="hlt">sisters</span> (five abused <span class="hlt">sister</span> dyads, and five abused and nonabused <span class="hlt">sister</span> dyads) who grew up in incestuous families. It examined the attributions of subjects regarding the general sibling group; victim selection and nonselection; and attributions regarding jealousy, protection,…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20110014117','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20110014117"><span>Analysis of Terminal Deletions using a Generalized Time-Dependent Model of Radiation-Induced Formation of Chromosomal <span class="hlt">Aberrations</span></span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ponomarev, Artem L.; George, K.; Cucinotta, Francis A.</p> <p>2011-01-01</p> <p>We have developed a model that can simulate different types of radiation induced chromosomal <span class="hlt">aberrations</span> (CA's) and can provide predictions on the frequency and size of chromosomes with terminal deletions. Chromosomes with terminal deletions lack telomeres and this can elicit <span class="hlt">sister</span> <span class="hlt">chromatid</span> unions and the prolonged breakage/fusion/bridge (B/F/B) cycles that have been observed in mammalian tumors. The loss of a single telomere has been shown to cause extensive genomic instability through the B/F/B cycle process. Our model uses a stochastic process of DNA broken end joining, in which a realistic spectrum of CA's is created from improperly joined DNA free ends formed by DNA double strand breaks (DSBs). The distribution of the DNA free ends is given by a mechanistic model that takes into account the chromatin structure and track structure for high-LET radiation. The model allows for DSB clustering from high-LET radiation and simulates the formation of CA's in stages that correspond to the actual time after radiation exposure. The time scale for CA formation is derived from experimental data on DSB repair kinetics. At any given time a nucleus may have intact chromosomes, CA's, and/or unrepaired fragments, some of which are defined as terminal deletions, if they are capped by one telomere. The model produces a spectrum of terminal deletions with their corresponding probabilities and size distributions for different heavy ions exposures for the first division after exposure. This data provides valuable information because there is limited experimental data available in the literature on the on the actual size of terminal deletions. We compare our model output to the available experimental data and make a reasonable extrapolation on the number of chromosomes lacking telomeres in human lymphocytes exposed to heavy ions. This model generates data which may lead to predictions on the rate of genomic instability in cells after exposure to high charge and energy nuclei</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23550483','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23550483"><span>Developing skills in clinical leadership for ward <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fenton, Katherine; Phillips, Natasha</p> <p></p> <p>The Francis report has called for a strengthening of the ward <span class="hlt">sister</span>'s role. It recommends that <span class="hlt">sisters</span> should operate in a supervisory capacity and should not be office bound. Effective ward leadership has been recognised as being vital to high-quality patient care and experience, resource management and interprofessional working. However, there is evidence that ward <span class="hlt">sisters</span> are ill equipped to lead effectively and lack confidence in their ability to do so. University College London Hospitals Foundation Trust has recognised that the job has become almost impossible in increasingly large and complex organisations. Ward <span class="hlt">sisters</span> spend less than 40% of their time on clinical leadership and the trust is undertaking a number of initiatives to support them in this role.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://pubs.usgs.gov/of/1999/0437/pdf/of1999-0437.pdf','USGSPUBS'); return false;" href="https://pubs.usgs.gov/of/1999/0437/pdf/of1999-0437.pdf"><span>Volcano hazards in the Three <span class="hlt">Sisters</span> region, Oregon</span></a></p> <p><a target="_blank" href="http://pubs.er.usgs.gov/pubs/index.jsp?view=adv">USGS Publications Warehouse</a></p> <p>Scott, William E.; Iverson, R.M.; Schilling, S.P.; Fisher, B.J.</p> <p>2001-01-01</p> <p>Three <span class="hlt">Sisters</span> is one of three potentially active volcanic centers that lie close to rapidly growing communities and resort areas in Central Oregon. Two types of volcanoes exist in the Three <span class="hlt">Sisters</span> region and each poses distinct hazards to people and property. South <span class="hlt">Sister</span>, Middle <span class="hlt">Sister</span>, and Broken Top, major composite volcanoes clustered near the center of the region, have erupted repeatedly over tens of thousands of years and may erupt explosively in the future. In contrast, mafic volcanoes, which range from small cinder cones to large shield volcanoes like North <span class="hlt">Sister</span> and Belknap Crater, are typically short-lived (weeks to centuries) and erupt less explosively than do composite volcanoes. Hundreds of mafic volcanoes scattered through the Three <span class="hlt">Sisters</span> region are part of a much longer zone along the High Cascades of Oregon in which birth of new mafic volcanoes is possible. This report describes the types of hazardous events that can occur in the Three <span class="hlt">Sisters</span> region and the accompanying volcano-hazard-zonation map outlines areas that could be at risk from such events. Hazardous events include landslides from the steep flanks of large volcanoes and floods, which need not be triggered by eruptions, as well as eruption-triggered events such as fallout of tephra (volcanic ash) and lava flows. A proximal hazard zone roughly 20 kilometers (12 miles) in diameter surrounding the Three <span class="hlt">Sisters</span> and Broken Top could be affected within minutes of the onset of an eruption or large landslide. Distal hazard zones that follow river valleys downstream from the Three <span class="hlt">Sisters</span> and Broken Top could be inundated by lahars (rapid flows of water-laden rock and mud) generated either by melting of snow and ice during eruptions or by large landslides. Slow-moving lava flows could issue from new mafic volcanoes almost anywhere within the region. Fallout of tephra from eruption clouds can affect areas hundreds of kilometers (miles) downwind, so eruptions at volcanoes elsewhere in the</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040141465&hterms=incubation&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3Dincubation','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040141465&hterms=incubation&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3Dincubation"><span>High-LET radiation-induced <span class="hlt">aberrations</span> in prematurely condensed G2 chromosomes of human fibroblasts</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Kawata, T.; Gotoh, E.; Durante, M.; Wu, H.; George, K.; Furusawa, Y.; Cucinotta, F. A.; Dicello, J. F. (Principal Investigator)</p> <p>2000-01-01</p> <p>PURPOSE: To determine the number of initial <span class="hlt">chromatid</span> breaks induced by low- or high-LET irradiations, and to compare the kinetics of <span class="hlt">chromatid</span> break rejoining for radiations of different quality. MATERIAL AND METHODS: Exponentially growing human fibroblast cells AG1522 were irradiated with gamma-rays, energetic carbon (290MeV/u), silicon (490MeV/u) and iron (200 and 600 MeV/u). Chromosomes were prematurely condensed using calyculin A. <span class="hlt">Chromatid</span> breaks and exchanges in G2 cells were scored. PCC were collected after several post-irradiation incubation times, ranging from 5 to 600 min. RESULTS: The kinetics of <span class="hlt">chromatid</span> break rejoining following low- or high-LET irradiation consisted of two exponential components representing a rapid and a slow time constant. <span class="hlt">Chromatid</span> breaks decreased rapidly during the first 10min after exposure, then continued to decrease at a slower rate. The rejoining kinetics were similar for exposure to each type of radiation. <span class="hlt">Chromatid</span> exchanges were also formed quickly. Compared to low-LET radiation, isochromatid breaks were produced more frequently and the proportion of unrejoined breaks was higher for high-LET radiation. CONCLUSIONS: Compared with gamma-rays, isochromatid breaks were observed more frequently in high-LET irradiated samples, suggesting that an increase in isochromatid breaks is a signature of high-LET radiation exposure.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28947820','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28947820"><span>Mps1 kinase-dependent Sgo2 centromere localisation mediates cohesin protection in mouse oocyte meiosis I.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>El Yakoubi, Warif; Buffin, Eulalie; Cladière, Damien; Gryaznova, Yulia; Berenguer, Inés; Touati, Sandra A; Gómez, Rocío; Suja, José A; van Deursen, Jan M; Wassmann, Katja</p> <p>2017-09-25</p> <p>A key feature of meiosis is the step-wise removal of cohesin, the protein complex holding <span class="hlt">sister</span> <span class="hlt">chromatids</span> together, first from arms in meiosis I and then from the centromere region in meiosis II. Centromeric cohesin is protected by Sgo2 from Separase-mediated cleavage, in order to maintain <span class="hlt">sister</span> <span class="hlt">chromatids</span> together until their separation in meiosis II. Failures in step-wise cohesin removal result in aneuploid gametes, preventing the generation of healthy embryos. Here, we report that kinase activities of Bub1 and Mps1 are required for Sgo2 localisation to the centromere region. Mps1 inhibitor-treated oocytes are defective in centromeric cohesin protection, whereas oocytes devoid of Bub1 kinase activity, which cannot phosphorylate H2A at T121, are not perturbed in cohesin protection as long as Mps1 is functional. Mps1 and Bub1 kinase activities localise Sgo2 in meiosis I preferentially to the centromere and pericentromere respectively, indicating that Sgo2 at the centromere is required for protection.In meiosis I centromeric cohesin is protected by Sgo2 from Separase-mediated cleavage ensuring that <span class="hlt">sister</span> <span class="hlt">chromatids</span> are kept together until their separation in meiosis II. Here the authors demonstrate that Bub1 and Mps1 kinase activities are required for Sgo2 localisation to the centromere region.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11255210','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11255210"><span>Chromosomal <span class="hlt">aberrations</span> in lymphocytes of employees in transformer and generator production exposed to electromagnetic fields and mineral oil.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Skyberg, K; Hansteen, I L; Vistnes, A I</p> <p>2001-04-01</p> <p>The objective was to study the risk of cytogenetic damage among high voltage laboratory workers exposed to electromagnetic fields and mineral oil. This is a cross sectional study of 24 exposed and 24 matched controls in a Norwegian transformer factory. The exposure group included employees in the high voltage laboratory and in the generator soldering department. Electric and magnetic fields and oil mist and vapor were measured. Blood samples were analyzed for chromosomal <span class="hlt">aberrations</span> in cultured lymphocytes. In addition to conventional cultures, the lymphocytes were also treated with hydroxyurea and caffeine. This procedure inhibits DNA synthesis and repair in vitro, revealing in vivo genotoxic lesions that are repaired during conventional culturing. In conventional cultures, the exposure group and the controls showed similar values for all cytogenetic parameters. In the DNA synthesis- and repair-inhibited cultures, generator welders showed no differences compared to controls. Among high voltage laboratory testers, compared to the controls, the median number of <span class="hlt">chromatid</span> breaks was doubled (5 vs. 2.5 per 50 cells; P<0.05) the median number of chromosome breaks was 2 vs. 0.5 (P>0.05) and the median number of <span class="hlt">aberrant</span> cells was 5 vs. 3.5 (P<0.05). Further analysis of the inhibited culture data from this and a previous study indicated that years of exposure and smoking increase the risk of <span class="hlt">aberrations</span>. We conclude that there was no increase in cytogenetic damage among exposed workers compared to controls in the conventional lymphocyte assay. In inhibited cultures, however, there were indications that electromagnetic fields in combination with mineral oil exposure may produce chromosomal <span class="hlt">aberrations</span>. Copyright 2001 Wiley-Liss, Inc.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_7");'>7</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li class="active"><span>9</span></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_9 --> <div id="page_10" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li class="active"><span>10</span></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="181"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29276124','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29276124"><span>Sex- and Gamete-Specific Patterns of X Chromosome Segregation in a Trioecious Nematode.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Tandonnet, Sophie; Farrell, Maureen C; Koutsovoulos, Georgios D; Blaxter, Mark L; Parihar, Manish; Sadler, Penny L; Shakes, Diane C; Pires-daSilva, Andre</p> <p>2018-01-08</p> <p>Three key steps in meiosis allow diploid organisms to produce haploid gametes: (1) homologous chromosomes (homologs) pair and undergo crossovers; (2) homologs segregate to opposite poles; and (3) <span class="hlt">sister</span> <span class="hlt">chromatids</span> segregate to opposite poles. The XX/XO sex determination system found in many nematodes [1] facilitates the study of meiosis because variation is easily recognized [2-4]. Here we show that meiotic segregation of X chromosomes in the trioecious nematode Auanema rhodensis [5] varies according to sex (hermaphrodite, female, or male) and type of gametogenesis (oogenesis or spermatogenesis). In this species, XO males exclusively produce X-bearing sperm [6, 7]. The unpaired X precociously separates into <span class="hlt">sister</span> <span class="hlt">chromatids</span>, which co-segregate with the autosome set to generate a functional haplo-X sperm. The other set of autosomes is discarded into a residual body. Here we explore the X chromosome behavior in female and hermaphrodite meioses. Whereas X chromosomes segregate following the canonical pattern during XX female oogenesis to yield haplo-X oocytes, during XX hermaphrodite oogenesis they segregate to the first polar body to yield nullo-X oocytes. Thus, crosses between XX hermaphrodites and males yield exclusively male progeny. During hermaphrodite spermatogenesis, the <span class="hlt">sister</span> <span class="hlt">chromatids</span> of the X chromosomes separate during meiosis I, and homologous X <span class="hlt">chromatids</span> segregate to the functional sperm to create diplo-X sperm. Given these intra-species, intra-individual, and intra-gametogenesis variations in the meiotic program, A. rhodensis is an ideal model for studying the plasticity of meiosis and how it can be modulated. Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23022599','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23022599"><span>Genetic damage in human cells exposed to non-ionizing radiofrequency fields: a meta-analysis of the data from 88 publications (1990-2011).</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Vijayalaxmi; Prihoda, Thomas J</p> <p>2012-12-12</p> <p>Based on the 'limited' evidence suggesting an association between exposure to radiofrequency fields (RF) emitted from mobile phones and two types of brain cancer, glioma and acoustic neuroma, the International Agency for Research on Cancer has classified RF as 'possibly carcinogenic to humans' in group 2B. In view of this classification and the positive correlation between increased genetic damage and carcinogenesis, a meta-analysis was conducted to determine whether a significant increase in genetic damage in human cells exposed to RF provides a potential mechanism for its carcinogenic potential. The extent of genetic damage in human cells, assessed from various end-points, viz., single-/double-strand breaks in the DNA, incidence of chromosomal <span class="hlt">aberrations</span>, micronuclei and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, reported in a total of 88 peer-reviewed scientific publications during 1990-2011 was considered in the meta-analysis. Among the several variables in the experimental protocols used, the influence of five specific variables related to RF exposure characteristics was investigated: (i) frequency, (ii) specific absorption rate, (iii) exposure as continuous wave, pulsed wave and occupationally exposed/mobile phone users, (iv) duration of exposure, and (v) different cell types. The data indicated the following. (1) The magnitude of difference between RF-exposed and sham-/un-exposed controls was small with some exceptions. (2) In certain RF exposure conditions there was a statistically significant increase in genotoxicity assessed from some end-points: the effect was observed in studies with small sample size and was largely influenced by publication bias. Studies conducted within the generally recommended RF exposure guidelines showed a smaller effect. (3) The multiple regression analyses and heterogeneity goodness of fit data indicated that factors other than the above five variables as well as the quality of publications have contributed to the overall results. (4) More</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8684405','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8684405"><span>In vitro studies on the genotoxicity of 2,4-dichloro-6-nitrophenol ammonium (DCNPA) and its major metabolite.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Heng, Z C; Ong, T; Nath, J</p> <p>1996-06-12</p> <p>2,4-dichloro-6-nitrophenol ammonium (DCNPA) is used as a herbicide. However, information on the potential health hazards of DCNPA is limited. In a previous study, we found that DCNPA is genotoxic to Bacillus subtilis and yeast. Further studies were performed to determine whether DCNPA and its major metabolite, 2,4-dichloro-6-aminophenol (DCAP), can induce reverse mutations in Salmonella, gene mutations at the HPRT locus, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) and micronuclei (MN) in V79 cells. Results show that DCNPA does not produce a positive response for any endpoint at concentrations tested. However, treatment of V79 cultures with DCAP caused a significant increase in SCEs and MN in a concentration-dependent manner. These results indicate that DCAP damages DNA and causes chromosomal <span class="hlt">aberrations</span> in V79 cells. Therefore, DCNPA could pose potential health hazards to populations exposed to this herbicide.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26738809','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26738809"><span>Assessment of in vitro genotoxic and cytotoxic effects of flurbiprofen on human cultured lymphocytes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Timocin, Taygun; Ila, Hasan Basri; Dordu, Tuba; Husunet, Mehmet Tahir; Tazehkand, Mostafa Norizadeh; Valipour, Ebrahim; Topaktas, Mehmet</p> <p>2016-01-01</p> <p>Flurbiprofen is non-steroidal anti-inflammatory drug which is commonly used for its analgesic, antipyretic, and anti-inflammatory effects. The purpose of the study was to explore the genotoxic and cytotoxic effects of flurbiprofen in human cultured lymphocytes by <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, chromosome <span class="hlt">aberration</span>, and cytokinesis-blocked micronucleus tests. 10, 20, 30, and 40 μg/mL concentrations of flurbiprofen (solvent is DMSO) were used to treatment of human cultured lymphocytes at two different treatment periods (24 and 48 h). Flurbiprofen had no significant genotoxic effect in any of these tests. But exposing to flurbiprofen for 24 and 48 h led to significant decrease on proliferation index, mitotic index, and nuclear division index (NDI). Also, all decreases were concentration-dependent (except NDI at 24 h treatment period). Consequently, the findings of this research showed that flurbiprofen had cytotoxic effects in human blood lymphocytes.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27618205','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27618205"><span>little <span class="hlt">sister</span>: An Afro-Temporal Solo-Play.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>De Berry, Misty</p> <p>2017-07-03</p> <p>little <span class="hlt">sister</span>: An Afro-Temporal Solo-Play is at once a memory-scape and a mytho-biography set to poetry, movement, and mixed media. A performance poem spanning from the Antebellum South to present-moment Chicago, it tells the story of a nomadic spirit named little-she who shape-shifts through the memories and imaginings of her <span class="hlt">sister</span>, the narrator. Through the characters little-she and the narrator, the solo-performance explores embodied ways to rupture and relieve the impact of macro forms of violence in the micro realm of the everyday. To this end, little <span class="hlt">sister</span> witnesses and disrupts the legacy of violence in the lives of queer Black women through a trans-temporal navigation of everyday encounters within familial, small groups and intimate partner spaces.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20354861','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20354861"><span>Interaction between a pair of gypsy insulators or between heterologous gypsy and Wari insulators modulates Flp site-specific recombination in Drosophila melanogaster.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Krivega, Margarita; Savitskaya, Ekaterina; Krivega, Ivan; Karakozova, Marina; Parshikov, Aleksander; Golovnin, Anton; Georgiev, Pavel</p> <p>2010-08-01</p> <p>Chromatin insulators block the action of transcriptional enhancers when interposed between an enhancer and a promoter. An Flp technology was used to examine interactions between Drosophila gypsy and Wari insulators in somatic and germ cells. The gypsy insulator consists of 12 binding sites for the Su(Hw) protein, while the endogenous Wari insulator, located on the 3' side of the white gene, is independent from the Su(Hw) protein. Insertion of the gypsy but not Wari insulator between FRT sites strongly blocks recombination between Flp dimers bound to FRT sites located on the same <span class="hlt">chromatid</span> (recombination in cis) or in <span class="hlt">sister</span> <span class="hlt">chromatids</span> (unequal recombination in trans). At the same time, the interaction between Wari and gypsy insulators regulates the efficiency of Flp-mediated recombination. Thus, insulators may have a role in controlling interactions between distantly located protein complexes (not only those involved in transcriptional gene regulation) on the same chromosome or on <span class="hlt">sister</span> <span class="hlt">chromatids</span> in somatic and germ cells. We have also found that the frequency of Flp-mediated recombination between FRT sites is strongly dependent on the relative orientation of gypsy insulators. Taken together, our results indicate that the interactions between insulators can be visualized by Flp technology and that insulators may be involved in blocking undesirable interactions between proteins at the two-<span class="hlt">chromatid</span> phase of the cell cycle.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title46-vol7/pdf/CFR-2010-title46-vol7-sec169-307.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title46-vol7/pdf/CFR-2010-title46-vol7-sec169-307.pdf"><span>46 CFR 169.307 - Plans for <span class="hlt">sister</span> vessels.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-10-01</p> <p>... 46 Shipping 7 2010-10-01 2010-10-01 false Plans for <span class="hlt">sister</span> vessels. 169.307 Section 169.307 Shipping COAST GUARD, DEPARTMENT OF HOMELAND SECURITY (CONTINUED) NAUTICAL SCHOOLS SAILING SCHOOL VESSELS Construction and Arrangement Plans § 169.307 Plans for <span class="hlt">sister</span> vessels. Plans are not required for any vessel...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title46-vol7/pdf/CFR-2011-title46-vol7-sec169-307.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title46-vol7/pdf/CFR-2011-title46-vol7-sec169-307.pdf"><span>46 CFR 169.307 - Plans for <span class="hlt">sister</span> vessels.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-10-01</p> <p>... 46 Shipping 7 2011-10-01 2011-10-01 false Plans for <span class="hlt">sister</span> vessels. 169.307 Section 169.307 Shipping COAST GUARD, DEPARTMENT OF HOMELAND SECURITY (CONTINUED) NAUTICAL SCHOOLS SAILING SCHOOL VESSELS Construction and Arrangement Plans § 169.307 Plans for <span class="hlt">sister</span> vessels. Plans are not required for any vessel...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=35277','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=35277"><span>The C-terminal domain of the Bloom syndrome DNA helicase is essential for genomic stability</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Yankiwski, Victor; Noonan, James P; Neff, Norma F</p> <p>2001-01-01</p> <p>Background Bloom syndrome is a rare cancer-prone disorder in which the cells of affected persons have a high frequency of somatic mutation and genomic instability. Bloom syndrome cells have a distinctive high frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and quadriradial formation. BLM, the protein altered in BS, is a member of the RecQ DNA helicase family, whose members share an average of 40% identity in the helicase domain and have divergent N-terminal and C-terminal flanking regions of variable lengths. The BLM DNA helicase has been shown to localize to the ND10 (nuclear domain 10) or PML (promyelocytic leukemia) nuclear bodies, where it associates with TOPIIIα, and to the nucleolus. Results This report demonstrates that the N-terminal domain of BLM is responsible for localization of the protein to the nuclear bodies, while the C-terminal domain directs the protein to the nucleolus. Deletions of the N-terminal domain of BLM have little effect on <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange frequency and chromosome stability as compared to helicase and C-terminal mutations which can increase SCE frequency and chromosome abnormalities. Conclusion The helicase activity and the C-terminal domain of BLM are critical for maintaining genomic stability as measured by the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay. The localization of BLM into the nucleolus by the C-terminal domain appears to be more important to genomic stability than localization in the nuclear bodies. PMID:11472631</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/10753184','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/10753184"><span>XPD polymorphisms: effects on DNA repair proficiency.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lunn, R M; Helzlsouer, K J; Parshad, R; Umbach, D M; Harris, E L; Sanford, K K; Bell, D A</p> <p>2000-04-01</p> <p>XPD codes for a DNA helicase involved in transcription and nucleotide excision repair. Rare XPD mutations diminish nucleotide excision repair resulting in hypersensitivity to UV light and increased risk of skin cancer. Several polymorphisms in this gene have been identified but their impact on DNA repair is not known. We compared XPD genotypes at codons 312 and 751 with DNA repair proficiency in 31 women. XPD genotypes were measured by PCR-RFLP. DNA repair proficiency was assessed using a cytogenetic assay that detects X-ray induced <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> (breaks and gaps). <span class="hlt">Chromatid</span> <span class="hlt">aberrations</span> were scored per 100 metaphase cells following incubation at 37 degrees C (1.5 h after irradiation) to allow for repair of DNA damage. Individuals with the Lys/Lys codon 751 XPD genotype had a higher number of <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> (132/100 metaphase cells) than those having a 751Gln allele (34/100 metaphase cells). Individuals having greater than 60 <span class="hlt">chromatid</span> breaks plus gaps were categorized as having sub-optimal repair. Possessing a Lys/Lys751 genotype increased the risk of sub-optimal DNA repair (odds ratio = 7.2, 95% confidence interval = 1.01-87.7). The Asp312Asn XPD polymorphism did not appear to affect DNA repair proficiency. These results suggest that the Lys751 (common) allele may alter the XPD protein product resulting in sub-optimal repair of X-ray-induced DNA damage.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040112575&hterms=cells+cancer&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3Dcells%2Bcancer','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040112575&hterms=cells+cancer&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3Dcells%2Bcancer"><span>Cell killing and <span class="hlt">chromatid</span> damage in primary human bronchial epithelial cells irradiated with accelerated 56Fe ions</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Suzuki, M.; Piao, C.; Hall, E. J.; Hei, T. K.</p> <p>2001-01-01</p> <p>We examined cell killing and <span class="hlt">chromatid</span> damage in primary human bronchial epithelial cells irradiated with high-energy 56Fe ions. Cells were irradiated with graded doses of 56Fe ions (1 GeV/nucleon) accelerated with the Alternating Gradient Synchrotron at Brookhaven National Laboratory. The survival curves for cells plated 1 h after irradiation (immediate plating) showed little or no shoulder. However, the survival curves for cells plated 24 h after irradiation (delayed plating) had a small initial shoulder. The RBE for 56Fe ions compared to 137Cs gamma rays was 1.99 for immediate plating and 2.73 for delayed plating at the D10. The repair ratio (delayed plating/immediate plating) was 1.67 for 137Cs gamma rays and 1.22 for 56Fe ions. The dose-response curves for initially measured and residual <span class="hlt">chromatid</span> fragments detected by the Calyculin A-mediated premature chromosome condensation technique showed a linear response. The results indicated that the induction frequency for initially measured fragments was the same for 137Cs gamma rays and 56Fe ions. On the other hand, approximately 85% of the fragments induced by 137Cs gamma rays had rejoined after 24 h of postirradiation incubation; the corresponding amount for 56Fe ions was 37%. Furthermore, the frequency of <span class="hlt">chromatid</span> exchanges induced by gamma rays measured 24 h after irradiation was higher than that induced by 56Fe ions. No difference in the amount of <span class="hlt">chromatid</span> damage induced by the two types of radiations was detected when assayed 1 h after irradiation. The results suggest that high-energy 56Fe ions induce a higher frequency of complex, unrepairable damage at both the cellular and chromosomal levels than 137Cs gamma rays in the target cells for radiation-induced lung cancers.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=sister+AND+cities&id=EJ437613','ERIC'); return false;" href="https://eric.ed.gov/?q=sister+AND+cities&id=EJ437613"><span>Building International Relations for Children through <span class="hlt">Sister</span> Schools.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Pryor, Carolyn B.</p> <p>1992-01-01</p> <p>Inspired by <span class="hlt">Sister</span> Cities International and the NASSP's school-to-school exchange program, "<span class="hlt">sister</span> school" pairings have proved to be workable educational programs with long-range impact on participants. Some post-cold war efforts include U.S.-USSR High School Academic Partnerships, Project Harmony, and Center for U.S.-USSR Initiatives.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=25194','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=25194"><span>The DNA Helicase Activity of BLM Is Necessary for the Correction of the Genomic Instability of Bloom Syndrome Cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Neff, Norma F.; Ellis, Nathan A.; Ye, Tian Zhang; Noonan, James; Huang, Kelly; Sanz, Maureen; Proytcheva, Maria</p> <p>1999-01-01</p> <p>Bloom syndrome (BS) is a rare autosomal recessive disorder characterized by growth deficiency, immunodeficiency, genomic instability, and the early development of cancers of many types. BLM, the protein encoded by BLM, the gene mutated in BS, is localized in nuclear foci and absent from BS cells. BLM encodes a DNA helicase, and proteins from three missense alleles lack displacement activity. BLM transfected into BS cells reduces the frequency of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and restores BLM in the nucleus. Missense alleles fail to reduce the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in transfected BS cells or restore the normal nuclear pattern. BLM complements a phenotype of a Saccharomyces cerevisiae sgs1 top3 strain, and the missense alleles do not. This work demonstrates the importance of the enzymatic activity of BLM for its function and nuclear localization pattern. PMID:10069810</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5963586','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5963586"><span>The <span class="hlt">Sister</span> Study Cohort: Baseline Methods and Participant Characteristics</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hodgson, M. Elizabeth; Deming-Halverson, Sandra L.; Juras, Paula S.; D’Aloisio, Aimee A.; Suarez, Lourdes M.; Kleeberger, Cynthia A.; Shore, David L.; DeRoo, Lisa A.; Taylor, Jack A.; Weinberg, Clarice R.</p> <p>2017-01-01</p> <p>Background: The <span class="hlt">Sister</span> Study was designed to address gaps in the study of environment and breast cancer by taking advantage of more frequent breast cancer diagnoses among women with a <span class="hlt">sister</span> history of breast cancer and the presumed enrichment of shared environmental and genetic exposures. Objective: The <span class="hlt">Sister</span> Study sought a large cohort of women never diagnosed with breast cancer but who had a <span class="hlt">sister</span> (full or half) diagnosed with breast cancer. Methods: A multifaceted national effort employed novel strategies to recruit a diverse cohort, and collected biological and environmental samples and extensive data on potential breast cancer risk factors. Results: The <span class="hlt">Sister</span> Study enrolled 50,884 U.S. and Puerto Rican women 35–74y of age (median 56 y). Although the majority were non-Hispanic white, well educated, and economically well off, substantial numbers of harder-to-recruit women also enrolled (race/ethnicity other than non-Hispanic white: 16%; no college degree: 35%; household income <$50,000: 26%). Although all had a biologic <span class="hlt">sister</span> with breast cancer, 16.5% had average or lower risk of breast cancer according to the Breast Cancer Risk Assessment Tool (Gail score). Most were postmenopausal (66%), parous with a first full-term pregnancy <30y of age (79%), never-smokers (56%) with body mass indexes (BMIs) of <29.9 kg/m2 (70%). Few (5%) reported any cancer prior to enrollment. Conclusions: The <span class="hlt">Sister</span> Study is a unique cohort designed to efficiently study environmental and genetic risk factors for breast cancer. Extensive exposure data over the life-course and baseline specimens provide important opportunities for studying breast cancer and other health outcomes in women. Collaborations are welcome. https://doi.org/10.1289/EHP1923 PMID:29373861</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20503771','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20503771"><span>[Two Dutch <span class="hlt">sisters</span> in analysis with Freud].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stroeken, Harry</p> <p>2010-01-01</p> <p>The author provides persuasive or at least plausible data for the identity of two patients recorded by Freud in his working season of 1910/11. They were two <span class="hlt">sisters</span>, living in The Hague/Leiden, who came from a rich banker's family, the van der Lindens. Whereas the treatment does not seem to have led to any decisive improvement for the older of the two, it may have encouraged the younger <span class="hlt">sister</span> to seek divorce.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=65716&keyword=donor+AND+blood&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50','EPA-EIMS'); return false;" href="https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=65716&keyword=donor+AND+blood&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50"><span>INDUCTION OF DNA STRAND BREAKS BY TRIHALOMETHANES IN PRIMARY HUMAN LUNG EPITHELIAL CELLS</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p><br>Abstract<br><br> Trihalomethanes (TEMs) are disinfection by-products and suspected human carcinogens present in chlorinated drinking water. Previous studies have shown that many THMs induce <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and DNA strand breaks in human peripheral blood lymphocyte...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/3802407','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/3802407"><span>High local carcinogenic activity of 1,3-dimethyl-3-phenyl-1-nitrosourea and its inactivation by intravenous application in rats: comparison of in vivo findings with the in vitro direct and a combined in vivo/in vitro <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay in V79-E cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Thust, R; Martin, J; Mendel, J; Schreiber, D</p> <p>1987-02-01</p> <p>1,3-Dimethyl-3-phenyl-1-nitrosourea (DMPNU) is a very potent local carcinogen in rats and induces a 100% frequency of forestomach carcinomas when applied i.g. in two different dosages (10 applications of 0.3 or 0.03 mmol/kg body wt, respectively, at 14-day intervals), but it is inactive upon i.v. administration (10 applications of 0.03 mmol/kg body wt at 14-day intervals). By means of the direct <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) assay in V79-E cells in the presence of rat blood, serum or plasma, respectively, as well as by a 'host-mediated' SCE assay (in which the agent was given i.v. to rats, and blood taken from the animal was checked for the recovery of genotoxic activity in cell cultures), we tried to elucidate the unexpected lack of carcinogenic activity of i.v. DMPNU. The direct SCE assay revealed a drastic reduction of DMPNU genotoxicity by rat blood, serum or plasma, respectively, which is abolished by the esterase inhibitor diisopropylfluorophosphate. In the 'host-mediated' SCE assay a genotoxic activity of DMPNU was only recoverable after a very high i.v. dose and when the blood added to the cell cultures had been taken from the rat heart within 1 min after DMPNU administration in vivo. 1-Methyl-1-nitrosourea (MNU) and 1-methyl-3-phenyl-1-nitrosourea (MPNU) were used as positive controls in these experiments and also gave a lower response than theoretically expected, but the relative loss of activity with the latter compounds was much lower than with DMPNU. It is assumed that an esterase in rat blood effectively decomposes this trisubstituted nitrosourea. Problems of the novel 'host-mediated' SCE assay are discussed.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5331533','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5331533"><span>Evidence of Some Natural Products with Antigenotoxic Effects. Part 1: Fruits and Polysaccharides</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Izquierdo-Vega, Jeannett Alejandra; Morales-González, José Antonio; Sánchez-Gutiérrez, Manuel; Betanzos-Cabrera, Gabriel; Sosa-Delgado, Sara M.; Sumaya-Martínez, María Teresa; Morales-González, Ángel; Paniagua-Pérez, Rogelio; Madrigal-Bujaidar, Eduardo; Madrigal-Santillán, Eduardo</p> <p>2017-01-01</p> <p>Cancer is one of the leading causes of deaths worldwide. The agents capable of causing damage to genetic material are known as genotoxins and, according to their mode of action, are classified into mutagens, carcinogens or teratogens. Genotoxins are involved in the pathogenesis of several chronic degenerative diseases including hepatic, neurodegenerative and cardiovascular disorders, diabetes, arthritis, cancer, chronic inflammation and ageing. In recent decades, researchers have found novel bioactive phytocompounds able to counteract the effects of physical and chemical mutagens. Several studies have shown potential antigenotoxicity in a variety of fruits. In this review (Part 1), we present an overview of research conducted on some fruits (grapefruit, cranberries, pomegranate, guava, pineapple, and mango) which are frequently consumed by humans, as well as the analysis of some phytochemicals extracted from fruits and yeasts which have demonstrated antigenotoxic capacity in various tests, including the Ames assay, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, chromosomal <span class="hlt">aberrations</span>, micronucleus and comet assay. PMID:28157162</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12616623','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12616623"><span>Antigenotoxic potential of certain dietary constituents.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Shukla, Yogeshwer; Arora, Annu; Taneja, Pankaj</p> <p>2003-01-01</p> <p>The human diet contains a variety of compounds that exhibit chemopreventive effects towards an array of xenobiotics. In the present study, the antigenotoxic potential of selected dietary constituents including Diallyl sulfide (DAS), Indole-3-carbinol (I3C), Curcumin (CUR), and Black tea polyphenols (BTP) has been evaluated in the Salmonella typhimurium reverse mutation and mammalian in vivo cytogenetic assays. In addition, the anticlastogenic effect of the above dietary constituents was identified towards Benzo(a)pyrene (BaP) and cyclophosphamide- (CP) induced cytogenetic damage in mouse bone marrow cells. The induction of BaP and CP induced chromosomal <span class="hlt">aberrations</span>, micronuclei formation, and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) were found to be inhibited in a dose-dependent manner by DAS, I3C, CUR, and BTP. Thus the study reveals the antimutagenic potential of these dietary compounds towards BaP- and CP-induced genotoxicity in microbial and mammalian test systems. Copyright 2003 Wiley-Liss, Inc.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15887256','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15887256"><span>Controversial cytogenetic observations in mammalian somatic cells exposed to extremely low frequency electromagnetic radiation: a review and future research recommendations.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Vijayalaxmi; Obe, Guenter</p> <p>2005-07-01</p> <p>During the years 1990-2003, a large number of investigations were conducted using animals, cultured rodent and human cells as well as freshly collected human blood lymphocytes to determine the genotoxic potential of exposure to nonionizing radiation emitted from extremely low frequency electromagnetic fields (EMF). Among the 63 peer reviewed scientific reports, the conclusions from 29 studies (46%) did not indicate increased damage to the genetic material, as assessed from DNA strand breaks, incidence of chromosomal <span class="hlt">aberrations</span> (CA), micronuclei (MN), and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE), in EMF exposed cells as compared with sham exposed and/or unexposed cells, while those from 14 investigations (22%) have suggested an increase in such damage in EMF exposed cells. The observations from 20 other studies (32%) were inconclusive. This study reviews the investigations published in peer reviewed scientific journals during 1990-2003 and attempts to identify probable reason(s) for the conflicting results. Recommendations are made for future research to address some of the controversial observations. Copyright 2005 Wiley-Liss, Inc.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_8");'>8</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li class="active"><span>10</span></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_10 --> <div id="page_11" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li class="active"><span>11</span></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="201"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16481348','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16481348"><span>Cytogenetic investigation of subjects professionally exposed to radiofrequency radiation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Maes, Annemarie; Van Gorp, Urbain; Verschaeve, Luc</p> <p>2006-03-01</p> <p>Nowadays, virtually everybody is exposed to radiofrequency radiation (RFR) from mobile phone base station antennas or other sources. At least according to some scientists, this exposure can have detrimental health effects. We investigated cytogenetic effects in peripheral blood lymphocytes from subjects who were professionally exposed to mobile phone electromagnetic fields in an attempt to demonstrate possible RFR-induced genetic effects. These subjects can be considered well suited for this purpose as their RFR exposure is 'normal' though rather high, and definitely higher than that of the 'general population'. The alkaline comet assay, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) and chromosome <span class="hlt">aberration</span> tests revealed no evidence of RFR-induced genetic effects. Blood cells were also exposed to the well known chemical mutagen mitomycin C in order to investigate possible combined effects of RFR and the chemical. No cooperative action was found between the electromagnetic field exposure and the mutagen using either the comet assay or SCE test.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1995Mercu..24e..23B','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1995Mercu..24e..23B"><span>The Prodigal <span class="hlt">Sister</span> - Venus</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Barlow, Nadine G.</p> <p>1995-09-01</p> <p>If you think Venus is a hellhole now, be thankful you weren't there 500 million years ago. Those were the days, many planetary scientists believe, of apocalypse on our <span class="hlt">sister</span> world: Volcanoes wracked the land, while greenhouse gases broiled the air. Is this the Earth's fate, too?</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3979685','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3979685"><span>Differential Radiosensitivity Phenotypes of DNA-PKcs Mutations Affecting NHEJ and HRR Systems following Irradiation with Gamma-Rays or Very Low Fluences of Alpha Particles</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Little, John B.; Kato, Takamitsu A.; Shih, Hung-Ying; Xie, Xian-Jin; Wilson Jr., Paul F.; Brogan, John R.; Kurimasa, Akihiro; Chen, David J.; Bedford, Joel S.; Chen, Benjamin P. C.</p> <p>2014-01-01</p> <p>We have examined cell-cycle dependence of chromosomal <span class="hlt">aberration</span> induction and cell killing after high or low dose-rate γ irradiation in cells bearing DNA-PKcs mutations in the S2056 cluster, the T2609 cluster, or the kinase domain. We also compared <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) production by very low fluences of α-particles in DNA-PKcs mutant cells, and in homologous recombination repair (HRR) mutant cells including Rad51C, Rad51D, and Fancg/xrcc9. Generally, chromosomal <span class="hlt">aberrations</span> and cell killing by γ-rays were similarly affected by mutations in DNA-PKcs, and these mutant cells were more sensitive in G1 than in S/G2 phase. In G1-irradiated DNA-PKcs mutant cells, both chromosome- and <span class="hlt">chromatid</span>-type breaks and exchanges were in excess than wild-type cells. For cells irradiated in late S/G2 phase, mutant cells showed very high yields of <span class="hlt">chromatid</span> breaks compared to wild-type cells. Few exchanges were seen in DNA-PKcs-null, Ku80-null, or DNA-PKcs kinase dead mutants, but exchanges in excess were detected in the S2506 or T2609 cluster mutants. SCE induction by very low doses of α-particles is resulted from bystander effects in cells not traversed by α-particles. SCE seen in wild-type cells was completely abolished in Rad51C- or Rad51D-deficient cells, but near normal in Fancg/xrcc9 cells. In marked contrast, very high levels of SCEs were observed in DNA-PKcs-null, DNA-PKcs kinase-dead and Ku80-null mutants. SCE induction was also abolished in T2609 cluster mutant cells, but was only slightly reduced in the S2056 cluster mutant cells. Since both non-homologous end-joining (NHEJ) and HRR systems utilize initial DNA lesions as a substrate, these results suggest the possibility of a competitive interference phenomenon operating between NHEJ and at least the Rad51C/D components of HRR; the level of interaction between damaged DNA and a particular DNA-PK component may determine the level of interaction of such DNA with a relevant HRR component. PMID:24714417</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21910232','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21910232"><span>Two <span class="hlt">sisters</span> resembling Gorlin-Chaudhry-Moss syndrome.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Aravena, Teresa; Passalacqua, Cristóbal; Pizarro, Oscar; Aracena, Mariana</p> <p>2011-10-01</p> <p>The Gorlin-Chaudhry-Moss syndrome (GCMS), was describe initially by Gorlin et al. [Gorlin et al. (1960)] in two <span class="hlt">sisters</span> with craniosynostosis, hypertrichosis, hypoplastic labia majora, dental defects, eye anomalies, patent ductus arteriosus, and normal intelligence. Two other sporadic instances have been documented. Here, we report on two <span class="hlt">sisters</span> with a condition with some similarities to GCMS as well as some differences, which could represent either previously unreported variability in GCMS, or it may represent a novel disorder. Copyright © 2011 Wiley-Liss, Inc.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/EJ1006063.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/EJ1006063.pdf"><span><span class="hlt">Sister</span> Mary Emil Penet, I.H.M.: Founder of the <span class="hlt">Sister</span> Formation Conference</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Glisky, Joan</p> <p>2006-01-01</p> <p>Mary Emil Penet, I.H.M., (1916-2001) used her talents and charisma to shape the first national organization of American women religious, the <span class="hlt">Sister</span> Formation Conference (SFC; 1954-1964), facilitating the integrated intellectual, spiritual, psychological, and professional development of vowed women religious. In the decade preceding Vatican II, her…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5088565','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5088565"><span>Mutations in genes encoding condensin complex proteins cause microcephaly through decatenation failure at mitosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Martin, Carol-Anne; Murray, Jennie E.; Carroll, Paula; Leitch, Andrea; Mackenzie, Karen J.; Halachev, Mihail; Fetit, Ahmed E.; Keith, Charlotte; Bicknell, Louise S.; Fluteau, Adeline; Gautier, Philippe; Hall, Emma A.; Joss, Shelagh; Soares, Gabriela; Silva, João; Bober, Michael B.; Duker, Angela; Wise, Carol A.; Quigley, Alan J.; Phadke, Shubha R.; Wood, Andrew J.; Vagnarelli, Paola; Jackson, Andrew P.</p> <p>2016-01-01</p> <p>Compaction of chromosomes is essential for accurate segregation of the genome during mitosis. In vertebrates, two condensin complexes ensure timely chromosome condensation, <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement, and maintenance of mitotic chromosome structure. Here, we report that biallelic mutations in NCAPD2, NCAPH, or NCAPD3, encoding subunits of these complexes, cause microcephaly. In addition, hypomorphic Ncaph2 mice have significantly reduced brain size, with frequent anaphase chromatin bridge formation observed in apical neural progenitors during neurogenesis. Such DNA bridges also arise in condensin-deficient patient cells, where they are the consequence of failed <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement during chromosome compaction. This results in chromosome segregation errors, leading to micronucleus formation and increased aneuploidy in daughter cells. These findings establish “condensinopathies” as microcephalic disorders, with decatenation failure as an additional disease mechanism for microcephaly, implicating mitotic chromosome condensation as a key process ensuring mammalian cerebral cortex size. PMID:27737959</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26923589','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26923589"><span>Structure of the Pds5-Scc1 Complex and Implications for Cohesin Function.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Muir, Kyle W; Kschonsak, Marc; Li, Yan; Metz, Jutta; Haering, Christian H; Panne, Daniel</p> <p>2016-03-08</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion is a fundamental prerequisite to faithful genome segregation. Cohesion is precisely regulated by accessory factors that modulate the stability with which the cohesin complex embraces chromosomes. One of these factors, Pds5, engages cohesin through Scc1 and is both a facilitator of cohesion, and, conversely also mediates the release of cohesin from chromatin. We present here the crystal structure of a complex between budding yeast Pds5 and Scc1, thus elucidating the molecular basis of Pds5 function. Pds5 forms an elongated HEAT repeat that binds to Scc1 via a conserved surface patch. We demonstrate that the integrity of the Pds5-Scc1 interface is indispensable for the recruitment of Pds5 to cohesin, and that its abrogation results in loss of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion and cell viability. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://pubs.usgs.gov/of/2007/1221/','USGSPUBS'); return false;" href="https://pubs.usgs.gov/of/2007/1221/"><span>Digital Data for Volcano Hazards of the Three <span class="hlt">Sisters</span> Region, Oregon</span></a></p> <p><a target="_blank" href="http://pubs.er.usgs.gov/pubs/index.jsp?view=adv">USGS Publications Warehouse</a></p> <p>Schilling, S.P.; Doelger, S.; Scott, W.E.; Iverson, R.M.</p> <p>2008-01-01</p> <p>Three <span class="hlt">Sisters</span> is one of three active volcanic centers that lie close to rapidly growing communities and resort areas in Central Oregon. The major composite volcanoes of this area are clustered near the center of the region and include South <span class="hlt">Sister</span>, Middle <span class="hlt">Sister</span>, and Broken Top. Additionally, hundreds of mafic volcanoes are scattered throughout the Three <span class="hlt">Sisters</span> area. These range from small cinder cones to large shield volcanoes like North <span class="hlt">Sister</span> and Belknap Crater. Hazardous events include landslides from the steep flanks of large volcanoes and floods, which need not be triggered by eruptions, as well as eruption-triggered events such as fallout of tephra (volcanic ash) and lava flows. A proximal hazard zone roughly 20 kilometers (12 miles) in diameter surrounding the Three <span class="hlt">Sisters</span> and Broken Top could be affected within minutes of the onset of an eruption or large landslide. Distal hazard zones that follow river valleys downstream from the Three <span class="hlt">Sisters</span> and Broken Top could be inundated by lahars (rapid flows of water-laden rock and mud) generated either by melting of snow and ice during eruptions or by large landslides. Slow-moving lava flows could issue from new mafic volcanoes almost anywhere within the region. Fallout of tephra from eruption clouds can affect areas hundreds of kilometers (miles) downwind, so eruptions at volcanoes elsewhere in the Cascade Range also contribute to volcano hazards in Central Oregon. Scientists at the Cascades Volcano Observatory created a geographic information system (GIS) data set which depicts proximal and distal lahar hazard zones as well as a regional lava flow hazard zone for Three <span class="hlt">Sisters</span> (USGS Open-File Report 99-437, Scott and others, 1999). The various distal lahar zones were constructed from LaharZ software using 20, 100, and 500 million cubic meter input flow volumes. Additionally, scientists used the depositional history of past events in the Three <span class="hlt">Sisters</span> Region as well as experience and judgment derived from the</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3374747','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3374747"><span>Spindle checkpoint–independent inhibition of mitotic chromosome segregation by Drosophila Mps1</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Althoff, Friederike; Karess, Roger E.; Lehner, Christian F.</p> <p>2012-01-01</p> <p>Monopolar spindle 1 (Mps1) is essential for the spindle assembly checkpoint (SAC), which prevents anaphase onset in the presence of misaligned chromosomes. Moreover, Mps1 kinase contributes in a SAC-independent manner to the correction of erroneous initial attachments of chromosomes to the spindle. Our characterization of the Drosophila homologue reveals yet another SAC-independent role. As in yeast, modest overexpression of Drosophila Mps1 is sufficient to delay progression through mitosis during metaphase, even though chromosome congression and metaphase alignment do not appear to be affected. This delay in metaphase depends on the SAC component Mad2. Although Mps1 overexpression in mad2 mutants no longer causes a metaphase delay, it perturbs anaphase. <span class="hlt">Sister</span> kinetochores barely move apart toward spindle poles. However, kinetochore movements can be restored experimentally by separase-independent resolution of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. We propose therefore that Mps1 inhibits <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation in a SAC-independent manner. Moreover, we report unexpected results concerning the requirement of Mps1 dimerization and kinase activity for its kinetochore localization in Drosophila. These findings further expand Mps1's significance for faithful mitotic chromosome segregation and emphasize the importance of its careful regulation. PMID:22553353</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22553353','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22553353"><span>Spindle checkpoint-independent inhibition of mitotic chromosome segregation by Drosophila Mps1.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Althoff, Friederike; Karess, Roger E; Lehner, Christian F</p> <p>2012-06-01</p> <p>Monopolar spindle 1 (Mps1) is essential for the spindle assembly checkpoint (SAC), which prevents anaphase onset in the presence of misaligned chromosomes. Moreover, Mps1 kinase contributes in a SAC-independent manner to the correction of erroneous initial attachments of chromosomes to the spindle. Our characterization of the Drosophila homologue reveals yet another SAC-independent role. As in yeast, modest overexpression of Drosophila Mps1 is sufficient to delay progression through mitosis during metaphase, even though chromosome congression and metaphase alignment do not appear to be affected. This delay in metaphase depends on the SAC component Mad2. Although Mps1 overexpression in mad2 mutants no longer causes a metaphase delay, it perturbs anaphase. <span class="hlt">Sister</span> kinetochores barely move apart toward spindle poles. However, kinetochore movements can be restored experimentally by separase-independent resolution of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. We propose therefore that Mps1 inhibits <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation in a SAC-independent manner. Moreover, we report unexpected results concerning the requirement of Mps1 dimerization and kinase activity for its kinetochore localization in Drosophila. These findings further expand Mps1's significance for faithful mitotic chromosome segregation and emphasize the importance of its careful regulation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2139799','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2139799"><span>Thrombopoietin-induced Polyploidization of Bone Marrow Megakaryocytes Is Due to a Unique Regulatory Mechanism in Late Mitosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Nagata, Yuka; Muro, Yoshinao; Todokoro, Kazuo</p> <p>1997-01-01</p> <p>Megakaryocytes undergo a unique differentiation program, becoming polyploid through repeated cycles of DNA synthesis without concomitant cell division. However, the mechanism underlying this polyploidization remains totally unknown. It has been postulated that polyploidization is due to a skipping of mitosis after each round of DNA replication. We carried out immunohistochemical studies on mouse bone marrow megakaryocytes during thrombopoietin- induced polyploidization and found that during this process megakaryocytes indeed enter mitosis and progress through normal prophase, prometaphase, metaphase, and up to anaphase A, but not to anaphase B, telophase, or cytokinesis. It was clearly observed that multiple spindle poles were formed as the polyploid megakaryocytes entered mitosis; the nuclear membrane broke down during prophase; the <span class="hlt">sister</span> <span class="hlt">chromatids</span> were aligned on a multifaced plate, and the centrosomes were symmetrically located on either side of each face of the plate at metaphase; and a set of <span class="hlt">sister</span> <span class="hlt">chromatids</span> moved into the multiple centrosomes during anaphase A. We further noted that the pair of spindle poles in anaphase were located in close proximity to each other, probably because of the lack of outward movement of spindle poles during anaphase B. Thus, the reassembling nuclear envelope may enclose all the <span class="hlt">sister</span> <span class="hlt">chromatids</span> in a single nucleus at anaphase and then skip telophase and cytokinesis. These observations clearly indicate that polyploidization of megakaryocytes is not simply due to a skipping of mitosis, and that the megakaryocytes must have a unique regulatory mechanism in anaphase, e.g., factors regulating anaphase such as microtubule motor proteins might be involved in this polyploidization process. PMID:9334347</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/478890-neuropsychological-profiles-three-sisters-homozygous-fragile-premutation','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/478890-neuropsychological-profiles-three-sisters-homozygous-fragile-premutation"><span>Neuropsychological profiles of three <span class="hlt">sisters</span> homozygous for the fragile X premutation</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Mazzocco, M.M.M.; Holden, J.J.A.</p> <p>1996-08-09</p> <p>Fragile X syndrome (fraX) is associated with an amplification of a CGG repeat within the fraX mental retardation (FMR-1) gene. We describe an exceptional family in which 3 adult <span class="hlt">sisters</span> are homozygous for the FMR-1 premutation. Each <span class="hlt">sister</span> inherited 2 premutation alleles (ca. 80 CGG repeats) from their biologically unrelated parents. The 3 <span class="hlt">sisters</span> were administered measures of executive function, visual spatial, memory, and verbal skills. Deficiencies in the first 2 of these domains have been reported among females with the full mutation. The <span class="hlt">sisters</span>` performances were compared with available normative data and with published group means for females affectedmore » by fraX. These women did not appear to have verbal or memory difficulties. None of the women demonstrated a global executive function deficit, and none had global deficits in spatial ability. The profiles of these <span class="hlt">sisters</span> are consistent with reports that the fragile X premutation does not affect cognitive performance. 31 refs., 1 fig., 4 tabs.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3348944','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3348944"><span>Having a Brother or <span class="hlt">Sister</span> with Down Syndrome: Perspectives from Siblings</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Skotko, Brian G.; Levine, Susan P.; Goldstein, Richard</p> <p>2012-01-01</p> <p>This study asks brothers and <span class="hlt">sisters</span> about their feelings and perceptions toward their sibling with Down syndrome. We analyzed valid and reliable surveys from 822 brothers and <span class="hlt">sisters</span> whose families were on the mailing lists of six non-profit Down syndrome organizations around the country. More than 96% of brothers/<span class="hlt">sisters</span> that responded to the survey indicated that they had affection toward their sibling with Down syndrome; and 94% of older siblings expressed feelings of pride. Less than 10% felt embarrassed, and less than 5% expressed a desire to trade their sibling in for another brother or <span class="hlt">sister</span> without Down syndrome. Among older siblings, 88% felt that they were better people because of their siblings with Down syndrome, and more than 90% plan to remain involved in their sibling’s lives as they become adults. The vast majority of brothers and <span class="hlt">sisters</span> describe their relationship with their sibling with Down syndrome as positive and enriching. PMID:21910244</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1931544','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1931544"><span>Meiotic Parthenogenesis in a Root-Knot Nematode Results in Rapid Genomic Homozygosity</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Liu, Qingli L.; Thomas, Varghese P.; Williamson, Valerie M.