Alpha-CaMKII plays a critical role in determining the aggressive behavior of human osteosarcoma

PubMed Central

Daft, Paul G.; Yuan, Kaiyu; Warram, Jason M.; Klein, Michael J.; Siegal, Gene P.; Zayzafoon, Majd

2013-01-01

Osteosarcoma is among the most frequently occurring primary bone tumors, primarily affecting adolescents and young adults. Despite improvements in osteosarcoma treatment, more specific molecular targets are needed as potential therapeutic options. One target of interest is alpha-Ca2+/calmodulin-dependent protein kinase II (α-CaMKII), a ubiquitous mediator of Ca2+-linked signaling, which has been shown to regulate tumor cell proliferation and differentiation. Here, we investigate the role of α-CaMKII in the growth and tumorigenicity of human osteosarcoma. We show that α-CaMKII is highly expressed in primary osteosarcoma tissue derived from 114 patients and is expressed in varying levels in different human osteosarcoma cell lines (HOS, MG-63, MNNG/HOS and 143B). To examine whether α-CaMKII regulates osteosarcoma tumorigenic properties, we genetically inhibited α-CaMKII in two osteosarcoma cell lines using two different α-CaMKII shRNAs delivered by lentiviral vectors and overexpressed α-CaMKII by retrovirus. The genetic deletion of α-CaMKII by shRNA in MG-63 and 143B cells resulted in decreased proliferation (50 and 41%), migration (22 and 25%) and invasion (95 and 90%), respectively. The overexpression of α-CaMKII in HOS cells resulted in increased proliferation (240%), migration (640%) and invasion (10,000%). Furthermore, α-CaMKII deletion in MG-63 cells significantly reduced tumor burden in vivo (65%), while α-CaMKII overexpression resulted in tumor formation in a previously non-tumor forming osteosarcoma cell line (HOS). Our results suggest that α-CaMKII plays a critical role in determining the aggressive phenotype of osteosarcoma, and its inhibition could be an attractive therapeutic target to combat this devastating adolescent disease. PMID:23364534

Alpha-CaMKII plays a critical role in determining the aggressive behavior of human osteosarcoma.

PubMed

Daft, Paul G; Yuan, Kaiyu; Warram, Jason M; Klein, Michael J; Siegal, Gene P; Zayzafoon, Majd

2013-04-01

Osteosarcoma is among the most frequently occurring primary bone tumors, primarily affecting adolescents and young adults. Despite improvements in osteosarcoma treatment, more specific molecular targets are needed as potential therapeutic options. One target of interest is α-Ca(2+)/calmodulin-dependent protein kinase II (α-CaMKII), a ubiquitous mediator of Ca(2+)-linked signaling, which has been shown to regulate tumor cell proliferation and differentiation. Here, we investigate the role of α-CaMKII in the growth and tumorigenicity of human osteosarcoma. We show that α-CaMKII is highly expressed in primary osteosarcoma tissue derived from 114 patients, and is expressed in varying levels in different human osteosarcoma (OS) cell lines [MG-63, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)/HOS, and 143B). To examine whether α-CaMKII regulates osteosarcoma tumorigenic properties, we genetically inhibited α-CaMKII in two osteosarcoma cell lines using two different α-CaMKII shRNAs delivered by lentiviral vectors and overexpressed α-CaMKII by retrovirus. The genetic deletion of α-CaMKII by short hairpin RNA (shRNA) in MG-63 and 143B cells resulted in decreased proliferation (50% and 41%), migration (22% and 25%), and invasion (95% and 90%), respectively. The overexpression of α-CaMKII in HOS cells resulted in increased proliferation (240%), migration (640%), and invasion (10,000%). Furthermore, α-CaMKII deletion in MG-63 cells significantly reduced tumor burden in vivo (65%), whereas α-CaMKII overexpression resulted in tumor formation in a previously nontumor forming osteosarcoma cell line (HOS). Our results suggest that α-CaMKII plays a critical role in determining the aggressive phenotype of osteosarcoma, and its inhibition could be an attractive therapeutic target to combat this devastating adolescent disease. ©2013 AACR.

CaMKII effects on inotropic but not lusitropic force frequency responses require phospholamban

PubMed Central

Wu, Yiming; Luczak, Elizabeth D; Lee, Eun-Jeong; Hidalgo, Carlos; Yang, Jinying; Gao, Zhan; Li, Jingdong; Wehrens, Xander; Granzier, Henk; Anderson, Mark E

2014-01-01

Increasing heart rate enhances cardiac contractility (force frequency relationship, FFR) and accelerates cardiac relaxation (frequency-dependent acceleration of relaxation, FDAR). The positive FFR together with FDAR promotes rapid filling and ejection of blood from the left ventricle (LV) at higher heart rates. Recent studies indicate that the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) is involved in regulating FFR and FDAR. We used isolated perfused mouse hearts to study the mechanisms of FFR and FDAR in different genetic models, including transgenic myocardial CaMKII inhibition (AC3-I) and phosphalamban knockout (PLN−/−). When the rate was increased from 360 beats/min to 630 beats/min in wild type mouse hearts, the LV developed pressure (LVDP) and the maximum rate of increase in pressure (dP/dt max) increased by 37.6 ± 4.7% and 77.0 ± 8.1%, respectively. However, hearts from AC3-I littermates showed no increase of LVDP and a relatively modest (20.4 ± 3.9 %) increase in dP/dt max. PLN−/− hearts had a negative FFR, and myocardial AC3-I expression did not change the FFR in PLN−/− mice. PLN−/− mouse hearts did not exhibit FDAR, while PLN−/−mice with myocardial AC3-I expression showed further frequency dependent reductions in cardiac relaxation, suggesting CaMKII targets in addition to PLN were critical to myocardial relaxation. We incubated a constitutively active form of CaMKII with chemically-skinned myocardium and found that several myofilament proteins were phosphorylated by CaMKII. However, CaMKII did not affect myofilament calcium sensitivity. Our study shows that CaMKII plays an important role in modulating FFR and FDAR in murine hearts and suggest that PLN is a critical target for CaMKII effects on FFR, while CaMKII effects on FDAR partially require PLN-alternative targets. PMID:22796260

CASK regulates CaMKII autophosphorylation in neuronal growth, calcium signaling, and learning

PubMed Central

Gillespie, John M.; Hodge, James J. L.

2013-01-01

Calcium (Ca2+)/calmodulin (CaM)-dependent kinase II (CaMKII) activity plays a fundamental role in learning and memory. A key feature of CaMKII in memory formation is its ability to be regulated by autophosphorylation, which switches its activity on and off during synaptic plasticity. The synaptic scaffolding protein CASK (calcium (Ca2+)/calmodulin (CaM) associated serine kinase) is also important for learning and memory, as mutations in CASK result in intellectual disability and neurological defects in humans. We show that in Drosophila larvae, CASK interacts with CaMKII to control neuronal growth and calcium signaling. Furthermore, deletion of the CaMK-like and L27 domains of CASK (CASK β null) or expression of overactive CaMKII (T287D) produced similar effects on synaptic growth and Ca2+ signaling. CASK overexpression rescues the effects of CaMKII overactivity, consistent with the notion that CASK and CaMKII act in a common pathway that controls these neuronal processes. The reduction in Ca2+ signaling observed in the CASK β null mutant caused a decrease in vesicle trafficking at synapses. In addition, the decrease in Ca2+ signaling in CASK mutants was associated with an increase in Ether-à-go-go (EAG) potassium (K+) channel localization to synapses. Reducing EAG restored the decrease in Ca2+ signaling observed in CASK mutants to the level of wildtype, suggesting that CASK regulates Ca2+ signaling via EAG. CASK knockdown reduced both appetitive associative learning and odor evoked Ca2+ responses in Drosophila mushroom bodies, which are the learning centers of Drosophila. Expression of human CASK in Drosophila rescued the effect of CASK deletion on the activity state of CaMKII, suggesting that human CASK may also regulate CaMKII autophosphorylation. PMID:24062638

Translocation of CaMKII to dendritic microtubules supports the plasticity of local synapses

PubMed Central

Lemieux, Mado; Labrecque, Simon; Tardif, Christian; Labrie-Dion, Étienne; LeBel, Éric

2012-01-01

The processing of excitatory synaptic inputs involves compartmentalized dendritic Ca2+ oscillations. The downstream signaling evoked by these local Ca2+ transients and their impact on local synaptic development and remodeling are unknown. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an important decoder of Ca2+ signals and mediator of synaptic plasticity. In addition to its known accumulation at spines, we observed with live imaging the dynamic recruitment of CaMKII to dendritic subdomains adjacent to activated synapses in cultured hippocampal neurons. This localized and transient enrichment of CaMKII to dendritic sites coincided spatially and temporally with dendritic Ca2+ transients. We show that it involved an interaction with microtubular elements, required activation of the kinase, and led to localized dendritic CaMKII autophosphorylation. This process was accompanied by the adjacent remodeling of spines and synaptic AMPA receptor insertion. Replacement of endogenous CaMKII with a mutant that cannot translocate within dendrites lessened this activity-dependent synaptic plasticity. Thus, CaMKII could decode compartmental dendritic Ca2+ transients to support remodeling of local synapses. PMID:22965911

Properties of Contextual Memory Formed in the Absence of αCaMKII Autophosphorylation

PubMed Central

2011-01-01

The alpha-isoform of calcium/calmodulin-dependent kinase II (αCaMKII) is a major synaptic kinase that undergoes autophosphorylation after NMDA receptor activation, switching the kinase into a calcium-independent activity state. This αCaMKII autophosphorylation is essential for NMDA receptor-dependent long-term potentiation (LTP), induced by a single tetanus, in hippocampal area CA1 and in neocortex. Furthermore, the αCaMKII autophosphorylation is essential for contextual long-term memory (LTM) formation after a single training trial but not after a massed training session. Here, we show that in the absence of αCaMKII autophosphorylation contextual fear conditioning is hippocampus dependent and that multi-tetanus-dependent late-LTP cannot be induced in hippocampal area CA1. Furthermore, we show that in the absence of αCaMKII autophosphorylation contextual LTM persists for 30 days, the latest time point tested. Additionally, contextual, but not cued, LTM formation in the absence of αCaMKII autophosphorylation appears to be impaired in 18 month-old mice. Taken together, our findings suggest that αCaMKII autophosphorylation-independent plasticity in the hippocampus is sufficient for contextual LTM formation and that αCaMKII autophosphorylation may be important for delaying age-related impairments in hippocampal memory formation. Furthermore, they propose that NMDA receptor-dependent LTP in hippocampal area CA1 is essential for contextual LTM formation after a single trial but not after massed training. Finally, our results challenge the proposal that NMDA receptor-dependent LTP in neocortex is required for remote contextual LTM. PMID:21276220

Diabetes increases mortality after myocardial infarction by oxidizing CaMKII

PubMed Central

Luo, Min; Guan, Xiaoqun; Luczak, Elizabeth D.; Lang, Di; Kutschke, William; Gao, Zhan; Yang, Jinying; Glynn, Patric; Sossalla, Samuel; Swaminathan, Paari D.; Weiss, Robert M.; Yang, Baoli; Rokita, Adam G.; Maier, Lars S.; Efimov, Igor R.; Hund, Thomas J.; Anderson, Mark E.

2013-01-01

Diabetes increases oxidant stress and doubles the risk of dying after myocardial infarction, but the mechanisms underlying increased mortality are unknown. Mice with streptozotocin-induced diabetes developed profound heart rate slowing and doubled mortality compared with controls after myocardial infarction. Oxidized Ca2+/calmodulin-dependent protein kinase II (ox-CaMKII) was significantly increased in pacemaker tissues from diabetic patients compared with that in nondiabetic patients after myocardial infarction. Streptozotocin-treated mice had increased pacemaker cell ox-CaMKII and apoptosis, which were further enhanced by myocardial infarction. We developed a knockin mouse model of oxidation-resistant CaMKIIδ (MM-VV), the isoform associated with cardiovascular disease. Streptozotocin-treated MM-VV mice and WT mice infused with MitoTEMPO, a mitochondrial targeted antioxidant, expressed significantly less ox-CaMKII, exhibited increased pacemaker cell survival, maintained normal heart rates, and were resistant to diabetes-attributable mortality after myocardial infarction. Our findings suggest that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction. PMID:23426181

Aging and CaMKII alter intracellular Ca2+ transients and heart rhythm in Drosophila melanogaster.

PubMed

Santalla, Manuela; Valverde, Carlos A; Harnichar, Ezequiel; Lacunza, Ezequiel; Aguilar-Fuentes, Javier; Mattiazzi, Alicia; Ferrero, Paola

2014-01-01

Aging is associated to disrupted contractility and rhythmicity, among other cardiovascular alterations. Drosophila melanogaster shows a pattern of aging similar to human beings and recapitulates the arrhythmogenic conditions found in the human heart. Moreover, the kinase CaMKII has been characterized as an important regulator of heart function and an arrhythmogenic molecule that participate in Ca2+ handling. Using a genetically engineered expressed Ca2+ indicator, we report changes in cardiac Ca2+ handling at two different ages. Aging prolonged relaxation, reduced spontaneous heart rate (HR) and increased the occurrence of arrhythmias, ectopic beats and asystoles. Alignment between Drosophila melanogaster and human CaMKII showed a high degree of conservation and indicates that relevant phosphorylation sites in humans are also present in the fruit fly. Inhibition of CaMKII by KN-93 (CaMKII-specific inhibitor), reduced HR without significant changes in other parameters. By contrast, overexpression of CaMKII increased HR and reduced arrhythmias. Moreover, it increased fluorescence amplitude, maximal rate of rise of fluorescence and reduced time to peak fluorescence. These results suggest that CaMKII in Drosophila melanogaster acts directly on heart function and that increasing CaMKII expression levels could be beneficial to improve contractility.

Mechanisms for localising calcineurin and CaMKII in dendritic spines.

PubMed

Penny, Christopher J; Gold, Matthew G

2018-05-27

Calcineurin and calmodulin-dependent protein kinase II (CaMKII) are both highly abundant in neurons, and both are activated by calmodulin at similar Ca 2+ concentrations in the test tube. However, they fulfill opposite functions in dendritic spines, with CaMKII activity driving long-term synaptic potentiation following large influxes of Ca 2+ through NMDA-type glutamate receptors (NMDARs), and calcineurin responding to smaller influxes of Ca 2+ through the same receptors to induce long-term depression. In this review, we explore the notion that precise dynamic localisation of the two enzymes at different sites within dendritic spines is fundamental to this behavior. We describe the structural basis of calcineurin and CaMKII localisation by their interaction with proteins including AKAP79, densin-180, α-actinin, and NMDARs. We then consider how interactions with these proteins likely position calcineurin and CaMKII at different distances from Ca 2+ microdomains emanating from the mouths of NMDARs in order to drive the divergent responses. We also highlight shortcomings in our current understanding of synaptic localisation of these two important signalling enzymes. Copyright © 2017. Published by Elsevier Inc.

Memory Erasure Experiments Indicate a Critical Role of CaMKII in Memory Storage.

PubMed

Rossetti, Tom; Banerjee, Somdeb; Kim, Chris; Leubner, Megan; Lamar, Casey; Gupta, Pooja; Lee, Bomsol; Neve, Rachael; Lisman, John

2017-09-27

The abundant synaptic protein CaMKII is necessary for long-term potentiation (LTP) and memory. However, whether CaMKII is required only during initial processes or whether it also mediates memory storage remains unclear. The most direct test of a storage role is the erasure test. In this test, a putative memory molecule is inhibited after learning. The key prediction is that this should produce persistent memory erasure even after the inhibitory agent is removed. We conducted this test using transient viral (HSV) expression of dominant-negative CaMKII-alpha (K42M) in the hippocampus. This produced persistent erasure of conditioned place avoidance. As an additional test, we found that expression of activated CaMKII (T286D/T305A/T306A) impaired place avoidance, a result not expected if a process other than CaMKII stores memory. Our behavioral results, taken together with prior experiments on LTP, strongly support a critical role of CaMKII in LTP maintenance and memory storage. Copyright © 2017 Elsevier Inc. All rights reserved.

Calcium signaling through CaMKII regulates hepatic glucose production in fasting and obesity.

PubMed

Ozcan, Lale; Wong, Catherine C L; Li, Gang; Xu, Tao; Pajvani, Utpal; Park, Sung Kyu Robin; Wronska, Anetta; Chen, Bi-Xing; Marks, Andrew R; Fukamizu, Akiyoshi; Backs, Johannes; Singer, Harold A; Yates, John R; Accili, Domenico; Tabas, Ira

2012-05-02

Hepatic glucose production (HGP) is crucial for glucose homeostasis, but the underlying mechanisms have not been fully elucidated. Here, we show that a calcium-sensing enzyme, CaMKII, is activated in a calcium- and IP3R-dependent manner by cAMP and glucagon in primary hepatocytes and by glucagon and fasting in vivo. Genetic deficiency or inhibition of CaMKII blocks nuclear translocation of FoxO1 by affecting its phosphorylation, impairs fasting- and glucagon/cAMP-induced glycogenolysis and gluconeogenesis, and lowers blood glucose levels, while constitutively active CaMKII has the opposite effects. Importantly, the suppressive effect of CaMKII deficiency on glucose metabolism is abrogated by transduction with constitutively nuclear FoxO1, indicating that the effect of CaMKII deficiency requires nuclear exclusion of FoxO1. This same pathway is also involved in excessive HGP in the setting of obesity. These results reveal a calcium-mediated signaling pathway involved in FoxO1 nuclear localization and hepatic glucose homeostasis. Copyright © 2012 Elsevier Inc. All rights reserved.

Calcium signaling through CaMKII regulates hepatic glucose production in fasting and obesity

PubMed Central

Ozcan, Lale; Wong, Catherine C.L.; Li, Gang; Xu, Tao; Pajvani, Utpal; Park, Sung Kyu Robin; Wronska, Anetta; Chen, Bi-Xing; Marks, Andrew R.; Fukamizu, Akiyoshi; Backs, Johannes; Singer, Harold A.; Yates, John R.; Accili, Domenico; Tabas, Ira

2012-01-01

SUMMARY Hepatic glucose production (HGP) is crucial for glucose homeostasis, but the underlying mechanisms have not been fully elucidated. Here we show that a calcium-sensing enzyme, CaMKII, is activated in a calcium- and IP3R-dependent manner by cAMP and glucagon in primary HCs and by glucagon and fasting in vivo. Genetic deficiency or inhibition of CaMKII blocks nuclear translocation of FoxO1 by affecting its phosphorylation, impairs fasting- and glucagon/cAMP-induced glycogenolysis and gluconeogenesis, and lowers blood glucose levels, while constitutively active CaMKII has the opposite effects. Importantly, the suppressive effect of CaMKII deficiency on glucose metabolism is abrogated by transduction with constitutively nuclear FoxO1, indicating that the effect of CaMKII deficiency requires nuclear exclusion of FoxO1. This same pathway is also involved in excessive HGP in the setting of obesity. These results reveal a calcium-mediated signaling pathway involved in FoxO1 nuclear localization and hepatic glucose homeostasis. PMID:22503562

Aging and CaMKII Alter Intracellular Ca2+ Transients and Heart Rhythm in Drosophila melanogaster

PubMed Central

Santalla, Manuela; Valverde, Carlos A.; Harnichar, Ezequiel; Lacunza, Ezequiel; Aguilar-Fuentes, Javier; Mattiazzi, Alicia; Ferrero, Paola

2014-01-01

Aging is associated to disrupted contractility and rhythmicity, among other cardiovascular alterations. Drosophila melanogaster shows a pattern of aging similar to human beings and recapitulates the arrhythmogenic conditions found in the human heart. Moreover, the kinase CaMKII has been characterized as an important regulator of heart function and an arrhythmogenic molecule that participate in Ca2+ handling. Using a genetically engineered expressed Ca2+ indicator, we report changes in cardiac Ca2+ handling at two different ages. Aging prolonged relaxation, reduced spontaneous heart rate (HR) and increased the occurrence of arrhythmias, ectopic beats and asystoles. Alignment between Drosophila melanogaster and human CaMKII showed a high degree of conservation and indicates that relevant phosphorylation sites in humans are also present in the fruit fly. Inhibition of CaMKII by KN-93 (CaMKII-specific inhibitor), reduced HR without significant changes in other parameters. By contrast, overexpression of CaMKII increased HR and reduced arrhythmias. Moreover, it increased fluorescence amplitude, maximal rate of rise of fluorescence and reduced time to peak fluorescence. These results suggest that CaMKII in Drosophila melanogaster acts directly on heart function and that increasing CaMKII expression levels could be beneficial to improve contractility. PMID:25003749

Activation-triggered subunit exchange between CaMKII holoenzymes facilitates the spread of kinase activity

PubMed Central

Stratton, Margaret; Lee, Il-Hyung; Bhattacharyya, Moitrayee; Christensen, Sune M; Chao, Luke H; Schulman, Howard; Groves, Jay T; Kuriyan, John

2014-01-01

The activation of the dodecameric Ca2+/calmodulin dependent kinase II (CaMKII) holoenzyme is critical for memory formation. We now report that CaMKII has a remarkable property, which is that activation of the holoenzyme triggers the exchange of subunits between holoenzymes, including unactivated ones, enabling the calcium-independent phosphorylation of new subunits. We show, using a single-molecule TIRF microscopy technique, that the exchange process is triggered by the activation of CaMKII, and that exchange is modulated by phosphorylation of two residues in the calmodulin-binding segment, Thr 305 and Thr 306. Based on these results, and on the analysis of molecular dynamics simulations, we suggest that the phosphorylated regulatory segment of CaMKII interacts with the central hub of the holoenzyme and weakens its integrity, thereby promoting exchange. Our results have implications for an earlier idea that subunit exchange in CaMKII may have relevance for information storage resulting from brief coincident stimuli during neuronal signaling. DOI: http://dx.doi.org/10.7554/eLife.01610.001 PMID:24473075

Subcellular Organization of CaMKII in Rat Hippocampal Pyramidal Neurons

PubMed Central

Ding, Jin-Dong; Kennedy, Mary B.; Weinberg, Richard J.

2015-01-01

Calcium/calmodulin-dependent protein kinase II (CaM-KII) plays a key role in N-methyl-D-aspartate (NMDA) receptor-dependent long-term synaptic plasticity; its location is critical for signal transduction, and may provide clues that further elucidate its function. We therefore examined the subcellular localization of CaMKII in CA1 stratum radiatum of adult rat hippocampus, by using immuno-electron microscopy after chemical fixation. When tissue was fixed quickly, the concentration of CaMKIIα (assessed by pre-embedding immunogold) was significantly higher in dendritic shafts than in spine heads. However, when tissue was fixed 5 minutes after perfusion with normal saline, the density of labeling decreased in dendritic shaft while increasing in spine heads, implying rapid translocation into the spine during brief perimortem stress. Likewise, in quickly fixed tissue, CaMKII within spine heads was found at comparable concentrations in the “proximal” half (adjacent to the spine neck) and the “distal” half (containing the postsynaptic density [PSD]), whereas after delayed fixation, label density increased in the distal side of the spine head, suggesting that CaMKII within the spine head moves toward the PSD during this interval. To estimate its distribution at the synapse in vivo, we performed postembedding immunogold staining for CaMKII in quick-fixed tissue, and found that the enzyme did not concentrate primarily within the central matrix of the PSD. Instead, labeling density peaked ∼40 nm inside the postsynaptic membrane, at the cytoplasmic fringe of the PSD. Labeling within 25 nm of the postsynaptic membrane concentrated at the lateral edge of the synapse. This lateral “PSD core” pool of CaMKII may play a special role in synaptic plasticity. PMID:23749614

Periodic Mechanical Stress INDUCES Chondrocyte Proliferation and Matrix Synthesis via CaMKII-Mediated Pyk2 Signaling.