</p> <p>2007-01-01</p> <p>Many isolates of the plant-parasitic nematode Meloidogyne hapla reproduce by facultative meiotic parthenogenesis. Sexual crosses can occur, but, in the absence of males, the diploid state appears to be restored by reuniting <span class="hlt">sister</span> chromosomes of a single meiosis. We have crossed inbred strains of M. hapla that differ in DNA markers and produced hybrids and F2 lines. Here we show that heterozygous M. hapla females, upon parthenogenetic reproduction, produce progeny that segregate 1:1 for the presence or absence of dominant DNA markers, as would be expected if <span class="hlt">sister</span> chromosomes are rejoined, rather than the 3:1 ratio typical of a Mendelian cross. Codominant markers also segregate 1:1 and heterozygotes are present at low frequency (<3%). Segregation patterns and recombinant analysis indicate that a homozygous condition is prevalent for markers flanking recombination events, suggesting that recombination occurs preferentially as four-strand exchanges at similar locations between both pairs of non-<span class="hlt">sister</span> <span class="hlt">chromatids</span>. With this mechanism, meiotic parthenogenesis would be expected to result in rapid genomic homozygosity. This type of high negative crossover interference coupled with positive <span class="hlt">chromatid</span> interference has not been observed in fungal or other animal systems in which it is possible to examine the <span class="hlt">sister</span> products of a single meiosis and may indicate that meiotic recombination in this nematode has novel features. PMID:17483427</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25352535','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25352535"><span>Generativity in Elderly Oblate <span class="hlt">Sisters</span> of Providence.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Black, Helen K; Hannum, Susan M; Rubinstein, Robert L; de Medeiros, Kate</p> <p>2016-06-01</p> <p>We explored how generativity and well-being merged in a group of childless older women: African and Hispanic Roman Catholic Religious <span class="hlt">Sisters</span>, linking two minority identity characteristics. We qualitatively interviewed 8 Oblate <span class="hlt">Sisters</span> of Providence (OSP), by providing a framework for examining the range of the women's generativity-cultural spheres in which generativity is rooted and outlets for generativity. Early negative experiences, such as fleeing despotism in Haiti and Cuba and racism within the Catholic Church, occurred alongside positive experiences-families who stressed education, and Caucasian Religious who taught children of color. This became a foundation for the <span class="hlt">Sister</span>'s generative commitment. Findings highlight that research gains from a phenomenological understanding of how religious faith promotes generative cognitions and emotions. Findings also reveal that the experiences of a subculture in society-African-American elderly women religious-add to theories and definitions of generativity. © The Author 2014. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4889787','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4889787"><span>GNE Myopathy in Turkish <span class="hlt">Sisters</span> with a Novel Homozygous Mutation</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Diniz, Gulden; Secil, Yaprak; Ceylaner, Serdar; Tokucoglu, Figen; Türe, Sabiha; Celebisoy, Mehmet; İncesu, Tülay Kurt; Akhan, Galip</p> <p>2016-01-01</p> <p>Background. Hereditary inclusion body myopathy is caused by biallelic defects in the GNE gene located on chromosome 9p13. It generally affects adults older than 20 years of age. Methods and Results. In this study, we present two Turkish <span class="hlt">sisters</span> with progressive myopathy and describe a novel mutation in the GNE gene. Both <span class="hlt">sisters</span> had slightly higher levels of creatine kinase (CK) and muscle weakness. The older <span class="hlt">sister</span> presented at 38 years of age with an inability to climb steps, weakness, and a steppage gait. Her younger <span class="hlt">sister</span> was 36 years old and had similar symptoms. The first symptoms of the disorder were seen when the <span class="hlt">sisters</span> were 30 and 34 years old, respectively. The muscle biopsy showed primary myopathic features and presence of rimmed vacuoles. DNA analysis demonstrated the presence of previously unknown homozygous mutations [c.2152 G>A (p.A718T)] in the GNE genes. Conclusion. Based on our literature survey, we believe that ours is the first confirmed case of primary GNE myopathy with a novel missense mutation in Turkey. These patients illustrate that the muscle biopsy is still an important method for the differential diagnosis of vacuolar myopathies in that the detection of inclusions is required for the definitive diagnosis. PMID:27298745</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29397502','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29397502"><span>Effects of Spirulina platensis on DNA damage and chromosomal <span class="hlt">aberration</span> against cadmium chloride-induced genotoxicity in rats.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Aly, Fayza M; Kotb, Ahmed M; Hammad, Seddik</p> <p>2018-04-01</p> <p>Todays, bioactive compounds extracted from Spirulina platensis have been intensively studied for their therapeutical values. Therefore, in the present study, we aimed to evaluate the effects of S. platensis extract on DNA damage and chromosomal <span class="hlt">aberrations</span> induced by cadmium in rats. Four groups of male albino rats (n = 7 rats) were used. The first group served as a control group and received distilled water. The second group was exposed intraperitoneally to cadmium chloride (CdCl 2 ) (3.5 mg/kg body weight dissolved in 2 ml distilled water). The third group included the rats that were orally treated with S. platensis extract (1 g/kg dissolved in 5 ml distilled water, every other day for 30 days). The fourth group included the rats that were intraperitoneally and orally exposed to cadmium chloride and S. platensis, respectively. The experiment in all groups was extended for 60 days. The results of cadmium-mediated toxicity revealed significant genetic effects (DNA fragmentation, deletion or disappearance of some base pairs of DNA, and appearance of few base pairs according to ISSR-PCR analysis). Moreover, chromosomes showed structural <span class="hlt">aberrations</span> such as reduction of chromosomal number, chromosomal ring, <span class="hlt">chromatid</span> deletions, chromosomal fragmentations, and dicentric chromosomes. Surprisingly, S. platensis extract plus CdCl 2 -treated group showed less genetic effects compared with CdCl 2 alone. Further, S. platensis extract upon CdCl 2 toxicity was associated with less chromosomal <span class="hlt">aberration</span> number and nearly normal appearance of DNA fragments as indicated by the bone marrow and ISSR-PCR analysis, respectively. In conclusion, the present novel study showed that co-treatment with S. platensis extract could reduce the genotoxic effects of CdCl 2 in rats.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23911859','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23911859"><span>Determination of <span class="hlt">aberration</span> center of Ronchigram for automated <span class="hlt">aberration</span> correctors in scanning transmission electron microscopy.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sannomiya, Takumi; Sawada, Hidetaka; Nakamichi, Tomohiro; Hosokawa, Fumio; Nakamura, Yoshio; Tanishiro, Yasumasa; Takayanagi, Kunio</p> <p>2013-12-01</p> <p>A generic method to determine the <span class="hlt">aberration</span> center is established, which can be utilized for <span class="hlt">aberration</span> calculation and axis alignment for <span class="hlt">aberration</span> corrected electron microscopes. In this method, decentering induced secondary <span class="hlt">aberrations</span> from inherent primary <span class="hlt">aberrations</span> are minimized to find the appropriate axis center. The fitness function to find the optimal decentering vector for the axis was defined as a sum of decentering induced secondary <span class="hlt">aberrations</span> with properly distributed weight values according to the <span class="hlt">aberration</span> order. Since the appropriate decentering vector is determined from the <span class="hlt">aberration</span> values calculated at an arbitrary center axis, only one <span class="hlt">aberration</span> measurement is in principle required to find the center, resulting in /very fast center search. This approach was tested for the Ronchigram based <span class="hlt">aberration</span> calculation method for <span class="hlt">aberration</span> corrected scanning transmission electron microscopy. Both in simulation and in experiments, the center search was confirmed to work well although the convergence to find the best axis becomes slower with larger primary <span class="hlt">aberrations</span>. Such <span class="hlt">aberration</span> center determination is expected to fully automatize the <span class="hlt">aberration</span> correction procedures, which used to require pre-alignment of experienced users. This approach is also applicable to automated aperture positioning. Copyright © 2013 Elsevier B.V. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/servlets/purl/6661008','SCIGOV-STC'); return false;" href="https://www.osti.gov/servlets/purl/6661008"><span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Harrison, F.L.; Rice, D.W. Jr.; Moore, D.H.</p> <p></p> <p>Traditional bioassays are unsuitable for assessing sublethal effects of low levels of radioactivity because mortality and phenotypic responses are not anticipated. We compared the usefulness of chromosomal <span class="hlt">aberration</span> (CA) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) induction as measures of low-level radiation effects in a sediment-dwelling marine worm, Neanthes arenaceodentata. Newly hatched larvae were exposed to two radiation exposure regimes. Groups of 100 larvae were exposed to either x rays delivered at high dose rates (0.7 Gy min/sup -1/) or to /sup 60/Co gamma rays delivered at low dose rates (4.8 X 10/sup -5/ to 1.2 X 10/sup -1/ Gy h/sup -1/).more » After irradiation, the larvae were exposed to 3 X 10/sup -5/M bromodeoxyuridine (BrdUrd) for 28 h (x-ray-irradiated larvae) or for 54 h (/sup 60/Co-irradiated larvae). Slides of larval cells were prepared for observation of CAs and SCEs. Frequencies of CAs were determined in first division cells; frequencies of SCEs were determined in second division cells. Results from x-ray irradiation indicated that dose-related increases occur in chromosome and <span class="hlt">chromatid</span> deletions, but an x-ray dose greater than or equal to 2 Gy was required to observe a significant increase. Worm larvae receiving /sup 60/Co irradiation showed elevated SCE frequencies; a significant increase in SCE frequency was observed at 0.6 Gy. 49 references, 2 figures.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27737959','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27737959"><span>Mutations in genes encoding condensin complex proteins cause microcephaly through decatenation failure at mitosis.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Martin, Carol-Anne; Murray, Jennie E; Carroll, Paula; Leitch, Andrea; Mackenzie, Karen J; Halachev, Mihail; Fetit, Ahmed E; Keith, Charlotte; Bicknell, Louise S; Fluteau, Adeline; Gautier, Philippe; Hall, Emma A; Joss, Shelagh; Soares, Gabriela; Silva, João; Bober, Michael B; Duker, Angela; Wise, Carol A; Quigley, Alan J; Phadke, Shubha R; Wood, Andrew J; Vagnarelli, Paola; Jackson, Andrew P</p> <p>2016-10-01</p> <p>Compaction of chromosomes is essential for accurate segregation of the genome during mitosis. In vertebrates, two condensin complexes ensure timely chromosome condensation, <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement, and maintenance of mitotic chromosome structure. Here, we report that biallelic mutations in NCAPD2, NCAPH, or NCAPD3, encoding subunits of these complexes, cause microcephaly. In addition, hypomorphic Ncaph2 mice have significantly reduced brain size, with frequent anaphase chromatin bridge formation observed in apical neural progenitors during neurogenesis. Such DNA bridges also arise in condensin-deficient patient cells, where they are the consequence of failed <span class="hlt">sister</span> <span class="hlt">chromatid</span> disentanglement during chromosome compaction. This results in chromosome segregation errors, leading to micronucleus formation and increased aneuploidy in daughter cells. These findings establish "condensinopathies" as microcephalic disorders, with decatenation failure as an additional disease mechanism for microcephaly, implicating mitotic chromosome condensation as a key process ensuring mammalian cerebral cortex size. © 2016 Martin et al.; Published by Cold Spring Harbor Laboratory Press.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_9");'>9</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li class="active"><span>11</span></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_11 --> <div id="page_12" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li class="active"><span>12</span></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="221"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5640152','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5640152"><span>Structural maintenance of chromosome complexes differentially compact mitotic chromosomes according to genomic context</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Schalbetter, S. A.; Goloborodko, A.; Fudenberg, G.; Belton, J.-M.; Miles, C.; Yu, M.; Dekker, J.; Mirny, L.; Baxter, J.</p> <p>2017-01-01</p> <p>Structural Maintenance of Chromosomes (SMC) protein complexes are key determinants of chromosome conformation. Using Hi-C and polymer modeling, we study how cohesin and condensin, two deeply conserved SMC complexes, organize chromosomes in the budding yeast Saccharomyces cerevisiae. The canonical role of cohesin is to co-align <span class="hlt">sister</span> <span class="hlt">chromatids</span> whilst condensin generally compacts mitotic chromosomes. We find strikingly different roles for the two complexes in budding yeast mitosis. First, cohesin is responsible for compacting mitotic chromosome arms, independently of <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. Polymer simulations demonstrate this role can be fully accounted for through cis-looping of chromatin. Second, condensin is generally dispensable for compaction along chromosome arms. Instead it plays a targeted role compacting the rDNA proximal regions and promoting resolution of peri-centromeric regions. Our results argue that the conserved mechanism of SMC complexes is to form chromatin loops and that distinct SMC-dependent looping activities are selectively deployed to appropriately compact chromosomes. PMID:28825700</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/12808731','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/12808731"><span>Paternity testing in case of brother-<span class="hlt">sister</span> incest.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Macan, Marijana; Uvodić, Petra; Botica, Vladimir</p> <p>2003-06-01</p> <p>We performed a paternity test in a case of incest between brother and <span class="hlt">sister</span>. DNA from blood samples of the alleged parents and their two children was obtained with Chelex DNA extraction method and quantified with Applied Biosystems QuantiBlot quantitation kit. Polymerase chain reaction (PCR) amplification of DNA samples was performed with AmpFlSTR SGM Plus PCR amplification kit and GenePrint PowerPlex PCR amplification kit. The amplified products were separated and detected by using the Perkin Elmer's ABI PRISM trade mark 310 Genetic Analyser. DNA and data analysis of 17 loci and Amelogenin confirmed the suspicion of brother-<span class="hlt">sister</span> incest. Since both children had inherited all of the obligate alleles from the alleged father, we could confirm with certainty of 99.999999% that the oldest brother in the family was the biological father of both children. Calculated data showed that even in a case of brother-<span class="hlt">sister</span> incest, paternity could be proved by the analysis of Amelogenin and 17 DNA loci.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://pubs.usgs.gov/sim/3186/data/pdf/sim3186_pamphlet.pdf','USGSPUBS'); return false;" href="https://pubs.usgs.gov/sim/3186/data/pdf/sim3186_pamphlet.pdf"><span>Geologic map of Three <span class="hlt">Sisters</span> volcanic cluster, Cascade Range, Oregon</span></a></p> <p><a target="_blank" href="http://pubs.er.usgs.gov/pubs/index.jsp?view=adv">USGS Publications Warehouse</a></p> <p>Hildreth, Wes; Fierstein, Judy; Calvert, Andrew T.</p> <p>2012-01-01</p> <p>The cluster of glaciated stratovolcanoes called the Three Sisters—South <span class="hlt">Sister</span>, Middle <span class="hlt">Sister</span>, and North Sister—forms a spectacular 20-km-long reach along the crest of the Cascade Range in Oregon. The three eponymous stratocones, though contiguous and conventionally lumped sororally, could hardly display less family resemblance. North <span class="hlt">Sister</span> (10,085 ft), a monotonously mafic edifice at least as old as 120 ka, is a glacially ravaged stratocone that consists of hundreds of thin rubbly lava flows and intercalated falls that dip radially and steeply; remnants of two thick lava flows cap its summit. Middle <span class="hlt">Sister</span> (10,047 ft), an andesite-basalt-dacite cone built between 48 and 14 ka, is capped by a thick stack of radially dipping, dark-gray, thin mafic lava flows; asymmetrically glaciated, its nearly intact west flank contrasts sharply with its steep east face. Snow and ice-filled South <span class="hlt">Sister</span> is a bimodal rhyolitic-intermediate edifice that was constructed between 50 ka and 2 ka; its crater (rim at 10,358 ft) was created between 30 and 22 ka, during the most recent of several explosive summit eruptions; the thin oxidized agglutinate that mantles its current crater rim protects a 150-m-thick pyroclastic sequence that helped fill a much larger crater. For each of the three, the eruptive volume is likely to have been in the range of 15 to 25 km³, but such estimates are fairly uncertain, owing to glacial erosion. The map area consists exclusively of Quaternary volcanic rocks and derivative surficial deposits. Although most of the area has been modified by glaciation, the volcanoes are young enough that the landforms remain largely constructional. Furthermore, twelve of the 145 eruptive units on the map are postglacial, younger than the deglaciation that was underway by about 17 ka. The most recent eruptions were of rhyolite near South <span class="hlt">Sister</span>, about 2,000 years ago, and of mafic magma near McKenzie Pass, about 1,500 years ago. As observed by trailblazing volcanologist</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title40-vol16/pdf/CFR-2011-title40-vol16-sec79-65.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title40-vol16/pdf/CFR-2011-title40-vol16-sec79-65.pdf"><span>40 CFR 79.65 - In vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-07-01</p> <p>... least five female and five male animals per experimental and control group shall be used. The use of a single sex or different number of animals shall be justified. (5) Positive control group. A single... making comparisons between treated and control groups. (2) Statistical evaluation. Data shall be...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2013-title40-vol17/pdf/CFR-2013-title40-vol17-sec79-65.pdf','CFR2013'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2013-title40-vol17/pdf/CFR-2013-title40-vol17-sec79-65.pdf"><span>40 CFR 79.65 - In vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2013&page.go=Go">Code of Federal Regulations, 2013 CFR</a></p> <p></p> <p>2013-07-01</p> <p>... least five female and five male animals per experimental and control group shall be used. The use of a single sex or different number of animals shall be justified. (5) Positive control group. A single... making comparisons between treated and control groups. (2) Statistical evaluation. Data shall be...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol17/pdf/CFR-2014-title40-vol17-sec79-65.pdf','CFR2014'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol17/pdf/CFR-2014-title40-vol17-sec79-65.pdf"><span>40 CFR 79.65 - In vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2014&page.go=Go">Code of Federal Regulations, 2014 CFR</a></p> <p></p> <p>2014-07-01</p> <p>... least five female and five male animals per experimental and control group shall be used. The use of a single sex or different number of animals shall be justified. (5) Positive control group. A single... making comparisons between treated and control groups. (2) Statistical evaluation. Data shall be...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol16/pdf/CFR-2010-title40-vol16-sec79-65.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol16/pdf/CFR-2010-title40-vol16-sec79-65.pdf"><span>40 CFR 79.65 - In vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-07-01</p> <p>... least five female and five male animals per experimental and control group shall be used. The use of a single sex or different number of animals shall be justified. (5) Positive control group. A single... making comparisons between treated and control groups. (2) Statistical evaluation. Data shall be...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2012-title40-vol17/pdf/CFR-2012-title40-vol17-sec79-65.pdf','CFR2012'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2012-title40-vol17/pdf/CFR-2012-title40-vol17-sec79-65.pdf"><span>40 CFR 79.65 - In vivo <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange assay.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2012&page.go=Go">Code of Federal Regulations, 2012 CFR</a></p> <p></p> <p>2012-07-01</p> <p>... least five female and five male animals per experimental and control group shall be used. The use of a single sex or different number of animals shall be justified. (5) Positive control group. A single... making comparisons between treated and control groups. (2) Statistical evaluation. Data shall be...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/3731084','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/3731084"><span>Abnormally banded chromosomal regions in doxorubicin-resistant B16-BL6 murine melanoma cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Slovak, M L; Hoeltge, G A; Ganapathi, R</p> <p>1986-08-01</p> <p>B16-BL6 murine melanoma cells were selected for cytogenetic evaluation during the stepwise development of increasing resistance in vitro to the antitumor antibiotic, doxorubicin (DOX). Karyotypic studies demonstrated extensive heteroploidy with both numerical and structural abnormalities which were not present in the parental DOX-sensitive B16-BL6 cells. Trypsin-Giemsa banding revealed the presence of several marker chromosomes containing abnormally banding regions (ABRs) in the 44-fold B16-BL6 DOX-resistant subline. These ABRs appeared to be more homogeneously staining at the higher DOX concentrations. Length measurements (ABR index) in seven banded metaphases indicated a direct correlation with increasing DOX concentration. When the DOX-resistant cells were grown in drug-free medium for 1 yr, the drug-resistant phenotype gradually declined in parallel with the level of resistance and the ABR index. DOX-induced cytogenetic damage examined by <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange methodology in parental B16-BL6 cells indicated a linear <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange:DOX dose-response relationship. However, after continuous treatment of parental B16-BL6 cells with DOX (0.01 microgram/ml) for 30 days, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange scores were found to return to base-line values. The B16-BL6 resistant cells demonstrated a cross-resistant phenotype with N-trifluoroacetyladriamycin-14-valerate, actinomycin D, and the Vinca alkaloids but not with 1-beta-D-arabinofuranosylcytosine. The results suggest that ABR-containing chromosomes in DOX-resistant sublines may represent cytogenetic alterations of specific amplified genes involved in the expression of DOX resistance. Further studies are required to identify and define the possible gene products and to correlate their relationship to the cytotoxic action of doxorubicin.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/22210259-sumo-protease-senp1-required-cohesion-maintenance-mitotic-arrest-following-spindle-poison-treatment','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/22210259-sumo-protease-senp1-required-cohesion-maintenance-mitotic-arrest-following-spindle-poison-treatment"><span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Era, Saho; Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606-8501; Abe, Takuya</p> <p></p> <p>Highlights: Black-Right-Pointing-Pointer SENP1 knockout chicken DT40 cells are hypersensitive to spindle poisons. Black-Right-Pointing-Pointer Spindle poison treatment of SENP1{sup -/-} cells leads to increased mitotic slippage. Black-Right-Pointing-Pointer Mitotic slippage in SENP1{sup -/-} cells associates with apoptosis and endoreplication. Black-Right-Pointing-Pointer SENP1 counteracts <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation during mitotic arrest. Black-Right-Pointing-Pointer Plk1-mediated cohesion down-regulation is involved in colcemid cytotoxicity. -- Abstract: SUMO conjugation is a reversible posttranslational modification that regulates protein function. SENP1 is one of the six SUMO-specific proteases present in vertebrate cells and its altered expression is observed in several carcinomas. To characterize SENP1 role in genome integrity, we generated Senp1 knockoutmore » chicken DT40 cells. SENP1{sup -/-} cells show normal proliferation, but are sensitive to spindle poisons. This hypersensitivity correlates with increased <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation, mitotic slippage, and apoptosis. To test whether the cohesion defect had a causal relationship with the observed mitotic events, we restored the cohesive status of <span class="hlt">sister</span> <span class="hlt">chromatids</span> by introducing the TOP2{alpha}{sup +/-} mutation, which leads to increased catenation, or by inhibiting Plk1 and Aurora B kinases that promote cohesin release from chromosomes during prolonged mitotic arrest. Although TOP2{alpha} is SUMOylated during mitosis, the TOP2{alpha}{sup +/-} mutation had no obvious effect. By contrast, inhibition of Plk1 or Aurora B rescued the hypersensitivity of SENP1{sup -/-} cells to colcemid. In conclusion, we identify SENP1 as a novel factor required for mitotic arrest and cohesion maintenance during prolonged mitotic arrest induced by spindle poisons.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3212099','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3212099"><span><span class="hlt">Sister</span> Circles as a Culturally Relevant Intervention for Anxious African American Women</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Neal-Barnett, Angela; Stadulis, Robert; Murray, Marsheena; Payne, Margaret Ralston; Thomas, Anisha; Salley, Bernadette B.</p> <p>2011-01-01</p> <p>Research on anxiety treatment with African American women reveals a need to develop interventions that address factors relevant to their lives. Such factors include feelings of isolation, multiple roles undertaken by Black women, and faith. A recurrent theme across treatment studies is the importance of having support from other Black women. <span class="hlt">Sister</span> circles are support groups that build upon existing friendships, fictive kin networks, and the sense of community found among African Americans females. <span class="hlt">Sister</span> circles appear to offer many of the components Black women desire in an anxiety intervention. In this article, we explore <span class="hlt">sister</span> circles as an intervention for anxious African American women. Culturally-infused aspects from our <span class="hlt">sister</span> circle work with middle-class African American women are presented. Further research is needed. PMID:22081747</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16766093','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16766093"><span>Women in-between' (Strathern, 1995): the ambiguous position of the <span class="hlt">sister</span> tutor, 1918-1960.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Brooks, Jane</p> <p>2007-02-01</p> <p>The purpose of this article is to explore the ambiguous position of <span class="hlt">sister</span> tutors, within the nursing and hospital hierarchy between 1918 and 1960. The function of the <span class="hlt">sister</span> tutor was to train the probationers (student nurses). However, I will argue that the students' education was to come second to the service needs of the hospital, the authority of the matron and desire of the medical profession to maintain control over the nursing curriculum and nursing practice. Therefore <span class="hlt">sister</span> tutors were caught 'in-between' several opposing forces which together militated against the individual <span class="hlt">sister</span> tutor's work and the ability of the nursing profession to recruit adequate numbers of senior nurses into the classroom. The recruitment issue was further hampered by the widespread knowledge that much of the <span class="hlt">sister</span> tutor's work was not student education at all, but organising lectures by medical staff and marking students' notes. In order to gauge the 'official' attitudes to the <span class="hlt">sister</span> tutors and also the experiences of those who either worked as <span class="hlt">sister</span> tutors or were taught by them, I used both archival and oral evidence in the research for this article. Pseudonyms have been used throughout for the oral history respondents.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-225.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-225.pdf"><span>20 CFR 725.225 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 3 2010-04-01 2010-04-01 false Determination of dependency; parent, brother, or <span class="hlt">sister</span>. 725.225 Section 725.225 Employees' Benefits EMPLOYMENT STANDARDS ADMINISTRATION... Benefits) § 725.225 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=mitosis&pg=2&id=EJ847053','ERIC'); return false;" href="https://eric.ed.gov/?q=mitosis&pg=2&id=EJ847053"><span>Using Long-Term Time-Lapse Imaging of Mammalian Cell Cycle Progression for Laboratory Instruction and Analysis</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Hinchcliffe, Edward H.</p> <p>2005-01-01</p> <p>Cinemicrography--the capture of moving cellular sequences through the microscope--has been influential in revealing the dynamic nature of cellular behavior. One of the more dramatic cellular events is mitosis, the division of <span class="hlt">sister</span> <span class="hlt">chromatids</span> into two daughter cells. Mitosis has been extensively studied in a variety of organisms, both…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20100039449&hterms=Genomes&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3DGenomes','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20100039449&hterms=Genomes&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D70%26Ntt%3DGenomes"><span>Interpreting Chromosome <span class="hlt">Aberration</span> Spectra</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Levy, Dan; Reeder, Christopher; Loucas, Bradford; Hlatky, Lynn; Chen, Allen; Cornforth, Michael; Sachs, Rainer</p> <p>2007-01-01</p> <p>Ionizing radiation can damage cells by breaking both strands of DNA in multiple locations, essentially cutting chromosomes into pieces. The cell has enzymatic mechanisms to repair such breaks; however, these mechanisms are imperfect and, in an exchange process, may produce a large-scale rearrangement of the genome, called a chromosome <span class="hlt">aberration</span>. Chromosome <span class="hlt">aberrations</span> are important in killing cells, during carcinogenesis, in characterizing repair/misrepair pathways, in retrospective radiation biodosimetry, and in a number of other ways. DNA staining techniques such as mFISH ( multicolor fluorescent in situ hybridization) provide a means for analyzing <span class="hlt">aberration</span> spectra by examining observed final patterns. Unfortunately, an mFISH observed final pattern often does not uniquely determine the underlying exchange process. Further, resolution limitations in the painting protocol sometimes lead to apparently incomplete final patterns. We here describe an algorithm for systematically finding exchange processes consistent with any observed final pattern. This algorithm uses <span class="hlt">aberration</span> multigraphs, a mathematical formalism that links the various aspects of <span class="hlt">aberration</span> formation. By applying a measure to the space of consistent multigraphs, we will show how to generate model-specific distributions of <span class="hlt">aberration</span> processes from mFISH experimental data. The approach is implemented by software freely available over the internet. As a sample application, we apply these algorithms to an <span class="hlt">aberration</span> data set, obtaining a distribution of exchange cycle sizes, which serves to measure <span class="hlt">aberration</span> complexity. Estimating complexity, in turn, helps indicate how damaging the <span class="hlt">aberrations</span> are and may facilitate identification of radiation type in retrospective biodosimetry.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://images.nasa.gov/#/details-PIA09263.html','SCIGOVIMAGE-NASA'); return false;" href="https://images.nasa.gov/#/details-PIA09263.html"><span>The Seven <span class="hlt">Sisters</span> Pose for Spitzer</span></a></p> <p><a target="_blank" href="https://images.nasa.gov/">NASA Image and Video Library</a></p> <p></p> <p>2007-04-16</p> <p>The Seven <span class="hlt">Sisters</span>, also known as the Pleiades star cluster, seem to float on a bed of feathers in a new infrared image from NASA Spitzer Space Telescope. Clouds of dust sweep around the stars, swaddling them in a cushiony veil.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2012-title20-vol4/pdf/CFR-2012-title20-vol4-sec725-225.pdf','CFR2012'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2012-title20-vol4/pdf/CFR-2012-title20-vol4-sec725-225.pdf"><span>20 CFR 725.225 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2012&page.go=Go">Code of Federal Regulations, 2012 CFR</a></p> <p></p> <p>2012-04-01</p> <p>... 20 Employees' Benefits 4 2012-04-01 2012-04-01 false Determination of dependency; parent, brother, or <span class="hlt">sister</span>. 725.225 Section 725.225 Employees' Benefits OFFICE OF WORKERS' COMPENSATION PROGRAMS... Benefits) § 725.225 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2013-title20-vol4/pdf/CFR-2013-title20-vol4-sec725-225.pdf','CFR2013'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2013-title20-vol4/pdf/CFR-2013-title20-vol4-sec725-225.pdf"><span>20 CFR 725.225 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2013&page.go=Go">Code of Federal Regulations, 2013 CFR</a></p> <p></p> <p>2013-04-01</p> <p>... 20 Employees' Benefits 4 2013-04-01 2013-04-01 false Determination of dependency; parent, brother, or <span class="hlt">sister</span>. 725.225 Section 725.225 Employees' Benefits OFFICE OF WORKERS' COMPENSATION PROGRAMS... Benefits) § 725.225 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2014-title20-vol4/pdf/CFR-2014-title20-vol4-sec725-225.pdf','CFR2014'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2014-title20-vol4/pdf/CFR-2014-title20-vol4-sec725-225.pdf"><span>20 CFR 725.225 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2014&page.go=Go">Code of Federal Regulations, 2014 CFR</a></p> <p></p> <p>2014-04-01</p> <p>... 20 Employees' Benefits 4 2014-04-01 2014-04-01 false Determination of dependency; parent, brother, or <span class="hlt">sister</span>. 725.225 Section 725.225 Employees' Benefits OFFICE OF WORKERS' COMPENSATION PROGRAMS... Benefits) § 725.225 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title20-vol3/pdf/CFR-2011-title20-vol3-sec725-225.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title20-vol3/pdf/CFR-2011-title20-vol3-sec725-225.pdf"><span>20 CFR 725.225 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-04-01</p> <p>... 20 Employees' Benefits 3 2011-04-01 2011-04-01 false Determination of dependency; parent, brother, or <span class="hlt">sister</span>. 725.225 Section 725.225 Employees' Benefits OFFICE OF WORKERS' COMPENSATION PROGRAMS... Benefits) § 725.225 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner...</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_10");'>10</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li class="active"><span>12</span></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_12 --> <div id="page_13" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li class="active"><span>13</span></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="241"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16689509','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16689509"><span>[Florence Nightingale and charity <span class="hlt">sisters</span>: revisiting the history].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Padilha, Maria Itayra Coelho de Souza; Mancia, Joel Rolim</p> <p>2005-01-01</p> <p>This study presents an historical analysis on the links between the nursing practice and the influence received from various religious orders/associations along the times, especially from Saint Vincent Paul's charity <span class="hlt">sisters</span>. The professional nursing which was pioneered by Florence Nightingale in the XlXth century, was directly influenced by the teachings of love and fraternity. In addition, other contributions from the religious orders/associations were the concepts of altruism, valorization of an adequate environment for the care of patients, and the division of work in nursing. The study shows the influence of Charity <span class="hlt">Sisters</span> on Florence Nightingale.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-215.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-215.pdf"><span>20 CFR 410.215 - Duration of entitlement; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false Duration of entitlement; parent, brother, or...; Duration of Entitlement; Filing of Claims and Evidence § 410.215 Duration of entitlement; parent, brother, or <span class="hlt">sister</span>. (a) parent, brother, or <span class="hlt">sister</span> is entitled to benefits beginning with the month all the...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-222.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-222.pdf"><span>20 CFR 725.222 - Conditions of entitlement; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 3 2010-04-01 2010-04-01 false Conditions of entitlement; parent, brother... Benefits) § 725.222 Conditions of entitlement; parent, brother, or <span class="hlt">sister</span>. (a) An individual is eligible for benefits as a surviving parent, brother or <span class="hlt">sister</span> if all of the following requirements are met: (1...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6657895-ntp-report-toxicity-studies-ethylbenzene-f344-rats-b6c3f1-mice-inhalation-studies-report-march-june','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6657895-ntp-report-toxicity-studies-ethylbenzene-f344-rats-b6c3f1-mice-inhalation-studies-report-march-june"><span>Ntp report on the toxicity studies of ethylbenzene in f344/n rats and b6c3f1 mice (inhalation studies). Report for 29 March-30 June 1988</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Chan, P.</p> <p>1992-03-01</p> <p>Inhalation toxicology studies of ethylbenzene (99% pure) were conducted by exposing groups of F344/N rats and B6C3F1 mice of each sex to ethylbenzene vapor at chamber concentrations of 0 to 1000 ppm, 6 hours per day, 5 days per week for 13 weeks. No rats or mice died during the 13-week exposure. Body weight gains were slightly lower in the high dose groups of male and female rats, but the differences were not statistically significant. Absolute and relative kidney, liver, and lung weights were increased in the exposed rats, while weight increases occurred only in the livers of exposed mice.more » No changes were observed in the evaluation of sperm or vaginal cytology in rats or mice. Ethylbenzene was not mutagenic in Salmonella and did not induce chromosomal <span class="hlt">aberrations</span> or <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges in Chinese hamster ovary (CHO) cells in vitro, though it did induce trifluorothymidine resistance in mouse lymphoma cells at the highest concentration tested. Micronuclei assays in peripheral blood of mice were negative.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21130826','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21130826"><span>The evaluation of the genotoxicity of two food preservatives: sodium benzoate and potassium benzoate.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zengin, N; Yüzbaşıoğlu, D; Unal, F; Yılmaz, S; Aksoy, H</p> <p>2011-04-01</p> <p>In this study, the genotoxic effects of sodium benzoate (SB) and potassium benzoate (PB) were investigated in cultured human peripheral lymphocytes using chromosomal <span class="hlt">aberrations</span> (CA), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE), and micronuclei (MN). The level of nuclear DNA damage of SB and PB were also evaluated using the comet assay. The lymphocytes were incubated with different concentrations of SB (6.25, 12.5, 25, 50, and 100 μg/ml) and PB (62.5, 125, 250, 500, and 1000 μg/ml). A significant increase was observed in CA, SCE, and MN, in almost all treatments compared to negative controls. SB and PB significantly decreased the mitotic index (MI) in all the treatments, compared to the negative controls. However, neither of the additives affected the replication index (RI). Although SB significantly increased DNA damage, PB did not cause a significant increase in DNA damage. The present results indicate that SB and PB are clastogenic, mutagenic and cytotoxic to human lymphocytes in vitro. Copyright © 2010 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2171634','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2171634"><span>Histone H1 is essential for mitotic chromosome architecture and segregation in Xenopus laevis egg extracts</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Maresca, Thomas J.; Freedman, Benjamin S.; Heald, Rebecca</p> <p>2005-01-01</p> <p>During cell division, condensation and resolution of chromosome arms and the assembly of a functional kinetochore at the centromere of each <span class="hlt">sister</span> <span class="hlt">chromatid</span> are essential steps for accurate segregation of the genome by the mitotic spindle, yet the contribution of individual chromatin proteins to these processes is poorly understood. We have investigated the role of embryonic linker histone H1 during mitosis in Xenopus laevis egg extracts. Immunodepletion of histone H1 caused the assembly of <span class="hlt">aberrant</span> elongated chromosomes that extended off the metaphase plate and outside the perimeter of the spindle. Although functional kinetochores assembled, aligned, and exhibited poleward movement, long and tangled chromosome arms could not be segregated in anaphase. Histone H1 depletion did not significantly affect the recruitment of known structural or functional chromosomal components such as condensins or chromokinesins, suggesting that the loss of H1 affects chromosome architecture directly. Thus, our results indicate that linker histone H1 plays an important role in the structure and function of vertebrate chromosomes in mitosis. PMID:15967810</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27888426','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27888426"><span>Evaluation of herbicides action on plant bioindicators by genetic biomarkers: a review.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>de Souza, Cleiton Pereira; Guedes, Thays de Andrade; Fontanetti, Carmem Silvia</p> <p>2016-12-01</p> <p>The use of pesticides has increased worldwide, owing to the demand for products of good quality and to satisfy a growing population. Herbicides represent almost half of the total amount of pesticides used. Although important to the reduction of costs and an increase of productivity, their indiscriminate use, as well as that of the other pesticides, is a global environmental problem, since they affect the living organisms. To evaluate the damage caused by herbicides to the environment, different organisms have been used as bioindicators, especially higher plants, due to several advantages. This is a literature review on herbicidal actions in plant bioindicators, as assessed by genetic biomarkers. Also, the present manuscript aimed to characterize the main organisms (Allium cepa, Vicia faba and Tradescantia spp.) and the most used biomarkers (mitotic index, chromosome <span class="hlt">aberrations</span>, micronuclei, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and mutations). We concluded that herbicides induce cytotoxicity and genotoxicity in the assessed bioindicators. The data corroborate the existing warnings of the risks that the indiscriminate and increasing use of pesticides poses to the environment and its biodiversity.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-224.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-224.pdf"><span>20 CFR 725.224 - Determination of relationship; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 3 2010-04-01 2010-04-01 false Determination of relationship; parent... Benefits) § 725.224 Determination of relationship; parent, brother, or <span class="hlt">sister</span>. (a) An individual will be considered to be the parent, brother, or <span class="hlt">sister</span> of a miner if the courts of the State in which the miner was...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/FR-2012-03-07/pdf/2012-5533.pdf','FEDREG'); return false;" href="https://www.gpo.gov/fdsys/pkg/FR-2012-03-07/pdf/2012-5533.pdf"><span>77 FR 13585 - Three <span class="hlt">Sisters</span> Irrigation District; Notice of Application Accepted for Filing and Soliciting...</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collection.action?collectionCode=FR">Federal Register 2010, 2011, 2012, 2013, 2014</a></p> <p></p> <p>2012-03-07</p> <p>...: The proposed Three <span class="hlt">Sisters</span> Irrigation District Hydroelectric Project would be located on the north pipe of the Three <span class="hlt">Sisters</span> Irrigation District's Main Canal Pipeline in Deschutes County, Oregon. The... of Project: The Three <span class="hlt">Sisters</span> Irrigation District Hydroelectric Project would consist of: (1) An...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-223.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol3/pdf/CFR-2010-title20-vol3-sec725-223.pdf"><span>20 CFR 725.223 - Duration of entitlement; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 3 2010-04-01 2010-04-01 false Duration of entitlement; parent, brother, or... Benefits) § 725.223 Duration of entitlement; parent, brother, or <span class="hlt">sister</span>. (a) A parent, <span class="hlt">sister</span>, or brother....222 are met. (b) The last month for which such parent is entitled to benefits is the month in which...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6572531-enhanced-g2-chromatid-radiosensitivity-early-stage-neoplastic-transformation-human-epidermal-keratinocytes-culture','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6572531-enhanced-g2-chromatid-radiosensitivity-early-stage-neoplastic-transformation-human-epidermal-keratinocytes-culture"><span>Enhanced G2 <span class="hlt">chromatid</span> radiosensitivity, an early stage in the neoplastic transformation of human epidermal keratinocytes in culture</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Gantt, R.; Sanford, K.K.; Parshad, R.</p> <p>1987-03-01</p> <p>A deficiency in DNA repair, manifest as enhanced <span class="hlt">chromatid</span> radiosensitivity during the G2 phase of the cell cycle, together with a proliferative stimulus such as that provided by active oncogenes may be necessary and sufficient for the malignant neoplastic transformation of human keratinocytes in culture. Normal epidermal keratinocytes established as continuous cell lines by transfection with pSV3-neo or infection with adeno 12-SV40 hybrid virus developed enhanced G2 <span class="hlt">chromatid</span> radiosensitivity after 18 passages in culture. In contrast to cells from primary or secondary culture, these cells could be transformed to malignant neoplastic cells by infection with Kirsten murine sarcoma virus containingmore » the Ki-ras oncogene or in one line by the chemical carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine; both of these agents produced a marked proliferative response. Cytological heterogeneity and karyotypic instability characterized the cells during their progression to neoplasia. These results are interpreted in terms of a mechanism for neoplastic transformation.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15024062','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15024062"><span>Securin is a target of the UV response pathway in mammalian cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Romero, Francisco; Gil-Bernabé, Ana M; Sáez, Carmen; Japón, Miguel A; Pintor-Toro, José A; Tortolero, María</p> <p>2004-04-01</p> <p>All eukaryotic cells possess elaborate mechanisms to protect genome integrity and ensure survival after DNA damage, ceasing proliferation and granting time for DNA repair. Securin is an inhibitory protein that is bound to a protease called Separase to inhibit <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation until the onset of anaphase. At the metaphase-to-anaphase transition, Securin is degraded by the anaphase-promoting complex or cyclosome, and Separase contributes to the release of cohesins from the chromosome, allowing for the segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> to opposite spindle poles. Here we provide evidence that human Securin (hSecurin) has a novel role in cell cycle arrest after exposure to UV light or ionizing radiation. In fact, irradiation downregulated the level of hSecurin protein, accelerating its degradation via the proteasome and reducing hSecurin mRNA translation, but the presence of hSecurin is necessary for cell proliferation arrest following UV treatment. Moreover, an alteration of UV-induced hSecurin downregulation could lead directly to the accumulation of DNA damage and the subsequent development of malignant tumors.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=371137','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=371137"><span>Securin Is a Target of the UV Response Pathway in Mammalian Cells†</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Romero, Francisco; Gil-Bernabé, Ana M.; Sáez, Carmen; Japón, Miguel A.; Pintor-Toro, José A.; Tortolero, María</p> <p>2004-01-01</p> <p>All eukaryotic cells possess elaborate mechanisms to protect genome integrity and ensure survival after DNA damage, ceasing proliferation and granting time for DNA repair. Securin is an inhibitory protein that is bound to a protease called Separase to inhibit <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation until the onset of anaphase. At the metaphase-to-anaphase transition, Securin is degraded by the anaphase-promoting complex or cyclosome, and Separase contributes to the release of cohesins from the chromosome, allowing for the segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> to opposite spindle poles. Here we provide evidence that human Securin (hSecurin) has a novel role in cell cycle arrest after exposure to UV light or ionizing radiation. In fact, irradiation downregulated the level of hSecurin protein, accelerating its degradation via the proteasome and reducing hSecurin mRNA translation, but the presence of hSecurin is necessary for cell proliferation arrest following UV treatment. Moreover, an alteration of UV-induced hSecurin downregulation could lead directly to the accumulation of DNA damage and the subsequent development of malignant tumors. PMID:15024062</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26399325','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26399325"><span>Bub1 autophosphorylation feeds back to regulate kinetochore docking and promote localized substrate phosphorylation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Asghar, Adeel; Lajeunesse, Audrey; Dulla, Kalyan; Combes, Guillaume; Thebault, Philippe; Nigg, Erich A; Elowe, Sabine</p> <p>2015-09-24</p> <p>During mitosis, Bub1 kinase phosphorylates histone H2A-T120 to promote centromere <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion through recruitment of shugoshin (Sgo) proteins. The regulation and dynamics of H2A-T120 phosphorylation are poorly understood. Using quantitative phosphoproteomics we show that Bub1 is autophosphorylated at numerous sites. We confirm mitosis-specific autophosphorylation of a several residues and show that Bub1 activation is primed in interphase but fully achieved only in mitosis. Mutation of a single autophosphorylation site T589 alters kinetochore turnover of Bub1 and results in uniform H2A-T120 phosphorylation and Sgo recruitment along chromosome arms. Consequently, improper <span class="hlt">sister</span> <span class="hlt">chromatid</span> resolution and chromosome segregation errors are observed. Kinetochore tethering of Bub1-T589A refocuses H2A-T120 phosphorylation and Sgo1 to centromeres. Recruitment of the Bub1-Bub3-BubR1 axis to kinetochores has recently been extensively studied. Our data provide novel insight into the regulation and kinetochore residency of Bub1 and indicate that its localization is dynamic and tightly controlled through feedback autophosphorylation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25601756','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25601756"><span>Interdependence of the rad50 hook and globular domain functions.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hohl, Marcel; Kochańczyk, Tomasz; Tous, Cristina; Aguilera, Andrés; Krężel, Artur; Petrini, John H J</p> <p>2015-02-05</p> <p>Rad50 contains a conserved Zn(2+) coordination domain (the Rad50 hook) that functions as a homodimerization interface. Hook ablation phenocopies Rad50 deficiency in all respects. Here, we focused on rad50 mutations flanking the Zn(2+)-coordinating hook cysteines. These mutants impaired hook-mediated dimerization, but recombination between <span class="hlt">sister</span> <span class="hlt">chromatids</span> was largely unaffected. This may reflect that cohesin-mediated <span class="hlt">sister</span> <span class="hlt">chromatid</span> interactions are sufficient for double-strand break repair. However, Mre11 complex functions specified by the globular domain, including Tel1 (ATM) activation, nonhomologous end joining, and DNA double-strand break end resection were affected, suggesting that dimerization exerts a broad influence on Mre11 complex function. These phenotypes were suppressed by mutations within the coiled-coil and globular ATPase domains, suggesting a model in which conformational changes in the hook and globular domains are transmitted via the extended coils of Rad50. We propose that transmission of spatial information in this manner underlies the regulation of Mre11 complex functions. Copyright © 2015 Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22732496','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22732496"><span>Shugoshins function as a guardian for chromosomal stability in nuclear division.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yao, Yixin; Dai, Wei</p> <p>2012-07-15</p> <p>Accurate chromosome segregation during mitosis and meiosis is regulated and secured by several distinctly different yet intricately connected regulatory mechanisms. As chromosomal instability is a hallmark of a majority of tumors as well as a cause of infertility for germ cells, extensive research in the past has focused on the identification and characterization of molecular components that are crucial for faithful chromosome segregation during cell division. Shugoshins, including Sgo1 and Sgo2, are evolutionarily conserved proteins that function to protect <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, thus ensuring chromosomal stability during mitosis and meiosis in eukaryotes. Recent studies reveal that Shugoshins in higher animals play an essential role not only in protecting centromeric cohesion of <span class="hlt">sister</span> <span class="hlt">chromatids</span> and assisting bi-orientation attachment at the kinetochores, but also in safeguarding centriole cohesion/engagement during early mitosis. Many molecular components have been identified that play essential roles in modulating/mediating Sgo functions. This review primarily summarizes recent advances on the mechanisms of action of Shugoshins in suppressing chromosomal instability during nuclear division in eukaryotic organisms.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16737721','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16737721"><span>Loss of heterozygosity in yeast can occur by ultraviolet irradiation during the S phase of the cell cycle.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Daigaku, Yasukazu; Mashiko, Satsuki; Mishiba, Keiichiro; Yamamura, Saburo; Ui, Ayako; Enomoto, Takemi; Yamamoto, Kazuo</p> <p>2006-08-30</p> <p>A CAN1/can1Delta heterozygous allele that determines loss of heterozygosity (LOH) was used to study recombination in Saccharomyces cerevisiae cells exposed to ultraviolet (UV) light at different points in the cell cycle. With this allele, recombination events can be detected as canavanine-resistant mutations after exposure of cells to UV radiation, since a significant fraction of LOH events appear to arise from recombination between homologous chromosomes. The radiation caused a higher level of LOH in cells that were in the S phase of the cell cycle relative to either cells at other points in the cell cycle or unsynchronized cells. In contrast, the inactivation of nucleotide excision repair abolished the cell cycle-specific induction by UV of LOH. We hypothesize that DNA lesions, if not repaired, were converted into double-strand breaks during stalled replication and these breaks could be repaired through recombination using a non-<span class="hlt">sister</span> <span class="hlt">chromatid</span> and probably also the <span class="hlt">sister</span> <span class="hlt">chromatid</span>. We argue that LOH may be an outcome used by yeast cells to recover from stalled replication at a lesion.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21768208','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21768208"><span>Evaluation of differential representative values between Chinese hamster cells and human lymphocytes in mitomycin C-induced cytogenetic assays and caspase-3 activity.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Liao, Pei-Hu; Lin, Ruey-Hseng; Yang, Ming-Ling; Li, Yi-Ching; Kuan, Yu-Hsiang</p> <p>2012-03-01</p> <p>Chinese hamster ovary (CHO) cells, its lung fibroblasts (V79), and human lymphocytes are routinely used in in vitro cytogenetic assays, which include micronuclei (MN), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE), and chromosome <span class="hlt">aberration</span> (CA) assays. Mitomycin C (MMC), a DNA cross-link alkylating agent, is both an anticancer medicine and a carcinogen. To study the differential representative values of cell types in MMC-treated cytogenetic assays and its upstream factor, cysteine aspartic acid-specific protease (caspase)-3. Among the chosen cell types, lymphocytes expressed the highest sensitivity in all three MMC-induced assays, whereas CHO and V79 showed varied sensitivity in different assays. In MN assay, the sensitivity of CHO is higher than or equal to V79; in SCE assay, the sensitivity of CHO is the same as V79; and in CA assay, the sensitivity of CHO is higher than V79. In-depth analysis of CA revealed that in <span class="hlt">chromatid</span> breaks and dicentrics formation, lymphocyte was the most sensitive of all and CHO was more sensitive than V79; and in acentrics and interchanges formation, lymphocyte was much more sensitive than the others. Furthermore, we found caspase-3 activity plays an important role in MMC-induced cytogenetic assays, with MMC-induced caspase-3 activity resulting in more sensitivity in lymphocytes than in CHO and V79. Based on these findings, lymphocyte will make a suitable predictive or representative control reference in cytogenetic assays and caspase-3 activity with its high specificity, positive predictive value, and sensitivity.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23590349','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23590349"><span>Brother-<span class="hlt">sister</span> incest: data from anonymous computer-assisted self interviews.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stroebel, Sandra S; O'Keefe, Stephen L; Beard, Keith W; Kuo, Shih-Ya; Swindell, Samuel; Stroupe, Walter</p> <p>2013-01-01</p> <p>Retrospective data were entered anonymously by 1,521 adult women using computer-assisted self interview. Forty were classified as victims of brother-<span class="hlt">sister</span> incest, 19 were classified as victims of father-daughter incest, and 232 were classified as victims of sexual abuse by an adult other than their father before reaching 18 years of age. The other 1,230 served as controls. The victims of brother-<span class="hlt">sister</span> incest had significantly more problematic outcomes than controls on many measures (e.g., more likely than the controls to endorse feeling like damaged goods, thinking that they had suffered psychological injury, and having undergone psychological treatment for childhood sexual abuse). However, victims of brother-<span class="hlt">sister</span> incest also had significantly less problematic outcomes than victims of father-daughter incest on some measures (e.g., significantly less likely than the father-daughter incest victims to endorse feeling like damaged goods, thinking that they had suffered psychological injury, and having undergone psychological treatment for childhood sexual abuse).</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2009SPIE.7379E..0PN','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2009SPIE.7379E..0PN"><span>Mask-induced <span class="hlt">aberration</span> in EUV lithography</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Nakajima, Yumi; Sato, Takashi; Inanami, Ryoichi; Nakasugi, Tetsuro; Higashiki, Tatsuhiko</p> <p>2009-04-01</p> <p>We estimated <span class="hlt">aberrations</span> using Zernike sensitivity analysis. We found the difference of the tolerated <span class="hlt">aberration</span> with line direction for illumination. The tolerated <span class="hlt">aberration</span> of perpendicular line for illumination is much smaller than that of parallel line. We consider this difference to be attributable to the mask 3D effect. We call it mask-induced <span class="hlt">aberration</span>. In the case of the perpendicular line for illumination, there was a difference in CD between right line and left line without <span class="hlt">aberration</span>. In this report, we discuss the possibility of pattern formation in NA 0.25 generation EUV lithography tool. In perpendicular pattern for EUV light, the dominant part of <span class="hlt">aberration</span> is mask-induced <span class="hlt">aberration</span>. In EUV lithography, pattern correction based on the mask topography effect will be more important.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_11");'>11</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li class="active"><span>13</span></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_13 --> <div id="page_14" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li class="active"><span>14</span></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="261"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.cancer.gov/publications/patient-education/sibling-has-cancer','NCI'); return false;" href="https://www.cancer.gov/publications/patient-education/sibling-has-cancer"><span>When Your Brother or <span class="hlt">Sister</span> Has Cancer</span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p>Help when a brother or <span class="hlt">sister</span> has cancer. Learn how families cope and find support when a sibling has cancer. Tips to help you talk with your friends, deal with stress, and take care of your mind and body are also shared.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2893262','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2893262"><span>Influence of homologous recombinational repair on cell survival and chromosomal <span class="hlt">aberration</span> induction during the cell cycle in γ-irradiated CHO cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Wilson, Paul F.; Hinz, John M.; Urbin, Salustra S.; Nham, Peter B.; Thompson, Larry H.</p> <p>2010-01-01</p> <p>The repair of DNA double-strand breaks (DSB) by homologous recombinational repair (HRR) underlies the high radioresistance and low mutability observed in S-phase mammalian cells. To evaluate the contributions of HRR and nonhomologous end-joining (NHEJ) to overall DSB repair capacity throughout the cell cycle after γ-irradiation, we compared HRR-deficient RAD51D-knockout 51D1 to CgRAD51D-complemented 51D1 (51D1.3) CHO cells for survival and chromosomal <span class="hlt">aberrations</span> (CAs). Asynchronous cultures were irradiated with 150 or 300 cGy and separated by cell size using centrifugal elutriation. Cell survival of each synchronous fraction (~20 fractions total from early G1 to late G2/M) was measured by colony formation. 51D1.3 cells were most resistant in S, while 51D1 cells were most resistant in early G1 (with survival and chromosome-type CA levels similar to 51D1.3) and became progressively more sensitive throughout S and G2. Both cell lines experienced significantly reduced survival from late S into G2. Metaphases were collected from every third elutriation fraction at the first post-irradiation mitosis and scored for CAs. 51D1 cells irradiated in S and G2 had ~2-fold higher <span class="hlt">chromatid</span>-type CAs and a remarkable ~25-fold higher level of complex <span class="hlt">chromatid</span>-type exchanges compared to 51D1.3 cells. Complex exchanges in 51D1.3 cells were only observed in G2. These results show an essential role for HRR in preventing gross chromosomal rearrangements in proliferating cells and, with our previous report of reduced survival of G2-phase NHEJ-deficient prkdc CHO cells [Hinz et al. DNA Repair 4, 782–792, 2005], imply reduced activity/efficiency of both HRR and NHEJ as cells transition from S to G2. PMID:20434408</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5957430','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5957430"><span>Dynamics and control of <span class="hlt">sister</span> kinetochore behavior during the meiotic divisions in Drosophila spermatocytes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p></p> <p>2018-01-01</p> <p><span class="hlt">Sister</span> kinetochores are connected to the same spindle pole during meiosis I and to opposite poles during meiosis II. The molecular mechanisms controlling the distinct behavior of <span class="hlt">sister</span> kinetochores during the two meiotic divisions are poorly understood. To study kinetochore behavior during meiosis, we have optimized time lapse imaging with Drosophila spermatocytes, enabling kinetochore tracking with high temporal and spatial resolution through both meiotic divisions. The correct bipolar orientation of chromosomes within the spindle proceeds rapidly during both divisions. Stable bi-orientation of the last chromosome is achieved within ten minutes after the onset of kinetochore-microtubule interactions. Our analyses of mnm and tef mutants, where univalents instead of bivalents are present during meiosis I, indicate that the high efficiency of normal bi-orientation depends on pronounced stabilization of kinetochore attachments to spindle microtubules by the mechanical tension generated by spindle forces upon bi-orientation. Except for occasional brief separation episodes, <span class="hlt">sister</span> kinetochores are so closely associated that they cannot be resolved individually by light microscopy during meiosis I, interkinesis and at the start of meiosis II. Permanent evident separation of <span class="hlt">sister</span> kinetochores during M II depends on spindle forces resulting from bi-orientation. In mnm and tef mutants, <span class="hlt">sister</span> kinetochore separation can be observed already during meiosis I in bi-oriented univalents. Interestingly, however, this <span class="hlt">sister</span> kinetochore separation is delayed until the metaphase to anaphase transition and depends on the Fzy/Cdc20 activator of the anaphase-promoting complex/cyclosome. We propose that univalent bi-orientation in mnm and tef mutants exposes a release of <span class="hlt">sister</span> kinetochore conjunction that occurs also during normal meiosis I in preparation for bi-orientation of dyads during meiosis II. PMID:29734336</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25163060','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25163060"><span>Camera processing with chromatic <span class="hlt">aberration</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Korneliussen, Jan Tore; Hirakawa, Keigo</p> <p>2014-10-01</p> <p>Since the refractive index of materials commonly used for lens depends on the wavelengths of light, practical camera optics fail to converge light to a single point on an image plane. Known as chromatic <span class="hlt">aberration</span>, this phenomenon distorts image details by introducing magnification error, defocus blur, and color fringes. Though achromatic and apochromatic lens designs reduce chromatic <span class="hlt">aberration</span> to a degree, they are complex and expensive and they do not offer a perfect correction. In this paper, we propose a new postcapture processing scheme designed to overcome these problems computationally. Specifically, the proposed solution is comprised of chromatic <span class="hlt">aberration</span>-tolerant demosaicking algorithm and post-demosaicking chromatic <span class="hlt">aberration</span> correction. Experiments with simulated and real sensor data verify that the chromatic <span class="hlt">aberration</span> is effectively corrected.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://medlineplus.gov/magazine/issues/fall08/articles/fall08pg14.html','NIH-MEDLINEPLUS'); return false;" href="https://medlineplus.gov/magazine/issues/fall08/articles/fall08pg14.html"><span>Cochlear Implants Keep Twin <span class="hlt">Sisters</span> Learning, Discovering Together</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePlus</a></p> <p></p> <p></p> <p>... University. Photo: Johns Hopkins University Keep Twin <span class="hlt">Sisters</span> Learning, Discovering Together Mia and Isabelle Jeppsen, 10, share ... her mother, gratefully, "There's the obvious benefit of learning to read, write and communicate with facility and ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4873764','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4873764"><span>Generativity in Elderly Oblate <span class="hlt">Sisters</span> of Providence</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Black, Helen K.; Hannum, Susan M.; Rubinstein, Robert L.; de Medeiros, Kate</p> <p>2016-01-01</p> <p>Purpose of the Study: We explored how generativity and well-being merged in a group of childless older women: African and Hispanic Roman Catholic Religious <span class="hlt">Sisters</span>, linking two minority identity characteristics. Design and Methods: We qualitatively interviewed 8 Oblate <span class="hlt">Sisters</span> of Providence (OSP), by providing a framework for examining the range of the women’s generativity—cultural spheres in which generativity is rooted and outlets for generativity. Results: Early negative experiences, such as fleeing despotism in Haiti and Cuba and racism within the Catholic Church, occurred alongside positive experiences—families who stressed education, and Caucasian Religious who taught children of color. This became a foundation for the Sister’s generative commitment. Implications: Findings highlight that research gains from a phenomenological understanding of how religious faith promotes generative cognitions and emotions. Findings also reveal that the experiences of a subculture in society—African-American elderly women religious—add to theories and definitions of generativity. PMID:25352535</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=nun+AND+study&pg=2&id=EJ377172','ERIC'); return false;" href="https://eric.ed.gov/?q=nun+AND+study&pg=2&id=EJ377172"><span><span class="hlt">Sisters</span> at Work: Career and Community Changes.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Briody, Elizabeth K.; Sullivan, Teresa A.</p> <p>1988-01-01</p> <p>The authors examine occupational differentiation of U.S. Catholic nuns before and since the Second Vatican Council. Data were collected from interviews with 30 <span class="hlt">sisters</span> representing 11 congregations. The analysis relates the diversification of their careers to changes in ideology and life-style and to the changing demographic and financial status…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/9355852','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/9355852"><span>Biodosimetry results from space flight Mir-18.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yang, T C; George, K; Johnson, A S; Durante, M; Fedorenko, B S</p> <p>1997-11-01</p> <p>Astronauts are classified as radiation workers due to the presence of ionizing radiation in space. For the assessment of health risks, physical dosimetry has been indispensable. However, the change of the location of dosimeters on the crew members, the variation in dose rate with location inside the spacecraft and the unknown biological effects of microgravity can introduce significant uncertainties in estimating exposure. To circumvent such uncertainty, a study on the cytogenetic effects of space radiation in human lymphocytes was proposed and conducted for Mir-18, a 115-day mission. This study used fluorescence in situ hybridization (FISH) with whole-chromosome painting probes to score chromosomal exchanges and the Giemsa staining method to determine the frequency of dicentrics. The growth kinetics of cells and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) were examined to ensure that chromosomal <span class="hlt">aberrations</span> were scored in the first mitosis and were induced primarily by space radiation. Our results showed that the frequency of chromosomal <span class="hlt">aberrations</span> increased significantly in postflight samples compared to samples drawn prior to flight, and that the frequency of SCEs was similar for both pre- and postflight samples. Based on a dose-response curve for preflight samples exposed to gamma rays, the absorbed dose received by crew members during the mission was estimated to be about 14.75 cSv. Because the absorbed dose measured by physical dosimeters is 5.2 cGy for the entire mission, the RBE is about 2.8.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040172870&hterms=mitosis&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D40%26Ntt%3Dmitosis','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040172870&hterms=mitosis&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D40%26Ntt%3Dmitosis"><span>Biodosimetry results from space flight Mir-18</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Yang, T. C.; George, K.; Johnson, A. S.; Durante, M.; Fedorenko, B. S.</p> <p>1997-01-01</p> <p>Astronauts are classified as radiation workers due to the presence of ionizing radiation in space. For the assessment of health risks, physical dosimetry has been indispensable. However, the change of the location of dosimeters on the crew members, the variation in dose rate with location inside the spacecraft and the unknown biological effects of microgravity can introduce significant uncertainties in estimating exposure. To circumvent such uncertainty, a study on the cytogenetic effects of space radiation in human lymphocytes was proposed and conducted for Mir-18, a 115-day mission. This study used fluorescence in situ hybridization (FISH) with whole-chromosome painting probes to score chromosomal exchanges and the Giemsa staining method to determine the frequency of dicentrics. The growth kinetics of cells and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) were examined to ensure that chromosomal <span class="hlt">aberrations</span> were scored in the first mitosis and were induced primarily by space radiation. Our results showed that the frequency of chromosomal <span class="hlt">aberrations</span> increased significantly in postflight samples compared to samples drawn prior to flight, and that the frequency of SCEs was similar for both pre- and postflight samples. Based on a dose-response curve for preflight samples exposed to gamma rays, the absorbed dose received by crew members during the mission was estimated to be about 14.75 cSv. Because the absorbed dose measured by physical dosimeters is 5.2 cGy for the entire mission, the RBE is about 2.8.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22885097','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22885097"><span>Cytogenetic analyses of Azadirachtin reveal absence of genotoxicity but marked antiproliferative effects in human lymphocytes and CHO cells in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mosesso, Pasquale; Bohm, Lothar; Pepe, Gaetano; Fiore, Mario; Carpinelli, Alice; Gäde, Gerd; Nagini, Siddavaram; Ottavianelli, Alessandro; Degrassi, Francesca</p> <p>2012-09-18</p> <p>In this work we have examined the genotoxic potential of the bioinsecticide Azadirachtin A (AZA) and its influence on cell proliferation on human lymphocytes and Chinese Hamster ovary (CHO) cells. AZA genotoxicity was assessed by the analysis of chromosomal <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) in the absence and presence of rat liver S9 metabolism. Primary DNA damage was also investigated by means of the comet assay. The results obtained clearly indicate that AZA is not genotoxic in mammalian cells. On the other hand, AZA proved to interfere with cell cycle progression as shown by modulation of frequencies of first (M1) and second division (M2) metaphases detected by 5-Bromo-2'-deoxyuridine labeling. Accumulation of M1 metaphases were more pronounced in human lymphocytes. In the transformed CHO cell line, however, significant increases of multinucleated interphases and polyploid cells were observed at long treatment time. At higher dose-levels, the incidence of polyploidy was close to 100%. Identification of spindle structure and number of centrosomes by fluorescent immunostaining with α- and γ-tubulin antibodies revealed <span class="hlt">aberrant</span> mitoses exhibiting multipolar spindles with several centrosomal signals. These findings suggest that AZA can act either through a stabilizing activity of microtubules or by inhibition of Aurora A, since both mechanisms are able to generate genetically unstable polyploid cells with multipolar spindles and multinucleated interphases. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5375655','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5375655"><span>The <span class="hlt">Sisters</span> of Mercy in the Crimean War: Lessons for Catholic health care</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Paradis, Mary Raphael; Hart, Edith Mary; O’Brien, Mary Judith</p> <p>2017-01-01</p> <p>In 1856, an appeal went out to nurses in both England and Ireland, and especially to religious nurses, to care for the troops fighting in the Crimean War. The <span class="hlt">Sisters</span> of Mercy, founded in 1831 by Venerable Catherine McAuley, answered that call. This article describes the enormous challenges the <span class="hlt">Sisters</span> faced in that mission, which was a test of their nursing skills, flexibility, organizational ability, and their spirit of mercy. The challenges they faced professionally and as religious <span class="hlt">Sisters</span>, the manner in which they faced those challenges, and their spiritual lives as religious women shaped their ability to give comprehensive care. Some applications are made to the challenges which religious communities and organizations working in health care face in our country at this time. Summary: This article describes the challenges faced by a group of <span class="hlt">Sisters</span> of Mercy from England and Ireland who volunteered to serve as nurses in the Crimean War from 1856 to 1858. Applications are made to challenges which are faced by religious communities and organizations in the current secular healthcare environment. PMID:28392597</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28392597','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28392597"><span>The <span class="hlt">Sisters</span> of Mercy in the Crimean War: Lessons for Catholic health care.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Paradis, Mary Raphael; Hart, Edith Mary; O'Brien, Mary Judith</p> <p>2017-02-01</p> <p>In 1856, an appeal went out to nurses in both England and Ireland, and especially to religious nurses, to care for the troops fighting in the Crimean War. The <span class="hlt">Sisters</span> of Mercy, founded in 1831 by Venerable Catherine McAuley, answered that call. This article describes the enormous challenges the <span class="hlt">Sisters</span> faced in that mission, which was a test of their nursing skills, flexibility, organizational ability, and their spirit of mercy. The challenges they faced professionally and as religious <span class="hlt">Sisters</span>, the manner in which they faced those challenges, and their spiritual lives as religious women shaped their ability to give comprehensive care. Some applications are made to the challenges which religious communities and organizations working in health care face in our country at this time. Summary: This article describes the challenges faced by a group of <span class="hlt">Sisters</span> of Mercy from England and Ireland who volunteered to serve as nurses in the Crimean War from 1856 to 1858. Applications are made to challenges which are faced by religious communities and organizations in the current secular healthcare environment.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/EJ1006059.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/EJ1006059.pdf"><span><span class="hlt">Sister</span> M. Madeleva Wolff, C.S.C.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Petit, M. Loretta</p> <p>2006-01-01</p> <p><span class="hlt">Sister</span> M. Madeleva Wolff, C.S.C., teacher, essayist, poet, and college administrator, through her creative ability and innovative practices made possible major contributions to Catholic education in her lifetime. Without her strong personality and boundless energy, many of her dreams for an ideal college curriculum would not have come to fruition.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/6650568','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/6650568"><span>Perrault's syndrome in two <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bösze, P; Skripeczky, K; Gaál, M; Tóth, A; László, J</p> <p>1983-10-01</p> <p>We report on two <span class="hlt">sisters</span> with Perrault's syndrome, i.e., autosomal recessive ovarian dysgenesis associated with sensorineural deafness. They were deaf-mute and of normal height with a few minor somatic anomalies. Both had streak gonads and an apparently normal female 46,XX chromosome constitution. The parents were apparently not consanguineous. The mother had normal hearing. Other relatives were not available for study. Epilepsy, which occurred in three relatives including one of the index patients, may have been inherited coincidentally from the mother's family.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4598568','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4598568"><span>Bub1 autophosphorylation feeds back to regulate kinetochore docking and promote localized substrate phosphorylation</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Asghar, Adeel; Lajeunesse, Audrey; Dulla, Kalyan; Combes, Guillaume; Thebault, Philippe; Nigg, Erich A.; Elowe, Sabine</p> <p>2015-01-01</p> <p>During mitosis, Bub1 kinase phosphorylates histone H2A-T120 to promote centromere <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion through recruitment of shugoshin (Sgo) proteins. The regulation and dynamics of H2A-T120 phosphorylation are poorly understood. Using quantitative phosphoproteomics we show that Bub1 is autophosphorylated at numerous sites. We confirm mitosis-specific autophosphorylation of a several residues and show that Bub1 activation is primed in interphase but fully achieved only in mitosis. Mutation of a single autophosphorylation site T589 alters kinetochore turnover of Bub1 and results in uniform H2A-T120 phosphorylation and Sgo recruitment along chromosome arms. Consequently, improper <span class="hlt">sister</span> <span class="hlt">chromatid</span> resolution and chromosome segregation errors are observed. Kinetochore tethering of Bub1-T589A refocuses H2A-T120 phosphorylation and Sgo1 to centromeres. Recruitment of the Bub1-Bub3-BubR1 axis to kinetochores has recently been extensively studied. Our data provide novel insight into the regulation and kinetochore residency of Bub1 and indicate that its localization is dynamic and tightly controlled through feedback autophosphorylation. PMID:26399325</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2171180','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2171180"><span>Recombination protein Tid1p controls resolution of cohesin-dependent linkages in meiosis in Saccharomyces cerevisiae</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kateneva, Anna V.; Konovchenko, Anton A.; Guacci, Vincent; Dresser, Michael E.</p> <p>2005-01-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion and interhomologue recombination are coordinated to promote the segregation of homologous chromosomes instead of <span class="hlt">sister</span> <span class="hlt">chromatids</span> at the first meiotic division. During meiotic prophase in Saccharomyces cerevisiae, the meiosis-specific cohesin Rec8p localizes along chromosome axes and mediates most of the cohesion. The mitotic cohesin Mcd1p/Scc1p localizes to discrete spots along chromosome arms, and its function is not clear. In cells lacking Tid1p, which is a member of the SWI2/SNF2 family of helicase-like proteins that are involved in chromatin remodeling, Mcd1p and Rec8p persist abnormally through both meiotic divisions, and chromosome segregation fails in the majority of cells. Genetic results indicate that the primary defect in these cells is a failure to resolve Mcd1p-mediated connections. Tid1p interacts with recombination enzymes Dmc1p and Rad51p and has an established role in recombination repair. We propose that Tid1p remodels Mcd1p-mediated cohesion early in meiotic prophase to facilitate interhomologue recombination and the subsequent segregation of homologous chromosomes. PMID:16230461</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29804664','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29804664"><span>Assays for the spindle assembly checkpoint in cell culture.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Marcozzi, Chiara; Pines, Jonathon</p> <p>2018-01-01</p> <p>The spindle assembly checkpoint (SAC) is crucial to maintain genomic stability since it prevents premature separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> in mitosis and ensures the fidelity of chromosome segregation. The SAC arrests cells in mitosis and is not satisfied until all kinetochores are stably attached to the mitotic spindle. Improperly attached kinetochores activate the SAC and catalyze the formation of the mitotic checkpoint complex (MCC), containing Mad2, Cdc20, BubR1, and Bub3 proteins. The MCC binds and thereby inhibits the APC/C E3 ubiquitin ligase until the last kinetochore has attached to microtubules. Once the SAC is satisfied, the APC/C promptly activates and targets cyclin B1 and securin for degradation, thus allowing <span class="hlt">sister</span> <span class="hlt">chromatids</span> to separate and the cell to exit mitosis. Our understanding of SAC signaling has increased thanks to the development of new genetic, biochemical, molecular, and structural biology techniques. Here, we describe how live-cell imaging microscopy in combination with gene-targeting strategies and biochemical assays can be exploited to investigate the intrinsic properties of the SAC in mammalian cultured cells. © 2018 Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1460327','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1460327"><span>The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 genes are required for tolerating irreparable, ultraviolet-induced DNA damage.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Paulovich, A G; Armour, C D; Hartwell, L H</p> <p>1998-01-01</p> <p>In wild-type Saccharomyces cerevisiae, a checkpoint slows the rate of progression of an ongoing S phase in response to exposure to a DNA-alkylating agent. Mutations that eliminate S phase regulation also confer sensitivity to alkylating agents, leading us to suggest that, by regulating the S phase rate, cells are either better able to repair or better able to replicate damaged DNA. In this study, we determine the effects of mutations that impair S phase regulation on the ability of excision repair-defective cells to replicate irreparably UV-damaged DNA. We assay survival after UV irradiation, as well as the genetic consequences of replicating a damaged template, namely mutation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange induction. We find that RAD9, RAD17, RAD24, and MEC3 are required for UV-induced (although not spontaneous) mutagenesis, and that RAD9 and RAD17 (but not REV3, RAD24, and MEC3) are required for maximal induction of replication-dependent <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange. Therefore, checkpoint genes not only control cell cycle progression in response to damage, but also play a role in accommodating DNA damage during replication. PMID:9725831</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/134375-interstitial-telomeric-sequences-human-chromosomes-cluster-common-fragile-sites-mutagen-sensitive-sites-viral-integration-sites-cancer-breakpoints-proto-oncogenes-breakpoints-involved-primate-evolution','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/134375-interstitial-telomeric-sequences-human-chromosomes-cluster-common-fragile-sites-mutagen-sensitive-sites-viral-integration-sites-cancer-breakpoints-proto-oncogenes-breakpoints-involved-primate-evolution"><span>Interstitial telomeric sequences in human chromosomes cluster with common fragile sites, mutagen sensitive sites, viral integration sites, cancer breakpoints, proto-oncogenes and breakpoints involved in primate evolution</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Adekunle, S.S.A.; Wyandt, H.; Mark, H.F.L.</p> <p>1994-09-01</p> <p>Recently we mapped the telomeric repeat sequences to 111 interstitial sites in the human genome and to sites of gaps and breaks induced by aphidicolin and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange sites detected by BrdU. Many of these sites correspond to conserved fragile sites in man, gorilla and chimpazee, to sites of conserved <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange in the mammalian X chromosome, to mutagenic sensitive sites, mapped locations of proto-oncogenes, breakpoints implicated in primate evolution and to breakpoints indicated as the sole anomaly in neoplasia. This observation prompted us to investigate if the interstitial telomeric sites cluster with these sites. An extensive literaturemore » search was carried out to find all the available published sites mentioned above. For comparison, we also carried out a statistical analysis of the clustering of the sites of the telomeric repeats with the gene locations where only nucleotide mutations have been observed as the only chromosomal abnormality. Our results indicate that the telomeric repeats cluster most with fragile sites, mutagenic sensitive sites and breakpoints implicated in primate evolution and least with cancer breakpoints, mapped locations of proto-oncogenes and other genes with nucleotide mutations.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/9725831','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/9725831"><span>The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 genes are required for tolerating irreparable, ultraviolet-induced DNA damage.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Paulovich, A G; Armour, C D; Hartwell, L H</p> <p>1998-09-01</p> <p>In wild-type Saccharomyces cerevisiae, a checkpoint slows the rate of progression of an ongoing S phase in response to exposure to a DNA-alkylating agent. Mutations that eliminate S phase regulation also confer sensitivity to alkylating agents, leading us to suggest that, by regulating the S phase rate, cells are either better able to repair or better able to replicate damaged DNA. In this study, we determine the effects of mutations that impair S phase regulation on the ability of excision repair-defective cells to replicate irreparably UV-damaged DNA. We assay survival after UV irradiation, as well as the genetic consequences of replicating a damaged template, namely mutation and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange induction. We find that RAD9, RAD17, RAD24, and MEC3 are required for UV-induced (although not spontaneous) mutagenesis, and that RAD9 and RAD17 (but not REV3, RAD24, and MEC3) are required for maximal induction of replication-dependent <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange. Therefore, checkpoint genes not only control cell cycle progression in response to damage, but also play a role in accommodating DNA damage during replication.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li class="active"><span>14</span></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_14 --> <div id="page_15" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li class="active"><span>15</span></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="281"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3208311','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3208311"><span>Non-redundant odor coding by <span class="hlt">sister</span> mitral cells revealed by light addressable glomeruli in the mouse</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Dhawale, Ashesh K.; Hagiwara, Akari; Bhalla, Upinder S.; Murthy, Venkatesh N.; Albeanu, Dinu F.</p> <p>2011-01-01</p> <p>Sensory inputs frequently converge on the brain in a spatially organized manner, often with overlapping inputs to multiple target neurons. Whether the responses of target neurons with common inputs become decorrelated depends on the contribution of local circuit interactions. We addressed this issue in the olfactory system using newly generated transgenic mice expressing channelrhodopsin-2 in all olfactory sensory neurons. By selectively stimulating individual glomeruli with light, we identified mitral/tufted (M/T) cells that receive common input (<span class="hlt">sister</span> cells). <span class="hlt">Sister</span> M/T cells had highly correlated responses to odors as measured by average spike rates, but their spike timing in relation to respiration was differentially altered. In contrast, non-<span class="hlt">sister</span> M/T cells correlated poorly on both these measures. We suggest that <span class="hlt">sister</span> M/T cells carry two different channels of information: average activity representing shared glomerular input, and phase-specific information that refines odor representations and is substantially independent for <span class="hlt">sister</span> M/T cells. PMID:20953197</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED332415.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED332415.pdf"><span>Brothers and <span class="hlt">Sisters</span> of Children with Disabilities: An Annotated Bibliography. Families as Allies Project.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Smieja, Linda L.; And Others</p> <p></p> <p>This annotated bibliography provides a comprehensive review of literature focusing on brothers and <span class="hlt">sisters</span> of children with emotional disorders. Some material addressing brothers and <span class="hlt">sisters</span> of children who have physical, mental, or developmental disabilities is also included. The bibliography lists approximately 80 references covering a 10-year…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4728446','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4728446"><span>Overlap microtubules link <span class="hlt">sister</span> k-fibres and balance the forces on bi-oriented kinetochores</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kajtez, Janko; Solomatina, Anastasia; Novak, Maja; Polak, Bruno; Vukušić, Kruno; Rüdiger, Jonas; Cojoc, Gheorghe; Milas, Ana; Šumanovac Šestak, Ivana; Risteski, Patrik; Tavano, Federica; Klemm, Anna H.; Roscioli, Emanuele; Welburn, Julie; Cimini, Daniela; Glunčić, Matko; Pavin, Nenad; Tolić, Iva M.</p> <p>2016-01-01</p> <p>During metaphase, forces on kinetochores are exerted by k-fibres, bundles of microtubules that end at the kinetochore. Interestingly, non-kinetochore microtubules have been observed between <span class="hlt">sister</span> kinetochores, but their function is unknown. Here we show by laser-cutting of a k-fibre in HeLa and PtK1 cells that a bundle of non-kinetochore microtubules, which we term ‘bridging fibre', bridges <span class="hlt">sister</span> k-fibres and balances the interkinetochore tension. We found PRC1 and EB3 in the bridging fibre, suggesting that it consists of antiparallel dynamic microtubules. By using a theoretical model that includes a bridging fibre, we show that the forces at the pole and at the kinetochore depend on the bridging fibre thickness. Moreover, our theory and experiments show larger relaxation of the interkinetochore distance for cuts closer to kinetochores. We conclude that the bridging fibre, by linking <span class="hlt">sister</span> k-fibres, withstands the tension between <span class="hlt">sister</span> kinetochores and enables the spindle to obtain a curved shape. PMID:26728792</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2002SPIE.4611..176M','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2002SPIE.4611..176M"><span>Correlations between corneal and total wavefront <span class="hlt">aberrations</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Mrochen, Michael; Jankov, Mirko; Bueeler, Michael; Seiler, Theo</p> <p>2002-06-01</p> <p>Purpose: Corneal topography data expressed as corneal <span class="hlt">aberrations</span> are frequently used to report corneal laser surgery results. However, the optical image quality at the retina depends on all optical elements of the eye such as the human lens. Thus, the aim of this study was to investigate the correlations between the corneal and total wavefront <span class="hlt">aberrations</span> and to discuss the importance of corneal <span class="hlt">aberrations</span> for representing corneal laser surgery results. Methods: Thirty three eyes of 22 myopic subjects were measured with a corneal topography system and a Tschernig-type wavefront analyzer after the pupils were dilated to at least 6 mm in diameter. All measurements were centered with respect to the line of sight. Corneal and total wavefront <span class="hlt">aberrations</span> were calculated up to the 6th Zernike order in the same reference plane. Results: Statistically significant correlations (p < 0.05) between the corneal and total wavefront <span class="hlt">aberrations</span> were found for the astigmatism (C3,C5) and all 3rd Zernike order coefficients such as coma (C7,C8). No statistically significant correlations were found for all 4th to 6th order Zernike coefficients except for the 5th order horizontal coma C18 (p equals 0.003). On average, all Zernike coefficients for the corneal <span class="hlt">aberrations</span> were found to be larger compared to Zernike coefficients for the total wavefront <span class="hlt">aberrations</span>. Conclusions: Corneal <span class="hlt">aberrations</span> are only of limited use for representing the optical quality of the human eye after corneal laser surgery. This is due to the lack of correlation between corneal and total wavefront <span class="hlt">aberrations</span> in most of the higher order <span class="hlt">aberrations</span>. Besides this, the data present in this study yield towards an <span class="hlt">aberration</span> balancing between corneal <span class="hlt">aberrations</span> and the optical elements within the eye that reduces the <span class="hlt">aberration</span> from the cornea by a certain degree. Consequently, ideal customized ablations have to take both, corneal and total wavefront <span class="hlt">aberrations</span>, into consideration.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/661839','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/661839"><span>Chromosome-damaging effect of betel leaf.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sadasivan, G; Rani, G; Kumari, C K</p> <p>1978-05-01</p> <p>The chewing of betel leaf with other ingredients is a widespread addiction in India. The chromosome damaging effect was studied in human leukocyte cultures. There was an increase in the frequency of <span class="hlt">chromatid</span> <span class="hlt">aberrations</span> when the leaf extract was added to cultures.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4041464','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4041464"><span>Requirement for Parp-1 and DNA ligases 1 or 3 but not of Xrcc1 in chromosomal translocation formation by backup end joining</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Soni, Aashish; Siemann, Maria; Grabos, Martha; Murmann, Tamara; Pantelias, Gabriel E.; Iliakis, George</p> <p>2014-01-01</p> <p>In mammalian cells, ionizing radiation (IR)-induced DNA double-strand breaks (DSBs) are repaired in all phases of the cell cycle predominantly by classical, DNA-PK-dependent nonhomologous end joining (D-NHEJ). Homologous recombination repair (HRR) is functional during the S- and G2-phases, when a <span class="hlt">sister</span> <span class="hlt">chromatid</span> becomes available. An error-prone, alternative form of end joining, operating as backup (B-NHEJ) functions robustly throughout the cell cycle and particularly in the G2-phase and is thought to backup predominantly D-NHEJ. Parp-1, DNA-ligases 1 (Lig1) and 3 (Lig3), and Xrcc1 are implicated in B-NHEJ. Chromosome and <span class="hlt">chromatid</span> translocations are manifestations of erroneous DSB repair and are crucial culprits in malignant transformation and IR-induced cell lethality. We analyzed shifts in translocation formation deriving from defects in D-NHEJ or HRR in cells irradiated in the G2-phase and identify B-NHEJ as the main DSB repair pathway backing up both of these defects at the cost of a large increase in translocation formation. Our results identify Parp-1 and Lig1 and 3 as factors involved in translocation formation and show that Xrcc1 reinforces the function of Lig3 in the process without being required for it. Finally, we demonstrate intriguing connections between B-NHEJ and DNA end resection in translocation formation and show that, as for D-NHEJ and HRR, the function of B-NHEJ facilitates the recovery from the G2-checkpoint. These observations advance our understanding of chromosome <span class="hlt">aberration</span> formation and have implications for the mechanism of action of Parp inhibitors. PMID:24748665</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11313115','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11313115"><span>Genotoxicity of dill (Anethum graveolens L.), peppermint (Menthaxpiperita L.) and pine (Pinus sylvestris L.) essential oils in human lymphocytes and Drosophila melanogaster.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lazutka, J R; Mierauskiene, J; Slapsyte, G; Dedonyte, V</p> <p>2001-05-01</p> <p>Genotoxic properties of the essential oils extracted from dill (Anethum graveolens L.) herb and seeds, peppermint (Menthaxpiperita L.) herb and pine (Pinus sylvestris L.) needles were studied using chromosome <span class="hlt">aberration</span> (CA) and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) tests in human lymphocytes in vitro, and Drosophila melanogaster somatic mutation and recombination test (SMART) in vivo. In the CA test, the most active essential oil was from dill seeds, then followed essential oils from dill herb, peppermint herb and pine needles, respectively. In the SCE test, the most active essential oils were from dill herb and seeds followed by essential oils from pine needles and peppermint herb. Essential oils from dill herb and seeds and pine needles induced CA and SCE in a clear dose-dependent manner, while peppermint essential oil induced SCE in a dose-independent manner. All essential oils were cytotoxic for human lymphocytes. In the SMART test, a dose-dependent increase in mutation frequency was observed for essential oils from pine and dill herb. Peppermint essential oil induced mutations in a dose-independent manner. Essential oil from dill seeds was almost inactive in the SMART test.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20306073','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20306073"><span>Genotoxicity surveillance programme in workers dismantling World War I chemical ammunition.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mateuca, R A; Carton, C; Roelants, M; Roesems, S; Lison, D; Kirsch-Volders, M</p> <p>2010-06-01</p> <p>To evaluate the effectiveness of personal protective measures in a dismantling plant for chemical weapons from World War I of the Belgian Defence. Seventeen NIOSH level B-equipped plant workers exposed to arsenic trichloride (AsCl(3)) in combination with phosgene or hydrogen cyanide (HCN) were compared to 24 NIOSH level C-protected field workers occasionally exposed to genotoxic chemicals (including AsCl(3)-phosgene/HCN) when collecting chemical ammunition, and 19 matched referents. Chromosomal <span class="hlt">aberrations</span> (CA), micronuclei (MNCB and MNMC), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) and high frequency cells (HFC) were analysed in peripheral blood lymphocytes. Urinary arsenic levels and genetic polymorphisms in major DNA repair enzymes (hOGG1(326), XRCC1(399), XRCC3(241)) were also assessed. SCE and HFC levels were significantly higher in plant-exposed versus referent subjects, but MNCB and MNMC were not different. MNCB, SCE and HFC levels were significantly higher and MNMC levels significantly lower in field-exposed workers versus referents. AsCl(3) exposure was not correlated with genotoxicity biomarkers. Protective measures for plant-exposed workers appear adequate, but protection for field-exposed individuals could be improved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23764456','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23764456"><span>Modulation of radiation-induced and mitomycin C-induced chromosome damage by apigenin in human lymphocytes in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sharma, Narinder K</p> <p>2013-09-01</p> <p>Apigenin (APG), a flavone, is known to exhibit antioxidant, antimutagenic and antitumorigenic activity, both in vivo and in vitro. The aim of this study is to investigate the modulatory effects of APG on human lymphocytes after irradiation with gamma rays (3 Gy) or treatment with the antineoplastic agent, mitomycin C (MMC), in vitro. Cytogenetic biomarkers such as chromosome <span class="hlt">aberrations</span> (CAs), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) and cytochalasin-B blocked micronuclei (CBMN), were studied in blood lymphocytes treated with radiation, or antineoplastic agent (MMC), and APG. Whole blood lymphocytes were cultured in vitro using a standard protocol. No significant differences were found in the frequency of CAs or micronuclei (MN) in human peripheral blood lymphocytes irradiated with gamma rays (3 Gy) and then post-treated with APG. There was an increase in the frequency of SCEs per cell in APG-treated samples compared with the controls. Lymphocytes treated with MMC in the presence of APG exhibited a significant decrease (P < 0.01) in the frequency of SCEs compared with MMC treatment alone. The data for the MN test indicated that APG treatment significantly reduced (P < 0.01) the frequency of MMC-induced MN.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3766282','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3766282"><span>Modulation of radiation-induced and mitomycin C-induced chromosome damage by apigenin in human lymphocytes in vitro</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Sharma, Narinder K.</p> <p>2013-01-01</p> <p>Apigenin (APG), a flavone, is known to exhibit antioxidant, antimutagenic and antitumorigenic activity, both in vivo and in vitro. The aim of this study is to investigate the modulatory effects of APG on human lymphocytes after irradiation with gamma rays (3 Gy) or treatment with the antineoplastic agent, mitomycin C (MMC), in vitro. Cytogenetic biomarkers such as chromosome <span class="hlt">aberrations</span> (CAs), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) and cytochalasin-B blocked micronuclei (CBMN), were studied in blood lymphocytes treated with radiation, or antineoplastic agent (MMC), and APG. Whole blood lymphocytes were cultured in vitro using a standard protocol. No significant differences were found in the frequency of CAs or micronuclei (MN) in human peripheral blood lymphocytes irradiated with gamma rays (3 Gy) and then post-treated with APG. There was an increase in the frequency of SCEs per cell in APG-treated samples compared with the controls. Lymphocytes treated with MMC in the presence of APG exhibited a significant decrease (P < 0.01) in the frequency of SCEs compared with MMC treatment alone. The data for the MN test indicated that APG treatment significantly reduced (P < 0.01) the frequency of MMC-induced MN. PMID:23764456</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6713508-ntp-technical-report-toxicity-studies-diethanolamine-cas-administered-topically-drinking-water-f344-rats-b6c3f1-mice-toxicity-report-series','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6713508-ntp-technical-report-toxicity-studies-diethanolamine-cas-administered-topically-drinking-water-f344-rats-b6c3f1-mice-toxicity-report-series"><span>NTP technical report on toxicity studies of diethanolamine (CAS No. 111-42-2) administered topically and in drinking water to F344/n rats and B6C3F1 mice. Toxicity report series</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Melnick, R.L.</p> <p>1992-10-01</p> <p>Diethanolamine is a high-production chemical used in cosmetics, in cutting fluids, as a dispersing agent for agricultural chemicals, and as an absorbent for acidic gases. Toxicology studies of diethanolamine were conducted in F344/N rats and B6C3F1 mice of both sexes for 2 weeks (5/sex/species/dose) and 13 weeks (10/sex/species/dose) to characterize and compare the effects of oral and dermal exposure. In addition to histopathology, evaluations included clinical pathology, urinalyses, and sperm morphology or vaginal cytology. In vitro genetic toxicity studies included assessments of mutagenicity in Salmonella typhimurium and mouse lymphoma L5178Y cells, analysis of chromosomal <span class="hlt">aberrations</span> and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange inmore » Chinese hamster ovary cells, and determination of micronuclei formed in mice during the 13 week dermal exposure study. In the 13-week drinking water study in mice, nephropathy and tubular necrosis were observed in males, and degeneration of cardiac myocytes, and hepatocellular necrosis were seen in males and females. Cytologic alteration in the submandibular salivary gland was noted in male and female mice. Hepatocyte cytologic alteration also was noted in all dosed groups of mice.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6641592-preliminary-study-effects-military-obscurant-smokes-flora-fauna-during-field-laboratory-exposures-final-technical-report','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6641592-preliminary-study-effects-military-obscurant-smokes-flora-fauna-during-field-laboratory-exposures-final-technical-report"><span>Preliminary study of effects of military obscurant smokes on flora and fauna during field and laboratory exposures. Final technical report</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Schaeffer, D.J.; Lower, W.R.; Kapila, S.</p> <p>1986-12-01</p> <p>Since continued routine use of obscurant smokes could be detrimental to the native flora and fauna of training sites, a preliminary biological and chemical study of smokes was conducted to determine whether tests could be developed to demonstrate measurable changes in organisms exposed to smokes and to evaluate whether short exposures to smokes produced measurable changes in the organisms tested. Fog oil, hexachloroethane, and tank diesel smokes were tested. Tradescantia clones were examined for mutagenic effects indicated by micronuclei induction in developing pollen and pink somatic mutations in stamen hairs. Photosynthetic perturbations were measured in Tradescantia and Ambrosia dumosa usingmore » variable fluorescence induction. Animals were examined for <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and chromosome <span class="hlt">aberrations</span>. It was found that all of the smokes tested exerted varying degrees of physiological and mutagenic effects in one or several of the assay systems at one or more of the exposure distances. These studies indicate that exposed ecological systems, or at least components of these systems, are at a higher risk than are control organisms for several types of damage attributed to obscurant smoke exposure.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24187132','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24187132"><span>Phosphorylation of microtubule-binding protein Hec1 by mitotic kinase Aurora B specifies spindle checkpoint kinase Mps1 signaling at the kinetochore.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhu, Tongge; Dou, Zhen; Qin, Bo; Jin, Changjiang; Wang, Xinghui; Xu, Leilei; Wang, Zhaoyang; Zhu, Lijuan; Liu, Fusheng; Gao, Xinjiao; Ke, Yuwen; Wang, Zhiyong; Aikhionbare, Felix; Fu, Chuanhai; Ding, Xia; Yao, Xuebiao</p> <p>2013-12-13</p> <p>The spindle assembly checkpoint (SAC) is a quality control device to ensure accurate chromosome attachment to spindle microtubule for equal segregation of <span class="hlt">sister</span> <span class="hlt">chromatid</span>. Aurora B is essential for SAC function by sensing chromosome bi-orientation via spatial regulation of kinetochore substrates. However, it has remained elusive as to how Aurora B couples kinetochore-microtubule attachment to SAC signaling. Here, we show that Hec1 interacts with Mps1 and specifies its kinetochore localization via its calponin homology (CH) domain and N-terminal 80 amino acids. Interestingly, phosphorylation of the Hec1 by Aurora B weakens its interaction with microtubules but promotes Hec1 binding to Mps1. Significantly, the temporal regulation of Hec1 phosphorylation orchestrates kinetochore-microtubule attachment and Mps1 loading to the kinetochore. Persistent expression of phosphomimetic Hec1 mutant induces a hyperactivation of SAC, suggesting that phosphorylation-elicited Hec1 conformational change is used as a switch to orchestrate SAC activation to concurrent destabilization of <span class="hlt">aberrant</span> kinetochore attachment. Taken together, these results define a novel role for Aurora B-Hec1-Mps1 signaling axis in governing accurate chromosome segregation in mitosis.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3861662','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3861662"><span>Phosphorylation of Microtubule-binding Protein Hec1 by Mitotic Kinase Aurora B Specifies Spindle Checkpoint Kinase Mps1 Signaling at the Kinetochore*</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zhu, Tongge; Dou, Zhen; Qin, Bo; Jin, Changjiang; Wang, Xinghui; Xu, Leilei; Wang, Zhaoyang; Zhu, Lijuan; Liu, Fusheng; Gao, Xinjiao; Ke, Yuwen; Wang, Zhiyong; Aikhionbare, Felix; Fu, Chuanhai; Ding, Xia; Yao, Xuebiao</p> <p>2013-01-01</p> <p>The spindle assembly checkpoint (SAC) is a quality control device to ensure accurate chromosome attachment to spindle microtubule for equal segregation of <span class="hlt">sister</span> <span class="hlt">chromatid</span>. Aurora B is essential for SAC function by sensing chromosome bi-orientation via spatial regulation of kinetochore substrates. However, it has remained elusive as to how Aurora B couples kinetochore-microtubule attachment to SAC signaling. Here, we show that Hec1 interacts with Mps1 and specifies its kinetochore localization via its calponin homology (CH) domain and N-terminal 80 amino acids. Interestingly, phosphorylation of the Hec1 by Aurora B weakens its interaction with microtubules but promotes Hec1 binding to Mps1. Significantly, the temporal regulation of Hec1 phosphorylation orchestrates kinetochore-microtubule attachment and Mps1 loading to the kinetochore. Persistent expression of phosphomimetic Hec1 mutant induces a hyperactivation of SAC, suggesting that phosphorylation-elicited Hec1 conformational change is used as a switch to orchestrate SAC activation to concurrent destabilization of <span class="hlt">aberrant</span> kinetochore attachment. Taken together, these results define a novel role for Aurora B-Hec1-Mps1 signaling axis in governing accurate chromosome segregation in mitosis. PMID:24187132</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27998191','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27998191"><span>In vitro potential cytogenetic and oxidative stress effects of roxithromycin.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Arslan, Mehmet; Timocin, Taygun; Ila, Hasan B</p> <p>2017-10-01</p> <p>Macrolide antibiotic roxithromycin was evaluated in terms of its genotoxic, cytotoxic and oxidative stress effects. For this purpose; 25, 50, 100 and 200 μg/mL concentrations of roxithromycin were dissolved in dimethyl sulfoxide and treated to human peripheral blood lymphocytes for two different treatment periods (24 and 48 h). In chromosome <span class="hlt">aberration</span> (CA) and micronucleus (MN) tests, roxithromycin did not show genotoxic effect. But it induced <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) at the highest concentration (200 μg/mL) for the 24-h treatment period and at all concentrations (except 25 μg/mL) for the 48-h treatment period. Looking at cytotoxic effect of roxithromycin, statistically insignificant decreases on mitotic index and proliferation index were observed. Roxithromycin decreased nuclear division index (NDI) at highest two concentrations (100 and 200 μg/mL) for the 24-h treatment period and at all concentrations (expect 25 μg/mL) for the 48-h treatment period. Total oxidant values, total antioxidant values and oxidative stress index did not change with roxithromycin treatment. Eventually, roxithromycin did not have genotoxic and oxidative stress effects in human-cultured lymphocytes.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/1383801','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/1383801"><span>Effect of 60-Hz magnetic fields on ultraviolet light-induced mutation and mitotic recombination in Saccharomyces cerevisiae.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ager, D D; Radul, J A</p> <p>1992-12-01</p> <p>The purpose of this study was to examine the effect of extremely low frequency (ELF) magnetic fields on the induction of genetic damage. In general, mutational studies involving ELF magnetic fields have proven negative. However, studies examining <span class="hlt">sister-chromatid</span> exchange and chromosome <span class="hlt">aberrations</span> have yielded conflicting results. In this study, we have examined whether 60-Hz magnetic fields are capable of inducing mutation or mitotic recombination in the yeast Saccharomyces cerevisiae. In addition we determined whether magnetic fields were capable of altering the genetic response of S. cerevisiae to UV (254 nm). We measured the frequencies of induced mutation, gene conversion and reciprocal mitotic crossing-over for exposures to magnetic fields alone (1 mT) or in combination with various UV exposures (2-50 J/m2). These experiments were performed using a repair-proficient strain (RAD+), as well as a strain of yeast (rad3) which is incapable of excising UV-induced thymine dimers. Magnetic field exposures did not induce mutation, gene conversion or reciprocal mitotic crossing-over in either of these strains, nor did the fields influence the frequencies of UV-induced genetic events.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=mental+AND+health+AND+siblings&pg=4&id=EJ626457','ERIC'); return false;" href="https://eric.ed.gov/?q=mental+AND+health+AND+siblings&pg=4&id=EJ626457"><span>Brothers and <span class="hlt">Sisters</span> of Adults with Mental Retardation: Gendered Nature of the Sibling Relationship.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Orsmond, Gael I.; Seltzer, Marsha Mailick</p> <p>2000-01-01</p> <p>Differences and similarities between 245 brothers and <span class="hlt">sisters</span> of adults with mental retardation in the sibling relationship were examined. <span class="hlt">Sisters</span> scored higher in the caregiving, companionship, and positive affect aspects of the sibling relationship. Sibling involvement increased over time, but was dependent upon changes in maternal health.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25194324','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25194324"><span>Identifying possible <span class="hlt">sister</span> groups of Cryptocercidae+Isoptera: a combined molecular and morphological phylogeny of Dictyoptera.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Djernæs, Marie; Klass, Klaus-Dieter; Eggleton, Paul</p> <p>2015-03-01</p> <p>Termites (Isoptera) offer an alternative model for the development of eusociality which is not dependent on a high degree of relatedness as found between <span class="hlt">sisters</span> in hymenopterans (bees, wasps, ants). Recent phylogenetic studies have established that termites belong within the cockroaches as <span class="hlt">sister</span> to the subsocial Cryptocercidae. Cryptocercidae shares several important traits with termites, thus we need to understand the phylogenetic position of Cryptocercidae+Isoptera to determine how these traits evolved. However, placement of Cryptocercidae+Isoptera is still uncertain. We used both molecular (12S, 16S, COII, 18S, 28S, H3) and morphological characters to reconstruct the phylogeny of Dictyoptera. We included all previously suggested <span class="hlt">sister</span> groups of Cryptocercidae+Isoptera as well as taxa which might represent additional major cockroach lineages. We used Bayes factors to test different <span class="hlt">sister</span> groups for Cryptocercidae+Isoptera and assessed character support for the consensus tree based on morphological characters and COII amino acid data. We used the molecular data and fossil calibration to estimate divergence times. We found the most likely <span class="hlt">sister</span> groups of Cryptocercidae+Isoptera to be Tryonicidae, Anaplecta or Tryonicidae+Anaplecta. Anaplecta has never previously been suggested as <span class="hlt">sister</span> group or even close to Cryptocercidae+Isoptera, but was formerly placed in Blaberoidea as <span class="hlt">sister</span> to the remaining taxa. Topological tests firmly supported our new placement of Anaplecta. We discuss the morphological characters (e.g. retractable genitalic hook) that have contributed to the previous placement of Anaplecta in Blaberoidea as well as the factors that might have contributed to a parallel development of genitalic features in Anaplecta and Blaberoidea. Cryptocercidae+Isoptera is placed in a clade with Tryonicidae, Anaplecta and possibly Lamproblattidae. Based on this, we suggest that wood-feeding, and the resultant need to conserve nitrogen, may have been an important</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2016APS..MARA41004R','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2016APS..MARA41004R"><span>On the robustness of SAC silencing in closed mitosis</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Ruth, Donovan; Liu, Jian</p> <p></p> <p>Mitosis equally partitions <span class="hlt">sister</span> <span class="hlt">chromatids</span> to two daughter cells. This is achieved by properly attaching these <span class="hlt">chromatids</span> via their kinetochores to microtubules that emanate from the spindle poles. Once the last kinetochore is properly attached, the spindle microtubules pull the <span class="hlt">sister</span> <span class="hlt">chromatids</span> apart. Due to the dynamic nature of microtubules, however, kinetochore-microtubule attachment often goes wrong. When this erroneous attachment occurs, it locally activates an ensemble of proteins, called the spindle assembly checkpoint proteins (SAC), which halts the mitotic progression until all the kinetochores are properly attached by spindle microtubules. The timing of SAC silencing thus determines the fidelity of chromosome segregation. We previously established a spatiotemporal model that addresses the robustness of SAC silencing in open mitosis for the first time. Here, we focus on closed mitosis by examining yeast mitosis as a model system. Though much experimental work has been done to study the SAC in cells undergoing closed mitosis, the processes responsible are not well understood. We leverage and extend our previous model to study SAC silencing mechanism in closed mitosis. We show that a robust signal of the SAC protein accumulation at the spindle pole body can be achieved. This signal is a nonlinear increasing function of number of kinetochore-microtubule attachments, and can thus serve as a robust trigger to time the SAC silencing. Together, our mechanism provides a unified framework across species that ensures robust SAC silencing and fidelity of chromosome segregation in mitosis. Intramural research program in NHLBI at NIH.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28777525','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28777525"><span>OF TRYPANOSOMATIDS. ENDOTRANSFORMATIONS AND <span class="hlt">ABERRATIONS</span>].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Frolov, A O; Malysheva, M N; Kostygov, A Yu</p> <p>2016-01-01</p> <p>Endotransformations and <span class="hlt">aberrations</span> of the life cycle in the evolutionary history of trypanosomatids (Kinetoplastea: Trypanosomatidae) are analyzed. We treat the term "endotransformations" as evolutionarily fixed changes of phases and/or developmental stages of parasites. By contrast, we treat <span class="hlt">aberrations</span> as evolutionary unstable, periodically arising deformations of developmental phases of trypanosomatids, never leading to life cycle changes. Various examples of life cycle endotransformations and <span class="hlt">aberrations</span> in representatives of the family Trypanosomatidae are discussed.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li class="active"><span>15</span></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_15 --> <div id="page_16" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li class="active"><span>16</span></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="301"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/437790','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/437790"><span>Chromosome mutations and chromosome stability in children treated with different regimes of immunosuppressive drugs.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schuler, D; Dobos, M; Fekete, G; Miltényi, M; Kalmár, L</p> <p>1979-01-01</p> <p>The chromosome mutations and the number of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges induced by different kinds of immunosuppressive treatment were investigated in children and adults with certain types of renal diseases. The aim of the study was to find among the treatment schedules those promising good therapeutic results with the least mutagenic effects. A slightly decreased chromosome stability was found in the patients treated by cyclophosphamide therapy.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4292170','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4292170"><span>DNA Strand Exchange and RecA Homologs in Meiosis</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Brown, M. Scott; Bishop, Douglas K.