PubMed

Liang, Wenwei; Li, Zeng; Wang, Zhen; Zhou, Jinchun; Song, Huanghe; Xu, Shun; Cui, Weiding; Wang, Qing; Chen, Zhefeng; Liu, Feng; Fan, Weimin

2017-01-01

Periodic mechanical stress can promote chondrocyte proliferation and matrix synthesis to improve the quality of tissue-engineered cartilage. Although the integrin β1-ERK1/2 signal cascade has been implicated in periodic mechanical stress-induced mitogenic effects in chondrocytes, the precise mechanisms have not been fully established. The current study was designed to probe the roles of CaMKII and Pyk2 signaling in periodic mechanical stress-mediated chondrocyte proliferation and matrix synthesis. Chondrocytes were subjected to periodic mechanical stress, proliferation was assessed by direct cell counting and CCK-8 assay; gene expressions were analyzed using quantitative real-time PCR, protein abundance by Western blotting. Mechanical stress, markedly enhanced the phosphorylation levels of Pyk2 at Tyr402 and CaMKII at Thr286. Both suppression of Pyk2 with Pyk2 inhibitor PF431396 or Pyk2 shRNA and suppression of CaMKII with CaMKII inhibitor KN-93 or CaMKII shRNA blocked periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis. Additionally, either pretreatment with KN-93 or shRNA targeted to CaMKII prevented the activation of ERK1/2 and Pyk2 under conditions of periodic mechanical stress. Interestingly, in relation to periodic mechanical stress, in the context of Pyk2 inhibition with PF431396 or its targeted shRNA, only the phosphorylation levels of ERK1/2 were abrogated, while CaMKII signal activation was not affected. Moreover, the phosphorylation levels of CaMKII- Thr286 and Pyk2- Tyr402 were abolished after pretreatment with blocking antibody against integrinβ1 exposed to periodic mechanical stress. Our results collectively indicate that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis through the integrinβ1-CaMKII-Pyk2-ERK1/2 signaling cascade. © 2017 The Author(s). Published by S. Karger AG, Basel.

CaMKII and CaMKIV mediate distinct prosurvival signaling pathways in response to depolarization in neurons

PubMed Central

Bok, Jinwoong; Wang, Qiong; Huang, Jie; Green, Steven H.

2007-01-01

By fusing the CaMKII inhibitory peptide AIP to GFP, we constructed a specific and effective CaMKII inhibitor, GFP-AIP. Expression of GFP-AIP and/or dominant-inhibitory CaMKIV in cultured neonatal rat spiral ganglion neurons (SGNs) shows that CaMKII and CaMKIV act additively and in parallel, to mediate the prosurvival effect of depolarization. Depolarization or expression of constitutively-active CaMKII functionally inactivates Bad, indicating that this is one means by which CaMKII promotes neuronal survival. CaMKIV, but not CaMKII, requires CREB to promote SGN survival, consistent with the exclusively nuclear localization of CaMKIV and indicating that the principal prosurvival function of CaMKIV is activation of CREB. Consistent with this, a constitutively-active CREB construct that provides a high level of CREB activity promotes SGN survival, although low levels of CREB activity did not do so. Also, in apoptotic SGNs, activation of CREB by depolarization is disabled, presumably as part of a cellular commitment to apoptosis. PMID:17651987

Oxidized CaMKII causes cardiac sinus node dysfunction in mice

PubMed Central

Swaminathan, Paari Dominic; Purohit, Anil; Soni, Siddarth; Voigt, Niels; Singh, Madhu V.; Glukhov, Alexey V.; Gao, Zhan; He, B. Julie; Luczak, Elizabeth D.; Joiner, Mei-ling A.; Kutschke, William; Yang, Jinying; Donahue, J. Kevin; Weiss, Robert M.; Grumbach, Isabella M.; Ogawa, Masahiro; Chen, Peng-Sheng; Efimov, Igor; Dobrev, Dobromir; Mohler, Peter J.; Hund, Thomas J.; Anderson, Mark E.

2011-01-01

Sinus node dysfunction (SND) is a major public health problem that is associated with sudden cardiac death and requires surgical implantation of artificial pacemakers. However, little is known about the molecular and cellular mechanisms that cause SND. Most SND occurs in the setting of heart failure and hypertension, conditions that are marked by elevated circulating angiotensin II (Ang II) and increased oxidant stress. Here, we show that oxidized calmodulin kinase II (ox-CaMKII) is a biomarker for SND in patients and dogs and a disease determinant in mice. In wild-type mice, Ang II infusion caused sinoatrial nodal (SAN) cell oxidation by activating NADPH oxidase, leading to increased ox-CaMKII, SAN cell apoptosis, and SND. p47–/– mice lacking functional NADPH oxidase and mice with myocardial or SAN-targeted CaMKII inhibition were highly resistant to SAN apoptosis and SND, suggesting that ox-CaMKII–triggered SAN cell death contributed to SND. We developed a computational model of the sinoatrial node that showed that a loss of SAN cells below a critical threshold caused SND by preventing normal impulse formation and propagation. These data provide novel molecular and mechanistic information to understand SND and suggest that targeted CaMKII inhibition may be useful for preventing SND in high-risk patients. PMID:21785215

Temporal and Region-Specific Requirements of αCaMKII in Spatial and Contextual Learning

PubMed Central

Achterberg, Katharina G.; Buitendijk, Gabriëlle H.S.; Kool, Martijn J.; Goorden, Susanna M.I.; Post, Laura; Slump, Denise E.; Silva, Alcino J.; van Woerden, Geeske M.

2014-01-01

The α isoform of the calcium/calmodulin-dependent protein kinase II (αCaMKII) has been implicated extensively in molecular and cellular mechanisms underlying spatial and contextual learning in a wide variety of species. Germline deletion of Camk2a leads to severe deficits in spatial and contextual learning in mice. However, the temporal and region-specific requirements for αCaMKII have remained largely unexplored. Here, we generated conditional Camk2a mutants to examine the influence of spatially restricted and temporally controlled expression of αCaMKII. Forebrain-specific deletion of the Camk2a gene resulted in severe deficits in water maze and contextual fear learning, whereas mice with deletion restricted to the cerebellum learned normally. Furthermore, we found that temporally controlled deletion of the Camk2a gene in adult mice is as detrimental as germline deletion for learning and synaptic plasticity. Together, we confirm the requirement for αCaMKII in the forebrain, but not the cerebellum, in spatial and contextual learning. Moreover, we highlight the absolute requirement for intact αCaMKII expression at the time of learning. PMID:25143599

CASK and CaMKII function in the mushroom body α'/β' neurons during Drosophila memory formation.

PubMed

Malik, Bilal R; Gillespie, John Michael; Hodge, James J L

2013-01-01

Ca(2+)/CaM serine/threonine kinase II (CaMKII) is a central molecule in mechanisms of synaptic plasticity and memory. A vital feature of CaMKII in plasticity is its ability to switch to a calcium (Ca(2+)) independent constitutively active state after autophosphorylation at threonine 287 (T287). A second pair of sites, T306 T307 in the calmodulin (CaM) binding region once autophosphorylated, prevent subsequent CaM binding and inactivates the kinase during synaptic plasticity and memory. Recently a synaptic molecule called Ca(2+)/CaM-dependent serine protein kinase (CASK) has been shown to control both sets of CaMKII autophosphorylation events and hence is well poised to be a key regulator of memory. We show deletion of full length CASK or just its CaMK-like and L27 domains disrupts middle-term memory (MTM) and long-term memory (LTM), with CASK function in the α'/β' subset of mushroom body neurons being required for memory. Likewise directly changing the levels of CaMKII autophosphorylation in these neurons removed MTM and LTM. The requirement of CASK and CaMKII autophosphorylation was not developmental as their manipulation just in the adult α'/β' neurons was sufficient to remove memory. Overexpression of CASK or CaMKII in the α'/β' neurons also occluded MTM and LTM. Overexpression of either Drosophila or human CASK in the α'/β' neurons of the CASK mutant completely rescued memory, confirming that CASK signaling in α'/β' neurons is necessary and sufficient for Drosophila memory formation and that the neuronal function of CASK is conserved between Drosophila and human. At the cellular level CaMKII overexpression in the α'/β' neurons increased activity dependent Ca(2+) responses while reduction of CaMKII decreased it. Likewise reducing CASK or directly expressing a phosphomimetic CaMKII T287D transgene in the α'/β' similarly decreased Ca(2+) signaling. Our results are consistent with CASK regulating CaMKII autophosphorylation in a pathway required for

α(2) noradrenergic receptor suppressed CaMKII signaling in spinal dorsal horn of mice with inflammatory pain.

PubMed

Wang, Xin-Tai; Lian, Xia; Xu, Ying-Ming; Suo, Zhan-Wei; Yang, Xian; Hu, Xiao-Dong

2014-02-05

Intrathecal application of α2 noradrenergic receptor agonists effectively alleviates the pathological pain induced by peripheral tissue injury. However, the spinal antinociceptive mechanisms of α2 noradrenergic receptors remain to be characterized. The present study performed immunohistochemistry and western blot to elucidate the signaling pathway initiated by α2 noradrenergic receptors in spinal dorsal horn of mice, and identified calcium/calmodulin-dependent protein kinase II (CaMKII) as an important target for noradrenergic suppression of inflammatory pain. Our data showed that intraplantar injection of Complete Freund's Adjuvant (CFA) substantially enhanced CaMKII autophosphorylation at Threonine 286, which could be abolished by intrathecal administration of α2 noradrenergic receptor agonist clonidine. Gi protein-coupled α2 noradrenergic receptor might inhibit cAMP-dependent protein kinase (PKA) to disturb CaMKII signaling. We found that pharmacological activation of PKA in intact mice also enhanced spinal CaMKII autophosphorylation level, which was completely antagonized by clonidine. Moreover, direct PKA inhibition in CFA-injected mice mimicked the suppressive effect of α2 noradrenergic receptors on CaMKII. PKA inhibition has been shown to downregulate CaMKII by enhancing protein phosphatase activity. Consistent with this notion, spinal treatment with protein phosphatase inhibitor okadaic acid ruled out clonidine-mediated CaMKII dephosphorylation in CFA-injected mice. Through PKA/protein phosphatase/CaMKII pathway, clonidine noticeably decreased CFA-evoked phosphorylation of N-methyl-d-aspartate subtype glutamate receptor GluN1 and GluN2B subunit as well as α-amino-3-hydroxy-5-methylisoxazole-4-propionic Acid subtype glutamate receptor GluA1 subunit. These data suggested that interference with CaMKII signaling might represent an important mechanism underlying noradrenergic suppression of inflammatory pain. Copyright © 2013 Elsevier B.V. All rights

αCaMKII Autophosphorylation Controls the Establishment of Alcohol Drinking Behavior

PubMed Central

Easton, Alanna C; Lucchesi, Walter; Lourdusamy, Anbarasu; Lenz, Bernd; Solati, Jalal; Golub, Yulia; Lewczuk, Piotr; Fernandes, Cathy; Desrivieres, Sylvane; Dawirs, Ralph R; Moll, Gunther H; Kornhuber, Johannes; Frank, Josef; Hoffmann, Per; Soyka, Michael; Kiefer, Falk; Schumann, Gunter; Peter Giese, K; Müller, Christian P

2013-01-01

The α-Ca2+/calmodulin-dependent protein kinase II (αCaMKII) is a crucial enzyme controlling plasticity in the brain. The autophosphorylation of αCaMKII works as a ‘molecular memory' for a transient calcium activation, thereby accelerating learning. We investigated the role of αCaMKII autophosphorylation in the establishment of alcohol drinking as an addiction-related behavior in mice. We found that alcohol drinking was initially diminished in αCaMKII autophosphorylation-deficient αCaMKIIT286A mice, but could be established at wild-type level after repeated withdrawals. The locomotor activating effects of a low-dose alcohol (2 g/kg) were absent in αCaMKIIT286A mice, whereas the sedating effects of high-dose (3.5 g/kg) were preserved after acute and subchronic administration. The in vivo microdialysis revealed that αCaMKIIT286A mice showed no dopamine (DA) response in the nucleus accumbens to acute or subchronic alcohol administration, but enhanced serotonin (5-HT) responses in the prefrontal cortex. The attenuated DA response in αCaMKIIT286A mice was in line with altered c-Fos activation in the ventral tegmental area after acute and subchronic alcohol administration. In order to compare findings in mice with the human condition, we tested 23 single-nucleotide polymorphisms (SNPs) in the CAMK2A gene for their association with alcohol dependence in a population of 1333 male patients with severe alcohol dependence and 939 controls. We found seven significant associations between CAMK2A SNPs and alcohol dependence, one of which in an autophosphorylation-related area of the gene. Together, our data suggest αCaMKII autophosphorylation as a facilitating mechanism in the establishment of alcohol drinking behavior with changing the DA–5-HT balance as a putative mechanism. PMID:23459588

On the brain of a crustacean: a morphological analysis of CaMKII expression and its relation to sensory and motor pathways.

PubMed

Ammar, Dib; Nazari, Evelise M; Müller, Yara M R; Allodi, Silvana

2013-01-01

Calcium/calmodulin kinase II (CaMKII) is a Ca(2+)-activated enzyme that is abundant in vertebrate and invertebrate brains. However, its characterization is poorly addressed in the nervous system of crustaceans, and, to our knowledge, no studies have determined the microanatomical location of CaMKII in a crustacean species. In this study, we found labeling of CaMKII in the eyestalk and brain of the prawn Macrobrachium acanthurus, by means of immunohistochemistry and Western blotting. Antibodies against neuron (ß tubulin III), glutamate receptor (GluA1), and FMRFamide were used in order to further characterize the CaMKII-labeled cells in the brain. In the eyestalk, strong labeling with CaMKII was observed in the photoreceptors. These cells, especially in the rhabdom, were also reactive to anti-ß tubulin III, whereas the pigment cells were labeled with anti-CaMKII. GluA1 co-located with CaMKII in the photoreceptors. Also, CaMKII appeared in the same sites as FMRFamide in the deutocerebrum, including the olfactory lobe, and in the tritocerebrum, specifically in the antennular neuropil, indicating that the synaptic areas in these regions may be related to sensory-motor processing. In the brain, the identification of cells and regions that express CaMKII contributes to the understanding of the processing of neural connections and the modulating role of CaMKII in decapod crustaceans.

The growth and aggressive behavior of human osteosarcoma is regulated by a CaMKII-controlled autocrine VEGF signaling mechanism.

PubMed

Daft, Paul G; Yang, Yang; Napierala, Dobrawa; Zayzafoon, Majd

2015-01-01

Osteosarcoma (OS) is a hyperproliferative malignant tumor that requires a high vascular density to maintain its large volume. Vascular Endothelial Growth Factor (VEGF) plays a crucial role in angiogenesis and acts as a paracrine and autocrine agent affecting both endothelial and tumor cells. The alpha-Ca2+/Calmodulin kinase two (α-CaMKII) protein is an important regulator of OS growth. Here, we investigate the role of α-CaMKII-induced VEGF in the growth and tumorigenicity of OS. We show that the pharmacologic and genetic inhibition of α-CaMKII results in decreases in VEGF gene expression (50%) and protein secretion (55%), while α- CaMKII overexpression increases VEGF gene expression (250%) and protein secretion (1,200%). We show that aggressive OS cells (143B) express high levels of VEGF receptor 2 (VEGFR-2) and respond to exogenous VEGF (100nm) by increasing intracellular calcium (30%). This response is ameliorated by the VEGFR inhibitor CBO-P11, suggesting that secreted VEGF results in autocrine stimulated α-CaMKII activation. Furthermore, we show that VEGF and α-CaMKII inhibition decreases the transactivation of the HIF-1α and AP-1 reporter constructs. Additionally, chromatin immunoprecipitation assay shows significantly decreased binding of HIF-1α and AP-1 to their responsive elements in the VEGF promoter. These data suggest that α-CaMKII regulates VEGF transcription by controlling HIF-1α and AP-1 transcriptional activities. Finally, CBO-P11, KN-93 (CaMKII inhibitor) and combination therapy significantly reduced tumor burden in vivo. Our results suggest that VEGF-induced OS tumor growth is controlled by CaMKII and dual therapy by CaMKII and VEGF inhibitors could be a promising therapy against this devastating adolescent disease.

The Growth and Aggressive Behavior of Human Osteosarcoma Is Regulated by a CaMKII-Controlled Autocrine VEGF Signaling Mechanism

PubMed Central

Daft, Paul G.; Yang, Yang; Napierala, Dobrawa; Zayzafoon, Majd

2015-01-01

Osteosarcoma (OS) is a hyperproliferative malignant tumor that requires a high vascular density to maintain its large volume. Vascular Endothelial Growth Factor (VEGF) plays a crucial role in angiogenesis and acts as a paracrine and autocrine agent affecting both endothelial and tumor cells. The alpha-Ca2+/Calmodulin kinase two (α-CaMKII) protein is an important regulator of OS growth. Here, we investigate the role of α-CaMKII-induced VEGF in the growth and tumorigenicity of OS. We show that the pharmacologic and genetic inhibition of α-CaMKII results in decreases in VEGF gene expression (50%) and protein secretion (55%), while α- CaMKII overexpression increases VEGF gene expression (250%) and protein secretion (1,200%). We show that aggressive OS cells (143B) express high levels of VEGF receptor 2 (VEGFR-2) and respond to exogenous VEGF (100nm) by increasing intracellular calcium (30%). This response is ameliorated by the VEGFR inhibitor CBO-P11, suggesting that secreted VEGF results in autocrine stimulated α-CaMKII activation. Furthermore, we show that VEGF and α-CaMKII inhibition decreases the transactivation of the HIF-1α and AP-1 reporter constructs. Additionally, chromatin immunoprecipitation assay shows significantly decreased binding of HIF-1α and AP-1 to their responsive elements in the VEGF promoter. These data suggest that α-CaMKII regulates VEGF transcription by controlling HIF-1α and AP-1 transcriptional activities. Finally, CBO-P11, KN-93 (CaMKII inhibitor) and combination therapy significantly reduced tumor burden in vivo. Our results suggest that VEGF-induced OS tumor growth is controlled by CaMKII and dual therapy by CaMKII and VEGF inhibitors could be a promising therapy against this devastating adolescent disease. PMID:25860662

Biochemical principles underlying the stable maintenance of LTP by the CaMKII/NMDAR complex.

PubMed

Lisman, John; Raghavachari, Sridhar

2015-09-24

Memory involves the storage of information at synapses by an LTP-like process. This information storage is synapse specific and can endure for years despite the turnover of all synaptic proteins. There must, therefore, be special principles that underlie the stability of LTP. Recent experimental results suggest that LTP is maintained by the complex of CaMKII with the NMDAR. Here we consider the specifics of the CaMKII/NMDAR molecular switch, with the goal of understanding the biochemical principles that underlie stable information storage by synapses. Consideration of a variety of experimental results suggests that multiple principles are involved. One switch requirement is to prevent spontaneous transitions from the off to the on state. The highly cooperative nature of CaMKII autophosphorylation by Ca(2+) (Hill coefficient of 8) and the fact that formation of the CaMKII/NMDAR complex requires release of CaMKII from actin are mechanisms that stabilize the off state. The stability of the on state depends critically on intersubunit autophosphorylation, a process that restores any loss of pT286 due to phosphatase activity. Intersubunit autophosphorylation is also important in explaining why on state stability is not compromised by protein turnover. Recent evidence suggests that turnover occurs by subunit exchange. Thus, stability could be achieved if a newly inserted unphosphorylated subunit was autophosphorylated by a neighboring subunit. Based on other recent work, we posit a novel mechanism that enhances the stability of the on state by protection of pT286 from phosphatases. We posit that the binding of the NMNDAR to CaMKII forces pT286 into the catalytic site of a neighboring subunit, thereby protecting pT286 from phosphatases. A final principle concerns the role of structural changes. The binding of CaMKII to the NMDAR may act as a tag to organize the binding of further proteins that produce the synapse enlargement that underlies late LTP. We argue that these

CASK and CaMKII function in the mushroom body α′/β′ neurons during Drosophila memory formation

PubMed Central

Malik, Bilal R.; Gillespie, John Michael; Hodge, James J. L.

2013-01-01

Ca2+/CaM serine/threonine kinase II (CaMKII) is a central molecule in mechanisms of synaptic plasticity and memory. A vital feature of CaMKII in plasticity is its ability to switch to a calcium (Ca2+) independent constitutively active state after autophosphorylation at threonine 287 (T287). A second pair of sites, T306 T307 in the calmodulin (CaM) binding region once autophosphorylated, prevent subsequent CaM binding and inactivates the kinase during synaptic plasticity and memory. Recently a synaptic molecule called Ca2+/CaM-dependent serine protein kinase (CASK) has been shown to control both sets of CaMKII autophosphorylation events and hence is well poised to be a key regulator of memory. We show deletion of full length CASK or just its CaMK-like and L27 domains disrupts middle-term memory (MTM) and long-term memory (LTM), with CASK function in the α′/β′ subset of mushroom body neurons being required for memory. Likewise directly changing the levels of CaMKII autophosphorylation in these neurons removed MTM and LTM. The requirement of CASK and CaMKII autophosphorylation was not developmental as their manipulation just in the adult α′/β′ neurons was sufficient to remove memory. Overexpression of CASK or CaMKII in the α′/β′ neurons also occluded MTM and LTM. Overexpression of either Drosophila or human CASK in the α′/β′ neurons of the CASK mutant completely rescued memory, confirming that CASK signaling in α′/β′ neurons is necessary and sufficient for Drosophila memory formation and that the neuronal function of CASK is conserved between Drosophila and human. At the cellular level CaMKII overexpression in the α′/β′ neurons increased activity dependent Ca2+ responses while reduction of CaMKII decreased it. Likewise reducing CASK or directly expressing a phosphomimetic CaMKII T287D transgene in the α′/β′ similarly decreased Ca2+ signaling. Our results are consistent with CASK regulating CaMKII autophosphorylation in a

γCaMKII shuttles Ca2+/CaM to the nucleus to trigger CREB phosphorylation and gene expression

PubMed Central

Ma, Huan; Groth, Rachel D.; Cohen, Samuel M.; Emery, John F.; Li, Bo-Xing; Hoedt, Esthelle; Zhang, Guo-An; Neubert, Thomas A.; Tsien, Richard W.

2014-01-01

SUMMARY Activity-dependent CREB phosphorylation and gene expression are critical for long-term neuronal plasticity. Local signaling at CaV1 channels triggers these events but how information is relayed onward to the nucleus remains unclear. Here we report a novel mechanism that mediates long-distance communication within cells: a shuttle that transports Ca2+/calmodulin from the surface membrane to the nucleus. We show that the shuttle protein is γCaMKII, that its phosphorylation at Thr287 by βCaMKII protects the Ca2+/CaM signal, and that CaN triggers its nuclear translocation. Both βCaMKII and CaN act in close proximity to CaV1 channels, supporting their dominance, while γCaMKII operates as a carrier, not as a kinase. Upon arrival within the nucleus, Ca2+/CaM activates CaMKK and its substrate CaMKIV, the CREB kinase. This mechanism resolves longstanding puzzles about CaM/CaMK-dependent signaling to the nucleus. The significance of the mechanism is emphasized by dysregulation of CaV1, γCaMKII, βCaMKII and CaN in multiple neuropsychiatric disorders. PMID:25303525

Phosphorylation of CaMKII in the rat dorsal raphe nucleus plays an important role in sleep-wake regulation.

PubMed

Cui, Su-Ying; Li, Sheng-Jie; Cui, Xiang-Yu; Zhang, Xue-Qiong; Yu, Bin; Sheng, Zhao-Fu; Huang, Yuan-Li; Cao, Qing; Xu, Ya-Ping; Lin, Zhi-Ge; Yang, Guang; Song, Jin-Zhi; Ding, Hui; Wang, Zi-Jun; Zhang, Yong-He

2016-02-01

The Ca(2+) modulation in the dorsal raphe nucleus (DRN) plays an important role in sleep-wake regulation. Calmodulin-dependent kinase II (CaMKII) is an important signal-transducing molecule that is activated by Ca(2+) . This study investigated the effects of intracellular Ca(2+) /CaMKII signaling in the DRN on sleep-wake states in rats. Maximum and minimum CaMKII phosphorylation was detected at Zeitgeber time 21 (ZT 21; wakefulness state) and ZT 3 (sleep state), respectively, across the light-dark rhythm in the DRN in rats. Six-hour sleep deprivation significantly reduced CaMKII phosphorylation in the DRN. Microinjection of the CAMKII activation inhibitor KN-93 (5 or 10 nmol) into the DRN suppressed wakefulness and enhanced rapid-eye-movement sleep (REMS) and non-REM sleep (NREMS). Application of a high dose of KN-93 (10 nmol) increased slow-wave sleep (SWS) time, SWS bouts, the mean duration of SWS, the percentage of SWS relative to total sleep, and delta power density during NREMS. Microinjection of CaCl2 (50 nmol) in the DRN increased CaMKII phosphorylation and decreased NREMS, SWS, and REMS. KN-93 abolished the inhibitory effects of CaCl2 on NREMS, SWS, and REMS. These data indicate a novel wake-promoting and sleep-suppressing role for the Ca(2+) /CaMKII signaling pathway in DRN neurons. We propose that the intracellular Ca(2+) /CaMKII signaling in the dorsal raphe nucleus (DRN) plays wake-promoting and sleep-suppressing role in rats. Intra-DRN application of KN-93 (CaMKII activation inhibitor) suppressed wakefulness and enhanced rapid-eye-movement sleep (REMS) and non-REMS (NREMS). Intra-DRN application of CaCl2 attenuated REMS and NREMS. We think these findings should provide a novel cellular and molecular mechanism of sleep-wake regulation. © 2015 International Society for Neurochemistry.

CaMKII prevents spontaneous acrosomal exocytosis in sperm through induction of actin polymerization.

PubMed

Shabtay, Ortal; Breitbart, Haim

2016-07-01

In order to interact with the egg and undergo acrosomal exocytosis or the acrosome reaction (AR), mammalian spermatozoa must undergo a series of biochemical changes in the female reproductive tract, collectively called capacitation. We showed that F-actin is formed during sperm capacitation and fast depolymerization occurs prior to the AR. We hypothesized that F-actin protects the sperm from undergoing spontaneous-AR (sAR) which decreases fertilization rate. We show that activation of the actin-severing protein gelsolin induces a significant increase in sAR. Moreover, inhibition of CaMKII or PLD during sperm capacitation, caused an increase in sAR and inhibition of F-actin formation. Spermine, which leads to PLD activation, was able to reverse the effects of CaMKII inhibition on sAR-increase and F-actin-decrease. Furthermore, the increase in sAR and the decrease in F-actin caused by the inactivation of the PLD-pathway, were reversed by activation of CaMKII using H2O2 or by inhibiting protein phosphatase 1 which enhance the phosphorylation and oxidation states of CaMKII. These results indicate that two distinct pathways lead to F-actin formation in the sperm capacitation process which prevents the occurrence of sAR. Copyright © 2016 Elsevier Inc. All rights reserved.

Calcium Input Frequency, Duration and Amplitude Differentially Modulate the Relative Activation of Calcineurin and CaMKII

PubMed Central

Li, Lu; Stefan, Melanie I.; Le Novère, Nicolas

2012-01-01

NMDA receptor dependent long-term potentiation (LTP) and long-term depression (LTD) are two prominent forms of synaptic plasticity, both of which are triggered by post-synaptic calcium elevation. To understand how calcium selectively stimulates two opposing processes, we developed a detailed computational model and performed simulations with different calcium input frequencies, amplitudes, and durations. We show that with a total amount of calcium ions kept constant, high frequencies of calcium pulses stimulate calmodulin more efficiently. Calcium input activates both calcineurin and Ca2+/calmodulin-dependent protein kinase II (CaMKII) at all frequencies, but increased frequencies shift the relative activation from calcineurin to CaMKII. Irrespective of amplitude and duration of the inputs, the total amount of calcium ions injected adjusts the sensitivity of the system to calcium input frequencies. At a given frequency, the quantity of CaMKII activated is proportional to the total amount of calcium. Thus, an input of a small amount of calcium at high frequencies can induce the same activation of CaMKII as a larger amount, at lower frequencies. Finally, the extent of activation of CaMKII signals with high calcium frequency is further controlled by other factors, including the availability of calmodulin, and by the potency of phosphatase inhibitors. PMID:22962589

Inhibitory phosphorylation of GSK-3 by CaMKII couples depolarization to neuronal survival.

PubMed

Song, Bin; Lai, Bingquan; Zheng, Zhihao; Zhang, Yuying; Luo, Jingyan; Wang, Chong; Chen, Yuan; Woodgett, James R; Li, Mingtao

2010-12-24

Glycogen synthase kinase-3 (GSK-3) plays a critical role in neuronal apoptosis. The two mammalian isoforms of the kinase, GSK-3α and GSK-3β, are inhibited by phosphorylation at Ser-21 and Ser-9, respectively. Depolarization, which is vital for neuronal survival, causes both an increase in Ser-21/9 phosphorylation and an inhibition of GSK-3α/β. However, the role of GSK-3 phosphorylation in depolarization-dependent neuron survival and the signaling pathway contributing to GSK-3 phosphorylation during depolarization remain largely unknown. Using several approaches, we showed that both isoforms of GSK-3 are important for mediating neuronal apoptosis. Nonphosphorylatable GSK-3α/β mutants (S21A/S9A) promoted apoptosis, whereas a peptide encompassing Ser-9 of GSK-3β protected neurons in a phosphorylation-dependent manner; these results indicate a critical role for Ser-21/9 phosphorylation on depolarization-dependent neuron survival. We found that Ser-21/9 phosphorylation of GSK-3 was mediated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but not by Akt/PKB, PKA, or p90(RSK). CaMKII associated with and phosphorylated GSK-3α/β. Furthermore, the pro-survival effect of CaMKII was mediated by GSK-3 phosphorylation and inactivation. These findings identify a novel Ca(2+)/calmodulin/CaMKII/GSK-3 pathway that couples depolarization to neuronal survival.

Nitric oxide and CaMKII: Critical steps in the cardiac contractile response To IGF-1 and swim training.

PubMed

Burgos, Juan I; Yeves, Alejandra M; Barrena, Jorge P; Portiansky, Enrique L; Vila-Petroff, Martín G; Ennis, Irene L

2017-11-01

Cardiac adaptation to endurance training includes improved contractility by a non-yet clarified mechanism. Since IGF-1 is the main mediator of the physiological response to exercise, we explored its effect on cardiac contractility and the putative involvement of nitric oxide (NO) and CaMKII in control and swim-trained mice. IGF-1 increased cardiomyocyte shortening (128.1±4.6% vs. basal; p˂0.05) and accelerated relaxation (time to 50% relengthening: 49.2±2.0% vs. basal; p˂0.05), effects abrogated by inhibition of: AKT with MK-2206, NO production with the NO synthase (NOS) inhibitor L-NAME and the specific NOS1 inhibitor nitroguanidine (NG), and CaMKII with KN-93. In agreement, an increase in NO in response to IGF-1 (133.8±2.2%) was detected and prevented by both L-NAME and NG but not KN-93, suggesting that CaMKII activation was downstream NO. In addition, we determined CaMKII activity (P-CaMKII) and phosphorylation of its target, Thr17-PLN. IGF-1, by a NO-dependent mechanism, significantly increased both (227.2±29.4% and 145.3±5.4%, respectively) while no changes in the CaMKII phosphorylation site of ryanodine receptor were evident. The improvement in contractility induced by IGF-1 was associated with increased Ca 2+ transient amplitude, rate of decay and SR content. Interestingly, this response was absent in cardiomyocytes from transgenic mice that express a CaMKII inhibitory peptide (AC3-I strain). Moreover, AC3-I mice subjected to swim training did develop physiological cardiac hypertrophy but not the contractile adaptation. Therefore, we conclude that NO-dependent CaMKII activation plays a critical role in the improvement in contractility induced by IGF-1 and exercise training. Interestingly, this pathway would not contribute to the adaptive hypertrophy. Copyright © 2017 Elsevier Ltd. All rights reserved.

Nitric oxide-dependent activation of CaMKII increases diastolic sarcoplasmic reticulum calcium release in cardiac myocytes in response to adrenergic stimulation.

PubMed

Curran, Jerry; Tang, Lifei; Roof, Steve R; Velmurugan, Sathya; Millard, Ashley; Shonts, Stephen; Wang, Honglan; Santiago, Demetrio; Ahmad, Usama; Perryman, Matthew; Bers, Donald M; Mohler, Peter J; Ziolo, Mark T; Shannon, Thomas R

2014-01-01

Spontaneous calcium waves in cardiac myocytes are caused by diastolic sarcoplasmic reticulum release (SR Ca(2+) leak) through ryanodine receptors. Beta-adrenergic (β-AR) tone is known to increase this leak through the activation of Ca-calmodulin-dependent protein kinase (CaMKII) and the subsequent phosphorylation of the ryanodine receptor. When β-AR drive is chronic, as observed in heart failure, this CaMKII-dependent effect is exaggerated and becomes potentially arrhythmogenic. Recent evidence has indicated that CaMKII activation can be regulated by cellular oxidizing agents, such as reactive oxygen species. Here, we investigate how the cellular second messenger, nitric oxide, mediates CaMKII activity downstream of the adrenergic signaling cascade and promotes the generation of arrhythmogenic spontaneous Ca(2+) waves in intact cardiomyocytes. Both SCaWs and SR Ca(2+) leak were measured in intact rabbit and mouse ventricular myocytes loaded with the Ca-dependent fluorescent dye, fluo-4. CaMKII activity in vitro and immunoblotting for phosphorylated residues on CaMKII, nitric oxide synthase, and Akt were measured to confirm activity of these enzymes as part of the adrenergic cascade. We demonstrate that stimulation of the β-AR pathway by isoproterenol increased the CaMKII-dependent SR Ca(2+) leak. This increased leak was prevented by inhibition of nitric oxide synthase 1 but not nitric oxide synthase 3. In ventricular myocytes isolated from wild-type mice, isoproterenol stimulation also increased the CaMKII-dependent leak. Critically, in myocytes isolated from nitric oxide synthase 1 knock-out mice this effect is ablated. We show that isoproterenol stimulation leads to an increase in nitric oxide production, and nitric oxide alone is sufficient to activate CaMKII and increase SR Ca(2+) leak. Mechanistically, our data links Akt to nitric oxide synthase 1 activation downstream of β-AR stimulation. Collectively, this evidence supports the hypothesis that CaMKII is

Inhibitions of late INa and CaMKII act synergistically to prevent ATX-II-induced atrial fibrillation in isolated rat right atria.

PubMed

Liang, Faquan; Fan, Peidong; Jia, Jessie; Yang, Suya; Jiang, Zhan; Karpinski, Serge; Kornyeyev, Dmytro; Pagratis, Nikos; Belardinelli, Luiz; Yao, Lina

2016-05-01

Increases in late Na(+) current (late INa) and activation of Ca(2+)/calmodulin-dependent protein kinase (CaMKII) are associated with atrial arrhythmias. CaMKII also phosphorylates Nav1.5, further increasing late INa. The combination of a CaMKII inhibitor with a late INa inhibitor may be superior to each compound alone to suppress atrial arrhythmias. Therefore, we investigated the effect of a CaMKII inhibitor in combination with a late INa inhibitor on anemone toxin II (ATX-II, a late INa enhancer)-induced atrial arrhythmias. Rat right atrial tissue was isolated and preincubated with either the CaMKII inhibitor autocamtide-2-related inhibitory peptide (AIP), the late INa inhibitor GS458967, or both, and then exposed to ATX-II. ATX-II increased diastolic tension and caused fibrillation of isolated right atrial tissue. AIP (0.3μmol/L) and 0.1μmol/L GS458967 alone inhibited ATX-II-induced arrhythmias by 20±3% (mean±SEM, n=14) and 34±5% (n=13), respectively, whereas the two compounds in combination inhibited arrhythmias by 81±4% (n=10, p<0.05, vs either AIP or GS458967 alone or the calculated sum of individual effects of both compounds). AIP and GS458967 also attenuated the ATX-induced increase of diastolic tension. Consistent with the mechanical and electrical data, 0.3μmol/L AIP and 0.1μmol/L GS458967 each inhibited ATX-II-induced CaMKII phosphorylation by 23±3% and 32±4%, whereas the combination of both compounds inhibited CaMKII phosphorylation completely. The effects of an enhanced late INa to induce arrhythmic activity and activation of CaMKII in atria are attenuated synergistically by inhibitors of late INa and CaMKII. Copyright © 2016 Elsevier Ltd. All rights reserved.

Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses

NASA Astrophysics Data System (ADS)

Pinto, Thiago M.; Schilstra, Maria J.; Steuber, Volker; Roque, Antonio C.

2015-12-01

Long-term plasticity at parallel fibre (PF)-Purkinje cell (PC) synapses is thought to mediate cerebellar motor learning. It is known that calcium-calmodulin dependent protein kinase II (CaMKII) is essential for plasticity in the cerebellum. Recently, Van Woerden et al. demonstrated that the β isoform of CaMKII regulates the bidirectional inversion of PF-PC plasticity. Because the cellular events that underlie these experimental findings are still poorly understood, our work aims at unravelling how β CaMKII controls the direction of plasticity at PF-PC synapses. We developed a bidirectional plasticity model that replicates the experimental observations by Van Woerden et al. Simulation results obtained from this model indicate the mechanisms that underlie the bidirectional inversion of cerebellar plasticity. As suggested by Van Woerden et al., the filamentous actin binding enables β CaMKII to regulate the bidirectional plasticity at PF-PC synapses. Our model suggests that the reversal of long-term plasticity in PCs is based on a combination of mechanisms that occur at different calcium concentrations.

Ionizing radiation regulates cardiac Ca handling via increased ROS and activated CaMKII.

PubMed

Sag, Can M; Wolff, Hendrik A; Neumann, Kay; Opiela, Marie-Kristin; Zhang, Juqian; Steuer, Felicia; Sowa, Thomas; Gupta, Shamindra; Schirmer, Markus; Hünlich, Mark; Rave-Fränk, Margret; Hess, Clemens F; Anderson, Mark E; Shah, Ajay M; Christiansen, Hans; Maier, Lars S

2013-11-01

Ionizing radiation (IR) is an integral part of modern multimodal anti-cancer therapies. IR involves the formation of reactive oxygen species (ROS) in targeted tissues. This is associated with subsequent cardiac dysfunction when applied during chest radiotherapy. We hypothesized that IR (i.e., ROS)-dependently impaired cardiac myocytes' Ca handling might contribute to IR-dependent cardiocellular dysfunction. Isolated ventricular mouse myocytes and the mediastinal area of anaesthetized mice (that included the heart) were exposed to graded doses of irradiation (sham 4 and 20 Gy) and investigated acutely (after ~1 h) as well as chronically (after ~1 week). IR induced a dose-dependent effect on myocytes' systolic function with acutely increased, but chronically decreased Ca transient amplitudes, which was associated with an acutely unaltered but chronically decreased sarcoplasmic reticulum (SR) Ca load. Likewise, in vivo echocardiography of anaesthetized mice revealed acutely enhanced left ventricular contractility (strain analysis) that declined after 1 week. Irradiated myocytes showed persistently increased diastolic SR Ca leakage, which was acutely compensated by an increase in SR Ca reuptake. This was reversed in the chronic setting in the face of slowed relaxation kinetics. As underlying cause, acutely increased ROS levels were identified to activate Ca/calmodulin-dependent protein kinase II (CaMKII). Accordingly, CaMKII-, but not PKA-dependent phosphorylation sites of the SR Ca release channels (RyR2, at Ser-2814) and phospholamban (at Thr-17) were found to be hyperphosphorylated following IR. Conversely, ROS-scavenging as well as CaMKII-inhibition significantly attenuated CaMKII-activation, disturbed Ca handling, and subsequent cellular dysfunction upon irradiation. Targeted cardiac irradiation induces a biphasic effect on cardiac myocytes Ca handling that is associated with chronic cardiocellular dysfunction. This appears to be mediated by increased oxidative

Autophosphorylation of [alpha]CaMKII is Differentially Involved in New Learning and Unlearning Mechanisms of Memory Extinction

ERIC Educational Resources Information Center

Kimura, Ryoichi; Silva, Alcino J.; Ohno, Masuo

2008-01-01

Accumulating evidence indicates the key role of [alpha]-calcium/calmodulin-dependent protein kinase II ([alpha]CaMKII) in synaptic plasticity and learning, but it remains unclear how this kinase participates in the processing of memory extinction. Here, we investigated the mechanism by which [alpha]CaMKII may mediate extinction by using…

CaMKII Regulates Synaptic NMDA Receptor Activity of Hypothalamic Presympathetic Neurons and Sympathetic Outflow in Hypertension.

PubMed

Li, De-Pei; Zhou, Jing-Jing; Zhang, Jixiang; Pan, Hui-Lin

2017-11-01

NMDAR activity in the hypothalamic paraventricular nucleus (PVN) is increased and critically involved in heightened sympathetic vasomotor tone in hypertension. Calcium/calmodulin-dependent protein kinase II (CaMKII) binds to and modulates NMDAR activity. In this study, we determined the role of CaMKII in regulating NMDAR activity of PVN presympathetic neurons in male spontaneously hypertensive rats (SHRs). NMDAR-mediated EPSCs and puff NMDA-elicited currents were recorded in spinally projecting PVN neurons in SHRs and male Wistar-Kyoto (WKY) rats. The basal amplitude of evoked NMDAR-EPSCs and puff NMDA currents in retrogradely labeled PVN neurons were significantly higher in SHRs than in WKY rats. The CaMKII inhibitor autocamtide-2-related inhibitory peptide (AIP) normalized the increased amplitude of NMDAR-EPSCs and puff NMDA currents in labeled PVN neurons in SHRs but had no effect in WKY rats. Treatment with AIP also normalized the higher frequency of NMDAR-mediated miniature EPSCs of PVN neurons in SHRs. CaMKII-mediated phosphorylation level of GluN2B serine 1303 (S1303) in the PVN, but not in the hippocampus and frontal cortex, was significantly higher in SHRs than in WKY rats. Lowering blood pressure with celiac ganglionectomy in SHRs did not alter the increased level of phosphorylated GluN2B S1303 in the PVN. In addition, microinjection of AIP into the PVN significantly reduced arterial blood pressure and lumbar sympathetic nerve discharges in SHRs. Our findings suggest that CaMKII activity is increased in the PVN and contributes to potentiated presynaptic and postsynaptic NMDAR activity to elevate sympathetic vasomotor tone in hypertension. SIGNIFICANCE STATEMENT Heightened sympathetic vasomotor tone is a major contributor to the development of hypertension. Although glutamate NMDA receptor (NMDAR)-mediated excitatory drive in the hypothalamus plays a critical role in increased sympathetic output in hypertension, the molecular mechanism involved in

Criteria for identifying the molecular basis of the engram (CaMKII, PKMzeta).

PubMed

Lisman, John

2017-11-29

The engram refers to the molecular changes by which a memory is stored in the brain. Substantial evidence suggests that memory involves learning-dependent changes at synapses, a process termed long-term potentiation (LTP). Thus, understanding the storages process that underlies LTP may provide insight into how the engram is stored. LTP involves induction, maintenance (storage), and expression sub-processes; special tests are required to specifically reveal properties of the storage process. The strongest of these is the Erasure test in which a transiently applied agent that attacks a putative storage molecule may lead to persistent erasure of previously induced LTP/memory. Two major hypotheses have been proposed for LTP/memory storage: the CaMKII and PKM-zeta hypotheses. After discussing the tests that can be used to identify the engram (Necessity test, Saturation/Occlusion test, Erasure test), the status of these hypotheses is evaluated, based on the literature on LTP and memory-guided behavior. Review of the literature indicates that all three tests noted above support the CaMKII hypothesis when done at both the LTP level and at the behavioral level. Taken together, the results strongly suggest that the engram is stored by an LTP process in which CaMKII is a critical memory storage molecule.

Inhibition of CaMKII activity in the nucleus accumbens shell blocks the reinstatement of morphine-seeking behavior in rats.

PubMed

Liu, Zhuo; Zhang, Jian-Jun; Liu, Xiao-Dong; Yu, Long-Chuan

2012-06-19

The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) may be a core component in the common molecular pathways for drug addiction. Moreover, studies using animal models of drug addiction have demonstrated that changing CaMKII activity or expression influences animals' responses to the drugs of abuse. Here, we explored the roles of CaMKII in the nucleus accumbens (NAc) shell in the extinction and reinstatement of morphine-seeking behavior. Rats were trained to obtain intravenous morphine infusions through poking hole on a fixed-ratio one schedule. Selective CaMKII inhibitor myristoylated autocamtide-2-inhibitory peptide (myr-AIP) was injected into the NAc shell of rats after the acquisition of morphine self-administration (SA) or before the reinstatement test. The results demonstrated that injection of myr-AIP after acquisition of morphine SA did not influence morphine-seeking in the following extinction days and the number of days spent for reaching extinction criterion. However, pretreatment with myr-AIP before the reinstatement test blocked the reinstatement of morphine-seeking behavior induced by morphine-priming. Our results strongly indicate that CaMKII activity in the NAc shell is essential to the relapse to morphine-seeking. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

CaMKII Signaling Stimulates Mef2c Activity In Vitro but Only Minimally Affects Murine Long Bone Development in vivo

PubMed Central

Amara, Chandra S.; Fabritius, Christine; Houben, Astrid; Wolff, Lena I.; Hartmann, Christine

2017-01-01

The long bones of vertebrate limbs form by endochondral ossification, whereby mesenchymal cells differentiate into chondrogenic progenitors, which then differentiate into chondrocytes. Chondrocytes undergo further differentiation from proliferating to prehypertrophic, and finally to hypertrophic chondrocytes. Several signaling pathways and transcription factors regulate this process. Previously, we and others have shown in chicken that overexpression of an activated form of Calcium/calmodulin-dependent kinase II (CaMKII) results in ectopic chondrocyte maturation. Here, we show that this is not the case in the mouse. Although, in vitro Mef2c activity was upregulated by about 55-fold in response to expression of an activated form of CaMKII (DACaMKII), transgenic mice that expressed a dominant-active form of CaMKII under the control of the Col2a1 regulatory elements display only a very transient and mild phenotype. Here, only the onset of chondrocyte hypertrophy at E12.5 is accelerated. It is also this early step in chondrocyte differentiation that is temporarily delayed around E13.5 in transgenic mice expressing the peptide inhibitor CaM-KIIN from rat (rKIIN) under the control of the Col2a1 regulatory elements. Yet, ultimately DACaMKII, as well as rKIIN transgenic mice are born with completely normal skeletal elements with regard to their length and growth plate organization. Hence, our in vivo analysis suggests that CaMKII signaling plays a minor role in chondrocyte maturation in mice. PMID:28361052

CaMKII knockdown affects both early and late phases of olfactory long-term memory in the honeybee.