</p> <p>2015-01-01</p> <p>Homology search and DNA strand–exchange reactions are central to homologous recombination in meiosis. During meiosis, these processes are regulated such that the probability of choosing a homolog <span class="hlt">chromatid</span> as recombination partner is enhanced relative to that of choosing a <span class="hlt">sister</span> <span class="hlt">chromatid</span>. This regulatory process occurs as homologous chromosomes pair in preparation for assembly of the synaptonemal complex. Two strand–exchange proteins, Rad51 and Dmc1, cooperate in regulated homology search and strand exchange in most organisms. Here, we summarize studies on the properties of these two proteins and their accessory factors. In addition, we review current models for the assembly of meiotic strand–exchange complexes and the possible mechanisms through which the interhomolog bias of recombination partner choice is achieved. PMID:25475089</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=freud&id=EJ827914','ERIC'); return false;" href="https://eric.ed.gov/?q=freud&id=EJ827914"><span>Freud on Brothers and <span class="hlt">Sisters</span>: A Neglected Topic</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Sherwin-White, Susan</p> <p>2007-01-01</p> <p>This paper explores Freud's developing thought on brothers and <span class="hlt">sisters</span>, and their importance in his psychoanalytical writings and clinical work. Freud's work on sibling psychology has been seriously undervalued. This paper aims to give due recognition to Freud's work in this area. (Contains 1 note.)</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1808341','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1808341"><span>Monochromatic ocular wave <span class="hlt">aberrations</span> in young monkeys</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ramamirtham, Ramkumar; Kee, Chea-su; Hung, Li-Fang; Qiao-Grider, Ying; Roorda, Austin; Smith, Earl L.</p> <p>2006-01-01</p> <p>High-order monochromatic <span class="hlt">aberrations</span> could potentially influence vision-dependent refractive development in a variety of ways. As a first step in understanding the effects of wave <span class="hlt">aberration</span> on refractive development, we characterized the maturational changes that take place in the high-order <span class="hlt">aberrations</span> of infant rhesus monkey eyes. Specifically, we compared the monochromatic wave <span class="hlt">aberrations</span> of infant and adolescent animals and measured the longitudinal changes in the high-order <span class="hlt">aberrations</span> of infant monkeys during the early period when emmetropization takes place. Our main findings were that (1) adolescent monkey eyes have excellent optical quality, exhibiting total RMS errors that were slightly better than those for adult human eyes that have the same numerical aperture and (2) shortly after birth, infant rhesus monkeys exhibited relatively larger magnitudes of high-order <span class="hlt">aberrations</span> predominately spherical <span class="hlt">aberration</span>, coma, and trefoil, which decreased rapidly to assume adolescent values by about 200 days of age. The results demonstrate that rhesus monkey eyes are a good model for studying the contribution of individual ocular components to the eye’s overall <span class="hlt">aberration</span> structure, the mechanisms responsible for the improvements in optical quality that occur during early ocular development, and the effects of high-order <span class="hlt">aberrations</span> on ocular growth and emmetropization. PMID:16750549</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol32/pdf/CFR-2014-title40-vol32-sec798-5375.pdf','CFR2014'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol32/pdf/CFR-2014-title40-vol32-sec798-5375.pdf"><span>40 CFR 798.5375 - In vitro mammalian cytogenetics.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2014&page.go=Go">Code of Federal Regulations, 2014 CFR</a></p> <p></p> <p>2014-07-01</p> <p>... mammalian cytogenetics. (a) Purpose. The in vitro cytogenetics test is a mutagenicity test system for the... first post-treatment mitosis and numerical <span class="hlt">aberrations</span> require at least one cell division to be... <span class="hlt">chromatids</span>. (c) Reference substances. Not applicable. (d) Test method—(1) Principle. In vitro cytogenetics...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2004ASAJ..115.2522M','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2004ASAJ..115.2522M"><span>Iteration of ultrasound <span class="hlt">aberration</span> correction methods</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Maasoey, Svein-Erik; Angelsen, Bjoern; Varslot, Trond</p> <p>2004-05-01</p> <p><span class="hlt">Aberration</span> in ultrasound medical imaging is usually modeled by time-delay and amplitude variations concentrated on the transmitting/receiving array. This filter process is here denoted a TDA filter. The TDA filter is an approximation to the physical <span class="hlt">aberration</span> process, which occurs over an extended part of the human body wall. Estimation of the TDA filter, and performing correction on transmit and receive, has proven difficult. It has yet to be shown that this method works adequately for severe <span class="hlt">aberration</span>. Estimation of the TDA filter can be iterated by retransmitting a corrected signal and re-estimate until a convergence criterion is fulfilled (adaptive imaging). Two methods for estimating time-delay and amplitude variations in receive signals from random scatterers have been developed. One method correlates each element signal with a reference signal. The other method use eigenvalue decomposition of the receive cross-spectrum matrix, based upon a receive energy-maximizing criterion. Simulations of iterating <span class="hlt">aberration</span> correction with a TDA filter have been investigated to study its convergence properties. A weak and strong human-body wall model generated <span class="hlt">aberration</span>. Both emulated the human abdominal wall. Results after iteration improve <span class="hlt">aberration</span> correction substantially, and both estimation methods converge, even for the case of strong <span class="hlt">aberration</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29797792','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29797792"><span>The effect of <span class="hlt">aberrant</span> expression and genetic polymorphisms of Rad21 on cervical cancer biology.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Xia, Li; Wang, Minjie; Li, Hongying; Tang, Xiangjing; Chen, Fei; Cui, Jinquan</p> <p>2018-05-24</p> <p>The therapeutic challenge of advanced, recurrent, and refractory cervical cancer (CC) needs to develop new molecularly targeted drugs. Rad21 is an important regulatory gene that maintains the correct dissociation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> during cell mitosis. The aim of this study was to investigate the effect of Rad21 on CC. Rad21 expression in CC and cervical intraepithelial neoplasia III was significantly increased. Women with the rs2289937 C genotype (CC+CT) of rs4570 and rs4579555 genotypes and haplotype 1 (TTTCAGGCGC) were significantly associated with CC risk, while women with low frequencies of haplotype 6 (TTTTAGGCGC) also increased the risk of CC.Rad21-specific shRNA decreased cancerous cell proliferation, migration, and invasion and increased the proportion of cells in G2/M phase as well as sensitivity to radiation. The Rad21 influenced the expression of XPO1, CyclinB1, CDK1, P21, P27, and P53 through up-and downregulating the Rad21 expression. The TCGA database of CC also showed that Rad21 expression was associated with poor disease survival and XPO1 expression. Moreover, the KEGG pathway indicated that Rad21 is broadly involved in the cell cycle and RNA transportation via XPO1. This suggests that Rad21 involves the development of cervical cancer possibly by participating in the regulation of cell cycle and the nuclear output of the tumor suppressor gene via XPO1. © 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2013AGUFMPA53A1906Q','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2013AGUFMPA53A1906Q"><span>EarthLabs Meet <span class="hlt">Sister</span> Corita Kent</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Quartini, E.; Ellins, K. K.; Cavitte, M. G.; Thirumalai, K.; Ledley, T. S.; Haddad, N.; Lynds, S. E.</p> <p>2013-12-01</p> <p>The EarthLabs project provides a framework to enhance high school students' climate literacy and awareness of climate change. The project provides climate science curriculum and teacher professional development, followed by research on students' learning as teachers implement EarthLabs climate modules in the classroom. The professional development targets high school teachers whose professional growth is structured around exposure to current climate science research, data observation collection and analysis. During summer workshops in Texas and Mississippi, teachers work through the laboratories, experiments, and hand-on activities developed for their students. In summer 2013, three graduate students from the University of Texas at Austin Institute for Geophysics with expertise in climate science participated in two weeklong workshops. The graduate students partnered with exemplary teacher leaders to provide scientific content and lead the EarthLabs learning activities. As an experiment, we integrated a visit to the Blanton Museum and an associated activity in order to motivate participants to think creatively, as well as analytically, about science. This exercise was inspired by the work and educational philosophy of <span class="hlt">Sister</span> Corita Kent. During the visit to the Blanton Museum, we steered participants towards specific works of art pre-selected to emphasize aspects of the climate of Texas and to draw participants' attention to ways in which artists convey different concepts. For example, artists use of color, lines, and symbols conjure emotional responses to imagery in the viewer. The second part of the exercise asked participants to choose a climate message and to convey this through a collage. We encouraged participants to combine their experience at the museum with examples of <span class="hlt">Sister</span> Corita Kent's artwork. We gave them simple guidelines for the project based on techniques and teaching of <span class="hlt">Sister</span> Corita Kent. Evaluation results reveal that participants enjoyed the</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22253761','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22253761"><span>Broad phylogenomic sampling and the <span class="hlt">sister</span> lineage of land plants.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Timme, Ruth E; Bachvaroff, Tsvetan R; Delwiche, Charles F</p> <p>2012-01-01</p> <p>The tremendous diversity of land plants all descended from a single charophyte green alga that colonized the land somewhere between 430 and 470 million years ago. Six orders of charophyte green algae, in addition to embryophytes, comprise the Streptophyta s.l. Previous studies have focused on reconstructing the phylogeny of organisms tied to this key colonization event, but wildly conflicting results have sparked a contentious debate over which lineage gave rise to land plants. The dominant view has been that 'stoneworts,' or Charales, are the <span class="hlt">sister</span> lineage, but an alternative hypothesis supports the Zygnematales (often referred to as "pond scum") as the <span class="hlt">sister</span> lineage. In this paper, we provide a well-supported, 160-nuclear-gene phylogenomic analysis supporting the Zygnematales as the closest living relative to land plants. Our study makes two key contributions to the field: 1) the use of an unbiased method to collect a large set of orthologs from deeply diverging species and 2) the use of these data in determining the <span class="hlt">sister</span> lineage to land plants. We anticipate this updated phylogeny not only will hugely impact lesson plans in introductory biology courses, but also will provide a solid phylogenetic tree for future green-lineage research, whether it be related to plants or green algae.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21695608','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21695608"><span>[Monochromatic <span class="hlt">aberration</span> in accommodation. Dynamic wavefront analysis].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fritzsch, M; Dawczynski, J; Jurkutat, S; Vollandt, R; Strobel, J</p> <p>2011-06-01</p> <p>Monochromatic <span class="hlt">aberrations</span> may influence the visual acuity of the eye. They are not stable and can be affected by different factors. The subject of the following paper is the dynamic investigation of the changes in wavefront <span class="hlt">aberration</span> with accommodation. Dynamic measurement of higher and lower order <span class="hlt">aberrations</span> was performed with a WASCA Wavefront Analyzer (Carl-Zeiss-Meditec) and a specially constructed target device for aligning objects in far and near distances on 25 subjects aged from 15 to 27 years old. Wavefront <span class="hlt">aberrations</span> showed some significant changes in accommodation. In addition to the characteristic sphere reaction accompanying miosis and changes in horizontal prism (Z(1) (1)) in the sense of a convergence movement of the eyeball also occurred. Furthermore defocus rose (Z(2) (0)) and astigmatism (Z(2) (-2)) changed. In higher-order <span class="hlt">aberrations</span> a decrease in coma-like Zernike polynomials (Z(3) (-1), Z(3) (1)) was found. The most obvious change appeared in spherical <span class="hlt">aberration</span> (Z(4) (0)) which increased and changed from positive to negative. In addition the secondary astigmatism (Z(4) (-2)) and quadrafoil (Z(4) (4)) rise also increased. The total root mean square (RMS), as well as the higher-order <span class="hlt">aberrations</span> (RMS-HO) significantly increased in accommodation which is associated with a theoretical reduction of visual acuity. An analysis of the influence of pupil size on <span class="hlt">aberrations</span> showed significant increases in defocus, spherical <span class="hlt">aberration</span>, quadrafoil, RMS and RMS HO by increasing pupil diameter. By accommodation-associated miosis, the growing <span class="hlt">aberrations</span> are partially compensated by focusing on near objects. Temporal analysis of the accommodation process with dynamic wavefront analysis revealed significant delays in pupil response and changing of prism in relation to the sphere reaction. In accommodation to near objects a discrete time ahead of third order <span class="hlt">aberrations</span> in relation to the sphere response was found. Using dynamic wavefront measurement</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25322219','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25322219"><span>Wavefront <span class="hlt">aberrations</span> of x-ray dynamical diffraction beams.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Liao, Keliang; Hong, Youli; Sheng, Weifan</p> <p>2014-10-01</p> <p>The effects of dynamical diffraction in x-ray diffractive optics with large numerical aperture render the wavefront <span class="hlt">aberrations</span> difficult to describe using the <span class="hlt">aberration</span> polynomials, yet knowledge of them plays an important role in a vast variety of scientific problems ranging from optical testing to adaptive optics. Although the diffraction theory of optical <span class="hlt">aberrations</span> was established decades ago, its application in the area of x-ray dynamical diffraction theory (DDT) is still lacking. Here, we conduct a theoretical study on the <span class="hlt">aberration</span> properties of x-ray dynamical diffraction beams. By treating the modulus of the complex envelope as the amplitude weight function in the orthogonalization procedure, we generalize the nonrecursive matrix method for the determination of orthonormal <span class="hlt">aberration</span> polynomials, wherein Zernike DDT and Legendre DDT polynomials are proposed. As an example, we investigate the <span class="hlt">aberration</span> evolution inside a tilted multilayer Laue lens. The corresponding Legendre DDT polynomials are obtained numerically, which represent balanced <span class="hlt">aberrations</span> yielding minimum variance of the classical <span class="hlt">aberrations</span> of an anamorphic optical system. The balancing of classical <span class="hlt">aberrations</span> and their standard deviations are discussed. We also present the Strehl ratio of the primary and secondary balanced <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2014ivs..conf..490X','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2014ivs..conf..490X"><span>On the Definition of <span class="hlt">Aberration</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Xu, Minghui; Wang, Guangli</p> <p>2014-12-01</p> <p>There was a groundbreaking step in the history of astronomy in 1728 when the effect of <span class="hlt">aberration</span> was discovered by James Bradley (1693-1762). Recently, the solar acceleration, due to the variations in the <span class="hlt">aberrational</span> effect of extragalactic sources caused by it, has been determined from VLBI observations with an uncertainty of about 0.5 mm{\\cdot}{s^{-1}}{\\cdot}{yr^{-1}} level. As a basic concept in astrometry with a nearly 300-year history, the definition of <span class="hlt">aberration</span>, however, is still equivocal and discordant in the literature. It has been under continuing debate whether it depends on the relative motion between the observer and the observed source or only on the motion of the observer with respect to the frame of reference. In this paper, we will review the debate and the inconsistency in the definition of the <span class="hlt">aberration</span> since the last century, and then discuss its definition in detail, which involves the discussions on the planetary <span class="hlt">aberration</span>, the stellar <span class="hlt">aberration</span>, the proper motion of an object during the travel time of light from the object to the observer, and the way of selecting the reference frame to express and distinguish the motions of the source and the observer. The <span class="hlt">aberration</span> is essentially caused by the transformation between coordinate systems, and consequently quantified by the velocity of the observer with respect to the selected reference frame, independent of the motion of the source. Obviously, this nature is totally different from that of the definition given by the IAU WG NFA (Capitaine, 2007) in 2006, which is stated as, ``the apparent angular displacement of the observed position of a celestial object from its geometric position, caused by the finite velocity of light in combination with the motions of the observer and of the observed object.''</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21838561','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21838561"><span>Psychopathology, childhood trauma, and personality traits in patients with borderline personality disorder and their <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Laporte, Lise; Paris, Joel; Guttman, Herta; Russell, Jennifer</p> <p>2011-08-01</p> <p>The aim of this study was to document and compare adverse childhood experiences, and personality profiles in women with borderline personality disorder (BPD) and their <span class="hlt">sisters</span>, and to determine how these factors impact current psychopathology. Fifty-six patients with BPD and their <span class="hlt">sisters</span> were compared on measures assessing psychopathology, personality traits, and childhood adversities. Most <span class="hlt">sisters</span> showed little evidence of psychopathology. Both groups reported dysfunctional parent-child relationships and a high prevalence of childhood trauma. Subjects with BPD reported experiencing more emotional abuse and intrafamilial sexual abuse, but more similarities than differences between probands and <span class="hlt">sisters</span> were found. In multilevel analyses, personality traits of affective instability and impulsivity predicted DIB-R scores and SCL-90-R scores, above and beyond trauma. There were few relationships between childhood adversities and other measures of psychopathology. Sensitivity to adverse experiences, as reflected in the development of psychopathology, appears to be influenced by personality trait profiles.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25985782','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25985782"><span>"If I only touch her cloak": the <span class="hlt">Sisters</span> of Charity of St. Joseph in New Orleans hospital, 1834-1860.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kong, Hyejung Grace; Kim, Ock-Joo</p> <p>2015-04-01</p> <p>This study is about the <span class="hlt">Sisters</span> of Charity of St. Joseph in New Orleans' Charity Hospital during the years between 1834 and 1860. The <span class="hlt">Sisters</span> of Charity of St. Joseph was founded in 1809 by Saint Elizabeth Ann Bailey Seton (first native-born North American canonized in 1975) in Emmitsburg, Maryland. Seton's <span class="hlt">Sisters</span> of Charity was the first community for religious women to be established in the United States and was later incorporated with the French Daughters of Charity of St. Vincent de Paul in 1850. A call to work in New Orleans' Charity Hospital in the 1830s meant a significant achievement for the <span class="hlt">Sisters</span> of Charity, since it was the second oldest continuously operating public hospitals in the United States until 2005, bearing the same name over the decades. In 1834, <span class="hlt">Sister</span> Regina Smith and other <span class="hlt">sisters</span> were officially called to Charity Hospital, in order to supersede the existing "nurses, attendants, and servants," and take a complete charge of the internal management of Charity Hospital. The existing scholarship on the history of hospitals and Catholic nursing has not integrated the concrete stories of the <span class="hlt">Sisters</span> of Charity into the broader histories of institutionalized medicine, gender, and religion. Along with a variety of primary sources, this study primarily relies on the Charity Hospital History Folder stored at the Daughters of Charity West Center Province Archives. Located in the "Queen city of the South," Charity Hospital was the center of the southern medical profession and the world's fair of people and diseases. Charity Hospital provided the <span class="hlt">sisters</span> with a unique situation that religion and medicine became intertwined. The <span class="hlt">Sisters</span>, as nurses, constructed a new atmosphere of caring for patients and even their families inside and outside the hospital, and built their own separate space within the hospital walls. As hospital managers, the <span class="hlt">Sisters</span> of Charity were put in complete charge of the hospital, which was never seen in other hospitals. By</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1995JOSAA..12.1637C','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1995JOSAA..12.1637C"><span>Effect of monochromatic <span class="hlt">aberrations</span> on photorefractive patterns</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Campbell, Melanie C. W.; Bobier, W. R.; Roorda, A.</p> <p>1995-08-01</p> <p>Photorefractive methods have become popular in the measurement of refractive and accommodative states of infants and children owing to their photographic nature and rapid speed of measurement. As in the case of any method that measures the refractive state of the human eye, monochromatic <span class="hlt">aberrations</span> will reduce the accuracy of the measurement. Monochromatic <span class="hlt">aberrations</span> cannot be as easily predicted or controlled as chromatic <span class="hlt">aberrations</span> during the measurement, and accordingly they will introduce measurement errors. This study defines this error or uncertainty by extending the existing paraxial optical analyses of coaxial and eccentric photorefraction. This new optical analysis predicts that, for the amounts of spherical <span class="hlt">aberration</span> (SA) reported for the human eye, there will be a significant degree of measurement uncertainty introduced for all photorefractive methods. The dioptric amount of this uncertainty may exceed the maximum amount of SA present in the eye. The calculated effects on photorefractive measurement of a real eye with a mixture of spherical <span class="hlt">aberration</span> and coma are shown to be significant. The ability, developed here, to predict photorefractive patterns corresponding to different amounts and types of monochromatic <span class="hlt">aberration</span> may in the future lead to an extension of photorefractive methods to the dual measurement of refractive states and <span class="hlt">aberrations</span> of individual eyes. <span class="hlt">aberration</span>, retinal image quality,</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040173044&hterms=Culture+differences&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D90%26Ntt%3DCulture%2Bdifferences','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040173044&hterms=Culture+differences&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D90%26Ntt%3DCulture%2Bdifferences"><span>Radiation-induced chromosomal instability in BALB/c and C57BL/6 mice: the difference is as clear as black and white</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ponnaiya, B.; Cornforth, M. N.; Ullrich, R. L.</p> <p>1997-01-01</p> <p>Genomic instability has been proposed to be the earliest step in radiation-induced tumorigenesis. It follows from this hypothesis that individuals highly susceptible to induction of tumors by radiation should exhibit enhanced radiation-induced instability. BALB/c white mice are considerably more sensitive to radiation-induced mammary cancer than C57BL/6 black mice. In this study, primary mammary epithelial cell cultures from these two strains were examined for the "delayed" appearance of chromosomal <span class="hlt">aberrations</span> after exposure to 137Cs gamma radiation, as a measure of radiation-induced genomic instability. As expected, actively dividing cultures from both strains showed a rapid decline of initial asymmetrical <span class="hlt">aberrations</span> with time postirradiation. However, after 16 population doublings, cells from BALB/c mice exhibited a marked increase in the frequency of <span class="hlt">chromatid</span>-type breaks and gaps which remained elevated throughout the time course of the experiment (28 doublings). No such effect was observed for the cells of C57BL/6 mice; after the rapid clearance of initial <span class="hlt">aberrations</span>, the frequency of <span class="hlt">chromatid</span>-type <span class="hlt">aberrations</span> in the irradiated population remained at or near those of nonirradiated controls. These results demonstrate a correlation between the latent expression of chromosomal damage in vitro and susceptibility for mammary tumors, and provide further support for the central role of radiation-induced instability in the process of tumorigenesis.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16698532','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16698532"><span><span class="hlt">Sister</span> Mary Joseph's nodule as the first presenting sign of primary fallopian tube adenocarcinoma.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kirshtein, Boris; Meirovitz, Mihai; Okon, Elimelech; Piura, Benjamin</p> <p>2006-01-01</p> <p>Umbilical metastasis (<span class="hlt">Sister</span> Mary Joseph's nodule) is often the first sign of intraabdominal and/or pelvic carcinoma. We describe the fourth case reported in the literature of <span class="hlt">Sister</span> Mary Joseph's nodule originating from fallopian tube carcinoma. In a 54-year-old woman, <span class="hlt">Sister</span> Mary Joseph's nodule was unexpectedly detected during umbilical hernia repair. Subsequent laparoscopy revealed a 2-cm friable tumor located at the fimbriated end of right fallopian tube and 1-cm peritoneal implant in the pouch of Douglas. Laparoscopic bilateral adnexectomy and resection of the peritoneal implant were performed. Because frozen section examination revealed fallopian tube carcinoma, the procedure was continued with laparotomy including total abdominal hysterectomy, omentectomy, and pelvic lymph node sampling. Final diagnosis was stage IIIB fallopian tube carcinoma. The patient received postoperative adjuvant chemotherapy with single-agent carboplatin and has remained alive and with no evidence of disease. It is concluded that in cases of <span class="hlt">Sister</span> Mary Joseph's nodule, laparoscopy can be a useful tool in the search of the primary tumor in the abdomen and/or pelvis. Laparoscopy can provide crucial information with respect to the location, size, and feasibility of optimal surgical resection of the intraabdominal and/or pelvic tumors.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23545961','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23545961"><span>Imaging characteristics of Zernike and annular polynomial <span class="hlt">aberrations</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mahajan, Virendra N; Díaz, José Antonio</p> <p>2013-04-01</p> <p>The general equations for the point-spread function (PSF) and optical transfer function (OTF) are given for any pupil shape, and they are applied to optical imaging systems with circular and annular pupils. The symmetry properties of the PSF, the real and imaginary parts of the OTF, and the modulation transfer function (MTF) of a system with a circular pupil <span class="hlt">aberrated</span> by a Zernike circle polynomial <span class="hlt">aberration</span> are derived. The interferograms and PSFs are illustrated for some typical polynomial <span class="hlt">aberrations</span> with a sigma value of one wave, and 3D PSFs and MTFs are shown for 0.1 wave. The Strehl ratio is also calculated for polynomial <span class="hlt">aberrations</span> with a sigma value of 0.1 wave, and shown to be well estimated from the sigma value. The numerical results are compared with the corresponding results in the literature. Because of the same angular dependence of the corresponding annular and circle polynomial <span class="hlt">aberrations</span>, the symmetry properties of systems with annular pupils <span class="hlt">aberrated</span> by an annular polynomial <span class="hlt">aberration</span> are the same as those for a circular pupil <span class="hlt">aberrated</span> by a corresponding circle polynomial <span class="hlt">aberration</span>. They are also illustrated with numerical examples.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2014SPIE.9293E..1VF','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2014SPIE.9293E..1VF"><span>Nodal <span class="hlt">aberration</span> theory applied to freeform surfaces</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Fuerschbach, Kyle; Rolland, Jannick P.; Thompson, Kevin P.</p> <p>2014-12-01</p> <p>When new three-dimensional packages are developed for imaging optical systems, the rotational symmetry of the optical system is often broken, changing its imaging behavior and making the optical performance worse. A method to restore the performance is to use freeform optical surfaces that compensate directly the <span class="hlt">aberrations</span> introduced from tilting and decentering the optical surfaces. In order to effectively optimize the shape of a freeform surface to restore optical functionality, it is helpful to understand the <span class="hlt">aberration</span> effect the surface may induce. Using nodal <span class="hlt">aberration</span> theory the <span class="hlt">aberration</span> fields induced by a freeform surface in an optical system are explored. These theoretical predications are experimentally validated with the design and implementation of an <span class="hlt">aberration</span> generating telescope.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20524537','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20524537"><span>Letters from a suicide: Van Gogh and his <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lester, David</p> <p>2010-04-01</p> <p>An analysis of trends over a 3-yr. period in the letters of Vincent Van Gogh to his <span class="hlt">sister</span> as the time of his suicide approached identified 8 trends, including an increase in words concerned with anxiety and words concerned with the past.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li class="active"><span>16</span></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_16 --> <div id="page_17" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li class="active"><span>17</span></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="321"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036906p/','SCIGOV-HHH'); return false;" href="https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036906p/"><span>14. UPPER THREE <span class="hlt">SISTERS</span> FALLS, LOOKING NORTHWEST Photocopy of photograph, ...</span></a></p> <p><a target="_blank" href="http://www.loc.gov/pictures/collection/hh/">Library of Congress Historic Buildings Survey, Historic Engineering Record, Historic Landscapes Survey</a></p> <p></p> <p></p> <p>14. UPPER THREE <span class="hlt">SISTERS</span> FALLS, LOOKING NORTHWEST Photocopy of photograph, 1930s National Park Service, National Capital Region files - Dumbarton Oaks Park, Thirty-second & R Streets Northwest, Washington, District of Columbia, DC</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4181439','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4181439"><span>Corneal spherical <span class="hlt">aberration</span> in Saudi population</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Al-Sayyari, Tarfah M.; Fawzy, Samah M.; Al-Saleh, Ahmed A.</p> <p>2014-01-01</p> <p>Purpose To find out the mean corneal spherical <span class="hlt">aberration</span> and its changes with age in Saudi population. Setting AlHokama Eye Specialist Center, Riyadh, Saudi Arabia. Methods Three hundred (300) eyes of 185 Saudi subjects (97 men and 88 women), whose age ranged from 15 to 85 years old, with matched refractive errors, were divided into three groups according to their age, 100 for each. All the subjects were included in measuring the spherical <span class="hlt">aberration</span> (SA) using pentacam HR (OCULUS, Germany) at the 6-mm optical zone. Results The mean corneal spherical <span class="hlt">aberration</span> (CSA) of the fourth order (Z40) of the whole groups was 0.252 ± 0.1154 μm. Patients from 15 to 35 years old have root mean square (RMS) of CSA of 0.2068 ± 0.07151 μm, 0.2370 ± 0.08023 μm was the RMS of CSA of the patients from 35 to 50 years old, while those from 50 to 85 years old have a CSA-RMS of 0.31511 ± 0.1503 μm (P < 0.0001). A positive correlation was found between the spherical <span class="hlt">aberration</span> (Z40) and the progress of age (r = 0.3429, P < 0.0001). The high order <span class="hlt">aberration</span> (HOA) presented 28.1% of the total corneal <span class="hlt">aberrations</span>. While the fourth order corneal spherical <span class="hlt">aberration</span> constituted 57% of the HOA and 16% of the total <span class="hlt">aberration</span>. The pupil diameter shows a negative correlation with the increase in age (P = 0.0012). Conclusion Our results showed a CSA (Z40) that is varied among the population, comparable to other studies, and significantly correlates to the progress of age. PMID:25278799</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=The+AND+Seven+AND+Sisters&id=EJ566969','ERIC'); return false;" href="https://eric.ed.gov/?q=The+AND+Seven+AND+Sisters&id=EJ566969"><span>The Racial Integration of the Seven <span class="hlt">Sister</span> Colleges.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Perkins, Linda M.</p> <p>1998-01-01</p> <p>Although the number of African-American women who attended the elite Seven <span class="hlt">Sisters</span> colleges prior to 1900 was small, these women were highly influential. Early integration is discussed for: (1) Wellesley College; (2) Radcliffe College; (3) Smith College; (4) Mount Holyoke College; (5) Bryn Mawr College; (6) Vassar College; and (7) Barnard College.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/254378-two-sisters-clinical-diagnosis-wiskott-aldrich-syndrome-condition-family-autosomal-recessive','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/254378-two-sisters-clinical-diagnosis-wiskott-aldrich-syndrome-condition-family-autosomal-recessive"><span>Two <span class="hlt">sisters</span> with clinical diagnosis of Wiskott-Aldrich Syndrome: Is the condition in the family autosomal recessive?</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Kondoh, T.; Hayashi, K.; Matsumoto, T.</p> <p>1995-10-09</p> <p>We report two <span class="hlt">sisters</span> in a family representing manifestations of Wiskott-Aldrich syndrome (WAS), an X-linked immunodeficiency disorder. An elder <span class="hlt">sister</span> had suffered from recurrent infections, small thrombocytopenic petechiae, purpura, and eczema for 7 years. The younger <span class="hlt">sister</span> had the same manifestations as the elder <span class="hlt">sister`s</span> for a 2-year period, and died of intracranial bleeding at age 2 years. All the laboratory data of the two patients were compatible with WAS, although they were females. Sialophorin analysis with the selective radioactive labeling method of this protein revealed that in the elder <span class="hlt">sister</span> a 115-KD band that should be specific for sialophorinmore » was reduced in quantity, and instead an additional 135-KD fragment was present as a main band. Polymerase chain reaction (PCR) analysis of the sialophorin gene and single-strand conformation polymorphism (SSCP) analysis of the PCR product demonstrated that there were no detectable size-change nor electrophoretic mobility change in the DNA from both patients. The results indicated that their sialophorin gene structure might be normal. Studies on the mother-daughter transmission of X chromosome using a pERT84-MaeIII polymorphic marker mapped at Xp21 and HPRT gene polymorphism at Xq26 suggested that each <span class="hlt">sister</span> had inherited a different X chromosome from the mother. Two explanations are plausible for the occurrence of the WAS in our patients: the WAS in the patients is attributable to an autosomal gene mutation which may regulate the sialophorin gene expression through the WAS gene, or, alternatively, the condition in this family is an autosomal recessive disorder separated etiologically from the X-linked WAS. 17 refs., 6 figs., 1 tab.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/22250970-transcranial-phase-aberration-correction-using-beam-simulations-mr-arfi','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/22250970-transcranial-phase-aberration-correction-using-beam-simulations-mr-arfi"><span>Transcranial phase <span class="hlt">aberration</span> correction using beam simulations and MR-ARFI</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Vyas, Urvi, E-mail: urvi.vyas@gmail.com; Kaye, Elena; Pauly, Kim Butts</p> <p>2014-03-15</p> <p>Purpose: Transcranial magnetic resonance-guided focused ultrasound surgery is a noninvasive technique for causing selective tissue necrosis. Variations in density, thickness, and shape of the skull cause <span class="hlt">aberrations</span> in the location and shape of the focal zone. In this paper, the authors propose a hybrid simulation-MR-ARFI technique to achieve <span class="hlt">aberration</span> correction for transcranial MR-guided focused ultrasound surgery. The technique uses ultrasound beam propagation simulations with MR Acoustic Radiation Force Imaging (MR-ARFI) to correct skull-caused phase <span class="hlt">aberrations</span>. Methods: Skull-based numerical <span class="hlt">aberrations</span> were obtained from a MR-guided focused ultrasound patient treatment and were added to all elements of the InSightec conformal bone focusedmore » ultrasound surgery transducer during transmission. In the first experiment, the 1024 <span class="hlt">aberrations</span> derived from a human skull were condensed into 16 <span class="hlt">aberrations</span> by averaging over the transducer area of 64 elements. In the second experiment, all 1024 <span class="hlt">aberrations</span> were applied to the transducer. The <span class="hlt">aberrated</span> MR-ARFI images were used in the hybrid simulation-MR-ARFI technique to find 16 estimated <span class="hlt">aberrations</span>. These estimated <span class="hlt">aberrations</span> were subtracted from the original <span class="hlt">aberrations</span> to result in the corrected images. Each <span class="hlt">aberration</span> experiment (16-<span class="hlt">aberration</span> and 1024-<span class="hlt">aberration</span>) was repeated three times. Results: The corrected MR-ARFI image was compared to the <span class="hlt">aberrated</span> image and the ideal image (image with zero <span class="hlt">aberrations</span>) for each experiment. The hybrid simulation-MR-ARFI technique resulted in an average increase in focal MR-ARFI phase of 44% for the 16-<span class="hlt">aberration</span> case and 52% for the 1024-<span class="hlt">aberration</span> case, and recovered 83% and 39% of the ideal MR-ARFI phase for the 16-<span class="hlt">aberrations</span> and 1024-<span class="hlt">aberration</span> case, respectively. Conclusions: Using one MR-ARFI image and noa priori information about the applied phase <span class="hlt">aberrations</span>, the hybrid simulation-MR-ARFI technique improved the maximum MR-ARFI phase of the beam's focus.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015SPIE.9409E..0MM','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015SPIE.9409E..0MM"><span>Anti-forensics of chromatic <span class="hlt">aberration</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Mayer, Owen; Stamm, Matthew C.</p> <p>2015-03-01</p> <p>Over the past decade, a number of information forensic techniques have been developed to identify digital image manipulation and falsification. Recent research has shown, however, that an intelligent forger can use anti-forensic countermeasures to disguise their forgeries. In this paper, an anti-forensic technique is proposed to falsify the lateral chromatic <span class="hlt">aberration</span> present in a digital image. Lateral chromatic <span class="hlt">aberration</span> corresponds to the relative contraction or expansion between an image's color channels that occurs due to a lens's inability to focus all wavelengths of light on the same point. Previous work has used localized inconsistencies in an image's chromatic <span class="hlt">aberration</span> to expose cut-and-paste image forgeries. The anti-forensic technique presented in this paper operates by estimating the expected lateral chromatic <span class="hlt">aberration</span> at an image location, then removing deviations from this estimate caused by tampering or falsification. Experimental results are presented that demonstrate that our anti-forensic technique can be used to effectively disguise evidence of an image forgery.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1991PhDT.......181K','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1991PhDT.......181K"><span>A Evaluation of Optical <span class="hlt">Aberrations</span> in Underwater Hologrammetry</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Kilpatrick, J. M.</p> <p></p> <p>Available from UMI in association with The British Library. An iterative ray-trace procedure is developed in conjunction with semi-analytic expressions for spherical <span class="hlt">aberration</span>, coma, and astigmatism in the reconstructed holographic images of underwater objects. An exact expression for the astigmatic difference is obtained, based on the geometry of the caustic for refraction. The geometrical characteristics of the <span class="hlt">aberrated</span> images associated with axial and non-axial field positions are represented by ray intersection diagrams. A third order expression for the wavefront <span class="hlt">aberration</span> introduced at a planar air/water boundary is given. The associated third order <span class="hlt">aberration</span> coefficients are used to obtain analytic expressions for the <span class="hlt">aberrations</span> observed in underwater hologrammetry. The results of the third order treatment are shown to give good agreement with the results obtained by geometrical ray tracing and by direct measurement on the reconstructed real image. The third order <span class="hlt">aberration</span> coefficients are employed to estimate the limit of resolution in the presence of the <span class="hlt">aberrations</span> associated with reconstruction in air. In concurrence with practical observations it is found that the estimated resolution is primarily limited by astigmatism. The limitations of the planar window in underwater imaging applications are outlined and various schemes are considered to effect a reduction in the extent of <span class="hlt">aberration</span>. The analogous problems encountered in underwater photography are examined in order to establish the grounds for a common solution based on a conventional optical corrector. The performance of one such system, the Ivanoff Corrector, is investigated. The spherical <span class="hlt">aberration</span> associated with axial image formation is evaluated. The equivalence of the third order wavefront <span class="hlt">aberration</span> introduced at a planar air/water boundary to that introduced upon reconstruction by an appropriate wavelength change is shown to provide a basis for the compensation of <span class="hlt">aberrations</span> in</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21142977','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21142977"><span>Geographic variance of cardiovascular risk factors among community women: the national <span class="hlt">Sister</span> to <span class="hlt">Sister</span> campaign.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Jarvie, Jennifer L; Johnson, Caitlin E; Wang, Yun; Wan, Yun; Aslam, Farhan; Athanasopoulos, Leonidas V; Pollin, Irene; Foody, JoAnne M</p> <p>2011-01-01</p> <p>There are substantial variations in cardiovascular disease (CVD) risk and outcomes among women. We sought to determine geographic variation in risk factor prevalence in a contemporary sample of U.S. women. Using 2008-2009 <span class="hlt">Sister</span> to <span class="hlt">Sister</span> (STS) free heart screening data from 17 U.S. cities, we compared rates of obesity (body mass index [BMI] ≥30 kg/m(2)), hypertension (HTN ≥140/90 mm Hg), low high-density lipoprotein cholesterol (HDL-C <40 mg/dL), and hyperglycemia (≥126 mg/dL) with national rates. In 18,892 women (mean age 49.8 ± 14.3 years, 37% black, 32% white, 14% Hispanic), compared to overall STS rates, significantly higher rates were observed for obesity in Baltimore (42.4%), Atlanta (40.0%), Dallas (37.9%), and Jacksonville (36.0%); for HTN in Atlanta (43.9%), Baltimore (42.5%), and New York (39.1%); for hyperglycemia in Jacksonville (20.3%), Philadelphia (18.1%), and Tampa (17.8%); and for HDL-C <40 mg/dL in Phoenix (37.4%), Dallas (26.5%), and Jacksonville (18.1%). Compared to national American Heart Association (AHA) 2010 update rates, most STS cities had higher rates of hyperglycemia and low HDL-C. In a large, community-based sample of women nationwide, this comprehensive analysis shows remarkable geographic variation in risk factors, which provides opportunities to improve and reduce a woman's CVD risk. Further investigation is required to understand the reasons behind such variation, which will provide insight toward tailoring preventive interventions to narrow gaps in CVD risk reduction in women.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/18688790','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/18688790"><span><span class="hlt">Sisters</span> in hereditary breast and ovarian cancer families: communal coping, social integration, and psychological well-being.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Koehly, Laura M; Peters, June A; Kuhn, Natalia; Hoskins, Lindsey; Letocha, Anne; Kenen, Regina; Loud, Jennifer; Greene, Mark H</p> <p>2008-08-01</p> <p>We investigated the association between psychological distress and indices of social integration and communal coping among <span class="hlt">sisters</span> from hereditary breast and ovarian cancer (HBOC) families. Sixty-five <span class="hlt">sisters</span> from 31 HBOC families completed the Brief Symptom Inventory-18 and the Colored Eco-Genetic Relationship Map, which identified members of participants' social support networks. Hierarchical linear models were used for all analyses to account for the clustering of <span class="hlt">sisters</span> within families. Intra-family correlation coefficients suggested that <span class="hlt">sisters</span> shared perceptions of breast cancer risk and worry, but not ovarian cancer risk and worry. Further, <span class="hlt">sisters</span> demonstrated shared levels of anxiety and somatization, but not depressive symptoms. Communal coping indices quantifying shared support resources were negatively related to anxiety and somatization. The number of persons with whom cancer risk information was shared exhibited a positive trend with somatization. Social integration, as measured by the size of participants' emotional support network, was negatively associated with anxiety. Lower depression scores were observed among participants with more persons playing multiple support roles and fewer persons providing tangible assistance. Understanding how support relationships impact well-being among persons adjusting to HBOC risk, and the particular role of family in that process, will facilitate developing appropriate management approaches to help cancer-prone families adjust to their cancer risk.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24077888','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24077888"><span>Identification and diversity of functional centromere satellites in the wild rice species Oryza brachyantha.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yi, Chuandeng; Zhang, Wenli; Dai, Xibin; Li, Xing; Gong, Zhiyun; Zhou, Yong; Liang, Guohua; Gu, Minghong</p> <p>2013-12-01</p> <p>The centromere is a key chromosomal component for <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion and is the site for kinetochore assembly and spindle fiber attachment, allowing each <span class="hlt">sister</span> <span class="hlt">chromatid</span> to faithfully segregate to each daughter cell during cell division. It is not clear what types of sequences act as functional centromeres and how centromere sequences are organized in Oryza brachyantha, an FF genome species. In this study, we found that the three classes of centromere-specific CentO-F satellites (CentO-F1, CentO-F2, and CentOF3) in O. brachyantha share no homology with the CentO satellites in Oryza sativa. The three classes of CentO-F satellites are all located within the chromosomal regions to which the spindle fibers attach and are characterized by megabase tandem arrays that are flanked by centromere-specific retrotransposons, CRR-F, in the O. brachyantha centromeres. Although these CentO-F satellites are quantitatively variable among 12 O. brachyantha centromeres, immunostaining with an antibody specific to CENH3 indicates that they are colocated with CENH3 in functional centromere regions. Our results demonstrate that the three classes of CentO-F satellites may be the major components of functional centromeres in O. brachyantha.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4790872','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4790872"><span>The Opposing Actions of Arabidopsis CHROMOSOME TRANSMISSION FIDELITY7 and WINGS APART-LIKE1 and 2 Differ in Mitotic and Meiotic Cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Mitra, Sayantan; Yang, Xiaohui</p> <p>2016-01-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatid</span> cohesion, which is mediated by the cohesin complex, is essential for the proper segregation of chromosomes during mitosis and meiosis. Stable binding of cohesin with chromosomes is regulated in part by the opposing actions of CTF7 (CHROMOSOME TRANSMISSION FIDELITY7) and WAPL (WINGS APART-LIKE). In this study, we characterized the interaction between Arabidopsis thaliana CTF7 and WAPL by conducting a detailed analysis of wapl1-1 wapl2 ctf7 plants. ctf7 plants exhibit major defects in vegetative growth and development and are completely sterile. Inactivation of WAPL restores normal growth, mitosis, and some fertility to ctf7 plants. This shows that the CTF7/WAPL cohesin system is not essential for mitosis in vegetative cells and suggests that plants may contain a second mechanism to regulate mitotic cohesin. WAPL inactivation restores cohesin binding and suppresses ctf7-associated meiotic cohesion defects, demonstrating that WAPL and CTF7 function as antagonists to regulate meiotic <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion. The ctf7 mutation only had a minor effect on wapl-associated defects in chromosome condensation and centromere association. These results demonstrate that WAPL has additional roles that are independent of its role in regulating chromatin-bound cohesin. PMID:26813623</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11139603','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11139603"><span>Termini of human chromosomes display elevated rates of mitotic recombination.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cornforth, M N; Eberle, R L</p> <p>2001-01-01</p> <p>The strand-specific in situ hybridization technique of CO-FISH was used to probe telomeres of human mitotic cells in order to determine the spontaneous frequency of crossover. This approach allowed the detection of recombinational crossovers occurring anywhere along the length of individual chromosomes, including reciprocal events taking place between <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Although the process of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) is the most prominent type of recombination in somatic mammalian cells, our results show that SCEs accounted for less than a third of the recombinational events revealed by CO-FISH. It is concluded that chromosomal regions near the termini of chromosome arms undergo extraordinarily high rates of spontaneous recombination, producing terminal crossovers whose small size precludes detection by standard cytogenetic methods. That similar results were observed for transformed epithelial cells, as well as primary fibroblasts, suggests that the phenomenon is a common characteristic of human cells. These findings are noteworthy because, although telomeric and subtelomeric DNA is known to be preferentially involved in certain types of recombination, the tips of somatic mammalian chromosomes have not previously been identified as preferred sites for crossover. Implications of these results are discussed in terms of limitations imposed on CO-FISH for its proposed use in directional hybridization mapping.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27996347','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27996347"><span>Oxcarbazepine-induced cytotoxicity and genotoxicity in human lymphocyte cultures with or without metabolic activation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Atlı Şekeroğlu, Zülal; Kefelioğlu, Haluk; Kontaş Yedier, Seval; Şekeroğlu, Vedat; Delmecioğlu, Berrin</p> <p>2017-03-01</p> <p>There has been considerable debate about the relationship between epilepsy and cancer. Oxcarbazepine (OXC) is used for treating certain types of seizures in patients with epilepsy. There have been no detailed investigations about genotoxicity of OXC and its metabolites. Therefore, the aim of this study is to investigate the cytotoxic and genotoxic effects of OXC and its metabolites on cultured human lymphocytes. The cytotoxicity and genotoxicity of OXC on human peripheral blood lymphocytes were examined in vitro by <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE), chromosomal <span class="hlt">aberration</span> (CA) and micronucleus (MN) tests. Cultures were treated with 125, 250 and 500 μg/ml of OXC in the presence (3 h treatment) and absence (24 h and 48 h treatment) of a metabolic activator (S9 mix). Dimethyl sulfoxide (DMSO) was used as a solvent control. OXC showed cytotoxic activities due to significant decreases in mitotic index (MI), proliferation index (PI) and nuclear division index (NDI) in the absence of S9 mix when compared with solvent control. Metabolites of OXC also significantly reduced MI and PI in cultures with S9 mix. OXC significantly increased the CAs, <span class="hlt">aberrant</span> cells, SCE and MN values in the presence and absence of S9 mix. Our results indicated that both OXC and its metabolites have cytotoxic, cytostatic and genotoxic potential on human peripheral blood lymphocyte cultures under the experimental conditions. Further studies are necessary to elucidate the relationship between cytotoxic, cytostatic and genotoxic effects, and to make a possible risk assessment in patients receiving therapy with this drug.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1470029','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1470029"><span>Biomarkers of human exposure to pesticides.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Anwar, W A</p> <p>1997-01-01</p> <p>For centuries, several hundred pesticides have been used to control insects. These pesticides differ greatly in their mode of action, uptake by the body, metabolism, elimination from the body, and toxicity to humans. Potential exposure from the environment can be estimated by environmental monitoring. Actual exposure (uptake) is measured by the biological monitoring of human tissues and body fluids. Biomarkers are used to detect the effects of pesticides before adverse clinical health effects occur. Pesticides and their metabolites are measured in biological samples, serum, fat, urine, blood, or breast milk by the usual analytical techniques. Biochemical responses to environmental chemicals provide a measure of toxic effect. A widely used biochemical biomarker, cholinesterase depression, measures exposure to organophosphorus insecticides. Techniques that measure DNA damage (e.g., detection of DNA adducts) provide a powerful tool in measuring environmental effects. Adducts to hemoglobin have been detected with several pesticides. Determination of chromosomal <span class="hlt">aberration</span> rates in cultured lymphocytes is an established method of monitoring populations occupationally or environmentally exposed to known or suspected mutagenic-carcinogenic agents. There are several studies on the cytogenetic effects of work with pesticide formulations. The majority of these studies report increases in the frequency of chromosomal <span class="hlt">aberrations</span> and/or <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges among the exposed workers. Biomarkers will have a major impact on the study of environmental risk factors. The basic aim of scientists exploring these issues is to determine the nature and consequences of genetic change or variation, with the ultimate purpose of predicting or preventing disease. PMID:9255564</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24851802','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24851802"><span>Childhood obsessive-compulsive traits in anorexia nervosa patients, their unaffected <span class="hlt">sisters</span> and healthy controls: a retrospective study.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Degortes, Daniela; Zanetti, Tatiana; Tenconi, Elena; Santonastaso, Paolo; Favaro, Angela</p> <p>2014-07-01</p> <p>Although there is evidence that childhood perfectionistic traits predate the onset of eating disorders, few studies to date have examined the prevalence and clinical correlates of these traits in patients with anorexia nervosa (AN) and their unaffected <span class="hlt">sisters</span>. The aim of this work was to study the prevalence of childhood obsessive-compulsive traits in patients with lifetime AN, their unaffected <span class="hlt">sisters</span> and healthy women. A total of 116 AN patients, 32 healthy <span class="hlt">sisters</span> and 119 controls were assessed by the EATATE Interview to assess traits such as perfectionism, inflexibility, rule-bound traits, drive for order and symmetry, and excessive doubt and cautiousness. Both self-report and maternal reports were collected. AN patients reported more childhood obsessive-compulsive traits than their healthy <span class="hlt">sisters</span> and controls. In contrast, no differences between healthy controls and unaffected <span class="hlt">sisters</span> emerged. In patients with AN, a dose-response relationship was found between the number of childhood obsessive-compulsive traits and psychopathology, including body image distortion, thus indicating that these traits are an important feature to be considered in assessing and treating eating disorders. Copyright © 2014 John Wiley & Sons, Ltd and Eating Disorders Association.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1996SPIE.2870...52A','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1996SPIE.2870...52A"><span><span class="hlt">Aberrated</span> laser beams in terms of Zernike polynomials</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Alda, Javier; Alonso, Jose; Bernabeu, Eusebio</p> <p>1996-11-01</p> <p>The characterization of light beams has devoted a lot of attention in the past decade. Several formalisms have been presented to treat the problem of parameter invariance and characterization in the propagation of light beam along ideal, ABCD, optical systems. The hard and soft apertured optical systems have been treated too. Also some <span class="hlt">aberrations</span> have been analyzed, but it has not appeared a formalism able to treat the problem as a whole. In this contribution we use a classical approach to describe the problem of <span class="hlt">aberrated</span>, and therefore apertured, light beams. The wavefront <span class="hlt">aberration</span> is included in a pure phase term expanded in terms of the Zernike polynomials. Then, we can use the relation between the lower order Zernike polynomia and the Seidel or third order <span class="hlt">aberrations</span>. We analyze the astigmatism, the spherical <span class="hlt">aberration</span> and the coma, and we show how higher order <span class="hlt">aberrations</span> can be taken into account. We have calculated the divergence, and the radius of curvature of such <span class="hlt">aberrated</span> beams and the influence of these <span class="hlt">aberrations</span> in the quality of the light beam. Some numerical simulations have been done to illustrate the method.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29567643','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29567643"><span>Structural centrosome <span class="hlt">aberrations</span> promote non-cell-autonomous invasiveness.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ganier, Olivier; Schnerch, Dominik; Oertle, Philipp; Lim, Roderick Yh; Plodinec, Marija; Nigg, Erich A</p> <p>2018-05-02</p> <p>Centrosomes are the main microtubule-organizing centers of animal cells. Although centrosome <span class="hlt">aberrations</span> are common in tumors, their consequences remain subject to debate. Here, we studied the impact of structural centrosome <span class="hlt">aberrations</span>, induced by deregulated expression of ninein-like protein (NLP), on epithelial spheres grown in Matrigel matrices. We demonstrate that NLP-induced structural centrosome <span class="hlt">aberrations</span> trigger the escape ("budding") of living cells from epithelia. Remarkably, all cells disseminating into the matrix were undergoing mitosis. This invasive behavior reflects a novel mechanism that depends on the acquisition of two distinct properties. First, NLP-induced centrosome <span class="hlt">aberrations</span> trigger a re-organization of the cytoskeleton, which stabilizes microtubules and weakens E-cadherin junctions during mitosis. Second, atomic force microscopy reveals that cells harboring these centrosome <span class="hlt">aberrations</span> display increased stiffness. As a consequence, mitotic cells are pushed out of mosaic epithelia, particularly if they lack centrosome <span class="hlt">aberrations</span>. We conclude that centrosome <span class="hlt">aberrations</span> can trigger cell dissemination through a novel, non-cell-autonomous mechanism, raising the prospect that centrosome <span class="hlt">aberrations</span> contribute to the dissemination of metastatic cells harboring normal centrosomes. © 2018 The Authors. Published under the terms of the CC BY NC ND 4.0 license.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15521268','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15521268"><span>Whole eye wavefront <span class="hlt">aberrations</span> in Mexican male subjects.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cantú, Roberto; Rosales, Marco A; Tepichín, Eduardo; Curioca, Andrée; Montes, Victor; Bonilla, Julio</p> <p>2004-01-01</p> <p>To analyze the characteristics, incidence, and appearance of wavefront <span class="hlt">aberrations</span> in undilated, normal, unoperated eyes. Eighty-eight eyes of 44 healthy male Mexican subjects (mean age 25.32 years, range 18 to 36 yr) were divided into three groups based on uncorrected visual acuity of greater than or equal to 20/20, 20/30, or 20/40. UCVA measurements were obtained using an Acuity Max computer screen chart. Wavefront <span class="hlt">aberrations</span> were measured with the Nidek OPD-Scan ARK 10000, Ver. 1.11b. All measurements were carried out at the same center by the same technician during a single session, following manufacturer instructions. Background illumination was 3 Lux. Wavefront <span class="hlt">aberration</span> measurements for each group were statistically analyzed using StatView; an average eye was characterized and the resulting <span class="hlt">aberrations</span> were simulated using MATLAB. We obtained wavefront <span class="hlt">aberration</span> maps for the 20/20 undilated normal unoperated eyes for total, low, and high order <span class="hlt">aberration</span> coefficients. Wavefront maps for right eyes were practically the same as those for left eyes. Higher <span class="hlt">aberrations</span> did not contribute substantially to total wavefront analysis. Average <span class="hlt">aberrations</span> of this "normal eye" will be used as criteria to decide the necessity of wavefront-guided ablation in our facilities. We will focus on the nearly zero average of high order <span class="hlt">aberrations</span> in this normal whole eye as a reference to be matched.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21317666','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21317666"><span>Accommodation to wavefront vergence and chromatic <span class="hlt">aberration</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wang, Yinan; Kruger, Philip B; Li, James S; Lin, Peter L; Stark, Lawrence R</p> <p>2011-05-01</p> <p>Longitudinal chromatic <span class="hlt">aberration</span> (LCA) provides a cue to accommodation with small pupils. However, large pupils increase monochromatic <span class="hlt">aberrations</span>, which may obscure chromatic blur. In this study, we examined the effect of pupil size and LCA on accommodation. Accommodation was recorded by infrared optometer while observers (nine normal trichromats) viewed a sinusoidally moving Maltese cross target in a Badal stimulus system. There were two illumination conditions: white (3000 K; 20 cd/m) and monochromatic (550 nm with 10 nm bandwidth; 20 cd/m) and two artificial pupil conditions (3 and 5.7 mm). Separately, static measurements of wavefront <span class="hlt">aberration</span> were made with the eye accommodating to targets between 0 and 4 D (COAS, Wavefront Sciences). Large individual differences in accommodation to wavefront vergence and to LCA are a hallmark of accommodation. LCA continues to provide a signal at large pupil sizes despite higher levels of monochromatic <span class="hlt">aberrations</span>. Monochromatic <span class="hlt">aberrations</span> may defend against chromatic blur at high spatial frequencies, but accommodation responds best to optical vergence and to LCA at 3 c/deg where blur from higher order <span class="hlt">aberrations</span> is less.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24748665','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24748665"><span>Requirement for Parp-1 and DNA ligases 1 or 3 but not of Xrcc1 in chromosomal translocation formation by backup end joining.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Soni, Aashish; Siemann, Maria; Grabos, Martha; Murmann, Tamara; Pantelias, Gabriel E; Iliakis, George</p> <p>2014-06-01</p> <p>In mammalian cells, ionizing radiation (IR)-induced DNA double-strand breaks (DSBs) are repaired in all phases of the cell cycle predominantly by classical, DNA-PK-dependent nonhomologous end joining (D-NHEJ). Homologous recombination repair (HRR) is functional during the S- and G2-phases, when a <span class="hlt">sister</span> <span class="hlt">chromatid</span> becomes available. An error-prone, alternative form of end joining, operating as backup (B-NHEJ) functions robustly throughout the cell cycle and particularly in the G2-phase and is thought to backup predominantly D-NHEJ. Parp-1, DNA-ligases 1 (Lig1) and 3 (Lig3), and Xrcc1 are implicated in B-NHEJ. Chromosome and <span class="hlt">chromatid</span> translocations are manifestations of erroneous DSB repair and are crucial culprits in malignant transformation and IR-induced cell lethality. We analyzed shifts in translocation formation deriving from defects in D-NHEJ or HRR in cells irradiated in the G2-phase and identify B-NHEJ as the main DSB repair pathway backing up both of these defects at the cost of a large increase in translocation formation. Our results identify Parp-1 and Lig1 and 3 as factors involved in translocation formation and show that Xrcc1 reinforces the function of Lig3 in the process without being required for it. Finally, we demonstrate intriguing connections between B-NHEJ and DNA end resection in translocation formation and show that, as for D-NHEJ and HRR, the function of B-NHEJ facilitates the recovery from the G2-checkpoint. These observations advance our understanding of chromosome <span class="hlt">aberration</span> formation and have implications for the mechanism of action of Parp inhibitors. © The Author(s) 2014. Published by Oxford University Press on behalf of Nucleic Acids Research.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li class="active"><span>17</span></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_17 --> <div id="page_18" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li class="active"><span>18</span></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="341"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28817615','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28817615"><span>Genotoxic effects of Roundup Full II® on lymphocytes of Chaetophractus villosus (Xenarthra, Mammalia): In vitro studies.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Luaces, Juan Pablo; Rossi, Luis Francisco; Chirino, Mónica Gabriela; Browne, Melanie; Merani, María Susana; Mudry, Marta Dolores</p> <p>2017-01-01</p> <p>In Argentina, Chaetophractus villosus has a wide distribution that overlaps with agricultural areas where soybean is the predominant crop. In such areas the pesticide Roundup Full II® (RU) is widely applied. The genotoxic effect of its active ingredient glyphosate (RU is 66.2% glyphosate) on the peripheral blood lymphocytes of C. villosus was tested over a range of concentrations (280, 420, 560, 1120 μmol/L). Culture medium without glyphosate served as negative control, while medium containing mitomycin C served as positive control. Genetic damage was characterized in terms of the percentage of cells with chromosome <span class="hlt">aberrations</span> (CA), the mean number of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE) per cell, and the modification of cell proliferation kinetics via the calculation of the replication index. Significant increases (p < 0.0001) were seen in the CA frequency and the mean number of SCEs per cell compared to negative controls at all the RU concentrations tested. <span class="hlt">Chromatid</span> breaks, the only form of CA observed, under the 560 μmol/L RU conditions and in presence of mitomycin C were four to five times more common than at lower concentrations, while no viable cells were seen in the 1120 μmol/L treatment. The mean number of SCEs per cell was significantly higher under the 280 μmol/L RU conditions than the 420 or 560 μmol/L RU conditions; cells cultivated in the presence of MMC also showed significantly more SCEs. All the RU concentrations tested (except in the 1120 μmol/L RU treatment [no viable cells]) induced a significant reduction in the replication index (p < 0.0001). The present results confirm the genotoxic effects of RU on C. villosus lymphocytes in vitro, strongly suggesting that exposure to RU could induce DNA damage in C. villosus wildlife.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036900p/','SCIGOV-HHH'); return false;" href="https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036900p/"><span>8. STREAMSIDE PATH NEAR MIDDLE OF THREE <span class="hlt">SISTERS</span> FALLS, LOOKING ...</span></a></p> <p><a target="_blank" href="http://www.loc.gov/pictures/collection/hh/">Library of Congress Historic Buildings Survey, Historic Engineering Record, Historic Landscapes Survey</a></p> <p></p> <p></p> <p>8. STREAM-SIDE PATH NEAR MIDDLE OF THREE <span class="hlt">SISTERS</span> FALLS, LOOKING WEST Photocopy of photograph, 1930s National Park Service, National Capital Region files - Dumbarton Oaks Park, Thirty-second & R Streets Northwest, Washington, District of Columbia, DC</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29043643','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29043643"><span>Imaging of DNA Ultrafine Bridges in Budding Yeast.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Quevedo, Oliver; Lisby, Michael</p> <p>2018-01-01</p> <p>DNA ultrafine bridges (UFBs) are a type of chromatin-free DNA bridges that connect <span class="hlt">sister</span> <span class="hlt">chromatids</span> in anaphase and pose a threat to genome stability. However, little is known about the origin of these structures, and how they are sensed and resolved by the cell. In this chapter, we review tools and methods for studying UFBs by fluorescence microscopy including chemical and genetic approaches to induce UFBs in the model organism Saccharomyces cerevisiae.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8186767','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8186767"><span>In vitro studies on chemoprotective effect of Purnark against benzo(a)pyrene-induced chromosomal damage in human lymphocytes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ghaisas, S D; Bhide, S V</p> <p>1994-01-01</p> <p>Human lymphocytes were used as an assay system to test chemopreventive activity of natural products. Purnark, a mixture of extracts of turmeric, betel leaf and catechu, was tested for its chemoprotective activity against BP induced DNA damage. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchange and micronuclei were used as markers to assess the protective activity of Purnark. Purnark gave 50-60% protection against BP induced SCEs and micronuclei. Purnark at 100 micrograms dose did not show any genotoxicity.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=improvement+AND+products&pg=3&id=EJ667313','ERIC'); return false;" href="https://eric.ed.gov/?q=improvement+AND+products&pg=3&id=EJ667313"><span>Clinical Design Sciences: A View from <span class="hlt">Sister</span> Design Efforts.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Zaritsky, Raul; Kelly, Anthony E.; Flowers, Woodie; Rogers, Everett; O'Neill, Patrick</p> <p>2003-01-01</p> <p>Asserts that the social sciences are clinical-like endeavors, and the way that "<span class="hlt">sister</span>" fields discover and validate their results may inform research practice in education. Describes three fields of design that confront similar societal demands for improvement (engineering product design, research on the diffusion of innovations, and…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29091641','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29091641"><span>Sixth-order wave <span class="hlt">aberration</span> theory of ultrawide-angle optical systems.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lu, Lijun; Cao, Yiqing</p> <p>2017-10-20</p> <p>In this paper, we develop sixth-order wave <span class="hlt">aberration</span> theory of ultrawide-angle optical systems like fisheye lenses. Based on the concept and approach to develop wave <span class="hlt">aberration</span> theory of plane-symmetric optical systems, we first derive the sixth-order intrinsic wave <span class="hlt">aberrations</span> and the fifth-order ray <span class="hlt">aberrations</span>; second, we present a method to calculate the pupil <span class="hlt">aberration</span> of such kind of optical systems to develop the extrinsic <span class="hlt">aberrations</span>; third, the relation of aperture-ray coordinates between adjacent optical surfaces is fitted with the second-order polynomial to improve the calculation accuracy of the wave <span class="hlt">aberrations</span> of a fisheye lens with a large acceptance aperture. Finally, the resultant <span class="hlt">aberration</span> expressions are applied to calculate the <span class="hlt">aberrations</span> of two design examples of fisheye lenses; the calculation results are compared with the ray-tracing ones with Zemax software to validate the <span class="hlt">aberration</span> expressions.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3125979','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3125979"><span><span class="hlt">Sisters</span> in hereditary breast and ovarian cancer families: communal coping, social integration, and psychological well-being†</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Koehly, Laura M.; Peters, June A.; Kuhn, Natalia; Hoskins, Lindsey; Letocha, Anne; Kenen, Regina; Loud, Jennifer; Greene, Mark H.</p> <p>2011-01-01</p> <p>Objective We investigated the association between psychological distress and indices of social integration and communal coping among <span class="hlt">sisters</span> from hereditary breast and ovarian cancer (HBOC) families. Sample and methods Sixty-five <span class="hlt">sisters</span> from 31 HBOC families completed the Brief Symptom Inventory-18 and the Colored Eco-Genetic Relationship Map, which identified members of participants’ social support networks. Hierarchical linear models were used for all analyses to account for the clustering of <span class="hlt">sisters</span> within families. Results Intra-family correlation coefficients suggested that <span class="hlt">sisters</span> shared perceptions of breast cancer risk and worry, but not ovarian cancer risk and worry. Further, <span class="hlt">sisters</span> demonstrated shared levels of anxiety and somatization, but not depressive symptoms. Communal coping indices quantifying shared support resources were negatively related to anxiety and somatization. The number of persons with whom cancer risk information was shared exhibited a positive trend with somatization. Social integration, as measured by the size of participants’ emotional support network, was negatively associated with anxiety. Lower depression scores were observed among participants with more persons playing multiple support roles and fewer persons providing tangible assistance. Conclusion Understanding how support relationships impact well-being among persons adjusting to HBOC risk, and the particular role of family in that process, will facilitate developing appropriate management approaches to help cancer-prone families adjust to their cancer risk. Published in 2008 by John Wiley & Sons Ltd. PMID:18688790</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036899p/','SCIGOV-HHH'); return false;" href="https://www.loc.gov/pictures/collection/hh/item/dc0640.photos.036899p/"><span>7. STREAMSIDE PATH BETWEEN THREE BRIDGE FALLS AND THREE <span class="hlt">SISTERS</span> ...</span></a></p> <p><a target="_blank" href="http://www.loc.gov/pictures/collection/hh/">Library of Congress Historic Buildings Survey, Historic Engineering Record, Historic Landscapes Survey</a></p> <p></p> <p></p> <p>7. STREAM-SIDE PATH BETWEEN THREE BRIDGE FALLS AND THREE <span class="hlt">SISTERS</span> FALLS, LOOKING WEST Photocopy of photograph, 1930s National Park Service, National Capital Region files - Dumbarton Oaks Park, Thirty-second & R Streets Northwest, Washington, District of Columbia, DC</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21595367','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21595367"><span>An illness in the family: Dr. Maude Abbott and her <span class="hlt">sister</span>, Alice Abbott.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Brookes, Barbara</p> <p>2011-01-01</p> <p>This paper explores Maude Abbott's internationally significant career in medicine and her parallel commitment to caring for her <span class="hlt">sister</span>, Alice Abbott. An examination of Abbott's life reveals the difficulties faced by an ambitious Canadian woman in medicine from the 1890s to the 1920s; difficulties compounded by caring for a <span class="hlt">sister</span> with a mental illness. The Abbott archive suggests that it was far more difficult for a woman doctor to make the kind of sharp distinction between public and private life that might be expected of professional men.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22045577','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22045577"><span>Spherical <span class="hlt">aberrations</span> of human astigmatic corneas.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhao, Huawei; Dai, Guang-Ming; Chen, Li; Weeber, Henk A; Piers, Patricia A</p> <p>2011-11-01</p> <p>To evaluate whether the average spherical <span class="hlt">aberration</span> of human astigmatic corneas is statistically equivalent to human nonastigmatic corneas. Spherical <span class="hlt">aberrations</span> of 445 astigmatic corneas prior to laser vision correction were retrospectively investigated to determine Zernike coefficients for central corneal areas 6 mm in diameter using CTView (Sarver and Associates). Data were divided into groups according to cylinder power (0.01 to 0.25 diopters [D], 0.26 to 0.75 D, 0.76 to 1.06 D, 1.07 to 1.53 D, 1.54 to 2.00 D, and >2.00 D) and according to age by decade. Spherical <span class="hlt">aberrations</span> were correlated with age and astigmatic power among groups and the entire population. Statistical analyses were conducted, and P<.05 was considered statistically significant. Mean patient age was 42.6±11 years. Astigmatic corneas had an average astigmatic power of 0.78±0.58 D and mean spherical <span class="hlt">aberration</span> was 0.25±0.13 μm for the entire population and approximately the same (0.27 μm) for individual groups, ranging from 0.23 to 0.29 μm (P>.05 for all tested groups). Mean spherical <span class="hlt">aberration</span> of astigmatic corneas was not correlated significantly with cylinder power or age (P>.05). Spherical <span class="hlt">aberrations</span> are similar to those of nonastigmatic corneas, permitting the use of these additional data in the design of aspheric toric intra-ocular lenses. Copyright 2011, SLACK Incorporated.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26260031','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26260031"><span>Siblings' experiences of their brother's or <span class="hlt">sister</span>'s cancer death: a nationwide follow-up 2-9 years later.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lövgren, Malin; Jalmsell, Li; Eilegård Wallin, Alexandra; Steineck, Gunnar; Kreicbergs, Ulrika</p> <p>2016-04-01</p> <p>The aim of this study was to examine siblings' experiences of their brother's or <span class="hlt">sister</span>'s cancer death and if these experiences influenced levels of anxiety 2-9 years later. This nationwide survey was conducted in Sweden in 2009. All siblings who had a brother/<span class="hlt">sister</span> who was diagnosed with cancer before the age of 17 years and who died before the age of 25 years during 2000-2007 were invited. Of those, 174 siblings participated (participation rate: 73%). Mixed data from the survey about the siblings' experiences of death were included as well as data from the Hospital Anxiety and Depression Scale. To examine the experiences, descriptive statistics and content analysis were used. Mann-Whitney U-test was conducted to investigate if the experiences influenced anxiety 2-9 years later. The siblings reported poor knowledge and experienced a lack of communication about their brother's/<span class="hlt">sister</span>'s death, for example, about the time frame, bodily changes near death, and about their own experiences. Siblings who reported that no one talked with them about what to expect when their brother/<span class="hlt">sister</span> was going to die reported higher levels of anxiety 2-9 years after the loss. Seventy percent reported that they witnessed their brother/<span class="hlt">sister</span> suffering in the last hours in life. Many of those who were not present during the illness period and at the time of death expressed regret. It is important to prepare siblings for their brother's/<span class="hlt">sister</span>'s illness and death as it may decrease anxiety and regrets later on. Copyright © 2015 John Wiley & Sons, Ltd.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2846563','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2846563"><span>Chromosomal instability in the lymphocytes of breast cancer patients</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Harsimran, Kaur; Kaur, Monga Gaganpreet; Nitika, Setia; Meena, Sudan; M. S., Uppal; Yamini; A. P. S., Batra; Vasudha, Sambyal</p> <p>2009-01-01</p> <p>Genomic instability in the tumor tissue has been correlated with tumor progression. In the present study, chromosomal <span class="hlt">aberrations</span> (CAs) in peripheral blood lymphocytes (PBLs) of breast tumor patients were studied to assess whether chromosomal instability (CIN) in PBLs correlates with aggressiveness of breast tumor (i.e., disease stage) and has any prognostic utility. Cultured blood lymphocyte metaphases were scored for <span class="hlt">aberrations</span> in 31 breast cancer patients and 20 healthy age and sex-matched controls. A variety of CAs, including aneuploidy, polyploidy, terminal deletions, acentric fragments, double minutes, <span class="hlt">chromatid</span> separations, ring chromosome, marker chromosome, <span class="hlt">chromatid</span> gaps, and breaks were seen in PBLs of the patients. The CAs in patients were higher than in controls. A comparison of the frequency of metaphases with <span class="hlt">aberrations</span> by grouping the patients according to the stage of advancement of disease did not reveal any consistent pattern of variation in lymphocytic CIN. Neither was any specific chromosomal abnormality found to be associated with the stage of cancer. This might be indicative of the fact that cancer patients have constitutional CIN, which predisposes them to the disease, and this inherent difference in the level of genomic instability might play a role in disease progression and response to treatment. PMID:20407644</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4539622','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4539622"><span>High order <span class="hlt">aberration</span> and straylight evaluation after cataract surgery with implantation of an aspheric, <span class="hlt">aberration</span> correcting monofocal intraocular lens</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kretz, Florian T A; Tandogan, Tamer; Khoramnia, Ramin; Auffarth, Gerd U</p> <p>2015-01-01</p> <p>AIM To evaluate the quality of vision in respect to high order <span class="hlt">aberrations</span> and straylight perception after implantation of an aspheric, <span class="hlt">aberration</span> correcting, monofocal intraocular lens (IOL). METHODS Twenty-one patients (34 eyes) aged 50 to 83y underwent cataract surgery with implantation of an aspheric, <span class="hlt">aberration</span> correcting IOL (Tecnis ZCB00, Abbott Medical Optics). Three months after surgery they were examined for uncorrected (UDVA) and corrected distance visual acuity (CDVA), contrast sensitivity (CS) under photopic and mesopic conditions with and without glare source, ocular high order <span class="hlt">aberrations</span> (HOA, Zywave II) and retinal straylight (C-Quant). RESULTS Postoperatively, patients achieved a postoperative CDVA of 0.0 logMAR or better in 97.1% of eyes. Mean values of high order abberations were +0.02±0.27 (primary coma components) and -0.04±0.16 (spherical <span class="hlt">aberration</span> term). Straylight values of the C-Quant were 1.35±0.44 log which is within normal range of age matched phakic patients. The CS measurements under mesopic and photopic conditions in combination with and without glare did not show any statistical significance in the patient group observed (P≥0.28). CONCLUSION The implantation of an aspherical <span class="hlt">aberration</span> correcting monofocal IOL after cataract surgery resulted in very low residual higher order <span class="hlt">aberration</span> (HOA) and normal straylight. PMID:26309872</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26123545','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26123545"><span>Extensive range overlap between heliconiine <span class="hlt">sister</span> species: evidence for sympatric speciation in butterflies?</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Rosser, Neil; Kozak, Krzysztof M; Phillimore, Albert B; Mallet, James</p> <p>2015-06-30</p> <p>Sympatric speciation is today generally viewed as plausible, and some well-supported examples exist, but its relative contribution to biodiversity remains to be established. We here quantify geographic overlap of <span class="hlt">sister</span> species of heliconiine butterflies, and use age-range correlations and spatial simulations of the geography of speciation to infer the frequency of sympatric speciation. We also test whether shifts in mimetic wing colour pattern, host plant use and climate niche play a role in speciation, and whether such shifts are associated with sympatry. Approximately a third of all heliconiine <span class="hlt">sister</span> species pairs exhibit near complete range overlap, and analyses of the observed patterns of range overlap suggest that sympatric speciation contributes 32%-95% of speciation events. Müllerian mimicry colour patterns and host plant choice are highly labile traits that seem to be associated with speciation, but we find no association between shifts in these traits and range overlap. In contrast, climatic niches of <span class="hlt">sister</span> species are more conserved. Unlike birds and mammals, <span class="hlt">sister</span> species of heliconiines are often sympatric and our inferences using the most recent comparative methods suggest that sympatric speciation is common. However, if <span class="hlt">sister</span> species spread rapidly into sympatry (e.g. due to their similar climatic niches), then assumptions underlying our methods would be violated. Furthermore, although we find some evidence for the role of ecology in speciation, ecological shifts did not show the associations with range overlap expected under sympatric speciation. We delimit species of heliconiines in three different ways, based on "strict and " "relaxed" biological species concepts (BSC), as well as on a surrogate for the widely-used "diagnostic" version of the phylogenetic species concept (PSC). We show that one reason why more sympatric speciation is inferred in heliconiines than in birds may be due to a different culture of species delimitation in the two</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3081412','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3081412"><span>Accommodation to Wavefront Vergence and Chromatic <span class="hlt">Aberration</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Wang, Yinan; Kruger, Philip B.; Li, James S.; Lin, Peter L.; Stark, Lawrence R.</p> <p>2011-01-01</p> <p>Purpose Longitudinal chromatic <span class="hlt">aberration</span> (LCA) provides a cue to accommodation with small pupils. However, large pupils increase monochromatic <span class="hlt">aberrations</span>, which may obscure chromatic blur. In the present study, we examined the effect of pupil size and LCA on accommodation. Methods Accommodation was recorded by infrared optometer while observers (nine normal trichromats) viewed a sinusoidally moving Maltese cross target in a Badal stimulus system. There were two illumination conditions: white (3000 K; 20 cd/m2) and monochromatic (550 nm with 10 nm bandwidth; 20 cd/m2) and two artificial pupil conditions (3 mm and 5.7 mm). Separately, static measurements of wavefront <span class="hlt">aberration</span> were made with the eye accommodating to targets between 0 and 4 D (COAS, Wavefront Sciences). Results Large individual differences in accommodation to wavefront vergence and to LCA are a hallmark of accommodation. LCA continues to provide a signal at large pupil sizes despite higher levels of monochromatic <span class="hlt">aberrations</span>. Conclusions Monochromatic <span class="hlt">aberrations</span> may defend against chromatic blur at high spatial frequencies, but accommodation responds best to optical vergence and to LCA at 3 c/deg where blur from higher order <span class="hlt">aberrations</span> is less. PMID:21317666</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2013JEOS....8E3061F','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2013JEOS....8E3061F"><span>Comparison of <span class="hlt">Aberrations</span> After Standard and Customized Refractive Surgery</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Fang, L.; He, X.; Wang, Y.</p> <p>2013-09-01</p> <p>To detect possible differences in residual wavefront <span class="hlt">aberrations</span> between standard and customized laser refractive surgery based onmathematical modeling, the residual optical <span class="hlt">aberrations</span> after conventional and customized laser refractive surgery were compared accordingto the ablation profile with transition zone. The results indicated that ablation profile has a significant impact on the residual <span class="hlt">aberrations</span>.The amount of residual <span class="hlt">aberrations</span> for conventional correction is higher than that for customized correction. Additionally, the residualaberrations for high myopia eyes are markedly larger than those for moderate myopia eyes. For a 5 mm pupil, the main residual aberrationterm is coma and yet it is spherical <span class="hlt">aberration</span> for a 7 mm pupil. When the pupil diameter is the same as optical zone or greater, themagnitudes of residual <span class="hlt">aberrations</span> is obviously larger than that for a smaller pupil. In addition, the magnitudes of the residual fifth orsixth order <span class="hlt">aberrations</span> are relatively large, especially secondary coma in a 6 mm pupil and secondary spherical <span class="hlt">aberration</span> in a 7 mm pupil.Therefore, the customized ablation profile may be superior to the conventional correction even though the transition zone and treatmentdecentration are taken into account. However, the customized ablation profile will still induce significant amount of residual <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2003APS..SES.EB008T','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2003APS..SES.EB008T"><span>Theoretical investigation of <span class="hlt">aberrations</span> upon ametropic human eyes</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Tan, Bo; Chen, Ying-Ling; Lewis, J. W. L.; Baker, Kevin</p> <p>2003-11-01</p> <p>The human eye <span class="hlt">aberrations</span> are important for visual acuity and ophthalmic diagnostics and surgical procedures. Reported monochromatic <span class="hlt">aberration</span> data of the normal 20/20 human eyes are scarce. There exist even fewer reports of the relation between ametropic conditions and <span class="hlt">aberrations</span>. We theoretically investigate the monochromatic and chromatic <span class="hlt">aberrations</span> of human eyes for refractive errors of -10 to +10 diopters. Schematic human eye models are employed using optical design software for axial, index, and refractive types of ametropia.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27701637','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27701637"><span>Anterior Corneal, Posterior Corneal, and Lenticular Contributions to Ocular <span class="hlt">Aberrations</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Atchison, David A; Suheimat, Marwan; Mathur, Ankit; Lister, Lucas J; Rozema, Jos</p> <p>2016-10-01</p> <p>To determine the corneal surfaces and lens contributions to ocular <span class="hlt">aberrations</span>. There were 61 healthy participants with ages ranging from 20 to 55 years and refractions -8.25 diopters (D) to +3.25 D. Anterior and posterior corneal topographies were obtained with an Oculus Pentacam, and ocular <span class="hlt">aberrations</span> were obtained with an iTrace aberrometer. Raytracing through models of corneas provided total corneal and surface component <span class="hlt">aberrations</span> for 5-mm-diameter pupils. Lenticular contributions were given as differences between ocular and corneal <span class="hlt">aberrations</span>. Theoretical raytracing investigated influence of object distance on <span class="hlt">aberrations</span>. Apart from defocus, the highest <span class="hlt">aberration</span> coefficients were horizontal astigmatism, horizontal coma, and spherical <span class="hlt">aberration</span>. Most correlations between lenticular and ocular parameters were positive and significant, with compensation of total corneal <span class="hlt">aberrations</span> by lenticular <span class="hlt">aberrations</span> for 5/12 coefficients. Anterior corneal <span class="hlt">aberrations</span> were approximately three times higher than posterior corneal <span class="hlt">aberrations</span> and usually had opposite signs. Corneal topographic centers were displaced from aberrometer pupil centers by 0.32 ± 0.19 mm nasally and 0.02 ± 0.16 mm inferiorly; disregarding corneal decentration relative to pupil center was significant for oblique astigmatism, horizontal coma, and horizontal trefoil. An object at infinity, rather than at the image in the anterior cornea, gave incorrect <span class="hlt">aberration</span> estimates of the posterior cornea. Corneal and lenticular <span class="hlt">aberration</span> magnitudes are similar, and <span class="hlt">aberrations</span> of the anterior corneal surface are approximately three times those of the posterior surface. Corneal decentration relative to pupil center has significant effects on oblique astigmatism, horizontal coma, and horizontal trefoil. When estimating component <span class="hlt">aberrations</span>, it is important to use correct object/image conjugates and heights at surfaces.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2016SPIE10154E..1WC','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2016SPIE10154E..1WC"><span>Nodal <span class="hlt">aberration</span> theory for wild-filed asymmetric optical systems</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Chen, Yang; Cheng, Xuemin; Hao, Qun</p> <p>2016-10-01</p> <p>Nodal <span class="hlt">Aberration</span> Theory (NAT) was used to calculate the zero field position in Full Field Display (FFD) for the given <span class="hlt">aberration</span> term. Aiming at wide-filed non-rotational symmetric decentered optical systems, we have presented the nodal geography behavior of the family of third-order and fifth-order <span class="hlt">aberrations</span>. Meanwhile, we have calculated the wavefront <span class="hlt">aberration</span> expressions when one optical element in the system is tilted, which was not at the entrance pupil. By using a three-piece-cellphone lens example in optical design software CodeV, the nodal geography is testified under several situations; and the wavefront <span class="hlt">aberrations</span> are calculated when the optical element is tilted. The properties of the nodal <span class="hlt">aberrations</span> are analyzed by using Fringe Zernike coefficients, which are directly related with the wavefront <span class="hlt">aberration</span> terms and usually obtained by real ray trace and wavefront surface fitting.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/servlets/purl/1435092','SCIGOV-STC'); return false;" href="https://www.osti.gov/servlets/purl/1435092"><span><span class="hlt">Aberration</span> corrected STEM by means of diffraction gratings</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Linck, Martin; Ercius, Peter A.; Pierce, Jordan S.</p> <p></p> <p>In the past 15 years, the advent of <span class="hlt">aberration</span> correction technology in electron microscopy has enabled materials analysis on the atomic scale. This is made possible by precise arrangements of multipole electrodes and magnetic solenoids to compensate the <span class="hlt">aberrations</span> inherent to any focusing element of an electron microscope. In this paper, we describe an alternative method to correct for the spherical <span class="hlt">aberration</span> of the objective lens in scanning transmission electron microscopy (STEM) using a passive, nanofabricated diffractive optical element. This holographic device is installed in the probe forming aperture of a conventional electron microscope and can be designed to removemore » arbitrarily complex <span class="hlt">aberrations</span> from the electron's wave front. In this work, we show a proof-of-principle experiment that demonstrates successful correction of the spherical <span class="hlt">aberration</span> in STEM by means of such a grating corrector (GCOR). Our GCOR enables us to record <span class="hlt">aberration</span>-corrected high-resolution high-angle annular dark field (HAADF-) STEM images, although yet without advancement in probe current and resolution. Finally, improvements in this technology could provide an economical solution for <span class="hlt">aberration</span>-corrected high-resolution STEM in certain use scenarios.« less</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li class="active"><span>18</span></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_18 --> <div id="page_19" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li class="active"><span>19</span></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="361"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/pages/biblio/1435092-aberration-corrected-stem-means-diffraction-gratings','SCIGOV-DOEP'); return false;" href="https://www.osti.gov/pages/biblio/1435092-aberration-corrected-stem-means-diffraction-gratings"><span><span class="hlt">Aberration</span> corrected STEM by means of diffraction gratings</span></a></p> <p><a target="_blank" href="http://www.osti.gov/pages">DOE PAGES</a></p> <p>Linck, Martin; Ercius, Peter A.; Pierce, Jordan S.; ...</p> <p>2017-06-12</p> <p>In the past 15 years, the advent of <span class="hlt">aberration</span> correction technology in electron microscopy has enabled materials analysis on the atomic scale. This is made possible by precise arrangements of multipole electrodes and magnetic solenoids to compensate the <span class="hlt">aberrations</span> inherent to any focusing element of an electron microscope. In this paper, we describe an alternative method to correct for the spherical <span class="hlt">aberration</span> of the objective lens in scanning transmission electron microscopy (STEM) using a passive, nanofabricated diffractive optical element. This holographic device is installed in the probe forming aperture of a conventional electron microscope and can be designed to removemore » arbitrarily complex <span class="hlt">aberrations</span> from the electron's wave front. In this work, we show a proof-of-principle experiment that demonstrates successful correction of the spherical <span class="hlt">aberration</span> in STEM by means of such a grating corrector (GCOR). Our GCOR enables us to record <span class="hlt">aberration</span>-corrected high-resolution high-angle annular dark field (HAADF-) STEM images, although yet without advancement in probe current and resolution. Finally, improvements in this technology could provide an economical solution for <span class="hlt">aberration</span>-corrected high-resolution STEM in certain use scenarios.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://ntrs.nasa.gov/search.jsp?R=20040170285&hterms=Cancer&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D90%26Ntt%3DCancer','NASA-TRS'); return false;" href="https://ntrs.nasa.gov/search.jsp?R=20040170285&hterms=Cancer&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D90%26Ntt%3DCancer"><span>Monitoring occupational exposure to cancer chemotherapy drugs</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Baker, E. S.; Connor, T. H.</p> <p>1996-01-01</p> <p>Reports of the health effects of handling cytotoxic drugs and compliance with guidelines for handling these agents are briefly reviewed, and studies using analytical and biological methods of detecting exposure are evaluated. There is little conclusive evidence of detrimental health effects from occupational exposure to cytotoxic drugs. Work practices have improved since the issuance of guidelines for handling these drugs, but compliance with the recommended practices is still inadequate. Of 64 reports published since 1979 on studies of workers' exposure to these drugs, 53 involved studies of changes in cellular or molecular endpoints (biological markers) and 12 described chemical analyses of drugs or their metabolites in urine (2 involved both, and 2 reported the same study). The primary biological markers used were urine mutagenicity, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, and chromosomal <span class="hlt">aberrations</span>; other studies involved formation of micronuclei and measurements of urinary thioethers. The studies had small sample sizes, and the methods were qualitative, nonspecific, subject to many confounders, and possibly not sensitive enough to detect most occupational exposures. Since none of the currently available biological and analytical methods is sufficiently reliable or reproducible for routine monitoring of exposure in the workplace, further studies using these methods are not recommended; efforts should focus instead on wide-spread implementation of improved practices for handling cytotoxic drugs.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25025061','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25025061"><span>Xanthium strumarium L. extracts produce DNA damage mediated by cytotoxicity in in vitro assays but does not induce micronucleus in mice.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Piloto Ferrer, Janet; Cozzi, Renata; Cornetta, Tommaso; Stano, Pasquale; Fiore, Mario; Degrassi, Francesca; De Salvia, Rosella; Remigio, Antonia; Francisco, Marbelis; Quiñones, Olga; Valdivia, Dayana; González, Maria L; Pérez, Carlos; Sánchez-Lamar, Angel</p> <p>2014-01-01</p> <p>Xanthium strumarium L. is a member of the Asteraceae commonly used in Cuba, mainly as diuretic. Some toxic properties of this plant have also been reported and, to date, very little is known about its genotoxic properties. The present work aims was to evaluate the potential cytotoxic and genotoxic risk of whole extract from Xanthium strumarium L. whole extract of aerial parts. No positive response was observed in a battery of four Salmonella typhimurium strains, when exposed to concentrations up to 5 mg/plate, with and without mammalian metabolic activation (liver microsomal S9 fraction from Wistar rats). In CHO cells, high concentrations (25-100 μg/mL) revealed significant reduction in cell viability. Results from <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, chromosome <span class="hlt">aberrations</span>, and comet assay showed that X. strumarium extract is genotoxic at the highest concentration used, when clear cytotoxic effects were also observed. On the contrary, no increase in micronuclei frequency in bone marrow cells was observed when the extract was orally administered to mice (100, 500, and 2000 mg/Kg doses). The data presented here constitute the most complete study on the genotoxic potential of X. strumarium L. and show that the extract can induce in vitro DNA damage at cytotoxic concentrations.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4082875','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4082875"><span>Xanthium strumarium L. Extracts Produce DNA Damage Mediated by Cytotoxicity in In Vitro Assays but Does Not Induce Micronucleus in Mice</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Piloto Ferrer, Janet; Cozzi, Renata; Cornetta, Tommaso; Stano, Pasquale; Fiore, Mario; Degrassi, Francesca; De Salvia, Rosella; Remigio, Antonia; Francisco, Marbelis; Quiñones, Olga; Valdivia, Dayana; González, Maria L.; Pérez, Carlos; Sánchez-Lamar, Angel</p> <p>2014-01-01</p> <p>Xanthium strumarium L. is a member of the Asteraceae commonly used in Cuba, mainly as diuretic. Some toxic properties of this plant have also been reported and, to date, very little is known about its genotoxic properties. The present work aims was to evaluate the potential cytotoxic and genotoxic risk of whole extract from Xanthium strumarium L. whole extract of aerial parts. No positive response was observed in a battery of four Salmonella typhimurium strains, when exposed to concentrations up to 5 mg/plate, with and without mammalian metabolic activation (liver microsomal S9 fraction from Wistar rats). In CHO cells, high concentrations (25–100 μg/mL) revealed significant reduction in cell viability. Results from <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges, chromosome <span class="hlt">aberrations</span>, and comet assay showed that X. strumarium extract is genotoxic at the highest concentration used, when clear cytotoxic effects were also observed. On the contrary, no increase in micronuclei frequency in bone marrow cells was observed when the extract was orally administered to mice (100, 500, and 2000 mg/Kg doses). The data presented here constitute the most complete study on the genotoxic potential of X. strumarium L. and show that the extract can induce in vitro DNA damage at cytotoxic concentrations. PMID:25025061</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22008529','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22008529"><span>Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Türkez, Hasan; Toğar, Başak</p> <p>2011-10-01</p> <p>The aim of this study was to investigate the protective effects of olive leaf extract (OLE) on genotoxicity and oxidative damage in cultured human blood cells treated with permethrin (PM) in the presence of a rat liver S9 mix containing cytochrome P 450 enzymes. Anti-genotoxic activities of OLE were studied using <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) and chromosome <span class="hlt">aberration</span> (CA) tests and furthermore total antioxidant capacity (TAC) and total oxidative status (TOS) were examined to determine the oxidative damage. Our results clearly revealed that treatment with PM (200 mg/l) alone increased SCE and CA rates and TOS level, decreased TAC level in cultured human blood cells. The OLE alone at the all tested doses did not induce any significant changes in the genotoxicity endpoint. However OLE leads to increases of plasma TAC level in vitro. OLE starts showing this positive effect at 100 mg/l. The combined treatment showed significant improvements in cytogenetic and biochemical parameters tested. Moreover, this improvement was more pronounced in the group received the high dose of the OLE. It could be concluded that the ethanol extract of OLE induced its genoprotective effect via the increase in the antioxidant capacity, inhibition of oxidative stress and scavenging of free radicals.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25552539','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25552539"><span>Genotoxicity in primary human peripheral lymphocytes after exposure to lithium titanate nanoparticles in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Akbaba, Giray B; Turkez, Hasan; Sönmez, Erdal; Tatar, Abdulgani; Yilmaz, Mehmet</p> <p>2016-08-01</p> <p>Lithium titanate (Li 2 TiO 3 ) nanoparticles (LTT NPs; <100 nm) are widely used in battery technology, porcelain enamels, and ceramic insulating bodies. With the increased applications of LTT NPs, the concerns about their potential human toxicity effects and their environmental impact were also increased. However, toxicity data for LTT NPs relating to human health are very limited. Therefore, the purpose of this study was to evaluate whether LTT NPs are able to induce genetic damage in human peripheral lymphocytes in vitro when taking into consideration that DNA damage plays an important role in carcinogenesis. With this aim, the chromosome <span class="hlt">aberrations</span> (CA), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE), and micronucleus (MN) assays were used as genotoxicity end points. Human peripheral lymphocytes obtained from five healthy male volunteers were exposed to LTT NPs at final dispersed concentrations ranging from 0 to 1000 μg/mL for 72 h at 37°C. The obtained results indicated that LTT NPs compound did not induce DNA damage in human peripheral lymphocytes as depicted by CA/cell, SCE/cell, and MN/1000 cell values in all concentrations tested. In summary, our results revealed that exposure to LTT NPs is not capable of inducing DNA lesions in human peripheral lymphocytes for the first time. © The Author(s) 2014.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1521169','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1521169"><span>Monitoring human exposure to urban air pollutants</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Barale, R.; Barrai, I.; Sbrana, I.; Migliore, L.; Marrazzini, A.; Scarcelli, V.; Bacci, E.; Di Sibio, A.; Tessa, A.; Cocchi, L.; Lubrano, V.; Vassalle, C.; He, J.</p> <p>1993-01-01</p> <p>A multidisciplinary study on a general population exposed to vehicle exhaust was undertaken in Pisa in 1991. Environmental factors such as air pollution and those associated with lifestyle were studied. Meanwhile, biological and medical indicators of health condition were investigated. Chromosomal <span class="hlt">aberrations</span>, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs), and micronuclei in lymphocytes were included for the assessment of the genotoxic risk. Because of the large number (3800) of subjects being investigated, standardization of protocols was compulsory. The results on data reproducibility are reported. To assess the reliability of the protocol on a large scale, the population of Porto Tolle, a village located in northeast Italy, was studied and compared to a subset of the Pisa population. Preliminary results showed that probable differences between the two populations and invididuals were present in terms of SCE frequencies. The study was potentially able to detect the effects of several factors such as age, smoking, genetics, and environment. The in vitro treatment of lymphocytes with diepoxybutane confirmed the presence of more responsive individuals and permitted us to investigate the genetic predisposition to genetic damage. The possible influence of environmental factors was studied by correlation analyses with external exposure to air pollutants as well as with several lifestyle factors. PMID:8143653</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25231917','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25231917"><span>Genotoxic evaluation of terbinafine in human lymphocytes in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Tolomeotti, Danielle; de Castro-Prado, Marialba Avezum Alves; de Sant'Anna, Juliane Rocha; Martins, Ana Beatriz Tozzo; Della-Rosa, Valter Augusto</p> <p>2015-01-01</p> <p>Terbinafine is an antimycotic drug usually used against several superficial fungal infections and with a potential application in the treatment of human cancers. Since to date there are few data on the genotoxic effects of terbinafine in mammalian cells, current study evaluated the potential genotoxic of such antifungal agent in cultured human peripheral blood lymphocytes. Terbinafine was used at the peak plasma concentration (1.0 μg/ml) and in four additional concentrations higher than the human plasmatic peak (5.0 μg/ml, 25.0 μg/ml, 50.0 μg/ml and 100.0 μg/ml). Chromosomal <span class="hlt">aberrations</span> (CA), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCE), micronuclei (MN), nucleoplasmic bridges (NP) and nuclear buds (NB) were scored as genetic endpoints. In all analysis no significant differences (α = 0.05, Kruskal-Wallis test) were observed. Complementary criterion adopted to obtain the final response in cytogenetic agreed with statistical results. Therefore, results of this study showed that terbinafine neither induced CA, SCE, MN, NP and NB nor affected significantly mitotic, replication and cytokinesis-block proliferation indices in any of the tested concentrations. It may be assumed that terbinafine was not genotoxic or cytotoxic to cultured human peripheral blood lymphocytes in our experimental conditions.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5176634-mutagens-cooked-foods-metabolism-genetic-toxicity','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/5176634-mutagens-cooked-foods-metabolism-genetic-toxicity"><span>Mutagens in cooked foods - metabolism and genetic toxicity</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Felton, J.S.; Bjeldanes, L.F.; Hatch, F.T.</p> <p>1984-02-17</p> <p>Recently developed in our laboratories is an efficient extraction procedure incorporating XAD resin adsorption which yields from 200/sup 0/C grilled ground beef an extract containing 230 Salmonella TA1538 revertants per g fresh weight of original ground beef. These mutagenic components are specific for frameshift-sensitive Salmonella strains and have an absolute requirement for metabolic activation. Normal-phase HPLC separation of methanol-extractable metabolites generated from reaction of 2-amino-3-methylimidazo (4,5-f)quinoline (IQ), a mutagenic component of broiled food with rat liver microsomes resulted in one direct-acting mutagenic peak and a second more polar peak still requiring metabolic activation. Two potent thermally-produced bacterial mutagens, 3-amino-1-methyl-5H-pyrido (4,3-b)more » indole (Trp-P-2) and IQ, were examined in mammalian cells. In excision repair-deficient CHO cells, Trp-P-2 exposure caused cytotoxicity, mutagenicity, <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange, and chromosomal <span class="hlt">aberrations</span> at concentrations more than 30-fold lower than those for IQ. In normal repair-proficient CHO cells Trp-P-2 was one-half as active and IQ was inactive. Relative to Trp-P-2, IQ is much more potent in the Salmonella bacterial system than in mammalian CHO cells.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26929995','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26929995"><span>Genotoxicity of monosodium glutamate.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ataseven, Nazmiye; Yüzbaşıoğlu, Deniz; Keskin, Ayten Çelebi; Ünal, Fatma</p> <p>2016-05-01</p> <p>Monosodium glutamate (MSG) is one of the most widely used flavor enhancers throughout the world. The aim of this study is to investigate the genotoxic potential of MSG by using chromosome <span class="hlt">aberrations</span> (CAs), <span class="hlt">sister-chromatid</span> exchanges (SCEs), cytokinesis-blocked micronucleus (CBMN), and random amplified polymorphic DNA-polimerase chain reaction (RAPD-PCR) in cultured human lymphocytes and alkaline comet assays in isolated human lymphocytes, which were incubated with six concentrations (250, 500, 1000, 2000, 4000 and 8000 μg/mL) of MSG. The result of this study indicated that MSG significantly and dose dependently increased the frequencies of CAs, SCE and MN in all treatments and times, compared with control. However, the replication (RI) and nuclear division indices (NDI) were not affected. In this paper, in vitro genotoxic effects of the MSG was also investigated on human peripheral lymphocytes by analysing the RAPD-PCR with arbitrary 10-mer primers. The changes occurring in RAPD profiles after MSG treatment include increase or decrease in band intensity and gain or loss of bands. In the comet assay, this additive caused DNA damage at all concentrations in isolated human lymphocytes after 1-h in vitro exposure. Our results demonstrate that MSG is genotoxic to the human peripheral blood lymphocytes in vitro. Copyright © 2016. Published by Elsevier Ltd.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2001SPIE.4510..218M','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2001SPIE.4510..218M"><span><span class="hlt">Aberration</span> correction for charged particle lithography</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Munro, Eric; Zhu, Xieqing; Rouse, John A.; Liu, Haoning</p> <p>2001-12-01</p> <p>At present, the throughput of projection-type charge particle lithography systems, such as PREVAIL and SCALPEL, is limited primarily by the combined effects of field curvature in the projection lenses and Coulomb interaction in the particle beam. These are fundamental physical limitations, inherent in charged particle optics, so there seems little scope for significantly improving the design of such systems, using conventional rotationally symmetric electron lenses. This paper explores the possibility of overcoming the field <span class="hlt">aberrations</span> of round electron lense, by using a novel <span class="hlt">aberration</span> corrector, proposed by Professor H. Rose of University of Darmstadt, called a hexapole planator. In this scheme, a set of round lenses is first used to simultaneously correct distortion and coma. The hexapole planator is then used to correct the field curvature and astigmatism, and to create a negative spherical <span class="hlt">aberration</span>. The size of the transfer lenses around the planator can then be adjusted to zero the residual spherical <span class="hlt">aberration</span>. In a way, an electron optical projection system is obtained that is free of all primary geometrical <span class="hlt">aberrations</span>. In this paper, the feasibility of this concept has been studied with a computer simulation. The simulations verify that this scheme can indeed work, for both electrostatic and magnetic projection systems. Two design studies have been carried out. The first is for an electrostatic system that could be used for ion beam lithography, and the second is for a magnetic projection system for electron beam lithography. In both cases, designs have been achieved in which all primary third-order geometrical <span class="hlt">aberrations</span> are totally eliminated.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.dtic.mil/docs/citations/AD1041922','DTIC-ST'); return false;" href="http://www.dtic.mil/docs/citations/AD1041922"><span><span class="hlt">Aberration</span> Compensation in Aplanatic Solid Immersion Lens Microscopy</span></a></p> <p><a target="_blank" href="http://www.dtic.mil/">DTIC Science & Technology</a></p> <p></p> <p>2013-11-08</p> <p>model and ray tracing software ( Zemax ) to understand how much <span class="hlt">aberrations</span> are in the system and how much can be compensated by the DM. Subsequently...<span class="hlt">aberration</span>. Table 2 shows the Zemax simulation on this particular case. With <span class="hlt">aberration</span> compensation, the finest resolvable group is at 252 nm</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21086039','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21086039"><span>Many functions of the meiotic cohesin.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bardhan, Amit</p> <p>2010-12-01</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatids</span> are held together from the time of their formation in S phase until they segregate in anaphase by the cohesin complex. In meiosis of most organisms, the mitotic Mcd1/Scc1/Rad21 subunit of the cohesin complex is largely replaced by its paralog named Rec8. This article reviews the specialized functions of Rec8 that are crucial for diverse aspects of chromosome dynamics in meiosis, and presents some speculations relating to meiotic chromosome organization.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2005NW.....92..586B','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2005NW.....92..586B"><span>Osteological evidence for <span class="hlt">sister</span> group relationship between pseudo-toothed birds (Aves: Odontopterygiformes) and waterfowls (Anseriformes)</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Bourdon, Estelle</p> <p>2005-12-01</p> <p>The phylogenetic affinities of the extinct pseudo-toothed birds have remained controversial. Some authors noted that they resemble both pelicans and allies (Pelecaniformes) and tube-nosed birds (Procellariiformes), but assigned them to a distinct taxon, the Odontopterygiformes. In most recent studies, the pseudo-toothed birds are referred to the family Pelagornithidae inside the Pelecaniformes. Here, I perform a cladistic analysis with five taxa of the pseudo-toothed birds including two undescribed new species from the Early Tertiary of Morocco. The present hypothesis strongly supports a <span class="hlt">sister</span> group relationship of pseudo-toothed birds (Odontopterygiformes) and waterfowls (Anseriformes). The Odontoanserae (Odontopterygiformes plus Anseriformes) are the <span class="hlt">sister</span> group of Neoaves. The placement of the landfowls (Galliformes) as the <span class="hlt">sister</span> taxon of all other neognathous birds does not support the consensus view that the Galloanserae (Galliformes plus Anseriformes) are monophyletic.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/FR-2012-08-15/pdf/2012-20067.pdf','FEDREG'); return false;" href="https://www.gpo.gov/fdsys/pkg/FR-2012-08-15/pdf/2012-20067.pdf"><span>77 FR 48993 - Proposed Collection; Comment Request; The <span class="hlt">Sister</span> Study: A Prospective Study of the Genetic and...</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collection.action?collectionCode=FR">Federal Register 2010, 2011, 2012, 2013, 2014</a></p> <p></p> <p>2012-08-15</p> <p>... Genetic and Environmental Risk Factors for Breast Cancer SUMMARY: In compliance with the requirement of... <span class="hlt">Sister</span> Study: A Prospective Study of the Genetic and Environmental Risk Factors for Breast Cancer. Type... the development of breast cancer in a high-risk cohort of <span class="hlt">sisters</span> of women who have had breast cancer...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/18831118','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/18831118"><span>Infant welfare, philanthropy and entrepreneurship in Glasgow: <span class="hlt">Sister</span> Laura's Infant Food Company.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Weaver, L T</p> <p>2008-06-01</p> <p>Laura Smith was <span class="hlt">sister</span>-in-charge of the Children's Dispensary in Glasgow from 1897 to 1922. In 1911 she established <span class="hlt">Sister</span> Laura's Infant Food Company to market a special milk formula of her own invention.The directors of the Dispensary were not amused. As the 'outdoor' department of the Royal Hospital for Sick Children (Yorkhill), the Dispensary was at the forefront of efforts to combat child ill health and malnutrition. This paper considers Laura Smith's initiative within the context of the health and care of infants of the time - high infant mortality, public and professional concerns for infant welfare, technological advances in food science, changing recommendations and practices of infant feeding and ambiguous relations between medicine and commerce.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=rooting&pg=6&id=EJ401034','ERIC'); return false;" href="https://eric.ed.gov/?q=rooting&pg=6&id=EJ401034"><span>Rooting Out <span class="hlt">Aberrant</span> Behavior in Training.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Kokalis, Jerry, Jr.; Paquin, Dave</p> <p>1989-01-01</p> <p>Discusses <span class="hlt">aberrant</span>, or disruptive, behavior in an industrial/business, classroom-based, instructor-led training setting. Three examples of <span class="hlt">aberrant</span> behavior are described, typical case studies are provided for each, and preventive (long-term) and corrective (on-the-spot) strategies for dealing with the problems are discussed. (LRW)</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28681436','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28681436"><span>Human eyes do not need monochromatic <span class="hlt">aberrations</span> for dynamic accommodation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bernal-Molina, Paula; Marín-Franch, Iván; Del Águila-Carrasco, Antonio J; Esteve-Taboada, Jose J; López-Gil, Norberto; Kruger, Philip B; Montés-Micó, Robert</p> <p>2017-09-01</p> <p>To determine if human accommodation uses the eye's own monochromatic <span class="hlt">aberrations</span> to track dynamic accommodative stimuli. Wavefront <span class="hlt">aberrations</span> were measured while subjects monocularly viewed a monochromatic Maltese cross moving sinusoidally around 2D of accommodative demand with 1D amplitude at 0.2 Hz. The amplitude and phase (delay) of the accommodation response were compared to the actual vergence of the stimulus to obtain gain and temporal phase, calculated from wavefront <span class="hlt">aberrations</span> recorded over time during experimental trials. The tested conditions were as follows: Correction of all the subject's <span class="hlt">aberrations</span> except defocus (C); Correction of all the subject's <span class="hlt">aberrations</span> except defocus and habitual second-order astigmatism (AS); Correction of all the subject's <span class="hlt">aberrations</span> except defocus and odd higher-order <span class="hlt">aberrations</span> (HOAs); Correction of all the subject's <span class="hlt">aberrations</span> except defocus and even HOAs (E); Natural <span class="hlt">aberrations</span> of the subject's eye, i.e., the adaptive-optics system only corrected the optical system's <span class="hlt">aberrations</span> (N); Correction of all the subject's <span class="hlt">aberrations</span> except defocus and fourth-order spherical <span class="hlt">aberration</span> (SA). The correction was performed at 20 Hz and each condition was repeated six times in randomised order. Average gain (±2 standard errors of the mean) varied little across conditions; between 0.55 ± 0.06 (SA), and 0.62 ± 0.06 (AS). Average phase (±2 standard errors of the mean) also varied little; between 0.41 ± 0.02 s (E), and 0.47 ± 0.02 s (O). After Bonferroni correction, no statistically significant differences in gain or phase were found in the presence of specific monochromatic <span class="hlt">aberrations</span> or in their absence. These results show that the eye's monochromatic <span class="hlt">aberrations</span> are not necessary for accommodation to track dynamic accommodative stimuli. © 2017 The Authors. Ophthalmic and Physiological Optics published by John Wiley & Sons Ltd on behalf of College of Optometrists.