PubMed

Scholl, Christina; Kübert, Natalie; Muenz, Thomas S; Rössler, Wolfgang

2015-12-01

Honeybees are able to solve complex learning tasks and memorize learned information for long time periods. The molecular mechanisms mediating long-term memory (LTM) in the honeybee Apis mellifera are, to a large part, still unknown. We approached this question by investigating the potential function of the calcium/calmodulin-dependent protein kinase II (CaMKII), an enzyme known as a 'molecular memory switch' in vertebrates. CaMKII is able to switch to a calcium-independent constitutively active state, providing a mechanism for a molecular memory and has further been shown to play an essential role in structural synaptic plasticity. Using a combination of knockdown by RNA interference and pharmacological manipulation, we disrupted the function of CaMKII during olfactory learning and memory formation. We found that learning, memory acquisition and mid-term memory were not affected, but all manipulations consistently resulted in an impaired LTM. Both early LTM (24 h after learning) and late LTM (72 h after learning) were significantly disrupted, indicating the necessity of CaMKII in two successive stages of LTM formation in the honeybee. © 2015. Published by The Company of Biologists Ltd.

Urotensin II induction of neonatal cardiomyocyte hypertrophy involves the CaMKII/PLN/SERCA 2a signaling pathway.

PubMed

Shi, Hongtao; Han, Qinghua; Xu, Jianrong; Liu, Wenyuan; Chu, Tingting; Zhao, Li

2016-05-25

Although studies have shown that Urotensin II (UII) can induce cardiomyocyte hypertrophy and UII-induced cardiomyocyte hypertrophy model has been widely used for hypertrophy research, but its precise mechanism remains unknown. Recent researches have demonstrated that UII-induced cardiomyocyte hypertrophy has a relationship with the changes of intracellular Ca(2+) concentration. Therefore, the aim of this study was to investigate the mechanisms of cardiomyocyte hypertrophy induced by UII and to explore whether the calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated up-regulating of phospholamban (PLN) Thr17-phosphorylation signaling pathway contributed to UII-induced cardiomyocyte hypertrophy. Primary cultures of neonatal rat cardiomyocytes were stimulated for 48h with UII. Cell size, protein/DNA contents and intracellular Ca(2+) were determined. Phosphorylated and total forms of CaMKII, PLN and the total amount of serco/endo-plasmic reticulum ATPases (SERCA 2a) were quantified by western blot. The responses of cardiomyocytes to UII were also evaluated after pretreatment with the CaMKII inhibitor, KN-93. These results showed that UII increased cell size, protein/DNA ratio and intracellular Ca(2+), consistent with a hypertrophic response. Furthermore, the phosphorylation of CaMKII and its downstream target PLN (Thr17), SERCA 2a levels were up-regulated by UII treatment. Conversely, treatment with KN-93 reversed all those effects of UII. Taken together, the results suggest that UII can induce cardiomyocyte hypertrophy through CaMKII-mediated up-regulating of PLN Thr17-phosphorylation signaling pathway. Copyright © 2016 Elsevier B.V. All rights reserved.

Perturbing NR2B-PSD-95 interaction relieves neuropathic pain by inactivating CaMKII-CREB signaling.

PubMed

Xu, Fangxia; Zhao, Xin; Liu, Lin; Song, Jia; Zhu, Yingjun; Chu, Shuaishuai; Shao, Xueming; Li, Xiuxiu; Ma, Zhengliang; Gu, Xiaoping

2017-09-06

Neuropathic pain is characterized by central sensitization. The interaction between N-methyl-D-aspartate receptors (NMDARs) and postsynaptic density protein-95 (PSD-95) plays a major role in central sensitization. Here, we aimed to investigate the analgesic effect of disruption of the interaction between NMDAR and PSD-95. Chronic dorsal root ganglia compression model rats were used to mimic sciatica. Thermal hyperalgesia and mechanical allodynia were evaluated. The expression of spinal phospho-NR2B, PSD-95, calcium/calmodulin-dependent protein kinase II (CaMKII), and cAMP response element binding protein (CREB) was measured using western blotting. A mimetic peptide Myr-NR2B9c was injected intrathecally to disrupt the interaction between PSD-95 and NR2B and detected by coimmunoprecipitation. Chronic dorsal root ganglia compression surgery induced thermal hyperalgesia and mechanical allodynia, and upregulated pain-related proteins such as phospho-NR2B, PSD-95, CaMKII, and CREB expressions in the spinal cord. Myr-NR2B9c disrupted the interaction between NR2B-containing NMDARs and PSD-95 in the spinal cord. Intrathecal administration of Myr-NR2B9c attenuated neuropathic pain behaviors and downregulated the expressions of phospho-NR2B, PSD-95, CaMKII, and CREB in the spinal cord. The present study indicates that dissociation of NR2B-containing NMDARs from PSD-95 inactivates CaMKII and CREB signaling and relieves pain.

Opposing Intermolecular Tuning of Ca2+ Affinity for Calmodulin by Neurogranin and CaMKII Peptides.

PubMed

Zhang, Pengzhi; Tripathi, Swarnendu; Trinh, Hoa; Cheung, Margaret S

2017-03-28

We investigated the impact of bound calmodulin (CaM)-target compound structure on the affinity of calcium (Ca 2+ ) by integrating coarse-grained models and all-atomistic simulations with nonequilibrium physics. We focused on binding between CaM and two specific targets, Ca 2+ /CaM-dependent protein kinase II (CaMKII) and neurogranin (Ng), as they both regulate CaM-dependent Ca 2+ signaling pathways in neurons. It was shown experimentally that Ca 2+ /CaM (holoCaM) binds to the CaMKII peptide with overwhelmingly higher affinity than Ca 2+ -free CaM (apoCaM); the binding of CaMKII peptide to CaM in return increases the Ca 2+ affinity for CaM. However, this reciprocal relation was not observed in the Ng peptide (Ng 13-49 ), which binds to apoCaM or holoCaM with binding affinities of the same order of magnitude. Unlike the holoCaM-CaMKII peptide, whose structure can be determined by crystallography, the structural description of the apoCaM-Ng 13-49 is unknown due to low binding affinity, therefore we computationally generated an ensemble of apoCaM-Ng 13-49 structures by matching the changes in the chemical shifts of CaM upon Ng 13-49 binding from nuclear magnetic resonance experiments. Next, we computed the changes in Ca 2+ affinity for CaM with and without binding targets in atomistic models using Jarzynski's equality. We discovered the molecular underpinnings of lowered affinity of Ca 2+ for CaM in the presence of Ng 13-49 by showing that the N-terminal acidic region of Ng peptide pries open the β-sheet structure between the Ca 2+ binding loops particularly at C-domain of CaM, enabling Ca 2+ release. In contrast, CaMKII peptide increases Ca 2+ affinity for the C-domain of CaM by stabilizing the two Ca 2+ binding loops. We speculate that the distinctive structural difference in the bound complexes of apoCaM-Ng 13-49 and holoCaM-CaMKII delineates the importance of CaM's progressive mechanism of target binding on its Ca 2+ binding affinities. Copyright © 2017

Differential regulation by ATP versus ADP further links CaMKII aggregation to ischemic conditions

PubMed Central

Vest, Rebekah S.; O’Leary, Heather; Bayer, K. Ulrich

2009-01-01

CaMKII, a major mediator of synaptic plasticity, forms extra-synaptic clusters under ischemic conditions. This study further supports self-aggregation of CaMKII holoenzymes as the underlying mechanism. Aggregation in vitro was promoted by mimicking ischemic conditions: low pH (6.8 or less), Ca2+ (and calmodulin), and low ATP and/or high ADP concentration. Mutational analysis showed that high ATP prevented aggregation by a mechanism involving T286 auto-phosphorylation, and indicated requirement for nucleotide binding but not auto-phosphorylation also for extra-synaptic clustering within neurons. These results clarify a previously apparent paradox in the nucleotide and phosphorylation requirement of aggregation, and support a mechanism that involves inter-holoenzyme T286-region/T-site interaction. PMID:19840793

Cardiac Protection of Valsartan on Juvenile Rats with Heart Failure by Inhibiting Activity of CaMKII via Attenuating Phosphorylation.

PubMed

Wu, Yao; Si, Feifei; Ji, Xiaojuan; Jiang, Kunfeng; Song, Sijie; Yi, Qijian

2017-01-01

Background . This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods . Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO). Simultaneously, the sham-operated rats were randomly given valsartan (Sham + Val) or placebo (Sham + PBO). After 4 weeks of treatment, Western blot analysis was employed to quantify CaMKII and relative calcium handling proteins (RyR2 and PLN) in all groups. Results . The deteriorated cardiac function was reversed by valsartan treatment. In ventricular muscle cells of group HF + PBO, Thr287 phosphorylation of CaMKII and S2808 phosphorylation of RyR2 and PLN were increased and S16 phosphorylation of PLN was decreased compared to the other groups, while Met281 oxidation was not significantly elevated. In addition, these changes in the expression of calcium handling proteins were ameliorated by valsartan administration. Conclusions . The phosphorylation of Thr286 is associated with the early activation of CaMKII rather than the oxidation of Met281.

Cardiac Protection of Valsartan on Juvenile Rats with Heart Failure by Inhibiting Activity of CaMKII via Attenuating Phosphorylation

PubMed Central

Wu, Yao; Si, Feifei; Ji, Xiaojuan; Jiang, Kunfeng; Song, Sijie

2017-01-01

Background. This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods. Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO). Simultaneously, the sham-operated rats were randomly given valsartan (Sham + Val) or placebo (Sham + PBO). After 4 weeks of treatment, Western blot analysis was employed to quantify CaMKII and relative calcium handling proteins (RyR2 and PLN) in all groups. Results. The deteriorated cardiac function was reversed by valsartan treatment. In ventricular muscle cells of group HF + PBO, Thr287 phosphorylation of CaMKII and S2808 phosphorylation of RyR2 and PLN were increased and S16 phosphorylation of PLN was decreased compared to the other groups, while Met281 oxidation was not significantly elevated. In addition, these changes in the expression of calcium handling proteins were ameliorated by valsartan administration. Conclusions. The phosphorylation of Thr286 is associated with the early activation of CaMKII rather than the oxidation of Met281. PMID:28536695

Late INa increases diastolic SR-Ca2+-leak in atrial myocardium by activating PKA and CaMKII

PubMed Central

Fischer, Thomas H.; Herting, Jonas; Mason, Fleur E.; Hartmann, Nico; Watanabe, Saera; Nikolaev, Viacheslav O.; Sprenger, Julia U.; Fan, Peidong; Yao, Lina; Popov, Aron-Frederik; Danner, Bernhard C.; Schöndube, Friedrich; Belardinelli, Luiz; Hasenfuss, Gerd; Maier, Lars S.; Sossalla, Samuel

2015-01-01

Aims Enhanced cardiac late Na current (late INa) and increased sarcoplasmic reticulum (SR)-Ca2+-leak are both highly arrhythmogenic. This study seeks to identify signalling pathways interconnecting late INa and SR-Ca2+-leak in atrial cardiomyocytes (CMs). Methods and results In murine atrial CMs, SR-Ca2+-leak was increased by the late INa enhancer Anemonia sulcata toxin II (ATX-II). An inhibition of Ca2+/calmodulin-dependent protein kinase II (Autocamide-2-related inhibitory peptide), protein kinase A (H89), or late INa (Ranolazine or Tetrodotoxin) all prevented ATX-II-dependent SR-Ca2+-leak. The SR-Ca2+-leak induction by ATX-II was not detected when either the Na+/Ca2+ exchanger was inhibited (KBR) or in CaMKIIδc-knockout mice. FRET measurements revealed increased cAMP levels upon ATX-II stimulation, which could be prevented by inhibition of adenylyl cyclases (ACs) 5 and 6 (NKY 80) but not by inhibition of phosphodiesterases (IBMX), suggesting PKA activation via an AC-dependent increase of cAMP levels. Western blots showed late INa-dependent hyperphosphorylation of CaMKII as well as PKA target sites at ryanodine receptor type-2 (-S2814 and -S2808) and phospholamban (-Thr17, -S16). Enhancement of late INa did not alter Ca2+-transient amplitude or SR-Ca2+-load. However, upon late INa activation and simultaneous CaMKII inhibition, Ca2+-transient amplitude and SR-Ca2+-load were increased, whereas PKA inhibition reduced Ca2+-transient amplitude and load and additionally slowed Ca2+ elimination. In atrial CMs from patients with atrial fibrillation, inhibition of late INa, CaMKII, or PKA reduced the SR-Ca2+-leak. Conclusion Late INa exerts distinct effects on Ca2+ homeostasis in atrial myocardium through activation of CaMKII and PKA. Inhibition of late INa represents a potential approach to attenuate CaMKII activation and decreases SR-Ca2+-leak in atrial rhythm disorders. The interconnection with the cAMP/PKA system further increases the antiarrhythmic potential of late

CaMKII Phosphorylation in Primary Somatosensory Cortical Neurons is Involved in the Inhibition of Remifentanil-induced Hyperalgesia by Lidocaine in Male Sprague-Dawley Rats.

PubMed

Cui, Weihua; Wang, Shanshan; Han, Ruquan; Wang, Qiang; Li, Junfa

2016-01-01

Previous clinical studies have shown that lidocaine can alleviate severe postoperative pain after remifentanil-based anesthesia. Experimental studies have also demonstrated that lidocaine can inhibit remifentanil-induced hyperalgesia, yet the mechanism remains unknown. The present study explored the role of the primary somatosensory (S1) cortex in remifentanil-induced hyperalgesia as well as its inhibition by lidocaine through evaluation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation and protein expression levels in S1 cortical neurons. Male Sprague-Dawley rats were randomly allocated to the following 3 groups: remifentanil only (R), lidocaine only (L), and remifentanil+lidocaine (RL). Experimentally naive animals were used as controls for immunoblotting and immunofluorescence evaluations. Via intravenous tail vein administration (24 G catheter), the animals received remifentanil at 2.4 μg/kg/min, lidocaine at 200 μg/kg/min, and remifentanil at 2.4 μg/kg/min plus lidocaine at 200 μg/kg/min for 2 hours. Paw withdrawal threshold (PWT) values for both mechanical and thermal hyperalgesia, along with immunoblotting and immunofluorescence, were used to measure remifentanil-induced hyperalgesia and changes in CaMKII phosphorylation (P-CaMKII) and total protein expression (T-CaMKII). There was a significant decrease in the PWT for mechanical stimulation at 0.5 and 2 hours after discontinuing infusion in groups R and RL (P<0.05, n=10 per group). However, there were no differences in thermal PWT in any group at any time period when compared with that of baseline. There was also a significant increase of P-CaMKII (not T-CaMKII) in S1 cortical neurons of group R (not L and RL groups) at 0 to 2 hours after discontinuing infusion when compared with that of the corresponding control group (P<0.05, n=6 per group) as determined by immunoblotting and immunofluorescence microscopy. These results suggested that the phosphorylation of CaMKII in S1

Potentiation of amygdala AMPA receptor activity selectively promotes escalated alcohol self-administration in a CaMKII-dependent manner.

PubMed

Cannady, Reginald; Fisher, Kristen R; Graham, Caitlin; Crayle, Jesse; Besheer, Joyce; Hodge, Clyde W

2017-05-01

Growing evidence indicates that drugs of abuse gain control over the individual by usurping glutamate-linked mechanisms of neuroplasticity in reward-related brain regions. Accordingly, we have shown that glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) activity in the amygdala is required for the positive reinforcing effects of alcohol, which underlie the initial stages of addiction. It is unknown, however, if enhanced AMPAR activity in the amygdala facilitates alcohol self-administration, which is a kernel premise of glutamate hypotheses of addiction. Here, we show that low-dose alcohol (0.6 g/kg/30 minutes) self-administration increases phosphorylation (activation) of AMPAR subtype GluA1 S831 (pGluA1 S831) in the central amygdala (CeA), basolateral amygdala and nucleus accumbens core (AcbC) of selectively bred alcohol-preferring P-rats as compared with behavior-matched (non-drug) sucrose controls. The functional role of enhanced AMPAR activity was assessed via site-specific infusion of the AMPAR positive modulator, aniracetam, in the CeA and AcbC prior to alcohol self-administration. Intra-CeA aniracetam increased alcohol-reinforced but not sucrose-reinforced responding and was ineffective following intra-AcbC infusion. Because GluA1 S831 is a Ca2+/calmodulin-dependent protein kinase II (CaMKII) substrate, we sought to determine if AMPAR regulation of enhanced alcohol self-administration is dependent on CaMKII activity. Intra-CeA infusion of the cell-permeable CaMKII peptide inhibitor myristolated autocamtide-2-related inhibitory peptide (m-AIP) dose-dependently reduced alcohol self-administration. A subthreshold dose of m-AIP also blocked the aniracetam-induced escalation of alcohol self-administration, demonstrating that AMPAR-mediated potentiation of alcohol reinforcement requires CaMKII activity in the amygdala. Enhanced activity of plasticity-linked AMPAR-CaMKII signaling in the amygdala may promote escalated alcohol use

Potentiation of amygdala AMPA receptor activity selectively promotes escalated alcohol self-administration in a CaMKII-dependent manner

PubMed Central

Cannady, Reginald; Fisher, Kristen R.; Graham, Caitlin; Crayle, Jesse; Besheer, Joyce; Hodge, Clyde W.

2015-01-01

Growing evidence indicates that drugs of abuse gain control over the individual by usurping glutamate-linked mechanisms of neuroplasticity in reward-related brain regions. Accordingly, we have shown that glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) activity in the amygdala is required for the positive reinforcing effects of alcohol, which underlie the initial stages of addiction. It is unknown, however, if enhanced AMPAR activity in the amygdala facilitates alcohol self-administration, which is a kernel premise of glutamate hypotheses of addiction. Here we show that low-dose alcohol (0.6 g/kg/30-min) self-administration increases phosphorylation (activation) of AMPAR subtype GluA1 S831 (pGluA1 S831) in the central amygdala (CeA), basolateral amygdala, and nucleus accumbens core (AcbC) of selectively bred alcohol-preferring P-rats as compared to behavior-matched (non-drug) sucrose controls. The functional role of enhanced AMPAR activity was assessed via site-specific infusion of the AMPAR positive modulator, aniracetam, in the CeA and AcbC prior to alcohol self-administration. Intra-CeA aniracetam increased alcohol- but not sucrose-reinforced responding, and was ineffective following intra-AcbC infusion. Since GluA1 S831 is a Ca2+/calmodulin-dependent protein kinase II (CaMKII) substrate, we sought to determine if AMPAR regulation of enhanced alcohol self-administration is dependent on CaMKII activity. Intra-CeA infusion of the cell-permeable CaMKII peptide inhibitor m-AIP dose-dependently reduced alcohol self-administration. A sub-threshold dose of m-AIP also blocked the aniracetam-induced escalation of alcohol self-administration, demonstrating that AMPAR-mediated potentiation of alcohol reinforcement requires CaMKII activity in the amygdala. Enhanced activity of plasticity-linked AMPAR-CaMKII signaling in the amygdala may promote escalated alcohol use via increased positive reinforcement during the initial stages of addiction

Mutation Induced Conformational Change In CaMKII Peptide Alters Binding Affinity to CaM Through Alternate Binding Site

NASA Astrophysics Data System (ADS)

Ezerski, Jacob; Cheung, Margaret

CaM forms distinct conformation states through modifications in its charge distribution upon binding to Ca2+ ions. The occurrence of protein structural change resulting from an altered charge distribution is paramount in the scheme of cellular signaling. Not only is charge induced structural change observed in CaM, it is also seen in an essential binding target: calmodulin-depended protein kinase II (CaMKII). In order to investigate the mechanism of selectivity in relation to changes in secondary structure, the CaM binding domain of CaMKII is isolated. Experimentally, charged residues of the CaMKII peptide are systematically mutated to alanine, resulting in altered binding kinetics between the peptide and the Ca2+ saturated state of CaM. We perform an all atom simulation of the wildtype (RRK) and mutated (AAA) CaMKII peptides and generate structures from the trajectory. We analyze RRK and AAA using DSSP and find significant structural differences due to the mutation. Structures from the RRK and AAA ensembles are then selected and docked onto the crystal structure of Ca2+ saturated CaM. We observe that RRK binds to CaM at the C-terminus, whereas the 3-residue mutation, AAA, shows increased patterns of binding to the N-terminus and linker regions of CaM. Due to the conformational change of the peptide ensemble from charged residue mutation, a distinct change in the binding site can be seen, which offers an explanation to experimentally observed changes in kinetic binding rates

Calmodulin and CaMKII modulate ENaC activity by regulating the association of MARCKS and the cytoskeleton with the apical membrane.

PubMed

Alli, Abdel A; Bao, Hui-Fang; Liu, Bing-Chen; Yu, Ling; Aldrugh, Summer; Montgomery, Darrice S; Ma, He-Ping; Eaton, Douglas C

2015-09-01

Phosphatidylinositol bisphosphate (PIP2) regulates epithelial sodium channel (ENaC) open probability. In turn, myristoylated alanine-rich C kinase substrate (MARCKS) protein or MARCKS-like protein 1 (MLP-1) at the plasma membrane regulates the delivery of PIP2 to ENaC. MARCKS and MLP-1 are regulated by changes in cytosolic calcium; increasing calcium promotes dissociation of MARCKS from the membrane, but the calcium-regulatory mechanisms are unclear. However, it is known that increased intracellular calcium can activate calmodulin and we show that inhibition of calmodulin with calmidazolium increases ENaC activity presumably by regulating MARCKS and MLP-1. Activated calmodulin can regulate MARCKS and MLP-1 in two ways. Calmodulin can bind to the effector domain of MARCKS or MLP-1, inactivating both proteins by causing their dissociation from the membrane. Mutations in MARCKS that prevent calmodulin association prevent dissociation of MARCKS from the membrane. Calmodulin also activates CaM kinase II (CaMKII). An inhibitor of CaMKII (KN93) increases ENaC activity, MARCKS association with ENaC, and promotes MARCKS movement to a membrane fraction. CaMKII phosphorylates filamin. Filamin is an essential component of the cytoskeleton and promotes association of ENaC, MARCKS, and MLP-1. Disruption of the cytoskeleton with cytochalasin E reduces ENaC activity. CaMKII phosphorylation of filamin disrupts the cytoskeleton and the association of MARCKS, MLP-1, and ENaC, thereby reducing ENaC open probability. Taken together, these findings suggest calmodulin and CaMKII modulate ENaC activity by destabilizing the association between the actin cytoskeleton, ENaC, and MARCKS, or MLP-1 at the apical membrane. Copyright © 2015 the American Physiological Society.