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29175744','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29175744"><span>Third-rank chromatic <span class="hlt">aberrations</span> of electron lenses.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Liu, Zhixiong</p> <p>2018-02-01</p> <p>In this paper the third-rank chromatic <span class="hlt">aberration</span> coefficients of round electron lenses are analytically derived and numerically calculated by Mathematica. Furthermore, the numerical results are cross-checked by the differential algebraic (DA) method, which verifies that all the formulas for the third-rank chromatic <span class="hlt">aberration</span> coefficients are completely correct. It is hoped that this work would be helpful for further chromatic <span class="hlt">aberration</span> correction in electron microscopy. Copyright © 2017 Elsevier B.V. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20110012712','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20110012712"><span>The Distribution of Chromosomal <span class="hlt">Aberrations</span> in Human Cells Predicted by a Generalized Time-Dependent Model of Radiation-Induced Formation of <span class="hlt">Aberrations</span></span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Ponomarev, Artem L.; George, K.; Cucinotta, F. A.</p> <p>2011-01-01</p> <p>New experimental data show how chromosomal <span class="hlt">aberrations</span> for low- and high-LET radiation are dependent on DSB repair deficiencies in wild-type, AT and NBS cells. We simulated the development of chromosomal <span class="hlt">aberrations</span> in these cells lines in a stochastic track-structure-dependent model, in which different cells have different kinetics of DSB repair. We updated a previously formulated model of chromosomal <span class="hlt">aberrations</span>, which was based on a stochastic Monte Carlo approach, to consider the time-dependence of DSB rejoining. The previous version of the model had an assumption that all DSBs would rejoin, and therefore we called it a time-independent model. The chromosomal-<span class="hlt">aberrations</span> model takes into account the DNA and track structure for low- and high-LET radiations, and provides an explanation and prediction of the statistics of rare and more complex <span class="hlt">aberrations</span>. We compared the program-simulated kinetics of DSB rejoining to the experimentally-derived bimodal exponential curves of the DSB kinetics. We scored the formation of translocations, dicentrics, acentric and centric rings, deletions, and inversions. The fraction of DSBs participating in <span class="hlt">aberrations</span> was studied in relation to the rejoining time. Comparisons of simulated dose dependence for simple <span class="hlt">aberrations</span> to the experimental dose-dependence for HF19, AT and NBS cells will be made.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li class="active"><span>19</span></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_19 --> <div id="page_20" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li class="active"><span>20</span></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="381"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/19930018142','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/19930018142"><span>Harmonic oscillator states in <span class="hlt">aberration</span> optics</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Wolf, Kurt Bernardo</p> <p>1993-01-01</p> <p>The states of the three-dimensional quantum harmonic oscillator classify optical <span class="hlt">aberrations</span> of axis-symmetric systems due to the isomorphism between the two mathematical structures. Cartesian quanta and angular momentum classifications have their corresponding <span class="hlt">aberration</span> classifications. The operation of concatenation of optical elements introduces a new operation between harmonic oscillator states.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2007up15.book..220H','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2007up15.book..220H"><span>Distortion of ultrashort pulses caused by <span class="hlt">aberrations</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Horváth, Z. L.; Kovács, A. P.; Bor, Zs.</p> <p></p> <p>The effect of the primary wave <span class="hlt">aberrations</span> (spherical <span class="hlt">aberration</span>, astigmatism and coma) on ultrashort pulses is studied by the Nijboer-Zernike theory. The results of the geometrical and the wave optical treatments are compared.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28476316','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28476316"><span><span class="hlt">Aberration</span>-free intraocular lenses - What does this really mean?</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Langenbucher, Achim; Schröder, Simon; Cayless, Alan; Eppig, Timo</p> <p>2017-09-01</p> <p>So-called <span class="hlt">aberration</span>-free intraocular lenses (IOLs) are well established in modern cataract surgery. Usually, they are designed to perfectly refract a collimated light beam onto the focal point. We show how much <span class="hlt">aberration</span> can be expected with such an IOL in a convergent light beam such as that found anterior to the human cornea. Additionally, the <span class="hlt">aberration</span> in a collimated beam is estimated for an IOL that has no <span class="hlt">aberrations</span> in the convergent beam. The convergent beam is modelled as the pencil of rays corresponding to the spherical wavefront resulting from a typical corneal power of 43m -1 . The IOLs are modelled as infinitely thin phase plates with 20m -1 optical power placed 5mm behind the cornea. Their <span class="hlt">aberrations</span> are reported in terms of optical path length difference and longitudinal spherical <span class="hlt">aberration</span> (LSA) of the marginal rays, as well as nominal spherical <span class="hlt">aberration</span> (SA) calculated based on a Zernike representation of the wavefront-error at the corneal plane within a 6mm aperture. The IOL designed to have no <span class="hlt">aberrations</span> in a collimated light beam has an optical path length difference of -1.8μm, and LSA of 0.15m -1 in the convergent beam of a typical eye. The corresponding nominal SA is 0.065μm. The IOL designed to have no <span class="hlt">aberrations</span> in a convergent light beam has an optical path length difference of 1.8μm, and LSA of -0.15m -1 in the collimated beam. An IOL designed to have no <span class="hlt">aberrations</span> in a collimated light beam will increase the SA of a patient's eye after implantation. Copyright © 2017. Published by Elsevier GmbH.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5027485','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5027485"><span>A defect in homologous recombination leads to increased translesion synthesis in E. coli</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Naiman, Karel; Pagès, Vincent; Fuchs, Robert P.</p> <p>2016-01-01</p> <p>DNA damage tolerance pathways allow cells to duplicate their genomes despite the presence of replication blocking lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS) and homology directed gap repair (HDGR). TLS pathways involve specialized DNA polymerases that are able to synthesize past DNA lesions with an intrinsic risk of causing point mutations. In contrast, HDGR pathways are essentially error-free as they rely on the recovery of missing information from the <span class="hlt">sister</span> <span class="hlt">chromatid</span> by RecA-mediated homologous recombination. We have investigated the genetic control of pathway choice between TLS and HDGR in vivo in Escherichia coli. In a strain with wild type RecA activity, the extent of TLS across replication blocking lesions is generally low while HDGR is used extensively. Interestingly, recA alleles that are partially impaired in D-loop formation confer a decrease in HDGR and a concomitant increase in TLS. Thus, partial defect of RecA's capacity to invade the homologous <span class="hlt">sister</span> <span class="hlt">chromatid</span> increases the lifetime of the ssDNA.RecA filament, i.e. the ‘SOS signal’. This increase favors TLS by increasing both the TLS polymerase concentration and the lifetime of the TLS substrate, before it becomes sequestered by homologous recombination. In conclusion, the pathway choice between error-prone TLS and error-free HDGR is controlled by the efficiency of homologous recombination. PMID:27257075</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22819078','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22819078"><span>A single mutation in Securin induces chromosomal instability and enhances cell invasion.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mora-Santos, Mar; Castilla, Carolina; Herrero-Ruiz, Joaquín; Giráldez, Servando; Limón-Mortés, M Cristina; Sáez, Carmen; Japón, Miguel Á; Tortolero, Maria; Romero, Francisco</p> <p>2013-01-01</p> <p>Pituitary tumour transforming gene (pttg1) encodes Securin, a protein involved in the inhibition of <span class="hlt">sister</span> <span class="hlt">chromatid</span> separation binding to Separase until the onset of anaphase. Separase is a cysteine-protease that degrades cohesin to segregate the <span class="hlt">sister</span> <span class="hlt">chromatids</span> to opposite poles of the cell. The amount of Securin is strongly regulated because it should allow Separase activation when it is degraded by the anaphase promoting complex/cyclosome, should arrest the cell cycle after DNA damage, when it is degraded through SKP1-CUL1-βTrCP ubiquitin ligase, and its overexpression induces tumour formation and correlates with metastasis in multiple tumours. Securin is a phosphoprotein that contains 32 potentially phosphorylatable residues. We mutated and analysed most of them, and found a single mutant, hSecT60A, that showed enhanced oncogenic properties. Our fluorescence activated cell sorting analysis, fluorescence in situ hybridisation assays, tumour cell migration and invasion experiments and gene expression by microarrays analysis clearly involved hSecT60A in chromosomal instability and cell invasion. These results show, for the first time, that a single mutation in pttg1 is sufficient to trigger the oncogenic properties of Securin. The finding of this point mutation in patients might be used as an effective strategy for early detection of cancer. Copyright © 2012 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25009111','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25009111"><span>The mitosis-regulating and protein-protein interaction activities of astrin are controlled by aurora-A-induced phosphorylation.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Chiu, Shao-Chih; Chen, Jo-Mei Maureen; Wei, Tong-You Wade; Cheng, Tai-Shan; Wang, Ya-Hui Candice; Ku, Chia-Feng; Lian, Chiao-Hsuan; Liu, Chun-Chih Jared; Kuo, Yi-Chun; Yu, Chang-Tze Ricky</p> <p>2014-09-01</p> <p>Cells display dramatic morphological changes in mitosis, where numerous factors form regulatory networks to orchestrate the complicated process, resulting in extreme fidelity of the segregation of duplicated chromosomes into two daughter cells. Astrin regulates several aspects of mitosis, such as maintaining the cohesion of <span class="hlt">sister</span> <span class="hlt">chromatids</span> by inactivating Separase and stabilizing spindle, aligning and segregating chromosomes, and silencing spindle assembly checkpoint by interacting with Src kinase-associated phosphoprotein (SKAP) and cytoplasmic linker-associated protein-1α (CLASP-1α). To understand how Astrin is regulated in mitosis, we report here that Astrin acts as a mitotic phosphoprotein, and Aurora-A phosphorylates Astrin at Ser(115). The phosphorylation-deficient mutant Astrin S115A abnormally activates spindle assembly checkpoint and delays mitosis progression, decreases spindle stability, and induces chromosome misalignment. Mechanistic analyses reveal that Astrin phosphorylation mimicking mutant S115D, instead of S115A, binds and induces ubiquitination and degradation of securin, which sequentially activates Separase, an enzyme required for the separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Moreover, S115A fails to bind mitosis regulators, including SKAP and CLASP-1α, which results in the mitotic defects observed in Astrin S115A-transfected cells. In conclusion, Aurora-A phosphorylates Astrin and guides the binding of Astrin to its cellular partners, which ensures proper progression of mitosis. Copyright © 2014 the American Physiological Society.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28514186','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28514186"><span>APC/C-Cdc20 mediates deprotection of centromeric cohesin at meiosis II in yeast.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Jonak, Katarzyna; Zagoriy, Ievgeniia; Oz, Tugce; Graf, Peter; Rojas, Julie; Mengoli, Valentina; Zachariae, Wolfgang</p> <p>2017-06-18</p> <p>Cells undergoing meiosis produce haploid gametes through one round of DNA replication followed by 2 rounds of chromosome segregation. This requires that cohesin complexes, which establish <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion during S phase, are removed in a stepwise manner. At meiosis I, the separase protease triggers the segregation of homologous chromosomes by cleaving cohesin's Rec8 subunit on chromosome arms. Cohesin persists at centromeres because the PP2A phosphatase, recruited by the shugoshin protein, dephosphorylates Rec8 and thereby protects it from cleavage. While <span class="hlt">chromatids</span> disjoin upon cleavage of centromeric Rec8 at meiosis II, it was unclear how and when centromeric Rec8 is liberated from its protector PP2A. One proposal is that bipolar spindle forces separate PP2A from Rec8 as cells enter metaphase II. We show here that <span class="hlt">sister</span> centromere biorientation is not sufficient to "deprotect" Rec8 at meiosis II in yeast. Instead, our data suggest that the ubiquitin-ligase APC/C Cdc20 removes PP2A from centromeres by targeting for degradation the shugoshin Sgo1 and the kinase Mps1. This implies that Rec8 remains protected until entry into anaphase II when it is phosphorylated concurrently with the activation of separase. Here, we provide further support for this model and speculate on its relevance to mammalian oocytes.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5499901','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5499901"><span>APC/C-Cdc20 mediates deprotection of centromeric cohesin at meiosis II in yeast</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Jonak, Katarzyna; Oz, Tugce; Graf, Peter; Rojas, Julie; Mengoli, Valentina; Zachariae, Wolfgang</p> <p>2017-01-01</p> <p>ABSTRACT Cells undergoing meiosis produce haploid gametes through one round of DNA replication followed by 2 rounds of chromosome segregation. This requires that cohesin complexes, which establish <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion during S phase, are removed in a stepwise manner. At meiosis I, the separase protease triggers the segregation of homologous chromosomes by cleaving cohesin's Rec8 subunit on chromosome arms. Cohesin persists at centromeres because the PP2A phosphatase, recruited by the shugoshin protein, dephosphorylates Rec8 and thereby protects it from cleavage. While <span class="hlt">chromatids</span> disjoin upon cleavage of centromeric Rec8 at meiosis II, it was unclear how and when centromeric Rec8 is liberated from its protector PP2A. One proposal is that bipolar spindle forces separate PP2A from Rec8 as cells enter metaphase II. We show here that <span class="hlt">sister</span> centromere biorientation is not sufficient to “deprotect” Rec8 at meiosis II in yeast. Instead, our data suggest that the ubiquitin-ligase APC/CCdc20 removes PP2A from centromeres by targeting for degradation the shugoshin Sgo1 and the kinase Mps1. This implies that Rec8 remains protected until entry into anaphase II when it is phosphorylated concurrently with the activation of separase. Here, we provide further support for this model and speculate on its relevance to mammalian oocytes. PMID:28514186</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2910038','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2910038"><span>Evidence that MEK1 positively promotes interhomologue double-strand break repair</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Terentyev, Yaroslav; Johnson, Rebecca; Neale, Matthew J.; Khisroon, Muhammad; Bishop-Bailey, Anna; Goldman, Alastair S. H.</p> <p>2010-01-01</p> <p>During meiosis there is an imperative to create sufficient crossovers for homologue segregation. This can be achieved during repair of programmed DNA double-strand breaks (DSBs), which are biased towards using a homologue rather than <span class="hlt">sister</span> <span class="hlt">chromatid</span> as a repair template. Various proteins contribute to this bias, one of which is a meiosis specific kinase Mek1. It has been proposed that Mek1 establishes the bias by creating a barrier to <span class="hlt">sister</span> <span class="hlt">chromatid</span> repair, as distinct from enforcing strand invasion with the homologue. We looked for evidence that Mek1 positively stimulates strand invasion of the homologue. This was done by analysing repair of DSBs induced by the VMA1-derived endonuclease (VDE) and flanked by directly repeated sequences that can be used for intrachromatid single-strand annealing (SSA). SSA competes with interhomologue strand invasion significantly more successfully when Mek1 function is lost. We suggest the increase in intrachromosomal SSA reflects an opportunistic default repair pathway due to loss of a MEK1 stimulated bias for strand invasion of the homologous chromosome. Making use of an inhibitor sensitive mek1-as1 allele, we found that Mek1 function influences the repair pathway throughout the first4–5 h of meiosis. Perhaps reflecting a particular need to create bias for successful interhomologue events before chromosome pairing is complete. PMID:20223769</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28819029','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28819029"><span>Loss of Tumor Suppressor STAG2 Promotes Telomere Recombination and Extends the Replicative Lifespan of Normal Human Cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Daniloski, Zharko; Smith, Susan</p> <p>2017-10-15</p> <p><span class="hlt">Sister</span> <span class="hlt">chromatids</span> are held together by cohesin, a tripartite ring with a peripheral SA1/2 subunit, where SA1 is required for telomere cohesion and SA2 for centromere cohesion. The STAG2 gene encoding SA2 is often inactivated in human cancer, but not in in a manner associated with aneuploidy. Thus, how these tumors maintain chromosomal cohesion and how STAG2 loss contributes to tumorigenesis remain open questions. Here we show that, despite a loss in centromere cohesion, <span class="hlt">sister</span> <span class="hlt">chromatids</span> in STAG2 mutant tumor cells maintain cohesion in mitosis at chromosome arms and telomeres. Telomere maintenance in STAG2 mutant tumor cells occurred by either telomere recombination or telomerase activation mechanisms. Notably, these cells were refractory to telomerase inhibitors, indicating recombination can provide an alternative means of telomere maintenance. STAG2 silencing in normal human cells that lack telomerase led to increased recombination at telomeres, delayed telomere shortening, and postponed senescence onset. Insofar as telomere shortening and replicative senescence prevent genomic instability and cancer by limiting the number of cell divisions, our findings suggest that extending the lifespan of normal human cells due to inactivation of STAG2 could promote tumorigenesis by extending the period during which tumor-driving mutations occur. Cancer Res; 77(20); 5530-42. ©2017 AACR . ©2017 American Association for Cancer Research.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25172298','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25172298"><span>Evaluation of cytogenetic and DNA damage in human lymphocytes treated with adrenaline in vitro.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Djelić, Ninoslav; Radaković, Milena; Spremo-Potparević, Biljana; Zivković, Lada; Bajić, Vladan; Stevanović, Jevrosima; Stanimirović, Zoran</p> <p>2015-02-01</p> <p>Catechol groups can be involved in redox cycling accompanied by generation of reactive oxygen species (ROS) which may lead to oxidative damage of cellular macromolecules including DNA. The objective of this investigation was to evaluate possible genotoxic effects of a natural catecholamine adrenaline in cultured human lymphocytes using cytogenetic (<span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and micronuclei) and the single cell gel electrophoresis (Comet) assay. In cytogenetic tests, six experimental concentrations of adrenaline were used in a range from 0.01-500 μM. There were no indications of genotoxic effects of adrenaline in <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange and micronucleus tests. However, at four highest concentrations of adrenaline (5 μM, 50 μM, 150 μM and 300 μM) we observed a decreased mitotic index and cell-cycle delay. In addition, in the Comet assay we used adrenaline in a range from 0.0005-500 μM, at two treatment times: 15 min or 60 min. In contrast to cytogenetic analysis, there was a dose-dependent increase of DNA damage detected in the Comet assay. These effects were significantly reduced by concomitant treatment with quercetin or catalase. Therefore, the obtained results indicate that adrenaline may exhibit genotoxic effects in cultured human lymphocytes, most likely due to production of reactive oxygen species. Copyright © 2014 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2011SPIE.8192E..51Q','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2011SPIE.8192E..51Q"><span>Effect of <span class="hlt">aberrations</span> in human eye on contrast sensitivity function</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Quan, Wei; Wang, Feng-lin; Wang, Zhao-qi</p> <p>2011-06-01</p> <p>The quantitative analysis of the effect of <span class="hlt">aberrations</span> in human eye on vision has important clinical value in the correction of <span class="hlt">aberrations</span>. The wave-front <span class="hlt">aberrations</span> of human eyes were measured with the Hartmann-Shack wave-front sensor and modulation transfer function (MTF) was computed from the wave-front <span class="hlt">aberrations</span>. Contrast sensitivity function (CSF) was obtained from MTF and the retinal aerial image modulation (AIM). It is shown that the 2nd, 3rd, 4th, 5th, 6th Zernike <span class="hlt">aberrations</span> deteriorate contrast sensitivity function. When the 2nd, 3rd, 4th, 5th, 6th Zernike <span class="hlt">aberrations</span> are corrected high contrast sensitivity function can be obtained.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22701050','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22701050"><span>The centenary of Janssens's chiasmatype theory.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Koszul, Romain; Meselson, Matthew; Van Doninck, Karine; Vandenhaute, Jean; Zickler, Denise</p> <p>2012-06-01</p> <p>The segregation and random assortment of characters observed by Mendel have their basis in the behavior of chromosomes in meiosis. But showing this actually to be the case requires a correct understanding of the meiotic behavior of chromosomes. This was achieved only gradually, over several decades, with much dispute and confusion along the way. One crucial step in the understanding of meiosis was provided in 1909 by Frans Alfons Janssens who published in La Cellule an article entitled "La théorie de la Chiasmatypie. Nouvelle interprétation des cinèses de maturation," which contains the first description of the chiasma structure. He observed that, of the four <span class="hlt">chromatids</span> present at the connection sites (chiasmata sites) at diplotene or anaphase of the first meiotic division, two crossed each other and two did not. He therefore postulated that the maternal and paternal <span class="hlt">chromatids</span> that crossed penetrated the other until they broke and rejoined in maternal and paternal segments new ways; the other two <span class="hlt">chromatids</span> remained free and thus intact. This allowed him also to propose that the <span class="hlt">chromatids</span> distributed in the four nuclei issued from the second meiotic division had various combinations of maternal and paternal segments of each chromosome. And conversely, permitted the appreciation that the laws of Mendelian segregation required breakage and joining (crossing over) between homologous non-<span class="hlt">sister</span> <span class="hlt">chromatids</span>. Although Janssens's article found a broad appreciative audience and had a large influence on the chromosomal theory at that time, his theory was resisted by both geneticists and cytologists for several decades. This Perspectives aims to highlight the novelty of Janssens's chiasmatype theory by examining the historical background and our actual understanding of meiotic recombination.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24931984','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24931984"><span>Detecting independent and recurrent copy number <span class="hlt">aberrations</span> using interval graphs.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Wu, Hsin-Ta; Hajirasouliha, Iman; Raphael, Benjamin J</p> <p>2014-06-15</p> <p>Somatic copy number <span class="hlt">aberrations</span> SCNAS: are frequent in cancer genomes, but many of these are random, passenger events. A common strategy to distinguish functional <span class="hlt">aberrations</span> from passengers is to identify those <span class="hlt">aberrations</span> that are recurrent across multiple samples. However, the extensive variability in the length and position of SCNA: s makes the problem of identifying recurrent <span class="hlt">aberrations</span> notoriously difficult. We introduce a combinatorial approach to the problem of identifying independent and recurrent SCNA: s, focusing on the key challenging of separating the overlaps in <span class="hlt">aberrations</span> across individuals into independent events. We derive independent and recurrent SCNA: s as maximal cliques in an interval graph constructed from overlaps between <span class="hlt">aberrations</span>. We efficiently enumerate all such cliques, and derive a dynamic programming algorithm to find an optimal selection of non-overlapping cliques, resulting in a very fast algorithm, which we call RAIG (Recurrent <span class="hlt">Aberrations</span> from Interval Graphs). We show that RAIG outperforms other methods on simulated data and also performs well on data from three cancer types from The Cancer Genome Atlas (TCGA). In contrast to existing approaches that employ various heuristics to select independent <span class="hlt">aberrations</span>, RAIG optimizes a well-defined objective function. We show that this allows RAIG to identify rare <span class="hlt">aberrations</span> that are likely functional, but are obscured by overlaps with larger passenger <span class="hlt">aberrations</span>. http://compbio.cs.brown.edu/software. © The Author 2014. Published by Oxford University Press.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1998SPIE.3219..124G','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1998SPIE.3219..124G"><span>Linear phase conjugation for atmospheric <span class="hlt">aberration</span> compensation</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Grasso, Robert J.; Stappaerts, Eddy A.</p> <p>1998-01-01</p> <p>Atmospheric induced <span class="hlt">aberrations</span> can seriously degrade laser performance, greatly affecting the beam that finally reaches the target. Lasers propagated over any distance in the atmosphere suffer from a significant decrease in fluence at the target due to these <span class="hlt">aberrations</span>. This is especially so for propagation over long distances. It is due primarily to fluctuations in the atmosphere over the propagation path, and from platform motion relative to the intended aimpoint. Also, delivery of high fluence to the target typically requires low beam divergence, thus, atmospheric turbulence, platform motion, or both results in a lack of fine aimpoint control to keep the beam directed at the target. To improve both the beam quality and amount of laser energy delivered to the target, Northrop Grumman has developed the Active Tracking System (ATS); a novel linear phase conjugation <span class="hlt">aberration</span> compensation technique. Utilizing a silicon spatial light modulator (SLM) as a dynamic wavefront reversing element, ATS undoes <span class="hlt">aberrations</span> induced by the atmosphere, platform motion or both. ATS continually tracks the target as well as compensates for atmospheric and platform motion induced <span class="hlt">aberrations</span>. This results in a high fidelity, near-diffraction limited beam delivered to the target.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2094213','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2094213"><span>Wave <span class="hlt">aberrations</span> in rhesus monkeys with vision-induced ametropias</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ramamirtham, Ramkumar; Kee, Chea-su; Hung, Li-Fang; Qiao-Grider, Ying; Huang, Juan; Roorda, Austin; Smith, Earl L.</p> <p>2007-01-01</p> <p>The purpose of this study was to investigate the relationship between refractive errors and high-order <span class="hlt">aberrations</span> in infant rhesus monkeys. Specifically, we compared the monochromatic wave <span class="hlt">aberrations</span> measured with a Shack-Hartman wavefront sensor between normal monkeys and monkeys with vision-induced refractive errors. Shortly after birth, both normal monkeys and treated monkeys reared with optically induced defocus or form deprivation showed a decrease in the magnitude of high-order <span class="hlt">aberrations</span> with age. However, the decrease in <span class="hlt">aberrations</span> was typically smaller in the treated animals. Thus, at the end of the lens-rearing period, higher than normal amounts of <span class="hlt">aberrations</span> were observed in treated eyes, both hyperopic and myopic eyes and treated eyes that developed astigmatism, but not spherical ametropias. The total RMS wavefront error increased with the degree of spherical refractive error, but was not correlated with the degree of astigmatism. Both myopic and hyperopic treated eyes showed elevated amounts of coma and trefoil and the degree of trefoil increased with the degree of spherical ametropia. Myopic eyes also exhibited a much higher prevalence of positive spherical <span class="hlt">aberration</span> than normal or treated hyperopic eyes. Following the onset of unrestricted vision, the amount of high-order <span class="hlt">aberrations</span> decreased in the treated monkeys that also recovered from the experimentally induced refractive errors. Our results demonstrate that high-order <span class="hlt">aberrations</span> are influenced by visual experience in young primates and that the increase in high-order <span class="hlt">aberrations</span> in our treated monkeys appears to be an optical byproduct of the vision-induced alterations in ocular growth that underlie changes in refractive error. The results from our study suggest that the higher amounts of wave <span class="hlt">aberrations</span> observed in ametropic humans are likely to be a consequence, rather than a cause, of abnormal refractive development. PMID:17825347</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2017OptCo.404..203A','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2017OptCo.404..203A"><span><span class="hlt">Aberrations</span> in stimulated emission depletion (STED) microscopy</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Antonello, Jacopo; Burke, Daniel; Booth, Martin J.</p> <p>2017-12-01</p> <p>Like all methods of super-resolution microscopy, stimulated emission depletion (STED) microscopy can suffer from the effects of <span class="hlt">aberrations</span>. The most important aspect of a STED microscope is that the depletion focus maintains a minimum, ideally zero, intensity point that is surrounded by a region of higher intensity. It follows that <span class="hlt">aberrations</span> that cause a non-zero value of this minimum intensity are the most detrimental, as they inhibit fluorescence emission even at the centre of the depletion focus. We present analysis that elucidates the nature of these effects in terms of the different polarisation components at the focus for two-dimensional and three-dimensional STED resolution enhancement. It is found that only certain low-order <span class="hlt">aberration</span> modes can affect the minimum intensity at the Gaussian focus. This has important consequences for the design of adaptive optics <span class="hlt">aberration</span> correction systems.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3409708','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3409708"><span>3D resolved mapping of optical <span class="hlt">aberrations</span> in thick tissues</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zeng, Jun; Mahou, Pierre; Schanne-Klein, Marie-Claire; Beaurepaire, Emmanuel; Débarre, Delphine</p> <p>2012-01-01</p> <p>We demonstrate a simple method for mapping optical <span class="hlt">aberrations</span> with 3D resolution within thick samples. The method relies on the local measurement of the variation in image quality with externally applied <span class="hlt">aberrations</span>. We discuss the accuracy of the method as a function of the signal strength and of the <span class="hlt">aberration</span> amplitude and we derive the achievable resolution for the resulting measurements. We then report on measured 3D <span class="hlt">aberration</span> maps in human skin biopsies and mouse brain slices. From these data, we analyse the consequences of tissue structure and refractive index distribution on <span class="hlt">aberrations</span> and imaging depth in normal and cleared tissue samples. The <span class="hlt">aberration</span> maps allow the estimation of the typical aplanetism region size over which <span class="hlt">aberrations</span> can be uniformly corrected. This method and data pave the way towards efficient correction strategies for tissue imaging applications. PMID:22876353</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2004OExpr..12..384B','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2004OExpr..12..384B"><span>Primary <span class="hlt">aberrations</span> in focused radially polarized vortex beams</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Biss, David P.; Brown, T. G.</p> <p>2004-02-01</p> <p>We study the effect of primary <span class="hlt">aberrations</span> on the 3-D polarization of the electric field in a focused lowest order radially polarized beam. A full vector diffraction treatment of the focused beams is used. Attention is given to the effects of primary spherical, astigmatic, and comatic <span class="hlt">aberrations</span> on the local polarization, Strehl ratio, and <span class="hlt">aberration</span> induced degradation of the longitudinal field at focus</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2017MsT..........7W','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2017MsT..........7W"><span>The Art of Optical <span class="hlt">Aberrations</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Wylde, Clarissa Eileen Kenney</p> <p></p> <p>Art and optics are inseparable. Though seemingly opposite disciplines, the combination of art and optics has significantly impacted both culture and science as they are now known. As history has run its course, in the sciences, arts, and their fruitful combinations, optical <span class="hlt">aberrations</span> have proved to be a problematic hindrance to progress. In an effort to eradicate <span class="hlt">aberrations</span> the simple beauty of these <span class="hlt">aberrational</span> forms has been labeled as undesirable and discarded. Here, rather than approach <span class="hlt">aberrations</span> as erroneous, these beautiful forms are elevated to be the photographic subject in a new body of work, On the Bright Side. Though many recording methods could be utilized, this work was composed on classic, medium-format, photographic film using white-light, Michelson interferometry. The resulting images are both a representation of the true light rays that interacted on the distorted mirror surfaces (data) and the artist's compositional eye for what parts of the interferogram are chosen and displayed. A detailed description of the captivating interdisciplinary procedure is documented and presented alongside the final artwork, CCD digital reference images, and deformable mirror contour maps. This alluring marriage between the arts and sciences opens up a heretofore minimally explored aspect of the inextricable art-optics connection. It additionally provides a fascinating new conversation on the importance of light and optics in photographic composition.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li class="active"><span>20</span></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_20 --> <div id="page_21" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li class="active"><span>21</span></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="401"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/7138370-analysis-mutagenic-activity-biohazardous-organics-kanawha-river-sediments-technical-completion-report','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/7138370-analysis-mutagenic-activity-biohazardous-organics-kanawha-river-sediments-technical-completion-report"><span>Analysis of mutagenic activity of biohazardous organics in Kanawha River sediments. Technical completion report</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>White, A.R.; Waldron, M.C.</p> <p>1988-01-01</p> <p>Residual chemical contamination of Kanawha River sediments may constitute a health hazard. Sediment cores have been analyzed using a coupled bioassay/chemical fractionation procedure. Both bacterial mutagenicity and <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) analyses were conducted on sediment samples. Pocatalico River sediments extracts showed no response in either bacterial mutagenicity assay or SCE assay. Extracts from Armour Creek and the Kanawha River induced mutagenicities in the presence of S9 enzymes. The same extracts produced a significant increase in human chromosomal cross-over events.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21479528','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21479528"><span>Bartter syndrome in two <span class="hlt">sisters</span> with a novel mutation of the CLCNKB gene, one with deafness.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Robitaille, Pierre; Merouani, Aicha; He, Ning; Pei, York</p> <p>2011-09-01</p> <p>This article describes two <span class="hlt">sisters</span> with type III Bartter syndrome (BS) due to a novel missense variant of the CLCNKB gene. The phenotypic expression of the disease was very different in these two siblings. In one <span class="hlt">sister</span>, the disease followed a very severe course, especially in the neonatal period and as a toddler. Both the classic symptoms and the biochemical features of the syndrome were striking. In addition, she presented with sensorineural deafness, a complication yet unreported in this subtype of BS In contrast, the least affected <span class="hlt">sister</span> was symptom free and the biochemical features of the disease although present remained discrete throughout the prolonged follow-up. It is suggested that such a difference in the phenotypic expression of the disease is possibly secondary to the modifier effect of a gene and/or results from environmental factor(s).</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=sibling+AND+relationship&id=EJ1069817','ERIC'); return false;" href="https://eric.ed.gov/?q=sibling+AND+relationship&id=EJ1069817"><span>Adult Sibling Relationships with Brothers and <span class="hlt">Sisters</span> with Severe Disabilities</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Rossetti, Zach; Hall, Sarah</p> <p>2015-01-01</p> <p>The purpose of this qualitative study was to examine perceptions of adult sibling relationships with a brother or <span class="hlt">sister</span> with severe disabilities and the contexts affecting the relationships. Adult siblings without disabilities (N = 79) from 19 to 72 years of age completed an online survey with four open-ended questions about their relationship…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8314713','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8314713"><span>Population dynamics of <span class="hlt">aberrant</span> chromosome 1 in mice.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sabantsev, I; Spitsin, O; Agulnik, S; Ruvinsky, A</p> <p>1993-05-01</p> <p>Natural populations of two semispecies of house mouse, Mus musculus domesticus and M.m. musculus, were found to be polymorphic for an <span class="hlt">aberrant</span> chromosome 1 bearing a large inserted block of homogeneously staining heterochromatin. Strong meiotic drive for the <span class="hlt">aberrant</span> chromosome from M.m. musculus was previously observed in heterozygous female mice. There are at least three meiotic drive levels determined by different allelic variants of distorter. Homozygotes had low viability and females showed low fertility. Both homo- and heterozygous males had normal fertility and their segregation patterns did not deviate from normal. Computer simulations were performed of the dynamics of <span class="hlt">aberrant</span> chromosome 1 in demes and populations. The data demonstrate that a spontaneous mutation (inversion) of an <span class="hlt">aberrant</span> chromosome 1, once arisen, has a high probability of spreading in a population at high coefficients of meiotic drive and migration. In the long-term, the population attains a stationary state which is determined by the drive level and migration intensity. The state of stable genotypic equilibrium is independent of deme and population size, as well as of the initial concentration of the <span class="hlt">aberrant</span> chromosome. As populations initially polymorphic for the distorters approach the stationary state, the stronger distorter is eliminated. The frequencies of the <span class="hlt">aberrant</span> chromosome determined by computer analysis agree well with those obtained for the studied Asian M.m. musculus populations. The evolutionary pathways for the origin and fixation of the <span class="hlt">aberrant</span> chromosome in natural populations are considered.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25608190','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25608190"><span><span class="hlt">Aberration</span> design of zoom lens systems using thick lens modules.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhang, Jinkai; Chen, Xiaobo; Xi, Juntong; Wu, Zhuoqi</p> <p>2014-12-20</p> <p>A systematic approach for the <span class="hlt">aberration</span> design of a zoom lens system using a thick lens module is presented. Each component is treated as a thick lens module at the beginning of the design. A thick lens module refers to a thick lens component with a real lens structure, like lens materials, lens curvatures, lens thicknesses, and lens interval distances. All nine third-order <span class="hlt">aberrations</span> of a thick lens component are considered during the design. The relationship of component <span class="hlt">aberrations</span> in different zoom positions can be approximated from the <span class="hlt">aberration</span> shift. After minimizing the <span class="hlt">aberrations</span> of the zoom lens system, the nine third-order <span class="hlt">aberrations</span> of every lens component can be determined. Then the thick lens structure of every lens component can be determined after optimization according to their first-order properties and third-order <span class="hlt">aberration</span> targets. After a third optimization for minimum practical third-order <span class="hlt">aberrations</span> of a zoom lens system, the <span class="hlt">aberration</span> design using the thick lens module is complete, which provides a practical zoom lens system with thick lens structures. A double-sided telecentric zoom lens system is designed using the thick lens module in this paper, which shows that this method is practical for zoom lens design.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3511620','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3511620"><span>Accuracy and reliability of self-reported weight and height in the <span class="hlt">Sister</span> Study</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Lin, Cynthia J; DeRoo, Lisa A; Jacobs, Sara R; Sandler, Dale P</p> <p>2012-01-01</p> <p>Objective To assess accuracy and reliability of self-reported weight and height and identify factors associated with reporting accuracy. Design Analysis of self-reported and measured weight and height from participants in the <span class="hlt">Sister</span> Study (2003–2009), a nationwide cohort of 50,884 women aged 35–74 in the United States with a <span class="hlt">sister</span> with breast cancer. Setting Weight and height were reported via computer-assisted telephone interview (CATI) and self-administered questionnaires, and measured by examiners. Subjects Early enrollees in the <span class="hlt">Sister</span> Study. There were 18,639 women available for the accuracy analyses and 13,316 for the reliability analyses. Results Using weighted kappa statistics, comparisons were made between CATI responses and examiner measures to assess accuracy and CATI and questionnaire responses to assess reliability. Polytomous logistic regression evaluated factors associated with over- or under-reporting. Compared to measured values, agreement was 96% for reported height (±1 inch; weighted kappa 0.84) and 67% for weight (±3 pounds; weighted kappa 0.92). Obese women [body mass index (BMI) ≥30 kg/m2)] were more likely than normal weight women to under-report weight by ≥5% and underweight women (BMI <18.5 kg/m2) were more likely to over-report. Among normal and overweight women (18.5 kgm2≤ BMI <30 kgm2), weight cycling and lifetime weight difference ≥50 pounds were associated with over-reporting. Conclusions U.S. women in the <span class="hlt">Sister</span> Study were reasonably reliable and accurate in reporting weight and height. Women with normal-range BMI reported most accurately. Overweight and obese women and those with weight fluctuations were less accurate, but even among obese women, few under-reported their weight by >10%. PMID:22152926</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23259587','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23259587"><span>High prevalence of metabolic syndrome in young Hispanic women: findings from the national <span class="hlt">Sister</span> to <span class="hlt">Sister</span> campaign.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Rodriguez, Fátima; Naderi, Sahar; Wang, Yun; Johnson, Caitlin E; Foody, JoAnne M</p> <p>2013-04-01</p> <p>Hispanics are the fastest growing segment of the U.S. population and have a higher prevalence of cardiometabolic risk factors as compared with non-Hispanic whites. Further data suggests that Hispanics have undiagnosed complications of metabolic syndrome, namely diabetes mellitus, at an earlier age. We sought to better understand the epidemiology of metabolic syndrome in Hispanic women using data from a large, community-based health screening program. Using data from the <span class="hlt">Sister</span> to <span class="hlt">Sister</span>: The Women's Heart Health Foundation community health fairs from 2008 to 2009 held in 17 U.S. cities, we sought to characterize how cardiometabolic risk profiles vary across age for women by race and ethnicity. Metabolic syndrome was defined using the updated National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines, which included three or more of the following: Waist circumference ≥35 inches, triglycerides ≥150 mg/dL, high-density lipoprotein (HDL) <50 mg/dL, systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥85 mmHg, or a fasting glucose ≥100 mg/dL. A total of 6843 community women were included in the analyses. Metabolic syndrome had a prevalence of 35%. The risk-adjusted odds ratio for metabolic syndrome in Hispanic women versus white women was 1.7 (95% confidence interval, 1.4, 2.0). Dyslipidemia was the strongest predictor of metabolic syndrome among Hispanic women. This disparity appeared most pronounced for younger women. Additional predictors of metabolic syndrome included black race, increasing age, and smoking. In a large, nationally representative sample of women, we found that metabolic syndrome was highly prevalent among young Hispanic women. Efforts specifically targeted to identifying these high-risk women are necessary to prevent the cardiovascular morbidity and mortality associated with metabolic syndrome.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-340.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-340.pdf"><span>20 CFR 410.340 - Determination of relationship; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false Determination of relationship; parent, brother, or <span class="hlt">sister</span>. 410.340 Section 410.340 Employees' Benefits SOCIAL SECURITY ADMINISTRATION FEDERAL COAL MINE HEALTH AND SAFETY ACT OF 1969, TITLE IV-BLACK LUNG BENEFITS (1969- ) Relationship and...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3659383','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3659383"><span>Narcolepsy with Cataplexy Mimicry: The Strange Case of Two <span class="hlt">Sisters</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Pizza, Fabio; Vandi, Stefano; Poli, Francesca; Moghadam, Keivan Kaveh; Franceschini, Christian; Bellucci, Claudia; Cipolli, Carlo; Ingravallo, Francesca; Natalini, Giuliana; Mignot, Emmanuel; Plazzi, Giuseppe</p> <p>2013-01-01</p> <p>We report on two <span class="hlt">sisters</span>, 17 and 12 years of age, with clinical features suggesting narcolepsy with cataplexy (NC): daytime sleepiness, spontaneous and emotionally triggered sudden falls to the ground, and overweight/obesity. MSLT showed borderline sleep latency, with 1 and 0 sleep onset REM periods. HLA typing disclosed the DQB1*0602 allele. Video-polygraphy of the spells ruled out NC diagnosis by demonstrating their easy elicitation by suggestion, with wake EEG, electromyo-graphic persistence of muscle tone, and stable presence of tendon reflexes (i.e., pseudo-cataplexy), together with normal cerebrospinal hypocretin-1 levels. Our cases emphasize the need of a clear depiction of cataplexy pattern at the different ages, the usefulness of examining ictal neurophysiology, and collecting all available disease markers in ambiguous cases. Citation: Pizza F; Vandi S; Poli F; Moghadam KK; Fran-ceschini C; Bellucci C; Cipolli C; Ingravallo F; Natalini G; Mignot E; Plazzi G. Narcolepsy with cataplexy mimicry: the strange case of two <span class="hlt">sisters</span>. J Clin Sleep Med 2013;9(6):611-612. PMID:23772196</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20192393','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20192393"><span><span class="hlt">Aberration</span> of a negative ion beam caused by space charge effect.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Miyamoto, K; Wada, S; Hatayama, A</p> <p>2010-02-01</p> <p><span class="hlt">Aberrations</span> are inevitable when the charged particle beams are extracted, accelerated, transmitted, and focused with electrostatic and magnetic fields. In this study, we investigate the <span class="hlt">aberration</span> of a negative ion accelerator for a neutral beam injector theoretically, especially the spherical <span class="hlt">aberration</span> caused by the negative ion beam expansion due to the space charge effect. The negative ion current density profiles with the spherical <span class="hlt">aberration</span> are compared with those without the spherical <span class="hlt">aberration</span>. It is found that the negative ion current density profiles in a log scale are tailed due to the spherical <span class="hlt">aberration</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29880909','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29880909"><span>Phylogenetic conservatism of thermal traits explains dispersal limitation and genomic differentiation of Streptomyces <span class="hlt">sister</span>-taxa.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Choudoir, Mallory J; Buckley, Daniel H</p> <p>2018-06-07</p> <p>The latitudinal diversity gradient is a pattern of biogeography observed broadly in plants and animals but largely undocumented in terrestrial microbial systems. Although patterns of microbial biogeography across broad taxonomic scales have been described in a range of contexts, the mechanisms that generate biogeographic patterns between closely related taxa remain incompletely characterized. Adaptive processes are a major driver of microbial biogeography, but there is less understanding of how microbial biogeography and diversification are shaped by dispersal limitation and drift. We recently described a latitudinal diversity gradient of species richness and intraspecific genetic diversity in Streptomyces by using a geographically explicit culture collection. Within this geographically explicit culture collection, we have identified Streptomyces <span class="hlt">sister</span>-taxa whose geographic distribution is delimited by latitude. These <span class="hlt">sister</span>-taxa differ in geographic distribution, genomic diversity, and ecological traits despite having nearly identical SSU rRNA gene sequences. Comparative genomic analysis reveals genomic differentiation of these <span class="hlt">sister</span>-taxa consistent with restricted gene flow across latitude. Furthermore, we show phylogenetic conservatism of thermal traits between the <span class="hlt">sister</span>-taxa suggesting that thermal trait adaptation limits dispersal and gene flow across climate regimes as defined by latitude. Such phylogenetic conservatism of thermal traits is commonly associated with latitudinal diversity gradients for plants and animals. These data provide further support for the hypothesis that the Streptomyces latitudinal diversity gradient was formed as a result of historical demographic processes defined by dispersal limitation and driven by paleoclimate dynamics.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED434287.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED434287.pdf"><span>The Effectiveness of Mentoring for Adolescent Mothers and Their Infants: A Comparative Study between <span class="hlt">Sister</span> Friend and Cal Learn.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Tebb, Kathleen P.</p> <p></p> <p>This study evaluated <span class="hlt">Sister</span> Friend, a mentoring program in Yolo County, California, serving low-income adolescent mothers and their infants. The primary objective was to determine if participating in the <span class="hlt">Sister</span> Friend program improved the adolescent mother's parenting class attendance, the home environment, parenting behavior, and child…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22344018','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22344018"><span><span class="hlt">Aberrant</span> regeneration of the third cranial nerve.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Shrestha, U D; Adhikari, S</p> <p>2012-01-01</p> <p><span class="hlt">Aberrant</span> regeneration of the third cranial nerve is most commonly due to its damage by trauma. A ten-month old child presented with the history of a fall from a four-storey building. She developed traumatic third nerve palsy and eventually the clinical features of <span class="hlt">aberrant</span> regeneration of the third cranial nerve. The adduction of the eye improved over time. She was advised for patching for the strabismic amblyopia as well. Traumatic third nerve palsy may result in <span class="hlt">aberrant</span> regeneration of the third cranial nerve. In younger patients, motility of the eye in different gazes may improve over time. © NEPjOPH.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29331234','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29331234"><span>Metabolic syndrome, hypertension, and hyperlipidemia in mothers, fathers, <span class="hlt">sisters</span>, and brothers of women with polycystic ovary syndrome: a systematic review and meta-analysis.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yilmaz, Bulent; Vellanki, Priyathama; Ata, Baris; Yildiz, Bulent Okan</p> <p>2018-02-01</p> <p>To provide an evidence-based assessment of metabolic syndrome, hypertension, and hyperlipidemia in first-degree relatives of women with polycystic ovary syndrome (PCOS). Systematic review and meta-analysis. Not applicable. Mothers, fathers, <span class="hlt">sisters</span>, and brothers of women with and without PCOS. An electronic-based search with the use of PubMed from 1960 to June 2015 and cross-checked references of relevant articles. Metabolic syndrome, hypertension and dyslipidemia, and surrogate markers, including systolic blood pressure (BP), diastolic BP, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. Fourteen of 3,346 studies were included in the meta-analysis. Prevalence of the following was significantly increased in relatives of women with PCOS: metabolic syndrome (risk ratio [RR] 1.78 [95% confidence interval 1.37, 2.30] in mothers, 1.43 [1.12, 1.81] in fathers, and 1.50 [1.12, 2.00] in <span class="hlt">sisters</span>), hypertension (RR 1.93 [1.58, 2.35] in fathers, 2.92 [1.92, 4.45] in <span class="hlt">sisters</span>), and dyslipidemia (RR 3.86 [2.54, 5.85] in brothers and 1.29 [1.11, 1.50] in fathers). Moreover, systolic BP (mothers, <span class="hlt">sisters</span>, and brothers), total cholesterol (mothers and <span class="hlt">sisters</span>), low-density lipoprotein cholesterol (<span class="hlt">sisters</span>), and triglycerides (mothers and <span class="hlt">sisters</span>) were significantly higher in first-degree relatives of PCOS probands than in controls. Our results show evidence of clustering for metabolic syndrome, hypertension, and dyslipidemia in mothers, fathers, <span class="hlt">sisters</span>, and brothers of women with PCOS. PROSPERO 2016 CRD42016048557. Copyright © 2017 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15222313','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15222313"><span>The use of convent archival records in medical research: the School <span class="hlt">Sisters</span> of Notre Dame archives and the nun study.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Patzwald, Gari-Anne; Wildt, Sister Carol Marie</p> <p>2004-01-01</p> <p>The School <span class="hlt">Sisters</span> of Notre Dame (SSND) archives program in a cooperative system for the arrangement and preservation of the records of the SSND provinces in North America, including records of individual <span class="hlt">sisters</span>. Archival records include autobiographies, school and college transcripts, employment histories, and family socioeconomic data. The Nun Study, a longitudinal study of Alzheimer's disease and aging in 678 SSND <span class="hlt">sisters</span>, compares data extracted from these records with data on late-life cognitive and physical function and postmortem brain neuropathology to explore early life factor that may affect late-life cognitive function and longevity.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=incest&id=EJ1011495','ERIC'); return false;" href="https://eric.ed.gov/?q=incest&id=EJ1011495"><span>Brother-<span class="hlt">Sister</span> Incest: Data from Anonymous Computer-Assisted Self Interviews</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Stroebel, Sandra S.; O'Keefe, Stephen L.; Beard, Keith W.; Kuo, Shih-Ya; Swindell, Samuel; Stroupe, Walter</p> <p>2013-01-01</p> <p>Retrospective data were entered anonymously by 1,521 adult women using computer-assisted self interview. Forty were classified as victims of brother-<span class="hlt">sister</span> incest, 19 were classified as victims of father-daughter incest, and 232 were classified as victims of sexual abuse by an adult other than their father before reaching 18 years of age. The…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4531603','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4531603"><span>Hydronephrosis by an <span class="hlt">Aberrant</span> Renal Artery: A Case Report</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Park, Byoung Seok; Jeong, Taek Kyun; Ma, Seong Kwon; Kim, Soo Wan; Kim, Nam Ho; Choi, Ki Chul; Jeong, Yong Yeon</p> <p>2003-01-01</p> <p>Ureteropelvic junction obstruction is usually intrinsic and is most common in children. <span class="hlt">Aberrant</span> renal arteries are present in about 30% of individuals. <span class="hlt">Aberrant</span> renal arteries to the inferior pole cross anteriorly to the ureter and may cause hydronephrosis. To the best of our knowledge, although there are some papers about <span class="hlt">aberrant</span> renal arteries producing ureteropelvic junction obstruction, there is no report of a case which is diagnosed by the new modalities, such as computed tomography angiogram (CTA) or magnetic resonance angiogram (MRA). We describe a 36-year-old woman with right hydronephrosis. Kidney ultrasonogram and excretory urogram revealed right hydronephrosis. CTA and MRA clearly displayed an <span class="hlt">aberrant</span> renal artery and hydronephrosis. The patient underwent surgical exploration. For the evaluation of hydronephrosis by an <span class="hlt">aberrant</span> renal artery, use of CTA and MRA is advocated. PMID:12760271</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=moral+AND+enhancement&id=EJ755531','ERIC'); return false;" href="https://eric.ed.gov/?q=moral+AND+enhancement&id=EJ755531"><span>Meanings of Sisterhood and Developmental Disability: Narratives from White Nondisabled <span class="hlt">Sisters</span></span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>McGraw, Lori A.; Walker, Alexis J.</p> <p>2007-01-01</p> <p>Integrating thought from critical feminist and disability theorists via a strategic social constructionist perspective, the authors analyzed 10 in-depth qualitative interviews to begin to understand the dialogue between (a) how nondisabled <span class="hlt">sisters</span> understand themselves and their siblings with developmental disabilities and (b) wider systems of…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25288226','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25288226"><span>Ocular higher-order <span class="hlt">aberrations</span> in a school children population.