Long-Term Potentiation Can Be Induced in the CA1 Region of Hippocampus in the Absence of aCaMKII T286-Autophosphorylation

ERIC Educational Resources Information Center

Villers, Agnès; Giese, Karl Peter; Ris, Lauerence

2014-01-01

a-calcium/calmodulin-dependent protein kinase (aCaMKII) T286-autophosphorylation provides a short-term molecular memory that was thought to be required for LTP and for learning and memory. However, it has been shown that learning can occur in aCaMKII-T286A mutant mice after a massed training protocol. This raises the question of whether there…

Cue-induced reinstatement of alcohol-seeking behavior is associated with increased CaMKII T286 phosphorylation in the reward pathway of mice☆

PubMed Central

Salling, Michael C.; Hodge, Christopher J.; Psilos, Kelly E.; Eastman, Vallari R.; Faccidomo, Sara P.; Hodge, Clyde W.

2018-01-01

Cue-induced reinstatement of alcohol-seeking is a hallmark behavioral pathology of addiction. Evidence suggests that reinstatement (e.g., relapse), may be regulated by cell signaling systems that underlie neuroplasticity. A variety of plasticity events require activation of calcium calmodulin-dependent protein kinase II (CaMKII) in components of the reward pathway, such as the nucleus accumbens and amygdala. We sought to determine if cue-induced reinstatement of alcohol-seeking behavior is associated with changes in the activation state (e.g., phosphorylation) of CaMKII-T286. Male C57BL/6J mice (n = 14) were trained to lever press on a fixed-ratio-4 schedule of sweetened alcohol (2% sucrose + 9% EtOH) reinforcement. After 14-d of extinction (no cues or reinforcers), mice underwent a response-contingent reinstatement (n = 7) vs. an additional day of extinction (n = 7). Brains were removed immediately after the test and processed for evaluation of pCaMKII-T286 immunoreactivity (IR). Number of pCaMKII-T286 positive cells/mm2 was quantified from coronal brain sections using Bioquant Image Analysis software. Mice emitted significantly more responses on the alcohol vs. the inactive lever throughout the baseline phase with average alcohol intake of 1.1 ± 0.03 g/kg/1-h. During extinction, responses on the alcohol lever decreased to inactive lever levels by day 7. Significant cue-induced reinstatement of alcohol-seeking was observed during a single test with no effects on the inactive lever. Reinstatement was associated with increased pCaMKII-T286 IR specifically in amygdala (LA and BLA), nucleus accumbens (AcbSh), lateral septum, mediodorsal thalamus, and piriform cortex as compared to extinction control. Brain regions showing no change included the dorsal striatum, medial septum, cingulate cortex, habenula, paraventricular thalamus, and ventral hypothalamus. These results show response contingent cue-induced reinstatement of alcohol-seeking behavior is associated with

Inward Rectifier K+ Currents Are Regulated by CaMKII in Endothelial Cells of Primarily Cultured Bovine Pulmonary Arteries.

PubMed

Qu, Lihui; Yu, Lei; Wang, Yanli; Jin, Xin; Zhang, Qianlong; Lu, Ping; Yu, Xiufeng; Zhong, Weiwei; Zheng, Xiaodong; Cui, Ningren; Jiang, Chun; Zhu, Daling

2015-01-01

Endothelium lines the interior surface of vascular walls and regulates vascular tones. The endothelial cells sense and respond to chemical and mechanical stimuli in the circulation, and couple the stimulus signals to vascular smooth muscles, in which inward rectifier K+ currents (Kir) play an important role. Here we applied several complementary strategies to determine the Kir subunit in primarily cultured pulmonary arterial endothelial cells (PAECs) that was regulated by the Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII). In whole-cell voltage clamp, the Kir currents were sensitive to micromolar concentrations of extracellular Ba2+. In excised inside-out patches, an inward rectifier K+ current was observed with single-channel conductance 32.43 ± 0.45 pS and Popen 0.27 ± 0.04, which were consistent with known unitary conductance of Kir 2.1. RT-PCR and western blot results showed that expression of Kir 2.1 was significantly stronger than that of other subtypes in PAECs. Pharmacological analysis of the Kir currents demonstrated that insensitivity to intracellular ATP, pinacidil, glibenclamide, pH, GDP-β-S and choleratoxin suggested that currents weren't determined by KATP, Kir2.3, Kir2.4 and Kir3.x. The currents were strongly suppressed by exposure to CaMKII inhibitor W-7 and KN-62. The expression of Kir2.1 was inhibited by knocking down CaMKII. Consistently, vasodilation was suppressed by Ba2+, W-7 and KN-62 in isolated and perfused pulmonary arterial rings. These results suggest that the PAECs express an inward rectifier K+ current that is carried dominantly by Kir2.1, and this K+ channel appears to be targeted by CaMKII-dependent intracellular signaling systems.

Metabolic regulation of oocyte cell death through the CaMKII-mediated phosphorylation of caspase-2.

PubMed

Nutt, Leta K; Margolis, Seth S; Jensen, Mette; Herman, Catherine E; Dunphy, William G; Rathmell, Jeffrey C; Kornbluth, Sally

2005-10-07

Vertebrate female reproduction is limited by the oocyte stockpiles acquired during embryonic development. These are gradually depleted over the organism's lifetime through the process of apoptosis. The timer that triggers this cell death is yet to be identified. We used the Xenopus egg/oocyte system to examine the hypothesis that nutrient stores can regulate oocyte viability. We show that pentose-phosphate-pathway generation of NADPH is critical for oocyte survival and that the target of this regulation is caspase-2, previously shown to be required for oocyte death in mice. Pentose-phosphate-pathway-mediated inhibition of cell death was due to the inhibitory phosphorylation of caspase-2 by calcium/calmodulin-dependent protein kinase II (CaMKII). These data suggest that exhaustion of oocyte nutrients, resulting in an inability to generate NADPH, may contribute to ooctye apoptosis. These data also provide unexpected links between oocyte metabolism, CaMKII, and caspase-2.

CaMKII activity is essential for improvement of memory-related behaviors by chronic rivastigmine treatment.

PubMed

Moriguchi, Shigeki; Tagashira, Hideaki; Sasaki, Yuzuru; Yeh, Jay Z; Sakagami, Hiroyuki; Narahashi, Toshio; Fukunaga, Kohji

2014-03-01

Because the cholinergic system is down-regulated in the brain of Alzheimer's disease patients, cognitive deficits in Alzheimer's disease patients are significantly improved by rivastigmine treatment. To address the mechanism underlying rivastigmine-induced memory improvements, we chronically treated olfactory bulbectomized (OBX) mice with rivastigmine. The chronic rivastigmine treatments for 12-13 days starting at 10 days after OBX operation significantly improved memory-related behaviors assessed by Y-maze task, novel object recognition task, passive avoidance task, and Barnes maze task, whereas the single rivastigmine treatment failed to improve the memory. Consistent with the improved memory-related behaviors, long-term potentiation in the hippocampal CA1 region was markedly restored by rivastigmine treatments. In immunoblotting analyses, the reductions of calcium/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and calcium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylation in the CA1 region in OBX mice were significantly restored by rivastigmine treatments. In addition, phosphorylation of AMPAR subunit glutamate receptor 1 (GluA1) (Ser-831) and cAMP-responsive element-binding protein (Ser-133) as downstream targets of CaMKII and CaMKIV, respectively, in the CA1 region was also significantly restored by chronic rivastigmine treatments. Finally, we confirmed that rivastigmine-induced improvements of memory-related behaviors and long-term potentiation were not obtained in CaMKIIα(+/-) mice. On the other hand, CaMKIV(-/-) mice did not exhibit the cognitive impairments. Taken together, the stimulation of CaMKII activity in the hippocampus is essential for rivastigmine-induced memory improvement in OBX mice. © 2013 International Society for Neurochemistry.

Metabotropic glutamate receptor 5 upregulates surface NMDA receptor expression in striatal neurons via CaMKII.

PubMed

Jin, Dao-Zhong; Xue, Bing; Mao, Li-Min; Wang, John Q

2015-10-22

Metabotropic and ionotropic glutamate receptors are closely clustered in postsynaptic membranes and are believed to interact actively with each other to control excitatory synaptic transmission. Metabotropic glutamate receptor 5 (mGluR5), for example, has been well documented to potentiate ionotropic NMDA receptor activity, although underlying mechanisms are poorly understood. In this study, we investigated the role of mGluR5 in regulating trafficking and subcellular distribution of NMDA receptors in adult rat striatal neurons. We found that the mGluR1/5 agonist DHPG concentration-dependently increased NMDA receptor GluN1 and GluN2B subunit expression in the surface membrane. Meanwhile, DHPG reduced GluN1 and GluN2B levels in the intracellular compartment. The effect of DHPG was blocked by an mGluR5 selective antagonist MTEP but not by an mGluR1 selective antagonist 3-MATIDA. Pretreatment with an inhibitor or a specific inhibitory peptide for synapse-enriched Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) also blocked the DHPG-stimulated redistribution of GluN1 and GluN2B. In addition, DHPG enhanced CaMKIIα activity and elevated GluN2B phosphorylation at a CaMKII-sensitive site (serine 1303). These results demonstrate that mGluR5 regulates trafficking of NMDA receptors in striatal neurons. Activation of mGluR5 appears to induce rapid trafficking of GluN1 and GluN2B to surface membranes through a signaling pathway involving CaMKII. Copyright © 2015 Elsevier B.V. All rights reserved.

Enriching the Environment of [alpha]CaMKII[superscript T286A] Mutant Mice Reveals that LTD Occurs in Memory Processing but Must be Subsequently Reversed by LTP

ERIC Educational Resources Information Center

Soto, Florentina; Giese, K. Peter; Edwards, Frances A.; Parsley, Stephanie L.; Pilgram, Sara M.

2007-01-01

[alpha]CaMKII[superscript T286A] mutant mice lack long-term potentiation (LTP) in the hippocampal CA1 region and are impaired in spatial learning. In situ hybridization confirms that the mutant mice show the same developmental expression of [alpha]CaMKII as their wild-type littermates. A simple hypothesis would suggest that if LTP is a substrate…

Oxidative stress activates the TRPM2-Ca2+-CaMKII-ROS signaling loop to induce cell death in cancer cells.

PubMed

Wang, Qian; Huang, Lihong; Yue, Jianbo

2017-06-01

High intracellular levels of reactive oxygen species (ROS) cause oxidative stress that results in numerous pathologies, including cell death. Transient potential receptor melastatin-2 (TRPM2), a Ca 2+ -permeable cation channel, is mainly activated by intracellular adenosine diphosphate ribose (ADPR) in response to oxidative stress. Here we studied the role and mechanisms of TRPM2-mediated Ca 2+ influx on oxidative stress-induced cell death in cancer cells. We found that oxidative stress activated the TRPM2-Ca 2+ -CaMKII cascade to inhibit early autophagy induction, which ultimately led to cell death in TRPM2 expressing cancer cells. On the other hand, TRPM2 knockdown switched cells from cell death to autophagy for survival in response to oxidative stress. Moreover, we found that oxidative stress activated the TRPM2-CaMKII cascade to further induce intracellular ROS production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential. In summary, our data demonstrated that oxidative stress activates the TRPM2-Ca 2+ -CaMKII-ROS signal loop to inhibit autophagy and induce cell death. Copyright © 2016 Elsevier B.V. All rights reserved.

Nitric Oxide Induces Ca2+-independent Activity of the Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII)*

PubMed Central

Coultrap, Steven J.; Bayer, K. Ulrich

2014-01-01

Both signaling by nitric oxide (NO) and by the Ca2+/calmodulin (CaM)-dependent protein kinase II α isoform (CaMKIIα) are implicated in two opposing forms of synaptic plasticity underlying learning and memory, as well as in excitotoxic/ischemic neuronal cell death. For CaMKIIα, these functions specifically involve also Ca2+-independent autonomous activity, traditionally generated by Thr-286 autophosphorylation. Here, we demonstrate that NO-induced S-nitrosylation of CaMKIIα also directly generated autonomous activity, and that CaMKII inhibition protected from NO-induced neuronal cell death. NO induced S-nitrosylation at Cys-280/289, and mutation of either site abolished autonomy, indicating that simultaneous nitrosylation at both sites was required. Additionally, autonomy was generated only when Ca2+/CaM was present during NO exposure. Thus, generation of this form of CaMKIIα autonomy requires simultaneous signaling by NO and Ca2+. Nitrosylation also significantly reduced subsequent CaMKIIα autophosphorylation specifically at Thr-286, but not at Thr-305. A previously described reduction of CaMKII activity by S-nitrosylation at Cys-6 was also observed here, but only after prolonged (>5 min) exposure to NO donors. These results demonstrate a novel regulation of CaMKII by another second messenger system and indicate its involvement in excitotoxic neuronal cell death. PMID:24855644

Release from meiotic arrest in ascidian eggs requires the activity of two phosphatases but not CaMKII

PubMed Central

Levasseur, Mark; Dumollard, Remi; Chambon, Jean-Philippe; Hebras, Celine; Sinclair, Maureen; Whitaker, Michael; McDougall, Alex

2013-01-01

The fertilising sperm triggers a transient Ca2+ increase that releases eggs from cell cycle arrest in the vast majority of animal eggs. In vertebrate eggs, Erp1, an APC/Ccdc20 inhibitor, links release from metaphase II arrest with the Ca2+ transient and its degradation is triggered by the Ca2+-induced activation of CaMKII. By contrast, many invertebrate groups have mature eggs that arrest at metaphase I, and these species do not possess the CaMKII target Erp1 in their genomes. As a consequence, it is unknown exactly how cell cycle arrest at metaphase I is achieved and how the fertilisation Ca2+ transient overcomes the arrest in the vast majority of animal species. Using live-cell imaging with a novel cyclin reporter to study cell cycle arrest and its release in urochordate ascidians, the closest living invertebrate group to the vertebrates, we have identified a new signalling pathway for cell cycle resumption in which CaMKII plays no part. Instead, we find that the Ca2+-activated phosphatase calcineurin (CN) is required for egg activation. Moreover, we demonstrate that parthenogenetic activation of metaphase I-arrested eggs by MEK inhibition, independent of a Ca2+ increase, requires the activity of a second egg phosphatase: PP2A. Furthermore, PP2A activity, together with CN, is required for normal egg activation during fertilisation. As ascidians are a sister group of the vertebrates, we discuss these findings in relation to cell cycle arrest and egg activation in chordates. PMID:24194472

A glitch in the Crab pulsar (PSR B0531+21)

NASA Astrophysics Data System (ADS)

Shaw, Benjamin; Lyne, Andrew; Bassa, Cees; Breton, Rene; Jordan, Christine; Keith, Michael; Mickaliger, Mitchell B.; Stappers, Benjamin; Weltevrede, Patrick

2018-05-01

We have detected a glitch in the Crab pulsar, B0531+21, on 2018-04-29. The Crab pulsar is regularly monitored with the 42-ft and Lovell telescopes at the Jodrell Bank Observatory as part of the pulsar timing programme.

Stimulation of ANP secretion by 2-Cl-IB-MECA through A(3) receptor and CaMKII.

PubMed

Yuan, Kuichang; Bai, Guang Yi; Park, Woo Hyun; Kim, Sung Zoo; Kim, Suhn Hee

2008-12-01

Adenosine is a potent mediator of myocardial protection against hypertrophy via A(1) or A(3) receptors that may be partly related to atrial natriuretic peptide (ANP) release. However, little is known about the possible involvement of the A(3) receptor on ANP release. We studied the effects of the A(3) receptor on atrial functions and its modification in hypertrophied atria. A selective A(3) receptor agonist, 2-chloro-N(6)-(3-iodobenzyl) adenosine-5'-N-methyluronamide (2-CI-IB-MECA), was perfused into isolated, beating rat atria with and without receptor modifiers. 2-CI-IB-MECA dose-dependently increased the ANP secretion, which was blocked by the A(3) receptor antagonist, but the increased atrial contractility and decreased cAMP levels induced by 30muM 2-CI-IB-MECA were not affected. The 100muM 2-(1-hexylnyl)-N-methyladenosine (HEMADO) and N(6)-(3-iodobenzyl) adenosine-5'-N-methyluronamide (IB-MECA), A(3) receptor agonist, also stimulated the ANP secretion without positive inotropy. The potency for the stimulation of ANP secretion was 2-CI-IB-MECA>IB-MECA=HEMADO. The inhibition of the ryanodine receptor or calcium/calmodulin-dependent kinase II (CaMKII) attenuated 2-CI-IB-MECA-induced ANP release, positive inotropy, and translocation of extracellular fluid. However, the inhibition of L-type Ca(2+) channels, sarcoplasmic reticulum Ca(2+)-reuptake, phospholipase C or inositol 1,4,5-triphosphate receptors did not affect these parameters. 2-CI-IB-MECA decreased cAMP level, which was blocked only with an inhibitor of CaMKII or adenylyl cyclase. These results suggest that 2-CI-IB-MECA increases the ANP secretion mainly via A(3) receptor activation and positive inotropy by intracellular Ca(2+) regulation via the ryanodine receptor and CaMKII.

Differential changes in hippocampal CaMKII and GluA1 activity after memory training involving different levels of adaptive forgetting

PubMed Central

Fraize, Nicolas; Hamieh, Al Mahdy; Joseph, Mickaël Antoine; Touret, Monique; Parmentier, Régis; Salin, Paul Antoine; Malleret, Gaël

2017-01-01

Phosphorylation of CaMKII and AMPA receptor GluA1 subunit has been shown to play a major role in hippocampal-dependent long-term/reference memory (RM) and in the expression of long-term synaptic potentiation (LTP). In contrast, it has been proposed that dephosphorylation of these proteins could be involved in the opposite phenomenon of hippocampal long-term synaptic depression (LTD) and in adaptive forgetting. Adaptive forgetting allows interfering old memories to be forgotten to give new ones the opportunity to be stored in memory, and in particular in short-term/working memory (WM) that was shown to be very sensitive to proactive interference. To determine the role of CaMKII and GluA1 in adaptive forgetting, we adopted a comparative approach to assess the relative quantity and phosphorylation state of these proteins in the brain of rats trained in one of three radial maze paradigms: a RM task, a WM task involving a high level of adaptive forgetting, or a WM involving a low level of adaptive forgetting. Surprisingly, Western blot analyses revealed that training in a WM task involving a high level of adaptive forgetting specifically increased the expression of AMPA receptor GluA1 subunit and the activity of CaMKII in the dentate gyrus. These results highlight that WM with proactive interference involves mechanisms of synaptic plasticity selectively in the dentate gyrus. PMID:28096498

Morphine- and CaMKII dependent enhancement of GIRK channel signaling in hippocampal neurons

PubMed Central

Nassirpour, Rounak; Bahima, Laia; Lalive, Arnaud L.; Lüscher, Christian; Luján, Rafael; Slesinger, Paul A.

2010-01-01

G protein-gated inwardly rectifying potassium (GIRK) channels, which help control neuronal excitability, are important for the response to drugs of abuse. Here, we describe a novel pathway for morphine-dependent enhancement of GIRK channel signaling in hippocampal neurons. Morphine treatment for ~20 h increased the colocalization of GIRK2 with PSD95, a dendritic spine marker. Western blot analysis and quantitative immuno-electron microscopy revealed an increase in GIRK2 protein and targeting to dendritic spines. In vivo administration of morphine also produced an upregulation of GIRK2 protein in the hippocampus. The mechanism engaged by morphine required elevated intracellular Ca2+ and was insensitive to pertussis toxin, implicating opioid receptors that may couple to Gq G proteins. met-enkephalin, but not the μ-selective (DAMGO) and δ-selective (DPDPE) opioid receptor agonists, mimicked the effect of morphine suggesting involvement of a heterodimeric opioid receptor complex. Peptide (KN-93) inhibition of CaMKII prevented the morphine-dependent change in GIRK localization while expression of a constitutively activated form of CaMKII mimicked the effects of morphine. Coincident with an increase in GIRK2 surface expression, functional analyses revealed that morphine-treatment increased the size of serotonin-activated GIRK currents and Ba2+-sensitive basal K+ currents in neurons. These results demonstrate plasticity in neuronal GIRK signaling that may contribute to the abusive effects of morphine. PMID:20926668

Differential changes in hippocampal CaMKII and GluA1 activity after memory training involving different levels of adaptive forgetting.

PubMed

Fraize, Nicolas; Hamieh, Al Mahdy; Joseph, Mickaël Antoine; Touret, Monique; Parmentier, Régis; Salin, Paul Antoine; Malleret, Gaël

2017-02-01

Phosphorylation of CaMKII and AMPA receptor GluA1 subunit has been shown to play a major role in hippocampal-dependent long-term/reference memory (RM) and in the expression of long-term synaptic potentiation (LTP). In contrast, it has been proposed that dephosphorylation of these proteins could be involved in the opposite phenomenon of hippocampal long-term synaptic depression (LTD) and in adaptive forgetting. Adaptive forgetting allows interfering old memories to be forgotten to give new ones the opportunity to be stored in memory, and in particular in short-term/working memory (WM) that was shown to be very sensitive to proactive interference. To determine the role of CaMKII and GluA1 in adaptive forgetting, we adopted a comparative approach to assess the relative quantity and phosphorylation state of these proteins in the brain of rats trained in one of three radial maze paradigms: a RM task, a WM task involving a high level of adaptive forgetting, or a WM involving a low level of adaptive forgetting. Surprisingly, Western blot analyses revealed that training in a WM task involving a high level of adaptive forgetting specifically increased the expression of AMPA receptor GluA1 subunit and the activity of CaMKII in the dentate gyrus. These results highlight that WM with proactive interference involves mechanisms of synaptic plasticity selectively in the dentate gyrus. © 2017 Fraize et al.; Published by Cold Spring Harbor Laboratory Press.

The role of low levels of fullerene C60 nanocrystals on enhanced learning and memory of rats through persistent CaMKII activation.

PubMed

Chen, Liang; Miao, Yanyan; Chen, Lin; Xu, Jing; Wang, Xinxing; Zhao, Han; Shen, Yi; Hu, Yi; Bian, Yunpeng; Shen, Yuanyuan; Chen, Jutao; Zha, Yingying; Wen, Long-Ping; Wang, Ming

2014-11-01

Engineered nanomaterials are known to exhibit diverse and sometimes unexpected biological effects. Fullerene nanoparticles have been reported to specifically bind to and elicit persistent activation of hippocampal Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), a multimeric intracellular serine/threonine kinase central to Ca(2+) signal transduction and critical for synaptic plasticity, but the functional consequence of that modulation is unknown. Here we show that low doses of fullerene C60 nanocrystals (Nano C60), delivered through intrahippocampal infusion and without any obvious cytotoxicity in hippocampal neuronal cells, enhance the long-term potentiation (LTP) of rats. Intraperitoneal injection of 320 μg/kg of Nano C60, once daily for 10 days, also enhanced spatial memory of rats in addition to an increase of LTP. In parallel, both the IH and IP administration of Nano C60 increased the autonomous activity and the level of threonine 286 (T286) autophosphorylation of CaMKII, enhanced post-synaptic AMPA/NMDA ratio, and triggered time-dependent activation of ERK and CREB. Our results reveal a striking and highly unexpected ability of Nano C60 in positively modulating learning and memory, an effect that is most likely manifested through locking CaMKII in an active conformation, and may have significant implications for the potential therapeutic applications of fullerene C60, a classic engineered nanomaterial. Copyright © 2014 Elsevier Ltd. All rights reserved.

Activation of NMDA receptors reduces metabotropic glutamate receptor-induced long-term depression in the nucleus accumbens via a CaMKII-dependent mechanism.

PubMed

Huang, Chiung-Chun; Hsu, Kuei-Sen

2012-12-01

Glutamate is the major excitatory neurotransmitter in the brain and exerts its actions through two distinct types of receptors, ionotropic and metabotropic glutamate receptors (mGluR). Although functional interplay between ionotropic N-methyl-d-aspartate receptors (NMDAR) and mGluR has been convincingly demonstrated in native and recombinant systems, the mechanism by which NMDAR activation leads to modulation of mGluR function has yet to be elucidated. Using whole-cell patch-clamp recordings in mouse nucleus accumbens (NAc) slices, we found that tetanic stimulation (TS) of excitatory afferents with a naturally occurring frequency (10 min at 13 Hz) reliably induces a mGluR1/5-dependent long-term depression (mGluR1/5-LTD) of excitatory synaptic transmission. Blockade of NMDAR during but not after TS showed enhanced mGluR1/5-LTD induction, which is associated with its antagonism of TS-induced calcium/calmodulin-dependent protein kinase II (CaMKII) activation. The ability of NMDAR antagonists to promote mGluR1/5-LTD induction was mimicked by a selective CaMKII inhibitor KN-62. However, the induction of mGluR1/5-LTD by bath-applied agonist (S)-3,5-dihydrophenylglycine was not affected by NMDAR blockade. We also observed that NMDAR or CaMKII blockade during TS significantly blunted TS-induced increased serine/threonine phosphorylation of the scaffold protein Homer1b/c and resulted in an increased interaction of mGluR5 with the Homer1b/c. These results indicate that synaptically released glutamate during TS of excitatory afferents can activate both NMDAR and mGluR1/5 in NAc neurons concomitantly and that activation of NMDAR may stimulate CaMKII-mediated phosphorylation of Homer1b/c and impair the interaction between mGluR5 and Homer1b/c, thereby attenuating mGluR1/5-LTD induction. This study provides a novel molecular mechanism by which NMDAR could regulate mGluR5 function. Copyright © 2012 Elsevier Ltd. All rights reserved.

CaMKII-dependent endoplasmic reticulum fission by whisker stimulation and during cortical spreading depolarization.

PubMed

Kucharz, Krzysztof; Lauritzen, Martin

2018-04-01

Cortical spreading depolarization waves, the cause underlying migraine aura, are also the markers and mechanism of pathology in the acutely injured human brain. Propagation of spreading depolarization wave uniquely depends on the interaction between presynaptic and postsynaptic glutamate N-methyl-d-aspartate receptors (NMDARs). In the normally perfused brain, even a single wave causes a massive depolarization of neurons and glia, which results in transient loss of neuronal function and depression of the ongoing electrocorticographic activity. Endoplasmic reticulum is the cellular organelle of particular importance for modulation of neurotransmission. Neuronal endoplasmic reticulum structure is assumed to be persistently continuous in neurons, but is rapidly lost within 1 to 2 min of global cerebral ischaemia, i.e. the organelle disintegrates by fission. This phenomenon appears to be timed with the cardiac arrest-induced cortical spreading depolarizations, rather than ensuing cell death. To what extent NMDAR-dependent processes may trigger neuronal endoplasmic reticulum fission and whether fission is reversible in the normally perfused brain is unknown. We used two-photon microscopy to examine neuronal endoplasmic reticulum structural dynamics during whisker stimulation and cortical spreading depolarizations in vivo. Somatosensory stimulation triggered loss of endoplasmic reticulum continuity, a likely outcome of constriction and fission, in dendritic spines within less than 10 s of stimulation, which was spontaneously reversible and recovery to normal took 5 min. The endoplasmic reticulum fission was inhibited by blockade of NMDAR and Ca2+/calmodulin-dependent protein kinase II (CaMKII) activated downstream of the NMDARs, whereas inhibition of guanosine triphosphate hydrolases hindered regain of endoplasmic reticulum continuity, i.e. fusion. In contrast to somatosensory stimulation, endoplasmic reticulum fission during spreading depolarization was widespread and

In vivo Post-Cardiac Arrest Myocardial Dysfunction is Supported by CaMKII-Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2

PubMed Central

Downey, Peter; Zalewski, Adrian; Rubio, Gabriel R.; Liu, Jing; Homburger, Julian R.; Grunwald, Zachary; Qi, Wei; Bollensdorff, Christian; Thanaporn, Porama; Ali, Ayyaz; Riemer, Kirk; Kohl, Peter; Mochly-Rosen, Daria; Gerstenfeld, Edward; Large, Stephen; Ali, Ziad; Ashley, Euan

2016-01-01

Background Survival after sudden cardiac arrest is limited by post-arrest myocardial dysfunction but understanding of this phenomenon is constrained by lack of data from a physiological model of disease. In this study, we established an in vivo model of cardiac arrest and resuscitation, characterized the biology of the associated myocardial dysfunction, and tested novel therapeutic strategies. Methods We developed rodent models of in vivo post-arrest myocardial dysfunction using extra-corporeal membrane oxygenation (ECMO) resuscitation followed by invasive hemodynamics measurement. In post-arrest isolated cardiomyocytes, we assessed mechanical load and Ca2+ induced Ca2+ release (CICR) simultaneously using the micro-carbon-fiber technique and observed reduced function and myofilament calcium sensitivity. We used a novel-designed fiber optic catheter imaging system, and a genetically encoded calcium sensor GCaMP6f, to image CICR in vivo. Results We found potentiation of CICR in isolated cells from this ECMO model and also in cells isolated from an ischemia-reperfusion Langendorff model perfused with oxygenated blood from an arrested animal, but not when reperfused in saline. We established that CICR potentiation begins in vivo. The augmented CICR observed post-arrest was mediated by the activation of Ca2+/calmodulin kinase II (CaMKII). Increased phosphorylation of CaMKII, phospholamban and ryanodine receptor 2 (RyR2) was detected in the post-arrest period. Exogenous adrenergic activation in vivo recapitulated Ca2+ potentiation but was associated with lesser CaMKII activation. Since oxidative stress and aldehydic adduct formation were high post arrest, we tested a small molecule activator of aldehyde dehydrogenase type 2, Alda-1, which reduced oxidative stress, restored calcium and CaMKII homeostasis, and improved cardiac function and post-arrest outcome in vivo. Conclusions Cardiac arrest and reperfusion lead to CaMKII activation and calcium long-term potentiation

Reconstruction of calmodulin single-molecule FRET states, dye interactions, and CaMKII peptide binding by MultiNest and classic maximum entropy

NASA Astrophysics Data System (ADS)

DeVore, Matthew S.; Gull, Stephen F.; Johnson, Carey K.

2013-08-01

We analyzed single molecule FRET burst measurements using Bayesian nested sampling. The MultiNest algorithm produces accurate FRET efficiency distributions from single-molecule data. FRET efficiency distributions recovered by MultiNest and classic maximum entropy are compared for simulated data and for calmodulin labeled at residues 44 and 117. MultiNest compares favorably with maximum entropy analysis for simulated data, judged by the Bayesian evidence. FRET efficiency distributions recovered for calmodulin labeled with two different FRET dye pairs depended on the dye pair and changed upon Ca2+ binding. We also looked at the FRET efficiency distributions of calmodulin bound to the calcium/calmodulin dependent protein kinase II (CaMKII) binding domain. For both dye pairs, the FRET efficiency distribution collapsed to a single peak in the case of calmodulin bound to the CaMKII peptide. These measurements strongly suggest that consideration of dye-protein interactions is crucial in forming an accurate picture of protein conformations from FRET data.

Reconstruction of Calmodulin Single-Molecule FRET States, Dye-Interactions, and CaMKII Peptide Binding by MultiNest and Classic Maximum Entropy

PubMed Central

DeVore, Matthew S.; Gull, Stephen F.; Johnson, Carey K.

2013-01-01

We analyze single molecule FRET burst measurements using Bayesian nested sampling. The MultiNest algorithm produces accurate FRET efficiency distributions from single-molecule data. FRET efficiency distributions recovered by MultiNest and classic maximum entropy are compared for simulated data and for calmodulin labeled at residues 44 and 117. MultiNest compares favorably with maximum entropy analysis for simulated data, judged by the Bayesian evidence. FRET efficiency distributions recovered for calmodulin labeled with two different FRET dye pairs depended on the dye pair and changed upon Ca2+ binding. We also looked at the FRET efficiency distributions of calmodulin bound to the calcium/calmodulin dependent protein kinase II (CaMKII) binding domain. For both dye pairs, the FRET efficiency distribution collapsed to a single peak in the case of calmodulin bound to the CaMKII peptide. These measurements strongly suggest that consideration of dye-protein interactions is crucial in forming an accurate picture of protein conformations from FRET data. PMID:24223465

Reconstruction of Calmodulin Single-Molecule FRET States, Dye-Interactions, and CaMKII Peptide Binding by MultiNest and Classic Maximum Entropy.

PubMed

Devore, Matthew S; Gull, Stephen F; Johnson, Carey K

2013-08-30

We analyze single molecule FRET burst measurements using Bayesian nested sampling. The MultiNest algorithm produces accurate FRET efficiency distributions from single-molecule data. FRET efficiency distributions recovered by MultiNest and classic maximum entropy are compared for simulated data and for calmodulin labeled at residues 44 and 117. MultiNest compares favorably with maximum entropy analysis for simulated data, judged by the Bayesian evidence. FRET efficiency distributions recovered for calmodulin labeled with two different FRET dye pairs depended on the dye pair and changed upon Ca 2+ binding. We also looked at the FRET efficiency distributions of calmodulin bound to the calcium/calmodulin dependent protein kinase II (CaMKII) binding domain. For both dye pairs, the FRET efficiency distribution collapsed to a single peak in the case of calmodulin bound to the CaMKII peptide. These measurements strongly suggest that consideration of dye-protein interactions is crucial in forming an accurate picture of protein conformations from FRET data.

Curcumin Modulates the NMDA Receptor Subunit Composition Through a Mechanism Involving CaMKII and Ser/Thr Protein Phosphatases.

PubMed

Mallozzi, Cinzia; Parravano, Mariacristina; Gaddini, Lucia; Villa, Marika; Pricci, Flavia; Malchiodi-Albedi, Fiorella; Matteucci, Andrea

2018-05-30

Curcumin is one of the major compounds contained in turmeric, the powdered rhizome of Curcuma longa. Results obtained in various experimental models indicate that curcumin has the potential to treat a large variety of neuronal diseases. Excitotoxicity, the toxicity due to pathological glutamate receptors stimulation, has been considered to be involved in several ocular pathologies including ischemia, glaucoma, and diabetic retinopathy. The NMDA receptor (NMDAR), a heteromeric ligand-gated ion channel, is composed of GluN1 and GluN2 subunits. There are four GluN2 subunits (GluN2A-D), which are major determinants of the functional properties of NMDARs. It is widely accepted that GluN2B has a pivotal role in excitotoxicity while the role of GluN2A remains controversial. We previously demonstrated that curcumin is neuroprotective against NMDA-induced excitotoxicity with a mechanism involving an increase of GluN2A subunit activity. In this paper, we investigate the mechanisms involved in curcumin-induced GluN2A increase in retinal cultures. Our results show that curcumin treatment activated CaMKII with a time-course that paralleled those of GluN2A increase. Moreover, KN-93, a CaMKII inhibitor, was able to block the effect of curcumin on GluN2A expression. Finally, in our experimental model, curcumin reduced ser/thr phosphatases activity. Using okadaic acid, a specific PP1 and PP2A blocker, we observed an increase in GluN2A levels in cultures. The ability of okadaic acid to mimic the effect of curcumin on GluN2A expression suggests that curcumin might regulate GluN2A expression through a phosphatase-dependent mechanism. In conclusion, our findings indicate curcumin modulation of CaMKII and/or ser/thr phosphatases activities as a mechanism involved in GluN2A expression and neuroprotection against excitotoxicity.

The Search for Extraterrestrial Intelligence

NASA Technical Reports Server (NTRS)

Tucher, A.

1985-01-01

The development of NASA's SETI project and strategies for searching radio signals are reviewed. A computer program was written in FORTRAN to set up data from observations taken at Jodrell Bank. These data are to be used with a larger program to find the average radio signal strength at each of the approximately 63,000 channels.

Differential Changes in Hippocampal CaMKII and GluA1 Activity after Memory Training Involving Different Levels of Adaptive Forgetting

ERIC Educational Resources Information Center

Fraize, Nicolas; Hamieh, Al Mahdy; Joseph, Mickael Antoine; Touret, Monique; Parmentier, Regis; Salin, Paul Antoine; Malleret, Gael

2017-01-01

Phosphorylation of CaMKII and AMPA receptor GluA1 subunit has been shown to play a major role in hippocampal-dependent long-term/reference memory (RM) and in the expression of long-term synaptic potentiation (LTP). In contrast, it has been proposed that dephosphorylation of these proteins could be involved in the opposite phenomenon of hippocampal…

Chronic renal failure induces cell death in rat hippocampal CA1 via upregulation of αCaMKII/NR2A synaptic complex and phosphorylated GluR1-containing AMPA receptor cascades.

PubMed

Kim, Jong Wan; Ha, Gyoung Yim; Jung, Yong Wook

2014-09-01

N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propinoic acid (AMPA) receptors bound to postsynaptic density-95 (PSD-95) and α isoform of calcium/calmodulin-dependent protein kinase II (αCaMKII) is fundamentally involved in the regulation of working memory. The aim of present study was to investigate the alterations of NMDA and AMPA receptors responsible for hippocampal synaptic dysfunction and selective neuronal cell death after chronic renal failure (CRF) which may be associated with impairment of working memory. Altered interactions between NMDA and AMPA receptors and PSD-95 and αCaMKII were analyzed in the cornu ammonis (CA) 1 and CA3/dentate gyrus (DG) subfields of the uremic rat hippocampi using the immunoblotting and immunoprecipitation methods. Uremia induced by CRF produced necrotic cell death and decreased neuronal nucleoli protein levels in the hippocampal CA1 subfield, but not in the CA3/DG subfields. The CA1 subfields of CRF rats exhibited significant decreases and increases, respectively, in the expressions of PSD-95/NR2B and αCaMKII/NR2A synaptic complex. Moreover, increased phosphorylation of glutamate receptor type 1 (GluR1) AMPA receptor at ser831 was observed in the CA1 subfield after CRF. These hippocampal CA1 neuronal vulnerability may be responsible for memory dysfunction after CRF as mediated by an increase in NR2A-containing NMDA receptors bound to αCaMKII and subsequent activation of GluR1-containing AMPA receptors caused by the phosphorylation of GluR1 at ser831.

Ozone (O{sub 3}) elicits neurotoxicity in spinal cord neurons (SCNs) by inducing ER Ca{sup 2+} release and activating the CaMKII/MAPK signaling pathway

DOE Office of Scientific and Technical Information (OSTI.GOV)

Li, Yun; Lin, Xiaowen; Zhao, XueJun

Ozone (O{sub 3}) is widely used in the treatment of spinal cord related diseases. Excess or accumulation of this photochemical air can however be neurotoxic. In this study, in vitro cultured Wister rat spinal cord neurons (SCNs) were used to investigate the detrimental effects and underlying mechanisms of O{sub 3}. Ozone in a dose-dependent manner inhibited cell viability at a range of 20 to 500 μg/ml, with the dose at 40 μg/ml resulting in a decrease of cell viability to 75%. The cell death after O{sub 3} exposure was related to endoplasmic reticulum (ER) calcium (Ca{sup 2+}) release. Intracellular Ca{supmore » 2+} chelator, ER stabilizer (inositol 1,4,5-trisphosphate receptor (IP3R) antagonist and ryanodine receptor (RyR) antagonist) and calcium/calmodulin-dependent protein kinase II (CaMKII) antagonist could effectively block Ca{sup 2+} mobilization and inhibit cell death following 40 μg/ml O{sub 3} exposure. In addition, ER Ca{sup 2+} release due to O{sub 3} exposure enhanced phospho-p38 and phospho-JNK levels and apoptosis of SCNs through activating CaMKII. Based on these results, we confirm that ozone elicits neurotoxicity in SCNs via inducing ER Ca{sup 2+} release and activating CaMKII/MAPK signaling pathway. Therefore, physicians should get attention to the selection of treatment concentrations of oxygen/ozone. And, approaches, such as chelating intracellular Ca{sup 2+} and stabilizing neuronal Ca{sup 2+} homeostasis could effectively ameliorate the neurotoxicity of O{sub 3}. - Highlights: • Exposure to O{sub 3} can reduce the viability of SCNs and cause the cell death. • Exposure to O{sub 3} can trigger RyR and IP3R dependent intracellular Ca{sup 2+} release. • Exposure to O{sub 3} can enhance the phospho-CaMKII, phospho-JNK and phospho-p38 levels.« less

Agmatine attenuates methamphetamine-induced passive avoidance learning and memory and CaMKII-α gene expression deteriorations in hippocampus of rat.

PubMed

Noorbakhshnia, Maryam; Rashidkaboli, Arsham; Pakatchian, Mahnaz; Beheshti, Siamak

2018-06-13

Methamphetamine (METH) abuse is one the most worldwide problems with wide-ranging effects on the central nervous system (CNS). Chronic METH abuse can associate with cognitive abnormalities and neurodegenerative changes in the brain. Agmatine, a cationic polyamine, has been proposed as a neuromodulator that modulates many effects of abused drugs. The aim of this study was to determine if agmatine can decrease the impairment effect of METH on memory and hippocampal CaMKII-α gene expression, a gene that plays a major role in memory. Male wistar rats (200-220 g) were allocated into 7 groups, including 5 groups of saline, METH (1, 2 mg/kg), Agmatine (5, 10 mg/kg) and 2 groups of agmatine (5, 10 mg/kg) with higher doses of METH (2 mg/kg) for 5 consecutive days (n = 8 in each group). All injections were done intraperitoneally and agmatine was administrated 10 min before METH treatment. Furthermore, Passive avoidance learning (PAL) test was assessed on the 5th day. Retention test was done 24 h after training and the rats were sacrificed immediately. Hippocampi were removed and stored at -80 °C. Finally, hippocampal CaMKII-α gene expression was measured using Quantitative Real-time PCR. Our data showed that chronic METH dose-dependently impaired PAL retrieval, as it decreased step-through latency (STL) and increased time spent in the dark compartment (TDC). While Agmatine with a higher dose (10 mg/kg) significantly decreased impairment effect of METH (2 mg/kg) on PAL and memory. Also, molecular results revealed that METH (2 mg/kg) markedly decreased hippocampal CaMKII-α gene expression while agmatine (10 mg/kg) coadminstration prevented it. Taken together, the results propose that agmatine may provide a potential therapy for learning and memory deficits induced by METH. Copyright © 2017. Published by Elsevier Inc.

Phosphorylation of Synaptic GTPase-activating Protein (synGAP) by Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII) and Cyclin-dependent Kinase 5 (CDK5) Alters the Ratio of Its GAP Activity toward Ras and Rap GTPases*

PubMed Central

Walkup, Ward G.; Washburn, Lorraine; Sweredoski, Michael J.; Carlisle, Holly J.; Graham, Robert L.; Hess, Sonja; Kennedy, Mary B.

2015-01-01

synGAP is a neuron-specific Ras and Rap GTPase-activating protein (GAP) found in high concentrations in the postsynaptic density (PSD) fraction from the mammalian forebrain. We have previously shown that, in situ in the PSD fraction or in recombinant form in Sf9 cell membranes, synGAP is phosphorylated by Ca2+/calmodulin-dependent protein kinase II (CaMKII), another prominent component of the PSD. Here, we show that recombinant synGAP (r-synGAP), lacking 102 residues at the N terminus, can be purified in soluble form and is phosphorylated by cyclin-dependent kinase 5 (CDK5) as well as by CaMKII. Phosphorylation of r-synGAP by CaMKII increases its HRas GAP activity by 25% and its Rap1 GAP activity by 76%. Conversely, phosphorylation by CDK5 increases r-synGAP's HRas GAP activity by 98% and its Rap1 GAP activity by 20%. Thus, phosphorylation by both kinases increases synGAP activity; CaMKII shifts the relative GAP activity toward inactivation of Rap1, and CDK5 shifts the relative activity toward inactivation of HRas. GAP activity toward Rap2 is not altered by phosphorylation by either kinase. CDK5 phosphorylates synGAP primarily at two sites, Ser-773 and Ser-802. Phosphorylation at Ser-773 inhibits r-synGAP activity, and phosphorylation at Ser-802 increases it. However, the net effect of concurrent phosphorylation of both sites, Ser-773 and Ser-802, is an increase in GAP activity. synGAP is phosphorylated at Ser-773 and Ser-802 in the PSD fraction, and its phosphorylation by CDK5 and CaMKII is differentially regulated by activation of NMDA-type glutamate receptors in cultured neurons. PMID:25533468

[The effects of methionine and choline on the expression levels of CaMKII and CREB mRNA and proteins in rats exposed to lead].

PubMed

Feng, Chang; Fan, Guang-qin; Wu, Feng-yun; Lin, Fen; Li, Yan-shu; Chen, Ying

2012-07-01

To study the effects of methionine and choline on the expression levels of CaMKII and CREB mRNA and proteins in hippocampus of rats exposed to lead. Male SD rats were divided into five groups. (1) control group, (2) group exposed to lead+2 by drinking water with 0.40 g/L lead acetate, (3) group exposed to methionine and choline (1:1, 400 mg/kg), (4) group exposed to 0.40 g/L lead acetate plus methionine and choline (1:1, 100 mg/kg), (5) group exposed to 0.40 g/L lead acetate plus methionine and choline (1:1, 400 mg/kg). In 8 weeks after exposure, all rats were killed. Then CREB mRNA and CaMK II mRNA expression levels in hippocampus were detected by real-time PCR, CREB and CaMK II protein expression levels in hippocampus were measured by western blot assay. The expression levels (0.743 ± 0.185 and 0.729 ± 0.199) of CaMKII mRNA and CREB mRNA in the hippocampus of lead group were significantly lower than those (0.950 ± 0.238 and 0.901 ± 0.232) of control group (P < 0.05), also the expression levels (0.271 ± 0.045 and 0.212 ± 0.058) of CREB protein and pCREB protein in the hippocampus of lead group were significantly lower than those (0.319 ± 0.058 and 0.506 ± 0.125) of control group (P < 0.05). The expression levels (1.014 ± 0.210 and 1.126 ± 0.379) of CaMKII mRNA and the expression levels (1.029 ± 0.335 and 0.932 ± 0.251) of CREB mRNA in the hippocampus of 2 groups exposed to lead acetate plus methionine and choline were significantly higher than those of lead group (P < 0.05). The expression levels (0.407 ± 0.951 and 0.563 ± 0.178) of CREB protein and pCREB protein in the hippocampus of group exposed to lead acetate plus 400 mg/kg methionine and choline were significantly higher than those of lead group (P < 0.05). Methionine and choline could decrease the inhibition effects of lead on the expression of CaMKII and CREB mRNA or CREB and pCREB proteins in the hippocampus of rats.

Archaeology and astronomy

NASA Astrophysics Data System (ADS)

2009-10-01

MEETING REPORT The interaction between archaeology and astronomy has a long, tangled and not entirely creditable history, marred by misunderstandings on both sides. But statistics and cultural awareness are bringing a better picture of how and why lasting monuments such as Stonehenge were built. Sue Bowler reports on a joint meeting of the Royal Astronomical Society and the Prehistoric Society, held at Jodrell Bank on 17 July 2009.