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Papamastorakis, George; Panagopoulou, Sophia; Tsilimbaris, Militadis K; Pallikaris, Ioannis G; Plainis, Sotiris</p> <p>2015-01-01</p> <p>The primary objective of the study was to explore the statistics of ocular higher-order <span class="hlt">aberrations</span> in a population of primary and secondary school children. A sample of 557 children aged 10-15 years were selected from two primary and two secondary schools in Heraklion, Greece. Children were classified by age in three subgroups: group I (10.7±0.5 years), group II (12.4±0.5 years) and group III (14.5±0.5 years). Ocular <span class="hlt">aberrations</span> were measured using a wavefront aberrometer (COAS, AMO Wavefront Sciences, USA) at mesopic light levels (illuminance at cornea was 4lux). Wavefront analysis was achieved for a 5mm pupil. Statistical analysis was carried out for the right eye only. The average coefficient of most high-order <span class="hlt">aberrations</span> did not differ from zero with the exception of vertical (0.076μm) and horizontal (0.018μm) coma, oblique trefoil (-0.055μm) and spherical <span class="hlt">aberration</span> (0.018μm). The most prominent change between the three groups was observed for the spherical <span class="hlt">aberration</span>, which increased from 0.007μm (SE 0.005) in group I to 0.011μm (SE 0.004) in group II and 0.030μm (SE 0.004) in group III. Significant differences were also found for the oblique astigmatism and the third-order coma <span class="hlt">aberrations</span>. Differences in the low levels of ocular spherical <span class="hlt">aberration</span> in young children possibly reflect differences in lenticular spherical <span class="hlt">aberration</span> and relate to the gradient refractive index of the lens. The evaluation of spherical <span class="hlt">aberration</span> at certain stages of eye growth may help to better understand the underlying mechanisms of myopia development. Copyright © 2014 Spanish General Council of Optometry. Published by Elsevier Espana. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4401828','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4401828"><span>Ocular higher-order <span class="hlt">aberrations</span> in a school children population</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Papamastorakis, George; Panagopoulou, Sophia; Tsilimbaris, Militadis K.; Pallikaris, Ioannis G.; Plainis, Sotiris</p> <p>2014-01-01</p> <p>Purpose The primary objective of the study was to explore the statistics of ocular higher-order <span class="hlt">aberrations</span> in a population of primary and secondary school children. Methods A sample of 557 children aged 10–15 years were selected from two primary and two secondary schools in Heraklion, Greece. Children were classified by age in three subgroups: group I (10.7 ± 0.5 years), group II (12.4 ± 0.5 years) and group III (14.5 ± 0.5 years). Ocular <span class="hlt">aberrations</span> were measured using a wavefront aberrometer (COAS, AMO Wavefront Sciences, USA) at mesopic light levels (illuminance at cornea was 4 lux). Wavefront analysis was achieved for a 5 mm pupil. Statistical analysis was carried out for the right eye only. Results The average coefficient of most high-order <span class="hlt">aberrations</span> did not differ from zero with the exception of vertical (0.076 μm) and horizontal (0.018 μm) coma, oblique trefoil (−0.055 μm) and spherical <span class="hlt">aberration</span> (0.018 μm). The most prominent change between the three groups was observed for the spherical <span class="hlt">aberration</span>, which increased from 0.007 μm (SE 0.005) in group I to 0.011 μm (SE 0.004) in group II and 0.030 μm (SE 0.004) in group III. Significant differences were also found for the oblique astigmatism and the third-order coma <span class="hlt">aberrations</span>. Conclusions Differences in the low levels of ocular spherical <span class="hlt">aberration</span> in young children possibly reflect differences in lenticular spherical <span class="hlt">aberration</span> and relate to the gradient refractive index of the lens. The evaluation of spherical <span class="hlt">aberration</span> at certain stages of eye growth may help to better understand the underlying mechanisms of myopia development. PMID:25288226</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li class="active"><span>21</span></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_21 --> <div id="page_22" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li class="active"><span>22</span></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="421"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/servlets/purl/15016780','SCIGOV-STC'); return false;" href="https://www.osti.gov/servlets/purl/15016780"><span>Generalized Alvarez lens for correction of laser <span class="hlt">aberrations</span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>LaFortune, K N</p> <p>2004-12-02</p> <p>The Alvarez lens (US Patent No. 3,305,294 [1]) is a compact <span class="hlt">aberration</span> corrector. The original design emphasized in the patent consists of a pair of adjacent optical elements that provide a variable focus. A lens system with a variable effective focal length is nothing new. Such systems are widely used in cameras, for example. It is the compactness and simplicity of operation that is the key advantage of the Alvarez lens. All of the complexity is folded into the design and fabrication of the optical elements. As mentioned in the Alvarez patent [1] and elaborated upon in Palusinski et al.more » [2], if one is willing to fold even more complexity into the optical elements, it is possible to correct higher-order <span class="hlt">aberrations</span> as well. There is no theoretical limit to the number or degree of wavefront distortions that can be corrected. The only limitation is that there must be a fixed relative magnitude of the <span class="hlt">aberrations</span>. Independent correction of each component of the higher-order <span class="hlt">aberrations</span> can not be performed without additional elements and degrees of freedom [3]. Under some circumstances, coupling may be observed between different <span class="hlt">aberrations</span>. This can be mitigated with the appropriate choice of design parameters. New methods are available today that increase the practicality of making higher-order <span class="hlt">aberration</span> correctors [4,5,6].« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/16048187','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/16048187"><span>Statistical estimation of ultrasonic propagation path parameters for <span class="hlt">aberration</span> correction.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Waag, Robert C; Astheimer, Jeffrey P</p> <p>2005-05-01</p> <p>Parameters in a linear filter model for ultrasonic propagation are found using statistical estimation. The model uses an inhomogeneous-medium Green's function that is decomposed into a homogeneous-transmission term and a path-dependent <span class="hlt">aberration</span> term. Power and cross-power spectra of random-medium scattering are estimated over the frequency band of the transmit-receive system by using closely situated scattering volumes. The frequency-domain magnitude of the <span class="hlt">aberration</span> is obtained from a normalization of the power spectrum. The corresponding phase is reconstructed from cross-power spectra of subaperture signals at adjacent receive positions by a recursion. The subapertures constrain the receive sensitivity pattern to eliminate measurement system phase contributions. The recursion uses a Laplacian-based algorithm to obtain phase from phase differences. Pulse-echo waveforms were acquired from a point reflector and a tissue-like scattering phantom through a tissue-mimicking <span class="hlt">aberration</span> path from neighboring volumes having essentially the same <span class="hlt">aberration</span> path. Propagation path <span class="hlt">aberration</span> parameters calculated from the measurements of random scattering through the <span class="hlt">aberration</span> phantom agree with corresponding parameters calculated for the same <span class="hlt">aberrator</span> and array position by using echoes from the point reflector. The results indicate the approach describes, in addition to time shifts, waveform amplitude and shape changes produced by propagation through distributed <span class="hlt">aberration</span> under realistic conditions.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title20-vol2/pdf/CFR-2011-title20-vol2-sec410-380.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title20-vol2/pdf/CFR-2011-title20-vol2-sec410-380.pdf"><span>20 CFR 410.380 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-04-01</p> <p>... 20 Employees' Benefits 2 2011-04-01 2011-04-01 false Determination of dependency; parent, brother... MINE HEALTH AND SAFETY ACT OF 1969, TITLE IV-BLACK LUNG BENEFITS (1969- ) Relationship and Dependency § 410.380 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner's...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-380.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-380.pdf"><span>20 CFR 410.380 - Determination of dependency; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false Determination of dependency; parent, brother... MINE HEALTH AND SAFETY ACT OF 1969, TITLE IV-BLACK LUNG BENEFITS (1969- ) Relationship and Dependency § 410.380 Determination of dependency; parent, brother, or <span class="hlt">sister</span>. An individual who is the miner's...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-214.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title20-vol2/pdf/CFR-2010-title20-vol2-sec410-214.pdf"><span>20 CFR 410.214 - Conditions of entitlement; parent, brother, or <span class="hlt">sister</span>.</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-04-01</p> <p>... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false Conditions of entitlement; parent, brother...; Duration of Entitlement; Filing of Claims and Evidence § 410.214 Conditions of entitlement; parent, brother, or <span class="hlt">sister</span>. An individual is entitled to benefits if: (a) Such individual: (1) Is the parent, brother...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29792816','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29792816"><span>The Physics of the Metaphase Spindle.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Oriola, David; Needleman, Daniel J; Brugués, Jan</p> <p>2018-05-20</p> <p>The assembly of the mitotic spindle and the subsequent segregation of <span class="hlt">sister</span> <span class="hlt">chromatids</span> are based on the self-organized action of microtubule filaments, motor proteins, and other microtubule-associated proteins, which constitute the fundamental force-generating elements in the system. Many of the components in the spindle have been identified, but until recently it remained unclear how their collective behaviors resulted in such a robust bipolar structure. Here, we review the current understanding of the physics of the metaphase spindle that is only now starting to emerge.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7188765','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7188765"><span>Sjögren-Larsson syndrome in dizygous twin <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>David, T J</p> <p>1980-01-01</p> <p>Two dizygous twin <span class="hlt">sisters</span> with the Sjögren-Larsson syndrome are described. There was parental consanguinity, and the condition is inherited as an autosomal recessive. The main features are mental retardation, spastic diplegia and ichthyosis. Sensory defects of gums and abnormal facial movements were found in the twins, these being recognised features of the syndrome. It is suggested that the condition may be due to an abnormality of the neural crest.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23285752','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23285752"><span>[Effects of oil-refining microbes (genus Acinetobacter) on cytogenetical structures of human lymphocytes in cell cultures].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Il'inskikh, N N; Il'inskikh, E N; Il'inskikh, I N</p> <p>2012-01-01</p> <p>The objective of this study was to assess ability of oil-refining bacteria Acinetobacter calcoaceticus and A. valentis to induce karyopathological abnormalities and chromosomal <span class="hlt">aberrations</span> in human lymphocyte cultures. It was found that the cultures infected with A. calcoaceticus showed significantly high frequencies of cytogenetical effects and chromosomal <span class="hlt">aberrant</span> cells as compared to the intact cultures and cultures infected with A. valentis. The most of chromosomal <span class="hlt">aberrations</span>, mainly <span class="hlt">chromatid</span> <span class="hlt">aberrations</span>, were located in 1 and 2 chromosomes. Moreover, the <span class="hlt">aberrations</span> were detected in some specific chromosome areas. Abnormalities of mitotic cell division and nucleus morphology were determined in lymphocyte cultures infected with A. calcoaceticus. There were found significantly high frequencies of cells with micronuclei, nucleus protrusions, anaphase or metaphase chromosome and chromosomal fragments lagging as well as multipolar and C-mitoses. Thus, the oil-refining bacteria A. calcoaceticus in contrast to A. valentis demonstrated strong genotoxic effects in human lymphocyte cultures in vitro.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4752329','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4752329"><span>Chromosome Synapsis Alleviates Mek1-Dependent Suppression of Meiotic DNA Repair</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Subramanian, Vijayalakshmi V.; MacQueen, Amy J.; Vader, Gerben; Shinohara, Miki; Sanchez, Aurore; Borde, Valérie; Shinohara, Akira; Hochwagen, Andreas</p> <p>2016-01-01</p> <p>Faithful meiotic chromosome segregation and fertility require meiotic recombination between homologous chromosomes rather than the equally available <span class="hlt">sister</span> <span class="hlt">chromatid</span>, a bias that in Saccharomyces cerevisiae depends on the meiotic kinase, Mek1. Mek1 is thought to mediate repair template bias by specifically suppressing <span class="hlt">sister</span>-directed repair. Instead, we found that when Mek1 persists on closely paired (synapsed) homologues, DNA repair is severely delayed, suggesting that Mek1 suppresses any proximal repair template. Accordingly, Mek1 is excluded from synapsed homologues in wild-type cells. Exclusion requires the AAA+-ATPase Pch2 and is directly coupled to synaptonemal complex assembly. Stage-specific depletion experiments further demonstrate that DNA repair in the context of synapsed homologues requires Rad54, a repair factor inhibited by Mek1. These data indicate that the <span class="hlt">sister</span> template is distinguished from the homologue primarily by its closer proximity to inhibitory Mek1 activity. We propose that once pairing or synapsis juxtaposes homologues, exclusion of Mek1 is necessary to avoid suppression of all templates and accelerate repair progression. PMID:26870961</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2008ChPhL..25.1309Z','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2008ChPhL..25.1309Z"><span>Influence of Misalignment on High-Order <span class="hlt">Aberration</span> Correction for Normal Human Eyes</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Zhao, Hao-Xin; Xu, Bing; Xue, Li-Xia; Dai, Yun; Liu, Qian; Rao, Xue-Jun</p> <p>2008-04-01</p> <p>Although a compensation device can correct <span class="hlt">aberrations</span> of human eyes, the effect will be degraded by its misalignment, especially for high-order <span class="hlt">aberration</span> correction. We calculate the positioning tolerance of correction device for high-order <span class="hlt">aberrations</span>, and within what degree the correcting effect is better than low-order <span class="hlt">aberration</span> (defocus and astigmatism) correction. With fixed certain misalignment within the positioning tolerance, we calculate the residual wavefront rms <span class="hlt">aberration</span> of the first-6 to first-35 terms along with the 3rd-5th terms of <span class="hlt">aberrations</span> corrected, and the combined first-13 terms of <span class="hlt">aberrations</span> are also studied under the same quantity of misalignment. However, the correction effect of high-order <span class="hlt">aberrations</span> does not meliorate along with the increase of the high-order terms under some misalignment, moreover, some simple combined terms correction can achieve similar result as complex combinations. These results suggest that it is unnecessary to correct too much the terms of high-order <span class="hlt">aberrations</span> which are difficult to accomplish in practice, and gives confidence to correct high-order <span class="hlt">aberrations</span> out of the laboratory.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/servlets/purl/873174','DOE-PATENT-XML'); return false;" href="https://www.osti.gov/servlets/purl/873174"><span>Determining orientation and direction of DNA sequences</span></a></p> <p><a target="_blank" href="http://www.osti.gov/doepatents">DOEpatents</a></p> <p>Goodwin, Edwin H.; Meyne, Julianne</p> <p>2000-01-01</p> <p>Determining orientation and direction of DNA sequences. A method by which fluorescence in situ hybridization can be made strand specific is described. Cell cultures are grown in a medium containing a halogenated nucleotide. The analog is partially incorporated in one DNA strand of each <span class="hlt">chromatid</span>. This substitution takes place in opposite strands of the two <span class="hlt">sister</span> <span class="hlt">chromatids</span>. After staining with the fluorescent DNA-binding dye Hoechst 33258, cells are exposed to long-wavelength ultraviolet light which results in numerous strand nicks. These nicks enable the substituted strand to be denatured and solubilized by heat, treatment with high or low pH aqueous solutions, or by immersing the strands in 2.times.SSC (0.3M NaCl+0.03M sodium citrate), to name three procedures. It is unnecessary to enzymatically digest the strands using Exo III or another exonuclease in order to excise and solubilize nucleotides starting at the sites of the nicks. The denaturing/solubilizing process removes most of the substituted strand while leaving the prereplication strand largely intact. Hybridization of a single-stranded probe of a tandem repeat arranged in a head-to-tail orientation will result in hybridization only to the <span class="hlt">chromatid</span> with the complementary strand present.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/21173827','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/21173827"><span>Orthonormal <span class="hlt">aberration</span> polynomials for anamorphic optical imaging systems with rectangular pupils.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mahajan, Virendra N</p> <p>2010-12-20</p> <p>The classical <span class="hlt">aberrations</span> of an anamorphic optical imaging system, representing the terms of a power-series expansion of its <span class="hlt">aberration</span> function, are separable in the Cartesian coordinates of a point on its pupil. We discuss the balancing of a classical <span class="hlt">aberration</span> of a certain order with one or more such <span class="hlt">aberrations</span> of lower order to minimize its variance across a rectangular pupil of such a system. We show that the balanced <span class="hlt">aberrations</span> are the products of two Legendre polynomials, one for each of the two Cartesian coordinates of the pupil point. The compound Legendre polynomials are orthogonal across a rectangular pupil and, like the classical <span class="hlt">aberrations</span>, are inherently separable in the Cartesian coordinates of the pupil point. They are different from the balanced <span class="hlt">aberrations</span> and the corresponding orthogonal polynomials for a system with rotational symmetry but a rectangular pupil.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=values+AND+school+AND+hidden+AND+curriculum&pg=5&id=EJ546582','ERIC'); return false;" href="https://eric.ed.gov/?q=values+AND+school+AND+hidden+AND+curriculum&pg=5&id=EJ546582"><span>Empowerment, Participation, and Democracy? -- The Hong Kong Big <span class="hlt">Sisters</span>' Guidance Programme.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Bottery, Mike; Siu, Shun-Mei</p> <p>1996-01-01</p> <p>Asserts that the Big <span class="hlt">Sisters</span> Programme in Hong Kong provides a good example of a scheme that transcends personal and school issues and facilitates a more participative and democratic view of society. Characterizes the program as a benign form of a "hidden curriculum" and recommends establishing it in secondary schools. (MJP)</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=human+AND+resource+AND+management+AND+diversity&pg=6&id=EJ604478','ERIC'); return false;" href="https://eric.ed.gov/?q=human+AND+resource+AND+management+AND+diversity&pg=6&id=EJ604478"><span>"Brothers and <span class="hlt">Sisters</span>": A Novel Way to Teach Human Resources Management.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Bumpus, Minnette</p> <p>2000-01-01</p> <p>The novel "Brothers and <span class="hlt">Sisters</span>" by Bebe Moore Campbell was used in a management course to explore human resource management issues, concepts, and theories. The course included prereading and postreading surveys, lecture, book review, and examination. Most of the students (92%) felt the novel was an appropriate way to meet course…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=Healthy+AND+organization&pg=2&id=EJ1150329','ERIC'); return false;" href="https://eric.ed.gov/?q=Healthy+AND+organization&pg=2&id=EJ1150329"><span>Exploring Undergraduate Black Womyn's Motivations for Engaging in "<span class="hlt">Sister</span> Circle" Organizations</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Croom, Natasha N.; Beatty, Cameron C.; Acker, Lorraine D.; Butler, Malika</p> <p>2017-01-01</p> <p>The purpose of this critical qualitative inquiry was to explore what motivated undergraduate Black womyn (UBW) to engage in "<span class="hlt">Sister</span> Circle"-type student organizations--or groups that center race and gender. Using a critical race feminist theoretical lens, data were collected through a combination of one-on-one interviews and focus…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3374303','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3374303"><span>The Centenary of Janssens’s Chiasmatype Theory</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Koszul, Romain; Meselson, Matthew; Van Doninck, Karine; Vandenhaute, Jean; Zickler, Denise</p> <p>2012-01-01</p> <p>The segregation and random assortment of characters observed by Mendel have their basis in the behavior of chromosomes in meiosis. But showing this actually to be the case requires a correct understanding of the meiotic behavior of chromosomes. This was achieved only gradually, over several decades, with much dispute and confusion along the way. One crucial step in the understanding of meiosis was provided in 1909 by Frans Alfons Janssens who published in La Cellule an article entitled “La théorie de la Chiasmatypie. Nouvelle interprétation des cinèses de maturation,” which contains the first description of the chiasma structure. He observed that, of the four <span class="hlt">chromatids</span> present at the connection sites (chiasmata sites) at diplotene or anaphase of the first meiotic division, two crossed each other and two did not. He therefore postulated that the maternal and paternal <span class="hlt">chromatids</span> that crossed penetrated the other until they broke and rejoined in maternal and paternal segments new ways; the other two <span class="hlt">chromatids</span> remained free and thus intact. This allowed him also to propose that the <span class="hlt">chromatids</span> distributed in the four nuclei issued from the second meiotic division had various combinations of maternal and paternal segments of each chromosome. And conversely, permitted the appreciation that the laws of Mendelian segregation required breakage and joining (crossing over) between homologous non-<span class="hlt">sister</span> <span class="hlt">chromatids</span>. Although Janssens’s article found a broad appreciative audience and had a large influence on the chromosomal theory at that time, his theory was resisted by both geneticists and cytologists for several decades. This Perspectives aims to highlight the novelty of Janssens’s chiasmatype theory by examining the historical background and our actual understanding of meiotic recombination. PMID:22701050</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25401809','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25401809"><span>Theory of <span class="hlt">aberration</span> fields for general optical systems with freeform surfaces.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fuerschbach, Kyle; Rolland, Jannick P; Thompson, Kevin P</p> <p>2014-11-03</p> <p>This paper utilizes the framework of nodal <span class="hlt">aberration</span> theory to describe the <span class="hlt">aberration</span> field behavior that emerges in optical systems with freeform optical surfaces, particularly φ-polynomial surfaces, including Zernike polynomial surfaces, that lie anywhere in the optical system. If the freeform surface is located at the stop or pupil, the net <span class="hlt">aberration</span> contribution of the freeform surface is field constant. As the freeform optical surface is displaced longitudinally away from the stop or pupil of the optical system, the net <span class="hlt">aberration</span> contribution becomes field dependent. It is demonstrated that there are no new <span class="hlt">aberration</span> types when describing the <span class="hlt">aberration</span> fields that arise with the introduction of freeform optical surfaces. Significantly it is shown that the <span class="hlt">aberration</span> fields that emerge with the inclusion of freeform surfaces in an optical system are exactly those that have been described by nodal <span class="hlt">aberration</span> theory for tilted and decentered optical systems. The key contribution here lies in establishing the field dependence and nodal behavior of each freeform term that is essential knowledge for effective application to optical system design. With this development, the nodes that are distributed throughout the field of view for each <span class="hlt">aberration</span> type can be anticipated and targeted during optimization for the correction or control of the <span class="hlt">aberrations</span> in an optical system with freeform surfaces. This work does not place any symmetry constraints on the optical system, which could be packaged in a fully three dimensional geometry, without fold mirrors.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4382745','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4382745"><span>Meiosis and Maternal Aging: Insights from Aneuploid Oocytes and Trisomy Births</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Herbert, Mary; Kalleas, Dimitrios; Cooney, Daniel; Lamb, Mahdi; Lister, Lisa</p> <p>2015-01-01</p> <p>In most organisms, genome haploidization requires reciprocal DNA exchanges (crossovers) between replicated parental homologs to form bivalent chromosomes. These are resolved to their four constituent <span class="hlt">chromatids</span> during two meiotic divisions. In female mammals, bivalents are formed during fetal life and remain intact until shortly before ovulation. Extending this period beyond ∼35 years greatly increases the risk of aneuploidy in human oocytes, resulting in a dramatic increase in infertility, miscarriage, and birth defects, most notably trisomy 21. Bivalent chromosomes are stabilized by cohesion between <span class="hlt">sister</span> <span class="hlt">chromatids</span>, which is mediated by the cohesin complex. In mouse oocytes, cohesin becomes depleted from chromosomes during female aging. Consistent with this, premature loss of centromeric cohesion is a major source of aneuploidy in oocytes from older women. Here, we propose a mechanistic framework to reconcile data from genetic studies on human trisomy and oocytes with recent advances in our understanding of the molecular mechanisms of chromosome segregation during meiosis in model organisms. PMID:25833844</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2018SPIE10620E..0CX','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2018SPIE10620E..0CX"><span>Image based method for <span class="hlt">aberration</span> measurement of lithographic tools</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Xu, Shuang; Tao, Bo; Guo, Yongxing; Li, Gongfa</p> <p>2018-01-01</p> <p>Information of lens <span class="hlt">aberration</span> of lithographic tools is important as it directly affects the intensity distribution in the image plane. Zernike polynomials are commonly used for a mathematical description of lens <span class="hlt">aberrations</span>. Due to the advantage of lower cost and easier implementation of tools, image based measurement techniques have been widely used. Lithographic tools are typically partially coherent systems that can be described by a bilinear model, which entails time consuming calculations and does not lend a simple and intuitive relationship between lens <span class="hlt">aberrations</span> and the resulted images. Previous methods for retrieving lens <span class="hlt">aberrations</span> in such partially coherent systems involve through-focus image measurements and time-consuming iterative algorithms. In this work, we propose a method for <span class="hlt">aberration</span> measurement in lithographic tools, which only requires measuring two images of intensity distribution. Two linear formulations are derived in matrix forms that directly relate the measured images to the unknown Zernike coefficients. Consequently, an efficient non-iterative solution is obtained.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5030025','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=5030025"><span>Minimum change in spherical <span class="hlt">aberration</span> that can be perceived</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Manzanera, Silvestre; Artal, Pablo</p> <p>2016-01-01</p> <p>It is important to know the visual sensitivity to optical blur from both a basic science perspective and a practical point of view. Of particular interest is the sensitivity to blur induced by spherical <span class="hlt">aberration</span> because it is being used to increase depth of focus as a component of a presbyopic solution. Using a flicker detection-based procedure implemented on an adaptive optics visual simulator, we measured the spherical <span class="hlt">aberration</span> thresholds that produce just-noticeable differences in perceived image quality. The thresholds were measured for positive and negative values of spherical <span class="hlt">aberration</span>, for best focus and + 0.5 D and + 1.0 D of defocus. At best focus, the SA thresholds were 0.20 ± 0.01 µm and −0.17 ± 0.03 µm for positive and negative spherical <span class="hlt">aberration</span> respectively (referred to a 6-mm pupil). These experimental values may be useful in setting spherical <span class="hlt">aberration</span> permissible levels in different ophthalmic techniques. PMID:27699113</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li class="active"><span>22</span></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_22 --> <div id="page_23" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li class="active"><span>23</span></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="441"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2010SPIE.7550E..2DB','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2010SPIE.7550E..2DB"><span>Surface geometry and optical <span class="hlt">aberrations</span> of ex-vivo crystalline lenses</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Bueno, Juan M.; Schwarz, Christina; Acosta, Eva; Artal, Pablo</p> <p>2010-02-01</p> <p>The shape of the surfaces of ex-vivo human crystalline lenses was measured using a shadow photography technique. From these data, the back-focal distance and the contribution of each surface to the main optical <span class="hlt">aberrations</span> of the lenses were estimated. The <span class="hlt">aberrations</span> of the lenses were measured separately with two complementary techniques: a Hartmann-Shack wavefront sensor and a point-diffraction interferometer. A laser scanning set-up was also used to measure the actual back-focal length as well as the phase <span class="hlt">aberration</span> in one meridian section of the lenses. Measured and predicted back-focal length agreed well within the experimental errors. The lens <span class="hlt">aberrations</span> computed with a ray-tracing approach from the measured surfaces and geometrical data only reproduce quantitatively the measured <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22611995','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22611995"><span>[The work of Moscow communities of <span class="hlt">Sisters</span> of Charity in own medical institutions].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zorin, K V</p> <p>2011-01-01</p> <p>The article analyses the medical activities of Moscow communities of <span class="hlt">Sisters</span> of Charity in curative and educational institutions organized by the communities themselves. The social ministration of communities on the territory of Moscow is considered.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2010Nanot..21c5102P','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2010Nanot..21c5102P"><span>Nanoceria have no genotoxic effect on human lens epithelial cells</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Pierscionek, Barbara K.; Li, Yuebin; Yasseen, Akeel A.; Colhoun, Liza M.; Schachar, Ronald A.; Chen, Wei</p> <p>2010-01-01</p> <p>There are no treatments for reversing or halting cataract, a disease of the structural proteins in the eye lens, that has associations with other age-related degenerative conditions such as Alzheimer's disease. The incidence of cataract and associated conditions is increasing as the average age of the population rises. Protein folding diseases are difficult to assess in vivo as proteins and their age-related changes are assessed after extraction. Nanotechnology can be used to investigate protein changes in the intact lens as well as for a potential means of drug delivery. Nanoparticles, such as cerium oxide (CeO2) which have antioxidant properties, may even be used as a means of treating cataract directly. Prior to use in treatments, nanoparticle genotoxicity must be tested to assess the extent of any DNA or chromosomal damage. <span class="hlt">Sister</span> <span class="hlt">chromatid</span> exchanges were measured and DNA damage investigated using the alkaline COMET assay on cultured human lens epithelial cells, exposed to 5 and 10 µg ml-1 of CeO2 nanoparticles (nanoceria). Nanoceria at these dosages did not cause any DNA damage or significant increases in the number of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges. The absence of genotoxic effects on lens cells suggests that nanoceria, in the doses and exposures tested in this study, are not deleterious to the eye lens and have the potential for use in studying structural alterations, in developing non-surgical cataract treatments and in investigating other protein folding diseases.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3389968','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3389968"><span>Ribosomal DNA Organization Before and After Magnification in Drosophila melanogaster</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Bianciardi, Alessio; Boschi, Manuela; Swanson, Ellen E.; Belloni, Massimo; Robbins, Leonard G.</p> <p>2012-01-01</p> <p>In all eukaryotes, the ribosomal RNA genes are stably inherited redundant elements. In Drosophila melanogaster, the presence of a Ybb− chromosome in males, or the maternal presence of the Ribosomal exchange (Rex) element, induces magnification: a heritable increase of rDNA copy number. To date, several alternative classes of mechanisms have been proposed for magnification: in situ replication or extra-chromosomal replication, either of which might act on short or extended strings of rDNA units, or unequal <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange. To eliminate some of these hypotheses, none of which has been clearly proven, we examined molecular-variant composition and compared genetic maps of the rDNA in the bb2 mutant and in some magnified bb+ alleles. The genetic markers used are molecular-length variants of IGS sequences and of R1 and R2 mobile elements present in many 28S sequences. Direct comparison of PCR products does not reveal any particularly intensified electrophoretic bands in magnified alleles compared to the nonmagnified bb2 allele. Hence, the increase of rDNA copy number is diluted among multiple variants. We can therefore reject mechanisms of magnification based on multiple rounds of replication of short strings. Moreover, we find no changes of marker order when pre- and postmagnification maps are compared. Thus, we can further restrict the possible mechanisms to two: replication in situ of an extended string of rDNA units or unequal exchange between <span class="hlt">sister</span> <span class="hlt">chromatids</span>. PMID:22505623</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26694509','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26694509"><span>Meiosis.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hillers, Kenneth J; Jantsch, Verena; Martinez-Perez, Enrique; Yanowitz, Judith L</p> <p>2017-05-04</p> <p>Sexual reproduction requires the production of haploid gametes (sperm and egg) with only one copy of each chromosome; fertilization then restores the diploid chromosome content in the next generation. This reduction in genetic content is accomplished during a specialized cell division called meiosis, in which two rounds of chromosome segregation follow a single round of DNA replication. In preparation for the first meiotic division, homologous chromosomes pair and synapse, creating a context that promotes formation of crossover recombination events. These crossovers, in conjunction with <span class="hlt">sister</span> <span class="hlt">chromatid</span> cohesion, serve to connect the two homologs and facilitate their segregation to opposite poles during the first meiotic division. During the second meiotic division, which is similar to mitosis, <span class="hlt">sister</span> <span class="hlt">chromatids</span> separate; the resultant products are haploid cells that become gametes. In Caenorhabditis elegans (and most other eukaryotes) homologous pairing and recombination are required for proper chromosome inheritance during meiosis; accordingly, the events of meiosis are tightly coordinated to ensure the proper execution of these events. In this chapter, we review the seminal events of meiosis: pairing of homologous chromosomes, the changes in chromosome structure that chromosomes undergo during meiosis, the events of meiotic recombination, the differentiation of homologous chromosome pairs into structures optimized for proper chromosome segregation at Meiosis I, and the ultimate segregation of chromosomes during the meiotic divisions. We also review the regulatory processes that ensure the coordinated execution of these meiotic events during prophase I.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11566579','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11566579"><span>Genotoxicity of mercury used in chromosome <span class="hlt">aberration</span> tests.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Akiyama, M; Oshima, H; Nakamura, M</p> <p>2001-01-01</p> <p>The purpose of this study was to investigate the genotoxic effects of Hg released from dental amalgams. The chromosome <span class="hlt">aberration</span> test was conducted using original extracts and their diluted solutions of conventional type amalgam and high copper amalgam. The concentrations of Hg, Cu and Ag in the original extract of high copper amalgam were 17.64, 7.97 and 43.90 microM, respectively. Those in the original extract of conventional type amalgam were 20.63, 7.87 and 14.79 microM, respectively. 10 and 30 microM Hg(2+) were also used for comparison. The frequency of chromosome <span class="hlt">aberrations</span> was below 5% with 0 microM Hg(2+) and with a triple dilution of high copper amalgam extract, containing 5.88 microM Hg, 14.63 microM Cu and 2.65 microM Ag. However, 9.5% of the cells showed chromosome <span class="hlt">aberrations</span> with a quadruple dilution of conventional type amalgam, containing 5.15 microM Hg, 3.69 microM Cu and 1.96 microM Ag. The amount of Hg in the quadruple dilution of conventional type amalgam was less than that in the triple dilution of high copper amalgam extract and 10 microM Hg(2+). A concentration of 30 microM Hg(2+) caused 34.5% of the cells to show chromosome <span class="hlt">aberrations</span> while with a two-thirds dilution of high copper amalgam extract, containing 11.76 microM Hg, 29.26 microM Cu and 5.31 microM Ag, 58.5% of the cells showed chromosome <span class="hlt">aberrations</span>. A two-thirds dilution of high copper amalgam extract induced more chromosome <span class="hlt">aberrations</span> than 30 microM Hg(2+), although the amount of Hg was less than 30 microM Hg(2+). A triple dilution of conventional type amalgam extract, original extracts of conventional type amalgam and high copper amalgam and 100 microM Hg(2+) were induced few metaphases. It was revealed that the conventional type amalgam induced chromosome <span class="hlt">aberrations</span> with quadruple dilution where cell viability was about 80% and that the high copper amalgam induced a high level of chromosome <span class="hlt">aberrations</span> with the two-thirds dilution. The effects of low level Hg on humans</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED452094.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED452094.pdf"><span><span class="hlt">Sisters</span> in Science: Using Sports as a Vehicle for Science Learning.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Hammrich, Penny L.; Richardson, Greer M.; Green, Tina Sloan; Livingston, Beverly</p> <p></p> <p>This paper describes a project for upper elementary and middle school minority girl students called the <span class="hlt">Sisters</span> in Sport Science (SISS). The SISS program addresses the needs of urban girls in gaining access to equal education in science and mathematics by using athletics as a vehicle for learning. The program provides a non-competitive and…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/1602972','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/1602972"><span>Differences in genotoxic activity of alpha-Ni3S2 on human lymphocytes from nickel-hypersensitized and nickel-unsensitized donors.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Arrouijal, F Z; Marzin, D; Hildebrand, H F; Pestel, J; Haguenoer, J M</p> <p>1992-05-01</p> <p>The genotoxic activity of alpha-Ni3S2 was assessed on human lymphocytes from nickel-hypersensitized (SSL) and nickel-unsensitized (USL) subjects. Three genotoxicity tests were performed: the <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) test, the metaphase analysis test and the micronucleus test. (i) The SCE test (3-100 micrograms/ml) showed a weak but statistically significant increase in the number of SCE in both lymphocyte types with respect to controls, USL presenting a slightly higher SCE incidence but only at one concentration. (ii) The metaphase analysis test demonstrated a high dose-dependent clastogenic activity of alpha-Ni3S2 in both lymphocyte types. The frequency of chromosomal anomalies was significantly higher in USL than in SSL for all concentrations applied. (iii) The micronucleus test confirmed the dose-dependent clastogenic activity of alpha-Ni3S2 and the differences already observed between USL and SSL, i.e. the number of cells with micronuclei was statistically higher in USL. Finally, the incorporation study with alpha-63Ni3S2 showed a higher uptake of its solubilized fraction by USL. This allows an explanation of the different genotoxic action of nickel on the two cell types. In this study we demonstrated that hypersensitivity has an influence on the incorporation of alpha-Ni3S2 and subsequently on the different induction of chromosomal <span class="hlt">aberrations</span> in human lymphocytes.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6018432-effects-chemical-smokes-flora-fauna-under-field-laboratory-exposures','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6018432-effects-chemical-smokes-flora-fauna-under-field-laboratory-exposures"><span>Effects of chemical smokes on flora and fauna under field and laboratory exposures</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Schaeffer, D.J.; Novak, E.W.; Lower, W.R.</p> <p>1987-06-01</p> <p>Various types of obscurant smokes are used routinely in training by the U.S. Army. Because continued routine use of the smokes could be detrimental to the native flora and fauna at training sites, a preliminary biological and chemical field study of fogoil, hexachloroethane, and tank diesel smokes was conducted. Smoke plumes were sampled and chemically analyzed at distances of 15-150 m from the smoke source where Tradescantia clones 4430 and 03 and the native plant Ambrosia dumosa and the native rodent Dipodomys merriami were exposed for 30 min. In addition, Tradescantia clone 4430 was exposed to tank diesel in themore » laboratory at concentration levels equivalent to exposure at 15 and 50 m. Tradescantia clones were examined for mutagenic effects indicated by micronuclei induction in developing pollen and pink somatic mutations in stamen hairs. Photosynthetic perturbations were measured in Tradescantia and A. dumosa using variable fluorescence induction. Animals were examined for <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and chromosome <span class="hlt">aberrations</span>. It was found that all of the smokes tested exerted varying degrees of physiological and mutagenic effects in one or more assay system at one or more exposure distance. The studies reported here indicate that exposed ecological systems, or at least components of these systems, are at a higher risk than are unexposed components (e.g., organisms) for several types of damage attributed to obscurant smoke exposure.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3609264','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3609264"><span>Evaluation of antigenotoxic effects of carotenoids from green algae Chlorococcum humicola using human lymphocytes</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Bhagavathy, S; Sumathi, P</p> <p>2012-01-01</p> <p>Objective To identify the available phytochemicals and carotenoids in the selected green algae and evaluate the potential genotoxic/antigenotoxic effect using lymphocytes. Methods Organic solvent extracts of Chlorococcum humicola (C. humicola) were used for the phytochemical analysis. The available carotenoids were assessed by HPLC, and LC-MS analysis. The genotoxicity was induced by the benzo(a)pyrene in the lymphocyte culture, the genotoxic and antigenotoxic effects of algal carotenoids with and without genotoxic inducer were evaluated by chromosomal <span class="hlt">aberration</span> (CA), <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) and micronucleus assay (MN). Results The results of the analysis showed that the algae were rich in carotenoids and fatty acids. In the total carotenoids lutein, β-carotene and α-carotene were found to be present in higher concentration. The frequency of CA and SCE increased by benzo(a)pyrene were significantly decreased by the carotenoids (P<0.05 for CA, P<0.001 for SCE). The MN frequencies of the cells were significantly decreased by the treatment with carotenoids when compared with the positive controls (P<0.05). Conclusions The findings of the present study demonstrate that, the green algae C. humicola is a rich source of bioactive compounds especially carotenoids which effectively fight against environmental genotoxic agents, the carotenoids itself is not a genotoxic substance and should be further considered for its beneficial effects. PMID:23569879</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28157162','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28157162"><span>Evidence of Some Natural Products with  Antigenotoxic Effects. Part 1: Fruits and  Polysaccharides.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Izquierdo-Vega, Jeannett Alejandra; Morales-González, José Antonio; SánchezGutiérrez, Manuel; Betanzos-Cabrera, Gabriel; Sosa-Delgado, Sara M; Sumaya-Martínez, María Teresa; Morales-González, Ángel; Paniagua-Pérez, Rogelio; Madrigal-Bujaidar, Eduardo; Madrigal-Santillán, Eduardo</p> <p>2017-02-02</p> <p>Cancer is one of the leading causes of deaths worldwide. The agents capable of causing damage to genetic material are known  as genotoxins and, according to their mode of action, are classified into mutagens, carcinogens or teratogens. Genotoxins are  involved in the pathogenesis of several chronic degenerative diseases including hepatic, neurodegenerative and cardiovascular  disorders, diabetes, arthritis, cancer, chronic inflammation and ageing. In recent decades, researchers have found novel bioactive  phytocompounds able to counteract the effects of physical and chemical mutagens. Several  studies  have  shown potential antigenotoxicity in a variety of fruits. In this review (Part 1), we present an overview of research conducted on some fruits (grapefruit, cranberries, pomegranate, guava, pineapple, and mango) which are frequentl consumed by humans, as well as  the  analysis of some phytochemicals extracted from fruits and yeasts which have demonstrated antigenotoxic capacity in various  tests, including the Ames assay, <span class="hlt">sister chromatid</span> exchange, chromosomal <span class="hlt">aberrations</span>, micronucleus and comet assay.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/2440659','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/2440659"><span>Effects of chemical smokes on flora and fauna under field and laboratory exposures.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schaeffer, D J; Novak, E W; Lower, W R; Yanders, A; Kapila, S; Wang, R</p> <p>1987-06-01</p> <p>Various types of obscurant smokes are used routinely in training by the U.S. Army. Because continued routine use of the smokes could be detrimental to the native flora and fauna at training sites, a preliminary biological and chemical field study of fogoil, hexachloroethane, and tank diesel smokes was conducted. Smoke plumes were sampled and chemically analyzed at distances of 15-150 m from the smoke source where Tradescantia clones 4430 and 03 and the native plant Ambrosia dumosa and the native rodent Dipodomys merriami were exposed for 30 min. In addition, Tradescantia clone 4430 was exposed to tank diesel in the laboratory at concentration levels equivalent to exposure at 15 and 50 m. Tradescantia clones were examined for mutagenic effects indicated by micronuclei induction in developing pollen and pink somatic mutations in stamen hairs. Photosynthetic perturbations were measured in Tradescantia and A. dumosa using variable fluorescence induction. Animals were examined for <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and chromosome <span class="hlt">aberrations</span>. It was found that all of the smokes tested exerted varying degrees of physiological and mutagenic effects in one or more assay system at one or more exposure distance. The studies reported here indicate that exposed ecological systems, or at least components of these systems, are at a higher risk than are unexposed components (e.g., organisms) for several types of damage attributed to obscurant smoke exposure.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2007PhDT........73T','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2007PhDT........73T"><span>Optical <span class="hlt">aberrations</span>, retinal image quality and eye growth: Experimentation and modeling</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Tian, Yibin</p> <p>2007-12-01</p> <p>Retinal image quality is important for normal eye growth. Optical <span class="hlt">aberrations</span> are of interest for two reasons: first, they degrade retinal images; second, they might provide some cues to defocus. Higher than normal ocular <span class="hlt">aberrations</span> have been previously associated with human myopia. However, these studies were cross-sectional in design, and only reported <span class="hlt">aberrations</span> in terms of root mean square (RMS) errors of Zernike coefficients, a poor metric of optical quality. This dissertation presents results from investigations of ocular optical <span class="hlt">aberrations</span>, retinal image quality and eye growth in chicks and humans. A number of techniques were utilized, including Shack-Hartmann aberrometry, high-frequency A-scan ultrasonography, ciliary nerve section (CNX), photorefractive keratectomy (PRK) as well as computer simulations and modeling. A technique to extract light scatter information from Shack-Hartmann images was also developed. The main findings of the dissertation are summarized below. In young chicks, most ocular <span class="hlt">aberrations</span> decreased with growth in both normal and CNX eyes, and there were diurnal fluctuations in some <span class="hlt">aberrations</span>. Modeling suggested active reduction in higher order <span class="hlt">aberrations</span> (HOAs) during early development. Although CNX eyes manifested greater than normal HOAs, they showed near normal growth. Retinal image degradation varied greatly among individual eyes post-PRK in young chicks. Including light scatter information into analyses of retinal image quality better estimated the latter. Albino eyes showed more severe retinal image degradation than normal eyes, due to increased optical <span class="hlt">aberrations</span> and light scatter, but their growth was similar to those of normal eyes, implying that they are relatively insensitive to retina image quality. Although the above results questioned the influence of optical <span class="hlt">aberrations</span> on early ocular growth, some optical quality metrics, derived from optical <span class="hlt">aberrations</span> data, could predict how much the eyes of young chicks</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/18041252','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/18041252"><span>Correcting highly <span class="hlt">aberrated</span> eyes using large-stroke adaptive optics.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sabesan, Ramkumar; Ahmad, Kamran; Yoon, Geunyoung</p> <p>2007-11-01</p> <p>To investigate the optical performance of a large-stroke deformable mirror in correcting large <span class="hlt">aberrations</span> in highly <span class="hlt">aberrated</span> eyes. A large-stroke deformable mirror (Mirao 52D; Imagine Eyes) and a Shack-Hartmann wavefront sensor were used in an adaptive optics system. Closed-loop correction of the static <span class="hlt">aberrations</span> of a phase plate designed for an advanced keratoconic eye was performed for a 6-mm pupil. The same adaptive optics system was also used to correct the <span class="hlt">aberrations</span> in one eye each of two moderate keratoconic and three normal human eyes for a 6-mm pupil. With closed-loop correction of the phase plate, the total root-mean-square (RMS) over a 6-mm pupil was reduced from 3.54 to 0.04 microm in 30 to 40 iterations, corresponding to 3 to 4 seconds. Adaptive optics closed-loop correction reduced an average total RMS of 1.73+/-0.998 to 0.10+/-0.017 microm (higher order RMS of 0.39+/-0.124 to 0.06+/-0.004 microm) in the three normal eyes and 2.73+/-1.754 to 0.10+/-0.001 microm (higher order RMS of 1.82+/-1.058 to 0.05+/-0.017 microm) in the two keratoconic eyes. <span class="hlt">Aberrations</span> in both normal and highly <span class="hlt">aberrated</span> eyes were successfully corrected using the large-stroke deformable mirror to provide almost perfect optical quality. This mirror can be a powerful tool to assess the limit of visual performance achievable after correcting the <span class="hlt">aberrations</span>, especially in eyes with abnormal corneal profiles.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1097741','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1097741"><span>Subjective face recognition difficulties, <span class="hlt">aberrant</span> sensibility, sleeping disturbances and <span class="hlt">aberrant</span> eating habits in families with Asperger syndrome</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Nieminen-von Wendt, Taina; Paavonen, Juulia E; Ylisaukko-Oja, Tero; Sarenius, Susan; Källman, Tiia; Järvelä, Irma; von Wendt, Lennart</p> <p>2005-01-01</p> <p>Background The present study was undertaken in order to determine whether a set of clinical features, which are not included in the DSM-IV or ICD-10 for Asperger Syndrome (AS), are associated with AS in particular or whether they are merely a familial trait that is not related to the diagnosis. Methods Ten large families, a total of 138 persons, of whom 58 individuals fulfilled the diagnostic criteria for AS and another 56 did not to fulfill these criteria, were studied using a structured interview focusing on the possible presence of face recognition difficulties, <span class="hlt">aberrant</span> sensibility and eating habits and sleeping disturbances. Results The prevalence for face recognition difficulties was 46.6% in individuals with AS compared with 10.7% in the control group. The corresponding figures for subjectively reported presence of <span class="hlt">aberrant</span> sensibilities were 91.4% and 46.6%, for sleeping disturbances 48.3% and 23.2% and for <span class="hlt">aberrant</span> eating habits 60.3% and 14.3%, respectively. Conclusion An <span class="hlt">aberrant</span> processing of sensory information appears to be a common feature in AS. The impact of these and other clinical features that are not incorporated in the ICD-10 and DSM-IV on our understanding of AS may hitherto have been underestimated. These associated clinical traits may well be reflected by the behavioural characteristics of these individuals. PMID:15826308</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=figure+AND+ground+AND+psychology&pg=2&id=EJ1003992','ERIC'); return false;" href="https://eric.ed.gov/?q=figure+AND+ground+AND+psychology&pg=2&id=EJ1003992"><span>Empirical Psycho-Aesthetics and Her <span class="hlt">Sisters</span>: Substantive and Methodological Issues--Part II</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Konecni, Vladimir J.</p> <p>2013-01-01</p> <p>Empirical psycho-aesthetics is approached in this two-part article from two directions. Part I, which appeared in the Winter 2012 issue of "JAE," addressed definitional and organizational issues, including the field's origins, its relation to "<span class="hlt">sister</span>" disciplines (experimental philosophy, cognitive neuroscience of art, and neuroaesthetics), and…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15295969','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15295969"><span>Spectral estimation for characterization of acoustic <span class="hlt">aberration</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Varslot, Trond; Angelsen, Bjørn; Waag, Robert C</p> <p>2004-07-01</p> <p>Spectral estimation based on acoustic backscatter from a motionless stochastic medium is described for characterization of <span class="hlt">aberration</span> in ultrasonic imaging. The underlying assumptions for the estimation are: The correlation length of the medium is short compared to the length of the transmitted acoustic pulse, an isoplanatic region of sufficient size exists around the focal point, and the backscatter can be modeled as an ergodic stochastic process. The motivation for this work is ultrasonic imaging with <span class="hlt">aberration</span> correction. Measurements were performed using a two-dimensional array system with 80 x 80 transducer elements and an element pitch of 0.6 mm. The f number for the measurements was 1.2 and the center frequency was 3.0 MHz with a 53% bandwidth. Relative phase of <span class="hlt">aberration</span> was extracted from estimated cross spectra using a robust least-mean-square-error method based on an orthogonal expansion of the phase differences of neighboring wave forms as a function of frequency. Estimates of cross-spectrum phase from measurements of random scattering through a tissue-mimicking <span class="hlt">aberrator</span> have confidence bands approximately +/- 5 degrees wide. Both phase and magnitude are in good agreement with a reference characterization obtained from a point scatterer.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19410348','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19410348"><span>[Familial pulmonary fibrosis in 2 Mexican <span class="hlt">sisters</span> with Hermansky-Pudlak syndrome].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zamora, Ana C; Alonso-Martínez, Delfino; Barrera, Lourdes; Mendoza, Felipe; Gaxiola, Miguel; Carrillo, Guillermo</p> <p>2009-08-01</p> <p>Hermansky-Pudlak syndrome is an autosomal recessive disorder commonly found in individuals of Puerto Rican ancestry. We present 2 cases of familial pulmonary fibrosis in 2 Mexican <span class="hlt">sisters</span> with Hermansky-Pudlak syndrome. Pulmonary fibrosis was biopsy-proven in 1 of the patients. This report shows that Hermansky-Pudlak syndrome may occur in individuals of Mexican ancestry.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=beans&pg=5&id=EJ797780','ERIC'); return false;" href="https://eric.ed.gov/?q=beans&pg=5&id=EJ797780"><span>Three <span class="hlt">Sisters</span>: Lessons of Traditional Story Honored in Assessment and Accreditation</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Chenault, Venida S.</p> <p>2008-01-01</p> <p>The three <span class="hlt">sisters</span> story is shared across many tribes. It explains the practice of planting corn, beans, and squash together. The corn stalks provide support for the bean vines; the beans provide nitrogen for the corn; and the squash prevents weed growth between the mounds. Such stories explain not only the science of agricultural methods in tribal…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19465021','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19465021"><span>A nucleolar protein RRS1 contributes to chromosome congression.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Gambe, Arni E; Matsunaga, Sachihiro; Takata, Hideaki; Ono-Maniwa, Rika; Baba, Akiko; Uchiyama, Susumu; Fukui, Kiichi</p> <p>2009-06-18</p> <p>We report here the functional analysis of human Regulator of Ribosome Synthesis 1 (RRS1) protein during mitosis. We demonstrate that RRS1 localizes in the nucleolus during interphase and is distributed at the chromosome periphery during mitosis. RNA interference experiments revealed that RRS1-depleted cells show abnormalities in chromosome alignment and spindle organization, which result in mitotic delay. RRS1 knockdown also perturbs the centromeric localization of Shugoshin 1 and results in premature separation of <span class="hlt">sister</span> <span class="hlt">chromatids</span>. Our results suggest that a nucleolar protein RRS1 contributes to chromosome congression.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li class="active"><span>23</span></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_23 --> <div id="page_24" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li class="active"><span>24</span></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="461"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/10593079','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/10593079"><span>First-generation physical map of the Culicoides variipennis (Diptera: Ceratopogonidae) genome.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nunamaker, R A; Brown, S E; McHolland, L E; Tabachnick, W J; Knudson, D L</p> <p>1999-11-01</p> <p>Recombinant cosmids labeled with biotin-11-dUTP or digoxigenin by nick translation were used as in situ hybridization probes to metaphase chromosomes of Culicoides variipennis (Coquillett). Paired fluorescent signals were detected on each arm of <span class="hlt">sister</span> <span class="hlt">chromatids</span> and were ordered along the 3 chromosomes. Thirty-three unique probes were mapped to the 3 chromosomes of C. variipennis (2n = 6): 7 to chromosome 1, 20 to chromosome 2, and 6 to chromosome 3. This work represents the first stage in generating a physical map of the genome of C. variipennis.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24028793','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24028793"><span>BAIT: Organizing genomes and mapping rearrangements in single cells.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hills, Mark; O'Neill, Kieran; Falconer, Ester; Brinkman, Ryan; Lansdorp, Peter M</p> <p>2013-01-01</p> <p>Strand-seq is a single-cell sequencing technique to finely map <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges (SCEs) and other rearrangements. To analyze these data, we introduce BAIT, software which assigns templates and identifies and localizes SCEs. We demonstrate BAIT can refine completed reference assemblies, identifying approximately 21 Mb of incorrectly oriented fragments and placing over half (2.6 Mb) of the orphan fragments in mm10/GRCm38. BAIT also stratifies scaffold-stage assemblies, potentially accelerating the assembling and finishing of reference genomes. BAIT is available at http://sourceforge.net/projects/bait/.