Polarization observations of four southern pulsars at 1560 MHz

NASA Astrophysics Data System (ADS)

Wu, Xin-Ji; Manchester, R. N.; Lyne, A. G.

1991-12-01

Some interesting results from the mean pulse polarization observations of four southern pulsars made at the Australian National Radio Astronomy Observatory, Parkes, using the 64-m telescope in June and July, 1988, are presented. The 2 x 16 x 5 MHz filter system from Jodrell Bank has proved excellent in dedispersing the pulse signals and measuring their polarization properties. Data for the four pulsars are given in some detail, and their spectral behavior is discussed.

Did the Crab Pulsar Undergo a Small Glitch in 2006 Late March/Early April?

NASA Astrophysics Data System (ADS)

Vivekanand, M.

2016-08-01

On 2006 August 23 the Crab Pulsar underwent a glitch, which was reported by the Jodrell Bank and the Xinjiang radio observatories. Neither data are available to the public. However, the Jodrell group publishes monthly arrival times of the Crab Pulsar pulse (their actual observations are done daily), and using these, it is shown that about 5 months earlier the Crab Pulsar probably underwent a small glitch, which has not been reported before. Neither observatory discusses the detailed analysis of data from 2006 March to August; either they may not have detected this small glitch, or they may have attributed it to timing noise in the Crab Pulsar. The above result is verified using X-ray data from RXTE. If this is indeed true, this is probably the smallest glitch observed in the Crab Pulsar so far, whose implications are discussed. This work addresses the confusion possible between small-magnitude glitches and timing noise in pulsars.

DID THE CRAB PULSAR UNDERGO A SMALL GLITCH IN 2006 LATE MARCH/EARLY APRIL?

DOE Office of Scientific and Technical Information (OSTI.GOV)

Vivekanand, M., E-mail: viv.maddali@gmail.com

2016-08-01

On 2006 August 23 the Crab Pulsar underwent a glitch, which was reported by the Jodrell Bank and the Xinjiang radio observatories. Neither data are available to the public. However, the Jodrell group publishes monthly arrival times of the Crab Pulsar pulse (their actual observations are done daily), and using these, it is shown that about 5 months earlier the Crab Pulsar probably underwent a small glitch, which has not been reported before. Neither observatory discusses the detailed analysis of data from 2006 March to August; either they may not have detected this small glitch, or they may have attributedmore » it to timing noise in the Crab Pulsar. The above result is verified using X-ray data from RXTE . If this is indeed true, this is probably the smallest glitch observed in the Crab Pulsar so far, whose implications are discussed. This work addresses the confusion possible between small-magnitude glitches and timing noise in pulsars.« less

Spinal IL-33/ST2 Signaling Contributes to Neuropathic Pain via Neuronal CaMKII-CREB and Astroglial JAK2-STAT3 Cascades in Mice.

PubMed

Liu, Shenbin; Mi, Wen-Li; Li, Qian; Zhang, Meng-Ting; Han, Ping; Hu, Shan; Mao-Ying, Qi-Liang; Wang, Yan-Qing

2015-11-01

Emerging evidence indicates that nerve damage-initiated neuroinflammation and immune responses, which are evidenced by the up-regulation of proinflammatory cytokines, contribute to the development of neuropathic pain. This study investigated the role of spinal interleukin (IL)-33 and its receptor ST2 in spared nerve injury (SNI)-induced neuropathic pain. The von Frey test and acetone test were performed to evaluate neuropathic pain behaviors (n = 8 to 12), and Western blot (n = 4 to 6), immunohistochemistry, real-time polymerase chain reaction (n = 5), and Bio-Plex (n = 5) assays were performed to understand the molecular mechanisms. Intrathecal administration of ST2-neutralizing antibody or ST2 gene knockout (ST2) significantly attenuated the SNI-induced mechanical and cold allodynia. On the 7th day after SNI, the expression of spinal IL-33 and ST2 was increased by 255.8 ± 27.3% and 266.4 ± 83.5% (mean ± SD), respectively. Mechanistic studies showed that the increased expression of the spinal N-methyl-D-aspartate (NMDA) receptor subunit 1 after SNI was reduced by ST2 antibody administration or ST2. The induction of nociceptive behaviors in naive mice due to recombinant IL-33 was reversed by the noncompetitive NMDA antagonist MK-801. ST2 antibody administration or ST2 markedly inhibited the increased activation of the astroglial janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) cascade and the neuronal calcium-calmodulin-dependent kinase II (CaMKII)-cyclic adenosine monophosphate response element-binding protein (CREB) cascade after SNI. Moreover, intrathecal pretreatment with the CaMKII inhibitor KN-93 or the JAK2-STAT3 cascade inhibitor AG490 attenuated recombinant IL-33-induced nociceptive behaviors and NMDA subunit 1 up-regulation in naive mice. Spinal IL-33/ST2 signaling contributes to neuropathic pain by activating the astroglial JAK2-STAT3 cascade and the neuronal CaMKII-CREB cascade.

Data on necrotic and apoptotic cell death in acute myocardial ischemia/reperfusion injury: the effects of CaMKII and angiotensin AT1 receptor inhibition.

PubMed

Rajtik, Tomas; Carnicka, Slavka; Szobi, Adrian; Giricz, Zoltan; O-Uchi, Jin; Hassova, Veronika; Svec, Pavel; Ferdinandy, Peter; Ravingerova, Tanya; Adameova, Adriana

2016-06-01

Content of particular proteins indicating cellular injury due to apoptosis and necrosis has been investigated in ischemic/reperfused (IR) hearts and ischemic/reperfused hearts treated with CaMKII inhibitor and/or AT1 receptor inhibitor. This data article provides information in support of the original research article "Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: a role of angiotensin AT1 receptor-NOX2 signaling axis" [1].

12 CFR 619.9140 - Farm Credit bank(s).

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Farm Credit bank(s). 619.9140 Section 619.9140 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9140 Farm Credit bank(s). Except as otherwise defined, the term Farm Credit bank(s) includes Farm Credit Banks...

12 CFR 619.9140 - Farm Credit bank(s).

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Farm Credit bank(s). 619.9140 Section 619.9140 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9140 Farm Credit bank(s). Except as otherwise defined, the term Farm Credit bank(s) includes Farm Credit Banks...

VizieR Online Data Catalog: Gravitational waves search from known PSR with LIGO (Abbott+, 2017)

NASA Astrophysics Data System (ADS)

Abbott, B. P.; Abbott, R.; Abbott, T. D.; Abernathy, M. R.; Acernese, F.; Ackley, K.; Adams, C.; Adams, T.; Addesso, P.; Adhikari, R. X.; Adya, V. B.; Affeldt, C.; Agathos, M.; Agatsuma, K.; Aggarwal, N.; Aguiar, O. D.; Aiello, L.; Ain, A.; Ajith, P.; Allen, B.; Allocca, A.; Altin, P. A.; Ananyeva, A.; Anderson, S. B.; Anderson, W. G.; Appert, S.; Arai, K.; Araya, M. C.; Areeda, J. S.; Arnaud, N.; Arun, K. G.; Ascenzi, S.; Ashton, G.; Ast, M.; Aston, S. M.; Astone, P.; Aufmuth, P.; Aulbert, C.; Avila-Alvarez, A.; Babak, S.; Bacon, P.; Bader, M. K. M.; Baker, P. T.; Baldaccini, F.; Ballardin, G.; Ballmer, S. W.; Barayoga, J. C.; Barclay, S. E.; Barish, B. C.; Barker, D.; Barone, F.; Barr, B.; Barsotti, L.; Barsuglia, M.; Barta, D.; Bartlett, J.; Bartos, I.; Bassiri, R.; Basti, A.; Batch, J. C.; Baune, C.; Bavigadda, V.; Bazzan, M.; Beer, C.; Bejger, M.; Belahcene, I.; Belgin, M.; Bell, A. S.; Berger, B. K.; Bergmann, G.; Berry, C. P. L.; Bersanetti, D.; Bertolini, A.; Betzwieser, J.; Bhagwat, S.; Bhandare, R.; Bilenko, I. A.; Billingsley, G.; Billman, C. R.; Birch, J.; Birney, R.; Birnho Ltz, O.; Biscans, S.; Bisht, A.; Bitossi, M.; Biwer, C.; Bizouard, M. A.; Blackburn, J. K.; Blackman, J.; Blair, C. D.; Blair, D. G.; Blair, R. M.; Bloemen, S.; Bock, O.; Boer, M.; Bogaert, G.; Bohe, A.; Bondu, F.; Bonnand, R.; Boom, B. A.; Bork, R.; Boschi, V.; Bose, S.; Bouffanais, Y.; Bozzi, A.; Bradaschia, C.; Brady, P. R.; Braginsky, V. B.; Branchesi, M.; Brau, J. E.; Briant, T.; Brillet, A.; Brinkmann, M.; Brisson, V.; Brockill, P.; Broida, J. E.; Brooks, A. F.; Brown, D. A.; Brown, D. D.; Brown, N. M.; Brunett, S.; Buchanan, C. C.; Buikema, A.; Bulik, T.; Bulten, H. J.; Buonanno, A.; Buskulic, D.; Buy, C.; Byer, R. L.; Cabero, M.; Cadonati, L.; Cagnoli, G.; Cahillane, C.; Calderon Bustillo, J.; Callister, T. A.; Calloni, E.; Camp, J. B.; Canepa, M.; Cannon, K. C.; Cao, H.; Cao, J.; Capano, C. D.; Capocasa, E.; Carbognani, F.; Caride, S.; Casanueva Diaz, J.; Casentini, C.; Caudill, S.; Cavaglia, M.; Cavalier, F.; Cavalieri, R.; Cella, G.; Cepeda, C. B.; Baiardi, L. C.; Cerretani, G.; Cesarini, E.; Chamberlin, S. J.; Chan, M.; Chao, S.; Charlton, P.; Chassande-Mottin, E.; Cheeseboro, B. D.; Chen, H. Y.; Chen, Y.; Cheng, H.-P.; Chincarini, A.; Chiummo, A.; Chmiel, T.; Cho, H. S.; Cho, M.; Chow, J. H.; Christensen, N.; Chu, Q.; Chua, A. J. K.; Chua, S.; Chung, S.; Ciani, G.; Clara, F.; Clark, J. A.; Cleva, F.; Cocchieri, C.; Coccia, E.; Cohadon, P.-F.; Colla, A.; Collette, C. G.; Cominsky, L.; Constancio, M.; Conti, L.; Cooper, S. J.; Corbitt, T. R.; Cornish, N.; Corsi, A.; Cortese, S.; Costa, C. A.; Coughlin, M. W.; Coughlin, S. B.; Coulon, J.-P.; Countryman, S. T.; Couvares, P.; Covas, P. B.; Cowan, E. E.; Coward, D. M.; Cowart, M. J.; Coyne, D. C.; Coyne, R.; Creighton, J. D. E.; Creighton, T. D.; Cripe, J.; Crowder, S. G.; Cullen, T. J.; Cumming, A.; Cunningham, L.; Cuoco, E.; Del Canton, T.; Danilishin, S. L.; D'Antonio, S.; Danzmann, K.; Dasgupta, A.; da Silva Costa, C. F.; Dattilo, V.; Dave, I.; Davier, M.; Davies, G. S.; Davis, D.; Daw, E. J.; Day, B.; Day, R.; de, S.; Debra, D.; Debreczeni, G.; Degallaix, J.; de Laurentis, M.; Deleglise, S.; Del Pozzo, W.; Denker, T.; Dent, T.; Dergachev, V.; De Rosa, R.; Derosa, R. T.; Desalvo, R.; Devenson, J.; Devine R. C, .; Dhurandhar, S.; Diaz, M. C.; di Fiore, L.; di Giovanni M.; di Girolamo, T.; di Lieto, A.; di Pace, S.; di Palma, I.; di Virgilio A.; Doctor, Z.; Dolique, V.; Donovan, F.; Dooley, K. L.; Doravari, S.; Dorrington, I.; Douglas, R.; Dovale Alvarez, M.; Downes, T. P.; Drago, M.; Drever, R. W. P.; Driggers, J. C.; Du, Z.; Ducrot, M.; Dwyer, S. E.; Edo, T. B.; Edwards, M. C.; Effler, A.; Eggenstein, H.-B.; Ehrens, P.; Eichholz, J.; Eikenberry, S. S.; Eisenstein, R. A.; Essick, R. C.; Etienne, Z.; Etzel, T.; Evans, M.; Evans, T. M.; Everett, R.; Factourovich, M.; Fafone, V.; Fair, H.; Fairhurst, S.; Fan, X.; Farinon, S.; Farr, B.; Farr, W. M.; Fauchon-Jones, E. J.; Favata, M.; Fays, M.; Fehrmann, H.; Fejer, M. M.; Fernandez Galiana, A.; Ferrante, I.; Ferreira, E. C.; Ferrini, F.; Fidecaro, F.; Fiori, I.; Fiorucci, D.; Fisher, R. P.; Flaminio, R.; Fletcher, M.; Fong, H.; Forsyth, S. S.; Fournier, J.-D.; Frasca, S.; Frasconi, F.; Frei, Z.; Freise, A.; Frey, R.; Frey, V.; Fries, E. M.; Fritschel, P.; Frolov, V. V.; Fulda, P.; Fyffe, M.; Gabbard, H.; Gadre, B. U.; Gaebel, S. M.; Gair, J. R.; Gammaitoni, L.; Gaonkar, S. G.; Garufi, F.; Gaur, G.; Gayathri, V.; Gehrels, N.; Gemme, G.; Genin, E.; Gennai, A.; George, J.; Gergely, L.; Germain, V.; Ghonge, S.; Ghosh, A.; Ghosh, A.; Ghosh, S.; Giaime, J. A.; Giardina, K. D.; Giazotto, A.; Gill, K.; Glaefke, A.; Goetz, E.; Goetz, R.; Gondan, L.; Gonzalez, G.; Gonzalez Castro, J. M.; Gopakumar, A.; Gorodetsky, M. L.; Gossan, S. E.; Gosselin, M.; Gouaty, R.; Grado, A.; Graef, C.; Granata, M.; Grant, A.; Gras, S.; Gray, C.; Greco, G.; Green, A. C.; Groot, P.; Grote, H.; Grunewald, S.; Guidi, G. M.; Guo, X.; Gupta, A.; Gupta, M. K.; Gushwa, K. E.; Gustafson, E. K.; Gustafson, R.; Hacker, J. J.; Hall, B. R.; Hall, E. D.; Hammond, G.; Haney, M.; Hanke, M. M.; Hanks, J.; Hanna, C.; Hanson, J.; Hardwick, T.; Harms, J.; Harry, G. M.; Harry, I. W.; Hart, M. J.; Hartman, M. T.; Haster, C.-J.; Haughian, K.; Healy, J.; Heidmann, A.; Heintze, M. C.; Heitmann, H.; Hello, P.; Hemming, G.; Hendry, M.; Heng, I. S.; Hennig, J.; Henry, J.; Heptonstall, A. W.; Heurs, M.; Hild, S.; Hoak, D.; Hofman, D.; Holt, K.; Holz, D. E.; Hopkins, P.; Hough, J.; Houston, E. A.; Howell, E. J.; Hu, Y. M.; Huerta, E. A.; Huet, D.; Hughey, B.; Husa, S.; Huttner, S. H.; Huynh-Dinh, T.; Indik, N.; Ingram, D. R.; Inta, R.; Isa, H. N.; Isac, J.-M.; Isi, M.; Isogai, T.; Iyer, B. R.; Izumi, K.; Jacqmin, T.; Jani, K.; Jaranowski, P.; Jawahar, S.; Jimenez-Forteza, F.; Johnson, W. W.; Jones, D. I.; Jones, R.; Jonker, R. J. G.; Ju, L.; Junker, J.; Kalaghatgi, C. V.; Kalogera, V.; Kandhasamy, S.; Kang, G.; Kanner, J. B.; Karki, S.; Karvinen, K. S.; Kasprzack, M.; Katsavounidis, E.; Katzman, W.; Kaufer, S.; Kaur, T.; Kawabe, K.; Kefelian, F.; Keitel, D.; Kelley, D. B.; Kennedy, R.; Key, J. S.; Khalili, F. Y.; Khan, I.; Khan, S.; Khan, Z.; Khazanov, E. A.; Kijbunchoo, N.; Kim, C.; Kim, J. C.; Kim, W.; Kim, W.; Kim, Y.-M.; Kimbrell, S. J.; King, E. J.; King, P. J.; Kirchhoff, R.; Kissel, J. S.; Klein, B.; Kleybolte, L.; Klimenko, S.; Koch, P.; Koehlenbeck, S. M.; Koley, S.; Kondrashov, V.; Kontos, A.; Korobko, M.; Korth, W. Z.; Kowalska, I.; Kozak, D. B.; Kramer, C.; Kringel, V.; Krishnan, B.; Krolak, A.; Kuehn, G.; Kumar, P.; Kumar, R.; Kuo, L.; Kutynia, A.; Lackey, B. D.; Landry, M.; Lang, R. N.; Lange, J.; Lantz, B.; Lanza, R. K.; Lartaux-Vollard, A.; Lasky, P. D.; Laxen, M.; Lazzarini, A.; Lazzaro, C.; Leaci, P.; Leavey, S.; Lebigot, E. O.; Lee, C. H.; Lee, H. K.; Lee, H. M.; Lee, K.; Lehmann, J.; Lenon, A.; Leonardi, M.; Leong, J. R.; Leroy, N.; Letendre, N.; Levin, Y.; Li, T. G. F.; Libson, A.; Littenberg, T. B.; Liu, J.; Lockerbie, N. A.; Lombardi, A. L.; London, L. T.; Lord, J. E.; Lorenzini, M.; Loriette, V.; Lormand, M.; Losurdo, G.; Lough, J. D.; Lousto, C. O.; Lovelace, G.; Luck, H.; Lundgren, A. P.; Lynch, R.; Ma, Y.; Macfoy, S.; Machenschalk, B.; Macinnis, M.; MacLeod, D. M.; Magana-Sandoval, F.; Majorana, E.; Maksimovic, I.; Malvezzi, V.; Man, N.; Mandic, V.; Mangano, V.; Mansell, G. L.; Manske, M.; Mantovani, M.; Marchesoni, F.; Marion, F.; Marka, S.; Marka, Z.; Markosyan, A. S.; Maros, E.; Martelli, F.; Martellini, L.; Martin, I. W.; Martynov, D. V.; Mason, K.; Masserot, A.; Massinger, T. J.; Masso-Reid, M.; Mastrogiovanni, S.; Matichard, F.; Matone, L.; Mavalvala, N.; Mazumder, N.; McCarthy, R.; McClelland, D. E.; McCormick, S.; McGra, Th C.; McGuire, S. C.; McIntyre, G.; McIver, J.; McManus, D. J.; McRae, T.; McWilliams, S. T.; Meacher, D.; Meadors, G. D.; Meidam, J.; Melatos, A.; Mendell, G.; Mendoza-Gandara, D.; Mercer, R. A.; Merilh, E. L.; Merzougui, M.; Meshkov, S.; Messenger, C.; Messick, C.; Metzdorff, R.; Meyers, P. M.; Mezzani, F.; Miao, H.; Michel, C.; Middleton, H.; Mikhailov, E. E.; Milano, L.; Miller, A. L.; Miller, A.; Miller, B. B.; Miller, J.; Millhouse, M.; Minenkov, Y.; Ming, J.; Mirshekari, S.; Mishra, C.; Mitra, S.; Mitrofanov, V. P.; Mitselmakher, G.; Mittleman, R.; Moggi, A.; Mohan, M.; Mohapatra, S. R. P.; Montani, M.; Moore, B. C.; Moore, C. J.; Moraru, D.; Moreno, G.; Morriss, S. R.; Mours, B.; Mow-Lowry, C. M.; Mueller, G.; Muir, A. W.; Mukherjee, A.; Mukherjee, D.; Mukherjee, S.; Mukund, N.; Mullavey, A.; Munch, J.; Muniz, E. A. M.; Murray, P. G.; Mytidis, A.; Napier, K.; Nardecchia, I.; Naticchioni, L.; Nelemans, G.; Nelson, T. J. N.; Neri, M.; Nery, M.; Neunzert, A.; Newport, J. M.; Newton, G.; Nguyen, T. T.; Nielsen, A. B.; Nissanke, S.; Nitz, A.; Noack, A.; Nocera, F.; Nolting, D.; Normandin, M. E. N.; Nuttall, L. K.; Oberling, J.; Ochsner, E.; Oelker, E.; Ogin, G. H.; Oh, J. J.; Oh, S. H.; Ohme, F.; Oliver, M.; Oppermann, P.; Oram, R. J.; O'Reilly, B.; O'Shaughnessy, R.; Ottaway, D. J.; Overmier, H.; Owen, B. J.; Pace, A. E.; Page, J.; Pai, A.; Pai, S. A.; Palamos, J. R.; Palashov, O.; Palomba, C.; Pal-Singh, A.; Pan, H.; Pankow, C.; Pannarale, F.; Pant, B. C.; Paoletti, F.; Paoli, A.; Papa, M. A.; Paris, H. R.; Parker, W.; Pascucci, D.; Pasqualetti, A.; Passaquieti, R.; Passuello, D.; Patricelli, B.; Pearlstone, B. L.; Pedraza, M.; Pedurand, R.; Pekowsky, L.; Pele, A.; Penn, S.; Perez, C. J.; Perreca, A.; Perri, L. M.; Pfeiffer, H. P.; Phelps, M.; Piccinni, O. J.; Pichot, M.; Piergiovanni, F.; Pierro, V.; Pillant, G.; Pinard, L.; Pinto, I. M.; Pitkin, M.; Poe, M.; Poggiani, R.; Popolizio, P.; Post, A.; Powell, J.; Prasad, J.; Pratt, J. W. W.; Predoi, V.; Prestegard, T.; Prijatelj, M.; Principe, M.; Privitera, S.; Prix, R.; Prodi, G. A.; Prokhorov, L. G.; Puncken, O.; Punturo, M.; Puppo, P.; Purrer, M.; Qi, H.; Qin, J.; Qiu, S.; Quetschke, V.; Quintero E. A.; QuitzoW-James, R.; Raab, F. J.; Rabeling, D. S.; Radkins, H.; Raffai, P.; Raja, S.; Rajan, C.; Rakhmanov, M.; Rapagnani, P.; Raymond, V.; Razzano, M.; Re, V.; Read, J.; Regimbau, T.; Rei, L.; Reid, S.; Reitze, D. H.; Rew, H.; Reyes, S. D.; Rhoades, E.; Ricci, F.; Riles, K.; Rizzo, M.; Robertson, N. A.; Robie, R.; Robinet, F.; Rocchi, A.; Rolland, L.; Rollins, J. G.; Roma, V. J.; Romano, R.; Romie, J. H.; Rosinska, D.; Rowan, S.; Rudiger, A.; Ruggi, P.; Ryan, K.; Sachdev, S.; Sadecki, T.; Sadeghian, L.; Sakellariadou, M.; Salconi, L.; Saleem, M.; Salemi, F.; Samajdar, A.; Sammut, L.; Sampson, L. M.; Sanchez, E. J.; Sandberg, V.; Sanders, J. R.; Sassolas, B.; Sathyaprakash, B. S.; Saulson, P. R.; Sauter, O.; Savage, R. L.; Sawadsky, A.; Schale, P.; Scheuer, J.; Schmidt, E.; Schmidt, J.; Schmidt, P.; Schnabel, R.; Schofield, R. M. S.; Schonbeck, A.; Schreiber, E.; Schuette, D.; Schutz, B. F.; Schwalbe, S. G.; Scott, J.; Scott, S. M.; Sellers, D.; Sengupta, A. S.; Sentenac, D.; Sequino, V.; Sergeev, A.; Setyawati, Y.; Shaddock, D. A.; Shaffer, T. J.; Shahriar, M. S.; Shapiro, B.; Shawhan P.; Sheperd, A.; Shoemaker, D. H.; Shoemaker, D. M.; Siellez, K.; Siemens, X.; Sieniawska, M.; Sigg, D.; Silva, A. D.; Singer, A.; Singer, L. P.; Singh, A.; Singh, R.; Singhal, A.; Sintes, A. M.; Slagmolen, B. J. J.; Smith, B.; Smith, J. R.; Smith, R. J. E.; Son, E. J.; Sorazu, B.; Sorrentino, F.; Souradeep, T.; Spencer, A. P.; Srivastava, A. K.; Staley, A.; Steinke, M.; Steinlechner, J.; Steinlechner, S.; Steinmeyer, D.; Stephens, B. C.; Stevenson, S. P.; Stone, R.; Strain, K. A.; Straniero, N.; Stratta, G.; Strigin, S. E.; Sturani, R.; Stuver, A. L.; Summerscales, T. Z.; Sun, L.; Sunil, S.; Sutton, P. J.; Swinkels, B. L.; Szczepanczyk, M. J.; Tacca, M.; Talukder, D.; Tanner, D. B.; Tapai, M.; Taracchini, A.; Taylor, R.; Theeg, T.; Thomas, E. G.; Thomas, M.; Thomas, P.; Thorne, K. A.; Thrane, E.; Tippens, T.; Tiwari, S.; Tiwari, V.; Tokmakov, K. V.; Toland, K.; Tomlinson, C.; Tonelli, M.; Tornasi, Z.; Torrie, C. I.; Toyra, D.; Travasso, F.; Traylor, G.; Trifiro, D.; Trinastic, J.; Tringali, M. C.; Trozzo, L.; Tse, M.; Tso, R.; Turconi, M.; Tuyenbayev, D.; Ugolini, D.; Unnikrishnan, C. S.; Urban, A. L.; Usman, S. A.; Vahlbruch, H.; Vajente, G.; Valdes, G.; van Bakel, N.; van Beuzekom, M.; van den Brand, J. F. J.; van den Broeck, C.; Vander-Hyde, D. C.; van der Schaaf, L.; van Heijningen, J. V.; van Veggel, A. A.; Vardaro, M.; Varma, V.; Vass, S.; Vasuth, M.; Vecchio, A.; Vedovato, G.; Veitch, J.; Veitch, P. J.; Venkateswara, K.; Venugopalan, G.; Verkindt, D.; Vetrano, F.; Vicere, A.; Viets, A. D.; Vinciguerra, S.; Vine, D. J.; Vinet, J.-Y.; Vitale, S.; Vo, T.; Vocca, H.; Vorvick, C.; Voss, D. V.; Vousden, W. D.; Vyatchanin, S. P.; Wade, A. R.; Wade, L. E.; Wade, M.; Walker, M.; Wallace, L.; Walsh, S.; Wang, G.; Wang, H.; Wang, M.; Wang, Y.; Ward, R. L.; Warner, J.; Was, M.; Watchi, J.; Weaver, B.; Wei, L.-W.; Weinert, M.; Weinstein, A. J.; Weiss, R.; Wen, L.; Wessels, P.; Westphal, T.; Wette, K.; Whelan, J. T.; Whiting, B. F.; Whittle, C.; Williams, D.; Williams, R. D.; Williamson, A. R.; Willis, J. L.; Willke, B.; Wimmer, M. H.; Winkler, W.; Wipf, C. C.; Wittel, H.; Woan, G.; Woehler, J.; Worden, J.; Wright, J. L.; Wu, D. S.; Wu, G.; Yam, W.; Yamamoto, H.; Yancey, C. C.; Yap, M. J.; Yu, H.; Yu, H.; Yvert, M.; Zadrozny, A.; Zangrando, L.; Zanolin, M.; Zendri, J.-P.; Zevin, M.; Zhang, L.; Zhang, M.; Zhang, T.; Zhang, Y.; Zhao, C.; Zhou, M.; Zhou, Z.; Zhu, S. J.; Zhu, X. J.; Zucker, M. E.; Zweizig, J.; Buchner, S.; Cognard, I.; Corongiu, A.; Freire, P. C. C.; Guillemot, L.; Hobbs, G. B.; Kerr, M.; Lyne, A. G.; Possenti, A.; Ridolfi, A.; Shannon, R. M.; Stappers, B. W.; Weltevrede, P.; (The Ligo Scientific Collaboration)