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3484706','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3484706"><span>Statistical virtual eye model based on wavefront <span class="hlt">aberration</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Wang, Jie-Mei; Liu, Chun-Ling; Luo, Yi-Ning; Liu, Yi-Guang; Hu, Bing-Jie</p> <p>2012-01-01</p> <p>Wavefront <span class="hlt">aberration</span> affects the quality of retinal image directly. This paper reviews the representation and reconstruction of wavefront <span class="hlt">aberration</span>, as well as the construction of virtual eye model based on Zernike polynomial coefficients. In addition, the promising prospect of virtual eye model is emphasized. PMID:23173112</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2004SPIE.5572..340L','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2004SPIE.5572..340L"><span>Double-pass measurement of human eye <span class="hlt">aberrations</span>: limitations and practical realization</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Letfullin, Renat R.; Belyakov, Alexey I.; Cherezova, Tatyana Y.; Kudryashov, Alexis V.</p> <p>2004-11-01</p> <p>The problem of correct eye <span class="hlt">aberrations</span> measurement is very important with the rising widespread of a surgical procedure for reducing refractive error in the eye, so called, LASIK (laser-assisted in situ keratomileusis). The double-pass technique commonly used for measuring <span class="hlt">aberrations</span> of a human eye involves some uncertainties. One of them is loosing the information about odd human eye <span class="hlt">aberrations</span>. We report about investigations of the applicability limit of the double-pass measurements depending upon the <span class="hlt">aberrations</span> status introduced by human eye and actual size of the entrance pupil. We evaluate the double-pass effects for various <span class="hlt">aberrations</span> and different pupil diameters. It is shown that for small pupils the double-pass effects are negligible. The testing and alignment of aberrometer was performed using the schematic eye, developed in our lab. We also introduced a model of human eye based on bimorph flexible mirror. We perform calculations to demonstrate that our schematic eye is capable of reproducing spatial-temporal statistics of <span class="hlt">aberrations</span> of living eye with normal vision or even myopic or hypermetropic or with high <span class="hlt">aberrations</span> ones.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6304772-induction-sister-chromatid-exchanges-inhibition-cellular-proliferation-vitro-caffeine','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6304772-induction-sister-chromatid-exchanges-inhibition-cellular-proliferation-vitro-caffeine"><span>Induction of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchanges and inhibition of cellular proliferation in vitro. I. Caffeine</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Guglielmi, G.E.; Vogt, T.F.; Tice, R.R.</p> <p>1982-01-01</p> <p>While many agents have been examined for their ability to induce SCE's, complete dose-response information has often been lacking. We have reexamined the ability of one such compound - caffeine - to induce SCEs and also to inhibit cellular proliferation in human peripheral lymphocytes in vitro. An acute exposure to caffeine prior to the DNA synthetic period did not affect either SCE frequency or the rate of cellular proliferation. Chronic exposure to caffeine throughout the culture period lead to both a dose-dependent increase in SCEs (SCE/sub d/ or doubling dose = 2.4 mM; SCE/sub 10/ or the dose capable ofmore » inducing 10 SCE = 1.4 mM) and a dose-dependent inhibition of cellular proliferation (IC/sub 50/ or the 50% inhibition concentration = 2.6 mM). The relative proportion of first generation metaphase cells, an assessment of proliferative inhibiton, increased linearly with increasing caffeine concentrations. However, SCE frequency increased nonlinearly over the same range of caffeine concentrations. Examination of the ratio of nonsymmetrical to symmetrical SCEs in third generation metaphase cells indicated that caffeine induced SCEs in equal frequency in each of three successive generations. The dependency of SCE induction and cellular proliferative inhibition on caffeine's presence during the DNA synthetic period suggests that caffeine may act as an antimetabolite in normal human cells.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27797077','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27797077"><span>Measuring <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Cohesion Protein Genome Occupancy in Drosophila melanogaster by ChIP-seq.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Dorsett, Dale; Misulovin, Ziva</p> <p>2017-01-01</p> <p>This chapter presents methods to conduct and analyze genome-wide chromatin immunoprecipitation of the cohesin complex and the Nipped-B cohesin loading factor in Drosophila cells using high-throughput DNA sequencing (ChIP-seq). Procedures for isolation of chromatin, immunoprecipitation, and construction of sequencing libraries for the Ion Torrent Proton high throughput sequencer are detailed, and computational methods to calculate occupancy as input-normalized fold-enrichment are described. The results obtained by ChIP-seq are compared to those obtained by ChIP-chip (genomic ChIP using tiling microarrays), and the effects of sequencing depth on the accuracy are analyzed. ChIP-seq provides similar sensitivity and reproducibility as ChIP-chip, and identifies the same broad regions of occupancy. The locations of enrichment peaks, however, can differ between ChIP-chip and ChIP-seq, and low sequencing depth can splinter broad regions of occupancy into distinct peaks.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.dtic.mil/docs/citations/ADA444255','DTIC-ST'); return false;" href="http://www.dtic.mil/docs/citations/ADA444255"><span>Linking <span class="hlt">Sister</span> <span class="hlt">Chromatid</span> Cohesion to Apoptosis and Aneuploidy in the Development of Breast Cancer</span></a></p> <p><a target="_blank" href="http://www.dtic.mil/">DTIC Science & Technology</a></p> <p></p> <p>2005-07-01</p> <p>antibody. Jurkat cells were ZE in wheat germ extract was .4 Claved fd21 transfected with blank vectors (B), treated with • • incubated in the presence...nonisotopic) hRad21 in wheat germ extracts by FPLC fractions 13-20. Samples were analyzed on an SDS-6% PAGE gel followed by Western bloting with hRda2l C...in vitro translated unlabelled hRad21 in wheat germ extracts and assaying the cleavage in Rad21 immunoblots (Fig. 5C). The broad-spectrum caspase</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1286223','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1286223"><span>Using <span class="hlt">aberrant</span> behaviors as reinforcers for autistic children.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Charlop, M H; Kurtz, P F; Casey, F G</p> <p>1990-01-01</p> <p>In a series of experiments, we assessed the efficacy of using autistic children's <span class="hlt">aberrant</span> behaviors as reinforcers to increase their correct task responding. In Experiment 1, reinforcer conditions of stereotypy, food, and varied (food or stereotypy) were compared. In Experiment 2, the conditions were delayed echolalia, food, and varied (food or delayed echolalia), and in Experiment 3, perseverative behavior was compared with stereotypy and food as potential reinforcers. A multielement design was used for all comparisons, and side-effect measures were recorded during and after teaching sessions as well as at home. Results indicated that, in general, task performance was highest when brief opportunities to engage in <span class="hlt">aberrant</span> behaviors were provided as reinforcers. Edibles were associated with the lowest performance. Furthermore, no negative side effects (e.g., an increase in <span class="hlt">aberrant</span> behaviors) occurred. The results are discussed in terms of suggesting a more pragmatic treatment approach by addressing the contingent use of autistic children's <span class="hlt">aberrant</span> behaviors as reinforcers. PMID:2373653</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/27391311','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/27391311"><span>Kindler syndrome: the case of two Iranian <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kargar, Saeed; Shiryazdi, Seyed M; Neamatzadeh, Hossein; Ramazani, Vahid</p> <p>2018-02-01</p> <p>Kindler syndrome is a rare autosomal recessive condition, characterized by multiple skin and mucosal abnormalities. Among the latter, esophageal involvement is an infrequent manifestation which may be completely asymptomatic or complicated by dysphagia. We report the case of two <span class="hlt">sisters</span> presenting with cutaneous features and severe dysphagia. Endoscopic examination showed that the patients were affected by a rare condition named "esophageal web". Both patients showed significant improvement after balloon dilation. Clinicians should be aware of the potential complications of this disease, and the approach by balloon dilation should be considered as primary therapy in Kindler syndrome patients with esophageal web.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3423812','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3423812"><span>Microcystin-LR, a protein phosphatase inhibitor, induces alterations in mitotic chromatin and microtubule organization leading to the formation of micronuclei in Vicia faba</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Beyer, Dániel; Tándor, Ildikó; Kónya, Zoltán; Bátori, Róbert; Roszik, Janos; Vereb, György; Erdődi, Ferenc; Vasas, Gábor; M-Hamvas, Márta; Jambrovics, Károly; Máthé, Csaba</p> <p>2012-01-01</p> <p>Background and Aims Microcystin-LR (MCY-LR) is a cyanobacterial toxin, a specific inhibitor of type 1 and 2A protein phosphatases (PP1 and PP2A) with significant impact on aquatic ecosystems. It has the potential to alter regulation of the plant cell cycle. The aim of this study was improved understanding of the mitotic alterations induced by cyanotoxin in Vicia faba, a model organism for plant cell biology studies. Methods Vicia faba seedlings were treated over the long and short term with MCY-LR purified in our laboratory. Short-term treatments were performed on root meristems synchronized with hydroxylurea. Sections of lateral root tips were labelled for chromatin, phosphorylated histone H3 and β-tubulin via histochemical and immunohistochemical methods. Mitotic activity and the occurrence of mitotic alterations were detected and analysed by fluorescence microscopy. The phosphorylation state of histone H3 was studied by Western blotting. Key Results Long-term MCY-LR exposure of lateral root tip meristems increased the percentage of either early or late mitosis in a concentration-dependent manner. We observed hypercondensed chromosomes and altered <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation (lagging chromosomes) leading to the formation of micronuclei, accompanied by the formation of disrupted, multipolar and monopolar spindles, disrupted phragmoplasts and the hyperphosphorylation of histone H3 at Ser10. Short-term MCY-LR treatment of synchronized cells showed that PP1 and PP2A inhibition delayed the onset of anaphase at 1 µg mL−1 MCY-LR, accelerated cell cycle at 10 µg mL−1 MCY-LR and induced the formation of lagging chromosomes. In this case mitotic microtubule alterations were not detected, but histone H3 was hyperphosphorylated. Conclusions MCY-LR delayed metaphase–anaphase transition. Consequently, it induced <span class="hlt">aberrant</span> <span class="hlt">chromatid</span> segregation and micronucleus formation that could be associated with both H3 hyperphosphorylation and altered microtubule organization</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22819947','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22819947"><span>Microcystin-LR, a protein phosphatase inhibitor, induces alterations in mitotic chromatin and microtubule organization leading to the formation of micronuclei in Vicia faba.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Beyer, Dániel; Tándor, Ildikó; Kónya, Zoltán; Bátori, Róbert; Roszik, Janos; Vereb, György; Erdodi, Ferenc; Vasas, Gábor; M-Hamvas, Márta; Jambrovics, Károly; Máthé, Csaba</p> <p>2012-09-01</p> <p>Microcystin-LR (MCY-LR) is a cyanobacterial toxin, a specific inhibitor of type 1 and 2A protein phosphatases (PP1 and PP2A) with significant impact on aquatic ecosystems. It has the potential to alter regulation of the plant cell cycle. The aim of this study was improved understanding of the mitotic alterations induced by cyanotoxin in Vicia faba, a model organism for plant cell biology studies. Vicia faba seedlings were treated over the long and short term with MCY-LR purified in our laboratory. Short-term treatments were performed on root meristems synchronized with hydroxylurea. Sections of lateral root tips were labelled for chromatin, phosphorylated histone H3 and β-tubulin via histochemical and immunohistochemical methods. Mitotic activity and the occurrence of mitotic alterations were detected and analysed by fluorescence microscopy. The phosphorylation state of histone H3 was studied by Western blotting. Long-term MCY-LR exposure of lateral root tip meristems increased the percentage of either early or late mitosis in a concentration-dependent manner. We observed hypercondensed chromosomes and altered <span class="hlt">sister</span> <span class="hlt">chromatid</span> segregation (lagging chromosomes) leading to the formation of micronuclei, accompanied by the formation of disrupted, multipolar and monopolar spindles, disrupted phragmoplasts and the hyperphosphorylation of histone H3 at Ser10. Short-term MCY-LR treatment of synchronized cells showed that PP1 and PP2A inhibition delayed the onset of anaphase at 1 µg mL(-1) MCY-LR, accelerated cell cycle at 10 µg mL(-1) MCY-LR and induced the formation of lagging chromosomes. In this case mitotic microtubule alterations were not detected, but histone H3 was hyperphosphorylated. MCY-LR delayed metaphase-anaphase transition. Consequently, it induced <span class="hlt">aberrant</span> <span class="hlt">chromatid</span> segregation and micronucleus formation that could be associated with both H3 hyperphosphorylation and altered microtubule organization. However, these two phenomena seemed to be independent</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/1990PhDT........59Z','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/1990PhDT........59Z"><span>Ocular Chromatic <span class="hlt">Aberrations</span> and Their Effects on Polychromatic Retinal Image Quality</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Zhang, Xiaoxiao</p> <p></p> <p>Previous studies of ocular chromatic <span class="hlt">aberrations</span> have concentrated on chromatic difference of focus (CDF). Less is known about the chromatic difference of image position (CDP) in the peripheral retina and no experimental attempt has been made to measure the ocular chromatic difference of magnification (CDM). Consequently, theoretical modelling of human eyes is incomplete. The insufficient knowledge of ocular chromatic <span class="hlt">aberrations</span> is partially responsible for two unsolved applied vision problems: (1) how to improve vision by correcting ocular chromatic <span class="hlt">aberration</span>? (2) what is the impact of ocular chromatic <span class="hlt">aberration</span> on the use of isoluminance gratings as a tool in spatial-color vision?. Using optical ray tracing methods, MTF analysis methods of image quality, and psychophysical methods, I have developed a more complete model of ocular chromatic <span class="hlt">aberrations</span> and their effects on vision. The ocular CDM was determined psychophysically by measuring the tilt in the apparent frontal parallel plane (AFPP) induced by interocular difference in image wavelength. This experimental result was then used to verify a theoretical relationship between the ocular CDM, the ocular CDF and the entrance pupil of the eye. In the retinal image after correcting the ocular CDF with existing achromatizing methods, two forms of chromatic <span class="hlt">aberration</span> (CDM and chromatic parallax) were examined. The CDM was predicted by theoretical ray tracing and measured with the same method used to determine ocular CDM. The chromatic parallax was predicted with a nodal ray model and measured with the two-color vernier alignment method. The influence of these two <span class="hlt">aberrations</span> on polychromatic MTF were calculated. Using this improved model of ocular chromatic <span class="hlt">aberration</span>, luminance artifacts in the images of isoluminance gratings were calculated. The predicted luminance artifacts were then compared with experimental data from previous investigators. The results show that: (1) A simple relationship exists between</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22722284','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22722284"><span>Orthonormal <span class="hlt">aberration</span> polynomials for anamorphic optical imaging systems with circular pupils.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mahajan, Virendra N</p> <p>2012-06-20</p> <p>In a recent paper, we considered the classical <span class="hlt">aberrations</span> of an anamorphic optical imaging system with a rectangular pupil, representing the terms of a power series expansion of its <span class="hlt">aberration</span> function. These <span class="hlt">aberrations</span> are inherently separable in the Cartesian coordinates (x,y) of a point on the pupil. Accordingly, there is x-defocus and x-coma, y-defocus and y-coma, and so on. We showed that the <span class="hlt">aberration</span> polynomials orthonormal over the pupil and representing balanced <span class="hlt">aberrations</span> for such a system are represented by the products of two Legendre polynomials, one for each of the two Cartesian coordinates of the pupil point; for example, L(l)(x)L(m)(y), where l and m are positive integers (including zero) and L(l)(x), for example, represents an orthonormal Legendre polynomial of degree l in x. The compound two-dimensional (2D) Legendre polynomials, like the classical <span class="hlt">aberrations</span>, are thus also inherently separable in the Cartesian coordinates of the pupil point. Moreover, for every orthonormal polynomial L(l)(x)L(m)(y), there is a corresponding orthonormal polynomial L(l)(y)L(m)(x) obtained by interchanging x and y. These polynomials are different from the corresponding orthogonal polynomials for a system with rotational symmetry but a rectangular pupil. In this paper, we show that the orthonormal <span class="hlt">aberration</span> polynomials for an anamorphic system with a circular pupil, obtained by the Gram-Schmidt orthogonalization of the 2D Legendre polynomials, are not separable in the two coordinates. Moreover, for a given polynomial in x and y, there is no corresponding polynomial obtained by interchanging x and y. For example, there are polynomials representing x-defocus, balanced x-coma, and balanced x-spherical <span class="hlt">aberration</span>, but no corresponding y-<span class="hlt">aberration</span> polynomials. The missing y-<span class="hlt">aberration</span> terms are contained in other polynomials. We emphasize that the Zernike circle polynomials, although orthogonal over a circular pupil, are not suitable for an anamorphic system as</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/19017705','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/19017705"><span>Birth weight and fetal growth in infants born to female hairdressers and their <span class="hlt">sisters</span>.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Axmon, A; Rylander, L</p> <p>2009-03-01</p> <p>To investigate birth weight and fetal growth in female hairdressers, while controlling for intergenerational effects and effects related to childhood exposures. A cohort of women who had attended vocational schools for hairdressers were compared to their <span class="hlt">sisters</span> with respect to birth weight and fetal growth (measured as small for gestational age (SGA) or large for gestational age (LGA), respectively) in their infants. In total, 6223 infants born to 3137 hairdressers and 8388 infants born to 3952 hairdressers' <span class="hlt">sisters</span> were studied. Among the infants born to the hairdressers' <span class="hlt">sisters</span>, the distribution of birth weights were wider than that among the infants born to the hairdressers. This was also reflected in that hairdresser cohort affiliation tended to be protective against both SGA (odds ratio 0.80; 95% confidence interval 0.49 to 1.31) and LGA (0.77; 0.54 to 1.09). For LGA, this effect was even more pronounced among women who had actually worked as hairdressers during at least one pregnancy (0.60; 0.39 to 0.92). The infants born to these women also had a significantly lower mean birth weight (3387 g vs 3419 g; p = 0.033). The results from the present study suggest that infants born to hairdressers have a decreased risk of being LGA. This is most likely not caused by a shift in birth weight distribution or abnormal glucose metabolism.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/6721582-comparison-cytological-effects-three-hypoxic-cell-radiosensitizers','SCIGOV-STC'); return false;" href="https://www.osti.gov/biblio/6721582-comparison-cytological-effects-three-hypoxic-cell-radiosensitizers"><span>A comparison of the cytological effects of three hypoxic cell radiosensitizers</span></a></p> <p><a target="_blank" href="http://www.osti.gov/search">DOE Office of Scientific and Technical Information (OSTI.GOV)</a></p> <p>Spunberg, J.J.; Geard, C.R.; Rutledge-Freeman, M.H.</p> <p>1982-07-01</p> <p>Misonidazole has entered Phase III clinical trials as a hypoxic cell radiosensitizer. Neurotoxocity is the major dose-limiting factor and has prompted the development of two further compounds with reduced lipophilicity and shorter half-life in vivo. Aside from the short-term problem of neurotoxicity, other potential long-term consequences should be considered. Such is the purpose of this investigation where the cytological effects of three radiosensitizers upon oxic and hypoxic Chinese hamster V-79 cells have been examined. Two newer compounds, desmethylmisonidazole and Stanford Research compound 2508, were compared with their clinically used predecessor misonidazole. Under aerated conditions, cell killing was increased with SR-2508more » in a concentration and time dependent manner, so as to exceed by more than three times the level produced by the other two drugs at 5 mM for 72 hours.Cell progression into mitosis was also markedly reduced by as much as 1/10,000 of control values. However, as the three compounds induced similar frequencies of <span class="hlt">sister</span> <span class="hlt">chromatid</span> exchange (SCE) and chromosome <span class="hlt">aberration</span>, the enhanced cytotoxic effect of SR-2508 appears to be mediated via an interphase rather than a post-mitotic cell death. Cells were made hypoxic and treated with the three drugs for 4 hr, then mitoses sequentially collected for 16 hr. The three compounds produced similar levels of cell killing, slowing of cell cycle progression, SCE's and chromosome <span class="hlt">aberrations</span>, with cycle-specific effect on S and G-I phase cells for SCE induction. These results indicate that desmethylmisonidazole and misonidazole have similar cytotoxic and clastogenic properties under oxic and hypoxic conditions. SR-2508 is relatively more toxic to aerated cells and may deserve close clinical observation for toxicity to normal tissues.« less</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26040382','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26040382"><span>[Nutritional status of two generations of brothers and <span class="hlt">sisters</span> <5 years of age beneficiaries from opportunities living in marginalized rural communities in Chiapas, Mexico].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>García-Parra, Esmeralda; Ochoa-Díaz-López, Héctor; García-Miranda, Rosario; Moreno-Altamirano, Laura; Morales, Helda; Estrada-Lugo, Erin Ingrid Jane; Solís-Hernández, Roberto</p> <p>2015-06-01</p> <p>Mexico, in recent decades, has developed several programs to eradicate the problem of infant malnutrition <5 years, primarily among those living in rural and indigenous areas. However, there is insufficient evidence on these programs’ impact on child health and nutrition. To describe the nutritional changes of two generations of brothers and <span class="hlt">sisters</span> living in rural communities of Chiapas and who are Oportunidades beneficiaries. Cross-sectional study. It was determined: underweight, stunting, wasting and overweight plus obesity. Older brothers and <span class="hlt">sisters</span> were evaluated in 2002-2003, for 2010-2011 younger brothers and <span class="hlt">sisters</span> were evaluated, both groups were <5 years of age at the time of data collection. Malnutrition, in its three types is a problem. 43.4% of brothers and <span class="hlt">sisters</span> evaluated in 2010-2011 showed stunting, underweight prevalence declined from 18% to 13.2%, wasting (low weight for height) increased from 8.1% to 10.4%. Overweight and obesity increased significantly by 12 percentage points among brothers and <span class="hlt">sisters</span>, from 24.8% in 2002-2003 to 36.8% in 2010-2011. Malnutrition among male children is lower than their brothers and <span class="hlt">sisters</span> from the 2002-2003 generation (stunting p=<0.05), overweight and obesity was 10.9 percentage points higher than their brothers and <span class="hlt">sisters</span> (26.4% to 37.3%). Children beneficiaries from Opportunities have not yet overcome chronic malnutrition problems. This study shows that there is not a clear impact in improving the nutritional status of the study population. Copyright AULA MEDICA EDICIONES 2014. Published by AULA MEDICA. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/26546904','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/26546904"><span>Familial Churg-Strauss Syndrome in a <span class="hlt">Sister</span> and Brother.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Alyasin, Soheyla; Khoshkhui, Maryam; Amin, Reza</p> <p>2015-06-01</p> <p>Churg-Strauss syndrome (CSS) is a granulomatous small vessel vasculitis. It is characterized by asthma, allergic granulomatosis and vasculitis. This syndrome is rare in children. A 5 years old boy was admitted with cough, fever and dyspnea for 2 weeks. On the basis of laboratory data (peripheral eosinophilia), associated with skin biopsy, and history of CSS in his <span class="hlt">sister</span>, this disease was eventually diagnosed. The patient had good response to corticosteroid. In every asthmatic patient with prolonged fever, eosinophilia and multisystemic involvment, CSS should be considered.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/29245820','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/29245820"><span>Numerical analysis of wavefront <span class="hlt">aberration</span> correction using multielectrode electrowetting-based devices.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zohrabi, Mo; Cormack, Robert H; Mccullough, Connor; Supekar, Omkar D; Gibson, Emily A; Bright, Victor M; Gopinath, Juliet T</p> <p>2017-12-11</p> <p>We present numerical simulations of multielectrode electrowetting devices used in a novel optical design to correct wavefront <span class="hlt">aberration</span>. Our optical system consists of two multielectrode devices, preceded by a single fixed lens. The multielectrode elements function as adaptive optical devices that can be used to correct <span class="hlt">aberrations</span> inherent in many imaging setups, biological samples, and the atmosphere. We are able to accurately simulate the liquid-liquid interface shape using computational fluid dynamics. Ray tracing analysis of these surfaces shows clear evidence of <span class="hlt">aberration</span> correction. To demonstrate the strength of our design, we studied three different input <span class="hlt">aberrations</span> mixtures that include astigmatism, coma, trefoil, and additional higher order <span class="hlt">aberration</span> terms, with amplitudes as large as one wave at 633 nm.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/23611288','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/23611288"><span>Stability of corneal topography and wavefront <span class="hlt">aberrations</span> in young Singaporeans.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhu, Mingxia; Collins, Michael J; Yeo, Anna C H</p> <p>2013-09-01</p> <p>The aim was to investigate the differences between and variations across time in corneal topography and ocular wavefront <span class="hlt">aberrations</span> in young Singaporean myopes and emmetropes. We used a videokeratoscope and wavefront sensor to measure the ocular surface topography and wavefront <span class="hlt">aberrations</span> of the total-eye optics in the morning, midday and late afternoon on two separate days. Topographic data were used to derive the corneal surface wavefront <span class="hlt">aberrations</span>. Both the corneal and total wavefronts were analysed up to the fourth radial order of the Zernike polynomial expansion and were centred on the entrance pupil (5.0 mm). The participants included 12 young progressing myopes, 13 young stable myopes and 15 young age-matched emmetropes. For all subjects considered together, there were significant changes in some of the <span class="hlt">aberrations</span> across the day, such as spherical <span class="hlt">aberration</span> ( Z(4 0)) and vertical coma ( Z (3 - 1)) (repeated measures analysis of variance, p < 0.05). The magnitude of positive spherical <span class="hlt">aberration</span> ( Z(4 0)) was significantly lower in the progressing myopic group than in the stable myopic (p = 0.04) and emmetropic (p = 0.02) groups. There were also significant interactions between refractive group and time of day for with and against-the-rule astigmatism ( Z(2 2)). Significantly lower fourth-order root mean square of ocular wavefront <span class="hlt">aberrations</span> were found in the progressing myopic group compared with the stable myopes and emmetropes (p < 0.01). These differences and variations in the corneal and total <span class="hlt">aberrations</span> may have significance for our understanding of refractive error development and for clinical applications requiring accurate wavefront measurements. © 2013 The Authors. Clinical and Experimental Optometry © 2013 Optometrists Association Australia.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22695313','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22695313"><span>Chromosomal <span class="hlt">aberrations</span> in 2000 couples of Indian ethnicity with reproductive failure.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Gada Saxena, S; Desai, K; Shewale, L; Ranjan, P; Saranath, D</p> <p>2012-08-01</p> <p>Constitutional chromosomal <span class="hlt">aberrations</span> contribute to infertility and repeated miscarriage leading to reproductive failure in couples. These <span class="hlt">aberrations</span> may show no obvious clinical manifestations and remain undetected across multiple generations. However, infertility or recurrent spontaneous pregnancy loss, and/or genotypic/phenotypic <span class="hlt">aberrations</span> may be manifested in the progeny during gametogenesis. The current study was a retrospective analysis to examine the chromosomal <span class="hlt">aberrations</span> and prevalence in 2000 couples of Indian ethnicity with reproductive failure. Cytogenetic analysis via conventional G-band karyotyping analysis was carried out on phytohaemagglutinin stimulated peripheral blood lymphocytes, cultured in RPMI1640 medium. The chromosomes were enumerated as per International System for Human Cytogenetic Nomenclature at 500-550 band resolution, and recorded in the screening sheets. Chromosomal <span class="hlt">aberrations</span> were detected in a total of 110 (2.78%) couples, with structural chromosomal <span class="hlt">aberrations</span> in 88 cases including reciprocal translocations in 56 cases, Robertsonian translocations in 16 cases, inversions in eight cases, deletions in three cases, derivative chromosomes in five cases and numerical chromosome <span class="hlt">aberrations</span> in 23 cases. The study emphasizes the importance of cytogenetic work up in both the partners associated with a history of reproductive failure. Genetic counselling with an option of prenatal diagnosis should be offered to couples with chromosomal <span class="hlt">aberrations</span>. Copyright © 2012 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li class="active"><span>24</span></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_24 --> <div id="page_25" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li class="active"><span>25</span></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="481"> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/25984643','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/25984643"><span>Dimensions of driving anger and their relationships with <span class="hlt">aberrant</span> driving.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhang, Tingru; Chan, Alan H S; Zhang, Wei</p> <p>2015-08-01</p> <p>The purpose of this study was to investigate the relationship between driving anger and <span class="hlt">aberrant</span> driving behaviours. An internet-based questionnaire survey was administered to a sample of Chinese drivers, with driving anger measured by a 14-item short Driving Anger Scale (DAS) and the <span class="hlt">aberrant</span> driving behaviours measured by a 23-item Driver Behaviour Questionnaire (DBQ). The results of Confirmatory Factor Analysis demonstrated that the three-factor model (hostile gesture, arrival-blocking and safety-blocking) of the DAS fitted the driving anger data well. The Exploratory Factor Analysis on DBQ data differentiated four types of <span class="hlt">aberrant</span> driving, viz. emotional violation, error, deliberate violation and maintaining progress violation. For the anger-<span class="hlt">aberration</span> relation, it was found that only "arrival-blocking" anger was a significant positive predictor for all four types of <span class="hlt">aberrant</span> driving behaviours. The "safety-blocking" anger revealed a negative impact on deliberate violations, a finding different from previously established positive anger-<span class="hlt">aberration</span> relation. These results suggest that drivers with different patterns of driving anger would show different behavioural tendencies and as a result intervention strategies may be differentially effective for drivers of different profiles. Copyright © 2015 Elsevier Ltd. All rights reserved.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED421602.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED421602.pdf"><span><span class="hlt">Sisters</span> in Science: A Model Program. Spotlight on Student Success, No. 201.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Hammrich, Penny L.</p> <p></p> <p>In an effort to promote females' achievement in science, the <span class="hlt">Sisters</span> in Science program was developed. Conducted in 2 schools in Philadelphia (Pennsylvania), the program's inaugural year involved 60 fourth-grade girls in 2 elementary schools, an intergenerational corps of 20 women volunteers, 150 undergraduate elementary education students, and 8…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2011JMOp...58.1681T','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2011JMOp...58.1681T"><span>Ocular wavefront <span class="hlt">aberration</span> and refractive error in pre-school children</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Thapa, Damber; Fleck, Andre; Lakshminarayanan, Vasudevan; Bobier, William R.</p> <p>2011-11-01</p> <p>Hartmann-Shack images taken from an archived collection of SureSight refractive measurements of pre-school children in Oxford County, Ontario, Canada were retrieved and re-analyzed. Higher-order <span class="hlt">aberrations</span> were calculated over the age range of 3 to 6 years. These higher-order <span class="hlt">aberrations</span> were compared with respect to magnitudes of ametropia. Subjects were classified as emmetropic (range -0.5 to + 0.5D), low hyperopic (+ 0.5 to +2D) and high hyperopic (+2D or more) based upon the resulting spherical equivalent. Higher-order <span class="hlt">aberrations</span> were found to increase with higher levels of hyperopia (p < 0.01). The strongest effect was for children showing more than +2.00D of hyperopia. The correlation coefficients were small in all of the higher-order <span class="hlt">aberrations</span>; however, they were significant (p < 0.01). These analyses indicate a weak association between refractive error and higher-order <span class="hlt">aberrations</span> in pre-school children.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2926285','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2926285"><span>Dynamic accommodation with simulated targets blurred with high order <span class="hlt">aberrations</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Gambra, Enrique; Wang, Yinan; Yuan, Jing; Kruger, Philip B.; Marcos, Susana</p> <p>2010-01-01</p> <p>High order <span class="hlt">aberrations</span> have been suggested to play a role in determining the direction of accommodation. We have explored the effect of retinal blur induced by high order <span class="hlt">aberrations</span> on dynamic accommodation by measuring the accommodative response to sinusoidal variations in accommodative demand (1–3 D). The targets were blurred with 0.3 and 1 μm (for a 3-mm pupil) of defocus, coma, trefoil and spherical <span class="hlt">aberration</span>. Accommodative gain decreased significantly when 1-μm of <span class="hlt">aberration</span> was induced. We found a strong correlation between the relative accommodative gain (and phase lag) and the contrast degradation imposed on the target at relevant spatial frequencies. PMID:20600230</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22773825','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22773825"><span>Fertility drugs and young-onset breast cancer: results from the Two <span class="hlt">Sister</span> Study.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fei, Chunyuan; Deroo, Lisa A; Sandler, Dale P; Weinberg, Clarice R</p> <p>2012-07-03</p> <p>Fertility drugs stimulate hyperovulation, which may have implications for breast cancer. We examined the association between use of fertility drugs (clomiphene citrate [CC] and follicle-stimulating hormone [FSH]) and subsequent risk of young-onset (<50 years at diagnosis) breast cancer. We conducted the Two <span class="hlt">Sister</span> Study, a <span class="hlt">sister</span>-matched case-control study, by enrolling 1422 women between September 2008 and December 2010, who were younger than age 50 years at diagnosis with breast cancer and were enrolled within 4 years of diagnosis, and 1669 breast cancer-free control <span class="hlt">sisters</span> from the <span class="hlt">Sister</span> Study. Participants reported their use of fertility drugs (CC and FSH) and ever-users reported whether a pregnancy had resulted that lasted 10 or more (10+) weeks. Conditional logistic regression was used to estimate confounder-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for fertility drug use with or without conception of a 10+ week pregnancy. A total of 288 participants reported having used ovulation-stimulating drugs (193 CC only, 29 FSH only, and 66 both). Overall, women who had used fertility drugs showed a non-statistically significantly decreased risk of breast cancer, compared with nonusers (OR = 0.82, 95% CI = 0.63 to 1.08). Women who had used fertility drugs but had not conceived a 10+ week pregnancy under treatment showed a statistically significantly decreased risk of breast cancer compared with nonusers (OR = 0.62, 95% CI = 0.43 to 0.89). Women who had used fertility drugs and conceived a 10+ week pregnancy under treatment showed a statistically significantly increased risk of breast cancer compared with unsuccessfully treated women (OR = 1.82, 95% CI = 1.10 to 3.00), although their risk was not increased compared with women who had not used fertility drugs (OR = 1.13, 95% CI = 0.78 to 1.64). In the absence of a 10+ week pregnancy under treatment, exposure to ovulation-stimulating fertility drugs was associated with reduced risk of young</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/FR-2011-01-04/pdf/2010-33090.pdf','FEDREG'); return false;" href="https://www.gpo.gov/fdsys/pkg/FR-2011-01-04/pdf/2010-33090.pdf"><span>76 FR 315 - <span class="hlt">Sisters</span> Ranger District; Deschutes National Forest; Oregon; Popper Vegetation Management Project</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collection.action?collectionCode=FR">Federal Register 2010, 2011, 2012, 2013, 2014</a></p> <p></p> <p>2011-01-04</p> <p>... would be located on National Forest System lands south of the city of <span class="hlt">Sisters</span>, Oregon; east of the Three... acre Cascade Timberlands property which is being considered as a future Community Forest. The legal...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/22760803','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/22760803"><span>Comparison of wavefront <span class="hlt">aberrations</span> under cycloplegic, scotopic and photopic conditions using WaveScan.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fan, Rong; He, Tao; Qiu, Yan; Di, Yu-Lan; Xu, Su-yun; Li, Yao-yu</p> <p>2012-01-01</p> <p>To evaluate the differences of wavefront <span class="hlt">aberrations</span> under cycloplegic, scotopic and photopic conditions. A total of 174 eyes of 105 patients were measured using the wavefront sensor (WaveScan® 3.62) under different pupil conditions: cycloplegic 8.58 ± 0.54 mm (6.4 mm - 9.5 mm), scotopic 7.53 ± 0.69 mm (5.7 mm - 9.1 mm) and photopic 6.08 ± 1.14 mm (4.1 mm - 8.8 mm). The pupil diameter, standard Zernike coefficients, root mean square of higher-order <span class="hlt">aberrations</span> and dominant <span class="hlt">aberrations</span> were compared between cycloplegic and scotopic conditions, and between scotopic and photopic conditions. The pupil diameter was 7.53 ± 0.69 mm under the scotopic condition, which reached the requirement of about 6.5 mm optical zone design in the wavefront-guided surgery and prevented measurement error due to the pupil centroid shift caused by mydriatics. Pharmacological pupil dilation induced increase of standard Zernike coefficients Z(3)(-3), Z(4)(0) and Z(5)(-5). The higher-order <span class="hlt">aberrations</span>, third-order <span class="hlt">aberration</span>, fourth-order <span class="hlt">aberration</span>, fifth-order <span class="hlt">aberration</span>, sixth-order <span class="hlt">aberration</span>, and spherical <span class="hlt">aberration</span> increased statistically significantly, compared to the scotopic condition (P<0.010). When the scotopic condition shifted to the photopic condition, the standard Zernike coefficients Z(4)(0), Z(4)(2), Z(6)(-4), Z(6)(-2), Z(6)(2) decreased and all the higher-order <span class="hlt">aberrations</span> decreased statistically significantly (P<0.010), demonstrating that accommodative miosis can significantly improve vision under the photopic condition. Under the three conditions, the vertical coma <span class="hlt">aberration</span> appears the most frequently within the dominant <span class="hlt">aberrations</span> without significant effect by pupil size variance, and the proportion of spherical <span class="hlt">aberrations</span> decreased with the decrease of the pupil size. The wavefront <span class="hlt">aberrations</span> are significantly different under cycloplegic, scotopic and photopic conditions. Using the wavefront sensor (VISX WaveScan) to measure scotopic wavefront <span class="hlt">aberrations</span> is</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4315771','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4315771"><span><span class="hlt">Aberrant</span> Salience, Self-Concept Clarity, and Interview-Rated Psychotic-Like Experiences</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Cicero, David C.; Docherty, Anna R.; Becker, Theresa M.; Martin, Elizabeth A.; Kerns, John G.</p> <p>2014-01-01</p> <p>Many social-cognitive models of psychotic-like symptoms posit a role for self-concept and <span class="hlt">aberrant</span> salience. Previous work has shown that the interaction between <span class="hlt">aberrant</span> salience and self-concept clarity is associated with self-reported psychotic-like experiences. In the current research with two structured interviews, the interaction between <span class="hlt">aberrant</span> salience and self-concept clarity was found to be associated withinterview-rated psychotic-like experiences. The interaction was associated withpsychotic-like experiences composite scores, delusional ideation, grandiosity, and perceptual anomalies. In all cases, self-concept clarity was negatively associated with psychotic-like experiences at high levels of <span class="hlt">aberrant</span> salience, but unassociated with psychotic-like experiences at low levels of <span class="hlt">aberrant</span> salience. The interaction was specific to positive psychotic-like experiences and not present for negative or disorganized ratings. The interaction was not mediated by self-esteem levels. These results provide further evidence that <span class="hlt">aberrant</span> salience and self-concept clarity play an important role in the generation of psychotic-like experiences. PMID:25102085</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4244149','PMC'); return false;" href="https://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4244149"><span>Using Ecological Niche Models and Niche Analyses to Understand Speciation Patterns: The Case of <span class="hlt">Sister</span> Neotropical Orchid Bees</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Silva, Daniel P.; Vilela, Bruno; De Marco, Paulo; Nemésio, André</p> <p>2014-01-01</p> <p>The role of past connections between the two major South American forested biomes on current species distribution has been recognized a long time ago. Climatic oscillations that further separated these biomes have promoted parapatric speciation, in which many species had their continuous distribution split, giving rise to different but related species (i.e., different potential distributions and realized niche features). The distribution of many <span class="hlt">sister</span> species of orchid bees follow this pattern. Here, using ecological niche models and niche analyses, we (1) tested the role of ecological niche differentiation on the divergence between <span class="hlt">sister</span> orchid-bees (genera Eulaema and Eufriesea) from the Amazon and Atlantic forests, and (2) highlighted interesting areas for new surveys. Amazonian species occupied different realized niches than their Atlantic <span class="hlt">sister</span> species. Conversely, species of sympatric but distantly related Eulaema bees occupied similar realized niches. Amazonian species had a wide potential distribution in South America, whereas Atlantic Forest species were more limited to the eastern coast of the continent. Additionally, we identified several areas in need of future surveys. Our results show that the realized niche of Atlantic-Amazonian <span class="hlt">sister</span> species of orchid bees, which have been previously treated as allopatric populations of three species, had limited niche overlap and similarity. These findings agree with their current taxonomy, which treats each of those populations as distinct valid species. PMID:25422941</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/15663107','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/15663107"><span>Recurrent branchial sinus tract with <span class="hlt">aberrant</span> extension.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Barret, J P</p> <p>2004-01-01</p> <p>Second branchial cysts are the commonest lesions among congenital lateral neck anomalies. Good knowledge of anatomy and embryology are necessary for proper treatment. Surgical treatment involves resection of all branchial remnants, which extend laterally in the neck, medial to the sternocleidomastoid muscle with cranial extension to the pharynx and ipsilateral tonsillar fosa. However, infections and previous surgery can distort anatomy, making the approach to branchial anomalies more difficult. We present a case of a 17-year-old patient who presented with a second branchial tract anomaly with an <span class="hlt">aberrant</span> extension to the midline and part of the contralateral neck. Previous surgical interventions and chronic infections may have been the primary cause for this <span class="hlt">aberrant</span> tract. All head and neck surgeons should bear in mind that <span class="hlt">aberrant</span> presentations may exist when reoperating on chronic branchial cysts fistulas.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/11424153','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/11424153"><span>Chromosomal <span class="hlt">aberrations</span> in peripheral lymphocytes of train engine drivers.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nordenson, I; Mild, K H; Järventaus, H; Hirvonen, A; Sandström, M; Wilén, J; Blix, N; Norppa, H</p> <p>2001-07-01</p> <p>Studies of Swedish railway employees have indicated that railroad engine drivers have an increased cancer morbidity and incidence of chronic lymphatic leukemia. The drivers are exposed to relatively high magnetic fields (MF), ranging from a few to over a hundred microT. Although the possible genotoxic potential of MF is unclear, some earlier studies have indicated that occupational exposure to MF may increase chromosome <span class="hlt">aberrations</span> in blood lymphocytes. Since an increased level of chromosomal <span class="hlt">aberrations</span> has been suggested to predict elevated cancer risk, we performed a cytogenetic analysis on cultured (48 h) peripheral lymphocytes of Swedish train engine drivers. A pilot study of 18 engine drivers indicated a significant difference in the frequency of cells with chromosomal <span class="hlt">aberrations</span> (gaps included or excluded) in comparison with seven concurrent referents (train dispatchers) and a control group of 16 office workers. The engine drivers had about four times higher frequency of cells with chromosome-type <span class="hlt">aberrations</span> (excluding gaps) than the office workers (P < 0.01) and the dispatchers (P < 0.05). Seventy-eight percent of the engine drivers showed at least one cell per 100 with chromosome-type <span class="hlt">aberrations</span> compared with 29% among the dispatchers and 31% among the office workers. In a follow-up study, another 30 engine drivers showed an increase (P < 0.05) in the frequency of cells with chromosome-type <span class="hlt">aberrations</span> (gaps excluded) as compared with 30 referent policemen. Sixty percent of the engine drivers had one or more cells (per 100 cells) with chromosome-type <span class="hlt">aberrations</span> compared with 30% among the policemen. In conclusion, the results of the two studies support the hypothesis that exposure to MF at mean intensities of 2-15 microT can induce chromosomal damage. Copyright 2001 Wiley-Liss, Inc.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/24270638','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/24270638"><span>In vivo longitudinal chromatic <span class="hlt">aberration</span> of pseudophakic eyes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Siedlecki, Damian; Jóźwik, Agnieszka; Zając, Marek; Hill-Bator, Aneta; Turno-Kręcicka, Anna</p> <p>2014-02-01</p> <p>To present the results of longitudinal chromatic <span class="hlt">aberration</span> measurements on two groups of pseudophakic eyes in comparison to healthy eyes. The longitudinal chromatic <span class="hlt">aberration</span> of the eye, defined as chromatic difference of refraction with disabled accommodation, was measured with the use of a visual refractometer with a custom-designed target illuminator consisting of a narrow-band RGB diode (blue λb = 470 ± 15 nm; green λg = 525 ± 18 nm; red λr = 660 ± 10 nm). The measurements were performed on nine eyes implanted with AcrySof IQ SN60WF, 14 eyes implanted with AcrySof SA60AT, and 10 phakic eyes under cycloplegia. The mean values of the longitudinal chromatic <span class="hlt">aberration</span> between 470 and 660 nm for the control group was 1.12 ± 0.14 D. For SA60AT group, it was 1.45 ± 0.42 D whereas for SN60WF it was 1.17 ± 0.52 D. The statistical test showed significant difference between SA60AT and the control group (p < 0.05) and no significant difference between SN60WF and the control groups (p = 0.64). The study showed that the longitudinal chromatic <span class="hlt">aberration</span> in vivo can be easily and reliably estimated with an adapted visual refractometer. The two groups of pseudophakic eyes measured in this study showed different values of chromatic <span class="hlt">aberration</span>. Its magnitude for SA60AT group was significantly larger than for the control group whereas for SN60WF the difference was not significant. The optical material used for intraocular lens design may have significant influence on the magnitude of the chromatic <span class="hlt">aberration</span> of the pseudophakic eye, and therefore on its optical and visual performance in polychromatic light.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=lens&pg=3&id=EJ963886','ERIC'); return false;" href="https://eric.ed.gov/?q=lens&pg=3&id=EJ963886"><span>Modified Matching Ronchi Test to Visualize Lens <span class="hlt">Aberrations</span></span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Hassani, Kh; Ziafi, H. Hooshmand</p> <p>2011-01-01</p> <p>We introduce a modification to the matching Ronchi test to visualize lens <span class="hlt">aberrations</span> with simple and inexpensive equipment available in educational optics labs. This method can help instructors and students to observe and estimate lens <span class="hlt">aberrations</span> in real time. It is also a semi-quantitative tool for primary tests in research labs. In this work…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.osti.gov/biblio/5371327','DOE-PATENT-XML'); return false;" href="https://www.osti.gov/biblio/5371327"><span>Sextupole system for the correction of spherical <span class="hlt">aberration</span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/doepatents">DOEpatents</a></p> <p>Crewe, A.V.; Kopf, D.A.</p> <p></p> <p>In an electron beam device in which an electron beam is developed and then focused by a lens to a particular spot, there is provided a means for eliminating spherical <span class="hlt">aberration</span>. A sextupole electromagnetic lens is positioned between two focusing lenses. The interaction of the sextupole with the beam compensates for spherical <span class="hlt">aberration</span>. (GHT)</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://eric.ed.gov/?q=Green+AND+behavior+AND+change&pg=5&id=EJ731689','ERIC'); return false;" href="https://eric.ed.gov/?q=Green+AND+behavior+AND+change&pg=5&id=EJ731689"><span>Persistence of Early Emerging <span class="hlt">Aberrant</span> Behavior in Children with Developmental Disabilities</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Green, Vanessa A.; O'Reilly, Mark; Itchon, Jonathan; Sigafoos, Jeff</p> <p>2005-01-01</p> <p>This study examined the persistence of early emerging <span class="hlt">aberrant</span> behavior in 13 preschool children with developmental disabilities. The severity of <span class="hlt">aberrant</span> behavior was assessed every 6 months over a 3-year period. Teachers completed the assessments using the <span class="hlt">Aberrant</span> Behavior Checklist [Aman, M. G., & Singh, N. N. (1986). "Aberrant…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2018ApPhL.112p3701E','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2018ApPhL.112p3701E"><span>Brillouin micro-spectroscopy through <span class="hlt">aberrations</span> via sensorless adaptive optics</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Edrei, Eitan; Scarcelli, Giuliano</p> <p>2018-04-01</p> <p>Brillouin spectroscopy is a powerful optical technique for non-contact viscoelastic characterizations which has recently found applications in three-dimensional mapping of biological samples. Brillouin spectroscopy performances are rapidly degraded by optical <span class="hlt">aberrations</span> and have therefore been limited to homogenous transparent samples. In this work, we developed an adaptive optics (AO) configuration designed for Brillouin scattering spectroscopy to engineer the incident wavefront and correct for <span class="hlt">aberrations</span>. Our configuration does not require direct wavefront sensing and the injection of a "guide-star"; hence, it can be implemented without the need for sample pre-treatment. We used our AO-Brillouin spectrometer in <span class="hlt">aberrated</span> phantoms and biological samples and obtained improved precision and resolution of Brillouin spectral analysis; we demonstrated 2.5-fold enhancement in Brillouin signal strength and 1.4-fold improvement in axial resolution because of the correction of optical <span class="hlt">aberrations</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/8249156','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/8249156"><span>[The clinical and cytogenetic characteristics of the children born to persons with a history of 1st- and 2d-degree acute radiation sickness as a result of the accident at the Chernobyl Atomic Electric Power Station].</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Stepanova, E I; Vaniurikhina, E A</p> <p>1993-01-01</p> <p>We have examined 15 children (born in 1987-1988), whose fathers liquidated the aftereffects of the accident at Chernobyl Nuclear Power Plant and suffered from acute radiation sickness of the 1st and 2nd stages and 50 children of the control group. The obtained data showed that the number of small developmental abnormalities (stigmas of dysembryogenesis) increased as well as the <span class="hlt">chromatid</span> <span class="hlt">aberration</span> frequency as compared with the control group.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/20040448','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/20040448"><span>A model of distributed phase <span class="hlt">aberration</span> for deblurring phase estimated from scattering.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Tillett, Jason C; Astheimer, Jeffrey P; Waag, Robert C</p> <p>2010-01-01</p> <p>Correction of <span class="hlt">aberration</span> in ultrasound imaging uses the response of a point reflector or its equivalent to characterize the <span class="hlt">aberration</span>. Because a point reflector is usually unavailable, its equivalent is obtained using statistical methods, such as processing reflections from multiple focal regions in a random medium. However, the validity of methods that use reflections from multiple points is limited to isoplanatic patches for which the <span class="hlt">aberration</span> is essentially the same. In this study, <span class="hlt">aberration</span> is modeled by an offset phase screen to relax the isoplanatic restriction. Methods are developed to determine the depth and phase of the screen and to use the model for compensation of <span class="hlt">aberration</span> as the beam is steered. Use of the model to enhance the performance of the noted statistical estimation procedure is also described. Experimental results obtained with tissue-mimicking phantoms that implement different models and produce different amounts of <span class="hlt">aberration</span> are presented to show the efficacy of these methods. The improvement in b-scan resolution realized with the model is illustrated. The results show that the isoplanatic patch assumption for estimation of <span class="hlt">aberration</span> can be relaxed and that propagation-path characteristics and <span class="hlt">aberration</span> estimation are closely related.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/7508088','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/7508088"><span>Chromosome damage in lymphocytes of stainless steel welders related to past and current exposure to manual metal arc welding fumes.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Jelmert, O; Hansteen, I L; Langård, S</p> <p>1994-02-01</p> <p>Cytogenetic damage was studied in lymphocytes from 42 welders using the manual metal arc (MMA) method on stainless steel (SS). A detailed characterization of previous exposure by job interviews, and for current exposure with personal air sampling and biological monitoring of chromium (Cr) and nickel (Ni) in blood and urine, was done for 32 of these welders. A subgroup of 20 welders was studied before and after 1-4 months of MMA/SS welding. A matched reference group I, and a larger reference group II were established for comparison. A significant increase in <span class="hlt">chromatid</span> breaks (1.4 vs. 0.9 and 0.8 for group I and II) and for cells with <span class="hlt">aberrations</span> (2.2 vs. 1.6 in group II) was found in the welders. An even larger difference was found when comparing non-smoking welders with their non-smoking referents. No synergistic effect between smoking and MMA/SS welding fumes was observed for any type of <span class="hlt">aberrations</span>. Current welding fume exposure during the week before sampling was not associated with increases in any type of cytogenetic damage. The results indicated that the increase in <span class="hlt">chromatid</span> breaks was associated with cumulated welding fume exposure for more than a year, and with not using respirators. Exposure to MMA/SS welding fumes for up to 4 months gave a slight, but significant increase in <span class="hlt">chromatid</span> breaks when using the welders as their own referents. However, when using matched referents in the study after exposure, no difference was found between these welders and their matched referents. No differences between the groups were observed in the DNA synthesis and repair-inhibited cultures or for SCE.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.ncbi.nlm.nih.gov/pubmed/28681906','PUBMED'); return false;" href="https://www.ncbi.nlm.nih.gov/pubmed/28681906"><span>Refractive Changes Induced by Spherical <span class="hlt">Aberration</span> in Laser Correction Procedures: An Adaptive Optics Study.</span></a></p> <p><a target="_blank" href="https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Amigó, Alfredo; Martinez-Sorribes, Paula; Recuerda, Margarita</p> <p>2017-07-01</p> <p>To study the effect on vision of induced negative and positive spherical <span class="hlt">aberration</span> within the range of laser vision correction procedures. In 10 eyes (mean age: 35.8 years) under cyclopegic conditions, spherical <span class="hlt">aberration</span> values from -0.75 to +0.75 µm in 0.25-µm steps were induced by an adaptive optics system. Astigmatism and spherical refraction were corrected, whereas the other natural <span class="hlt">aberrations</span> remained untouched. Visual acuity, depth of focus defined as the interval of vision for which the target was still perceived acceptable, contrast sensitivity, and change in spherical refraction associated with the variation in pupil diameter from 6 to 2.5 mm were measured. A refractive change of 1.60 D/µm of induced spherical <span class="hlt">aberration</span> was obtained. Emmetropic eyes became myopic when positive spherical <span class="hlt">aberration</span> was induced and hyperopic when negative spherical <span class="hlt">aberration</span> was induced (R 2 = 81%). There were weak correlations between spherical <span class="hlt">aberration</span> and visual acuity or depth of focus (R 2 = 2% and 3%, respectively). Contrast sensitivity worsened with the increment of spherical <span class="hlt">aberration</span> (R 2 = 59%). When pupil size decreased, emmetropic eyes became hyperopic when preexisting spherical <span class="hlt">aberration</span> was positive and myopic when spherical <span class="hlt">aberration</span> was negative, with an average refractive change of 0.60 D/µm of spherical <span class="hlt">aberration</span> (R 2 = 54%). An inverse linear correlation exists between the refractive state of the eye and spherical <span class="hlt">aberration</span> induced within the range of laser vision correction. Small values of spherical <span class="hlt">aberration</span> do not worsen visual acuity or depth of focus, but positive spherical <span class="hlt">aberration</span> may induce night myopia. In addition, the changes in spherical refraction when the pupil constricts may worsen near vision when positive spherical <span class="hlt">aberration</span> is induced or improve it when spherical <span class="hlt">aberration</span> is negative. [J Refract Surg. 2017;33(7):470-474.]. 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