2017-11-01

We have obtained timings for 200 known pulsars. Timing was performed using the 42ft telescope and Lovell telescope at Jodrell Bank (UK), the 26m telescope at Hartebeesthoek (South Africa), the Parkes radio telescope (Australia), the Nancay Decimetric Radio Telescope (France), the Arecibo Observatory (Puerto Rico) and the Fermi Large Area Telescope (LAT). Of these, 122 have been targeted in previous campaigns (Aasi+ 2014, J/ApJ/785/119), while 78 are new to this search. (1 data file).

Vorinostat ameliorates impaired fear extinction possibly via the hippocampal NMDA-CaMKII pathway in an animal model of posttraumatic stress disorder.

PubMed

Matsumoto, Yasutaka; Morinobu, Shigeru; Yamamoto, Shigeto; Matsumoto, Tomoya; Takei, Shiro; Fujita, Yosuke; Yamawaki, Shigeto

2013-09-01

Given that impairment of fear extinction plays a pivotal role in the pathophysiology of posttraumatic stress disorder (PTSD), drugs that facilitate fear extinction may be useful as novel treatments for PTSD. Histone deacetylase (HDAC) inhibitors have recently been shown to enhance fear extinction in animal studies. Using a single prolonged stress (SPS) paradigm, an animal model of PTSD, we examined whether the HDAC inhibitor vorinostat can facilitate fear extinction in rats, and elucidated the mechanism by which vorinostat enhanced fear extinction, focusing on the N-methyl-D-aspartate (NMDA) receptor signals in the hippocampus. Seven days after SPS, rats received contextual fear conditioning, followed by 2-day extinction training. Vorinostat was intraperitoneally injected immediately after second extinction training session. Contextual fear response was assessed 24 h after vorinostat injection. Hippocampal tissues were dissected 2 h after vorinostat injection. The levels of mRNA and protein tested were measured by RT-PCR or western blotting, respectively. Systemic administration of vorinostat with extinction training significantly enhanced fear extinction in SPS rats as compared with the controls. Furthermore, vorinostat enhanced the hippocampal levels of NR2B and calcium/calmodulin kinase II (CaMKII) α and β proteins, accompanied by increases in the levels of acetylated histone H3 and H4. These findings suggest that vorinostat ameliorated the impaired fear extinction in SPS rats, and this effect was associated with an increase in histone acetylation and thereby enhancement of NR2B and CaMKII in the hippocampus. Our results may provide new insight into the molecular and therapeutic mechanisms of PTSD.

The aniracetam metabolite 2-pyrrolidinone induces a long-term enhancement in AMPA receptor responses via a CaMKII pathway.

PubMed

Nishizaki, Tomoyuki; Matsumura, Takuro

2002-01-31

The present study was conducted to assess the effect of aniracetam and its metabolites, such as 2-pyrrolidinone, p-anisic acid, and anisamide butyrate, on the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, heteromerically formed of GluR1,2 (GluR1 and GluR2), GluR1,3 (GluR1 and GluR3), and GluR1,2,3 (GluR1, GluR2, and GluR3), expressed in Xenopus oocytes. 2-Pyrrolidinone potentiated kainate-evoked currents through GluR1,2,3 channels in a bell-shaped dose-dependent manner at concentrations ranged from 1 nM to 300 microM, with a maximal effect at 100 microM. The potentiation was long-lasting, reaching approximately 180% of basal levels 60 min after 5-min treatment with 2-pyrrolidinone at 100 microM. 2-Pyrrolidinone (100 microM) potentiated GluR1,3 channel currents as observed in GluR1,2,3, but instead it depressed GluR1,2 currents. Aniracetam and p-anisic acid potentiated GluR1,2,3 channel currents, but to a lesser extent, each about 130 and 103% of basal levels 60 min after treatment at 100 microM. In contrast, anisamide butyrate had no potentiating effect on the currents. Potentiation of GluR1,2,3 channel currents obtained with 2-pyrrolidinone was inhibited by KN-93, a selective inhibitor of calcium/calmodulin-dependent protein kinase (CaMKII), while it was not affected by GF109203X, a selective inhibitor of protein kinase C or H-89, a selective inhibitor of cAMP-dependent protein kinase. The results of the present study suggest that 2-pyrrolidinone persistently enhances activity of the Ca2+-permeable AMPA receptors, GluR1,3 and GluR1,2,3, by interacting with CaMKII.

Trafficking of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor (AMPA) Receptor Subunit GluA2 from the Endoplasmic Reticulum Is Stimulated by a Complex Containing Ca2+/Calmodulin-activated Kinase II (CaMKII) and PICK1 Protein and by Release of Ca2+ from Internal Stores*

PubMed Central

Lu, Wei; Khatri, Latika; Ziff, Edward B.

2014-01-01

The GluA2 subunit of the AMPA receptor (AMPAR) dominantly blocks AMPAR Ca2+ permeability, and its trafficking to the synapse regulates AMPAR-dependent synapse Ca2+ permeability. Here we show that GluA2 trafficking from the endoplasmic reticulum (ER) to the plasma membrane of cultured hippocampal neurons requires Ca2+ release from internal stores, the activity of Ca2+/calmodulin activated kinase II (CaMKII), and GluA2 interaction with the PDZ protein, PICK1. We show that upon Ca2+ release from the ER via the IP3 and ryanodine receptors, CaMKII that is activated enters a complex that contains PICK1, dependent upon the PICK1 BAR (Bin-amphiphysin-Rvs) domain, and that interacts with the GluA2 C-terminal domain and stimulates GluA2 ER exit and surface trafficking. This study reveals a novel mechanism of regulation of trafficking of GluA2-containing receptors to the surface under the control of intracellular Ca2+ dynamics and CaMKII activity. PMID:24831007

Simulating Retail Banking for Banking Students

ERIC Educational Resources Information Center

Supramaniam, Mahadevan; Shanmugam, Bala

2009-01-01

The purpose of this study was to examine the implementation flow and development of retail bank management simulation based training system which could provide a comprehensive knowledge about the operations and management of banks for the banking students. The prototype of a Retail banking simulation based training system was developed based on…

Critical role for free radicals on sprint exercise-induced CaMKII and AMPKα phosphorylation in human skeletal muscle.

PubMed

Morales-Alamo, David; Ponce-González, Jesús Gustavo; Guadalupe-Grau, Amelia; Rodríguez-García, Lorena; Santana, Alfredo; Cusso, Roser; Guerrero, Mario; Dorado, Cecilia; Guerra, Borja; Calbet, José A L

2013-03-01

The extremely high energy demand elicited by sprint exercise is satisfied by an increase in O2 consumption combined with a high glycolytic rate, leading to a marked lactate accumulation, increased AMP-to-ATP ratio, and reduced NAD(+)/NADH.H(+) and muscle pH, which are accompanied by marked Thr(172) AMP-activated protein kinase (AMPK)-α phosphorylation during the recovery period by a mechanism not fully understood. To determine the role played by reactive nitrogen and oxygen species (RNOS) on Thr(172)-AMPKα phosphorylation in response to cycling sprint exercise, nine voluntary participants performed a single 30-s sprint (Wingate test) on two occasions: one 2 h after the ingestion of placebo and another after the intake of antioxidants (α-lipoic acid, vitamin C, and vitamin E) in a double-blind design. Vastus lateralis muscle biopsies were obtained before, immediately postsprint, and 30 and 120 min postsprint. Performance and muscle metabolism were similar during both sprints. The NAD(+)-to-NADH.H(+) ratio was similarly reduced (84%) and the AMP-to-ATP ratio was similarly increased (×21-fold) immediately after the sprints. Thr(286) Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and Thr(172)-AMPKα phosphorylations were increased after the control sprint (with placebo) but not when the sprints were preceded by the ingestion of antioxidants. Ser(485)-AMPKα1/Ser(491)-AMPKα2 phosphorylation, a known inhibitory mechanism of Thr(172)-AMPKα phosphorylation, was increased only with antioxidant ingestion. In conclusion, RNOS play a crucial role in AMPK-mediated signaling after sprint exercise in human skeletal muscle. Antioxidant ingestion 2 h before sprint exercise abrogates the Thr(172)-AMPKα phosphorylation response observed after the ingestion of placebo by reducing CaMKII and increasing Ser(485)-AMPKα1/Ser(491)-AMPKα2 phosphorylation. Sprint performance, muscle metabolism, and AMP-to-ATP and NAD(+)-to-NADH.H(+) ratios are not affected by the acute

12 CFR 209.2 - Banks desiring to become member banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Banks desiring to become member banks. 209.2 Section 209.2 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM ISSUE AND CANCELLATION OF FEDERAL RESERVE BANK CAPITAL STOCK (REGULATION I) § 209.2 Banks desiring to...

12 CFR 615.5144 - Banks for cooperatives and agricultural credit banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Banks for cooperatives and agricultural credit banks. 615.5144 Section 615.5144 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM FUNDING....5144 Banks for cooperatives and agricultural credit banks. As may be authorized by the banks for...

75 FR 20848 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-04-21

... Carolina, Seneca National Bank, Seneca, South Carolina, and The Peoples National Bank, Easley, South... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

75 FR 49493 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-13

... Peoples Bank and Trust Company, both of North Carrollton, Mississippi. B. Federal Reserve Bank of Dallas... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

75 FR 54148 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-09-03

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 9414 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-03-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 39016 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-07-07

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 51814 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-23

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 33810 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-06-15

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 3904 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-01-25

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 10484 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-03-08

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 53968 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-09-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 5322 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-02-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

75 FR 51073 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-18

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

Phase Evolution of the Crab Pulsar between Radio and X-Ray

DOE Office of Scientific and Technical Information (OSTI.GOV)

Yan, L. L.; Ge, M. Y.; Zheng, S. J.

We study the X-ray phases of the Crab pulsar utilizing the 11-year observations from the Rossi X-ray Timing Explorer , 6-year radio observations from Nanshan Telescope, and the ephemeris from Jodrell Bank Observatory. It is found that the X-ray phases in different energy bands and the radio phases from the Nanshan Telescope show similar behaviors, including long-time evolution and short-time variations. Such strong correlations between the X-ray and radio phases imply that the radio and X-ray timing noises are both generated from the pulsar spin that cannot be well described by the the monthly ephemeris from the Jodrell Bank observatory.more » When using the Nanshan phases as references to study the X-ray timing noise, it has a significantly smaller variation amplitude and shows no long-time evolution, with a change rate of (−1.1 ± 1.1) × 10{sup −7} periods per day. These results show that the distance of the X-ray and radio emission regions on the Crab pulsar has no detectable secular change, and it is unlikely that the timing noises resulted from any unique physical processes in the radio or X-ray emitting regions. The similar behaviors of the X-ray and radio timing noises also imply that the variation of the interstellar medium is not the origin of the Crab pulsar’s timing noises, which is consistent with the results obtained from the multi-frequency radio observations of PSR B1540−06.« less

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells.

PubMed

Huang, Chun-Yin; Chang, An-Chen; Chen, Hsien-Te; Wang, Shih-Wei; Lo, Yuan-Shun; Tang, Chih-Hsin

2016-09-01

Chondrosarcoma is the second most frequently occurring type of bone malignancy characterized by distant metastatic propensity. Vascular endothelial growth factor-C (VEGF-C) is the major lymphangiogenic factor, and makes crucial contributions to tumour lymphangiogenesis and lymphatic metastasis. Adiponectin is a protein hormone secreted predominantly by differentiated adipocytes. In recent years, adiponectin has also been indicated as facilitating tumorigenesis, angiogenesis and metastasis. However, the effect of adiponectin on VEGF-C regulation and lymphangiogenesis in chondrosarcoma has remained largely a mystery. In the present study, we have shown a clinical correlation between adiponectin and VEGF-C, as well as tumour stage, in human chondrosarcoma tissues. We further demonstrated that adiponectin promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium from adiponectin-treated cells significantly induced tube formation and migration of human lymphatic endothelial cells. In addition, adiponectin knock down inhibited lymphangiogenesis in vitro and in vivo We also found that adiponectin-induced VEGF-C is mediated by the calmodulin-dependent protein kinase II (CaMKII), AMP-activated protein kinase (AMPK) and p38 signaling pathway. Furthermore, the expression of miR-27b was negatively regulated by adiponectin via the CaMKII, AMPK and p38 cascade. The present study is the first to describe the mechanism of adiponectin-promoted lymphangiogenesis by up-regulating VEGF-C expression in chondrosarcomas. Thus, adiponectin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis. © 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.

12 CFR 614.4352 - Farm Credit Banks and agricultural credit banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Farm Credit Banks and agricultural credit banks. 614.4352 Section 614.4352 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4352 Farm Credit Banks and agricultural credit...

12 CFR 614.4352 - Farm Credit Banks and agricultural credit banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Farm Credit Banks and agricultural credit banks. 614.4352 Section 614.4352 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4352 Farm Credit Banks and agricultural credit...

76 FR 59396 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-09-26

... control of Bank of Odessa, both in Odessa, Missouri, Commercial Bank of Oak Grove, Oak Grove, Missouri... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Wheeler, David L

2007-01-01

GenBank (R) is a comprehensive database that contains publicly available nucleotide sequences for more than 240 000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the EMBL Data Library in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage (www.ncbi.nlm.nih.gov).

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Wheeler, David L

2006-01-01

GenBank (R) is a comprehensive database that contains publicly available DNA sequences for more than 205 000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the Web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the EMBL Data Library in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, go to the NCBI Homepage at www.ncbi.nlm.nih.gov.

GenBank

PubMed Central

Benson, Dennis A.; Karsch-Mizrachi, Ilene; Lipman, David J.; Ostell, James; Wheeler, David L.

2007-01-01

GenBank (R) is a comprehensive database that contains publicly available nucleotide sequences for more than 240 000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the EMBL Data Library in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage (). PMID:17202161

75 FR 31788 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-06-04

... voting shares of Chino Commercial Bank, N.A., both of Chino, California. Board of Governors of the... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

About Banking.

ERIC Educational Resources Information Center

Pieslak, Raymond F.

The student manual for high school level special needs students was prepared to provide deaf students with the basic fundamentals of banking. Five units are presented covering the topics of banks and banking services, checking accounts, other services of banks, savings accounts, and other investments. Each lesson was carefully written for easy…

12 CFR 250.200 - Investment in bank premises by holding company banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Investment in bank premises by holding company banks. 250.200 Section 250.200 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS... bank premises by holding company banks. (a) The Board of Governors has been asked whether, in...

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Sayers, Eric W

2011-01-01

GenBank® is a comprehensive database that contains publicly available nucleotide sequences for more than 380,000 organisms named at the genus level or lower, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects, including whole genome shotgun (WGS) and environmental sampling projects. Most submissions are made using the web-based BankIt or standalone Sequin programs, and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the European Nucleotide Archive (ENA) and the DNA Data Bank of Japan (DDBJ) ensures worldwide coverage. GenBank is accessible through the NCBI Entrez retrieval system that integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage: www.ncbi.nlm.nih.gov.

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Sayers, Eric W

2009-01-01

GenBank is a comprehensive database that contains publicly available nucleotide sequences for more than 300,000 organisms named at the genus level or lower, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs, and accession numbers are assigned by GenBank(R) staff upon receipt. Daily data exchange with the European Molecular Biology Laboratory Nucleotide Sequence Database in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through the National Center for Biotechnology Information (NCBI) Entrez retrieval system, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage: www.ncbi.nlm.nih.gov.

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Wheeler, David L

2005-01-01

GenBank is a comprehensive database that contains publicly available DNA sequences for more than 165,000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the EMBL Data Library in the UK and the DNA Data Bank of Japan helps to ensure worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, go to the NCBI Homepage at http://www.ncbi.nlm.nih.gov.

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Wheeler, David L

2008-01-01

GenBank (R) is a comprehensive database that contains publicly available nucleotide sequences for more than 260 000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the European Molecular Biology Laboratory Nucleotide Sequence Database in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage: www.ncbi.nlm.nih.gov.

GenBank

PubMed Central

Benson, Dennis A.; Karsch-Mizrachi, Ilene; Lipman, David J.; Ostell, James; Wheeler, David L.

2008-01-01

GenBank (R) is a comprehensive database that contains publicly available nucleotide sequences for more than 260 000 named organisms, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Most submissions are made using the web-based BankIt or standalone Sequin programs and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the European Molecular Biology Laboratory Nucleotide Sequence Database in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through NCBI's retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI Homepage: www.ncbi.nlm.nih.gov PMID:18073190

12 CFR 250.200 - Investment in bank premises by holding company banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Investment in bank premises by holding company banks. 250.200 Section 250.200 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS... premises without prior Board approval, a State member bank, which is owned by a registered bank holding...

78 FR 37541 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-21

..., North Dakota, as trustees/administrators, to retain voting shares of the Commercial Bank of Mott Employee Stock Ownership Plan, and thereby indirectly retain voting shares of Commercial Bank of Mott, both... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

12 CFR 614.4070 - Loans and chartered territory-Farm Credit Banks, agricultural credit banks, Federal land bank...

Code of Federal Regulations, 2010 CFR

2010-01-01

..., agricultural credit banks, Federal land bank associations, Federal land credit associations, production credit associations, and agricultural credit associations. 614.4070 Section 614.4070 Banks and Banking FARM CREDIT... land credit associations, production credit associations, and agricultural credit associations. (a) A...

77 FR 14368 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-09

... thereby indirectly acquire voting shares of Peoples Community Bank, both in Bremen, Georgia. B. Federal... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 26280 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-05-03

... thereby indirectly acquire voting shares of Peoples Community Bank, both in Bremen, Georgia. Board of... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 13323 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-06

... thereby indirectly acquire additional voting shares of Peoples State Bank, both in Lake City, Florida. B... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 60996 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-05

... shares of Anchor Commercial Bank, Juno Beach, Florida. Board of Governors of the Federal Reserve System... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 64498 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-10-29

... Peoples Savings Bank, both in Indianola, Iowa. 2. David H. McKee, individually, and as special voting... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 15014 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-03-08

... acquire voting shares of Peoples State Bank, McDonald, Kansas. Board of Governors of the Federal Reserve... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 34384 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-07

... Johnson Bank as trustee, both of Racine, Wisconsin; to join the existing Johnson Family Control Group and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

GenBank.

PubMed

Benson, Dennis A; Karsch-Mizrachi, Ilene; Lipman, David J; Ostell, James; Sayers, Eric W

2010-01-01

GenBank is a comprehensive database that contains publicly available nucleotide sequences for more than 300,000 organisms named at the genus level or lower, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects, including whole genome shotgun (WGS) and environmental sampling projects. Most submissions are made using the web-based BankIt or standalone Sequin programs, and accession numbers are assigned by GenBank staff upon receipt. Daily data exchange with the European Molecular Biology Laboratory Nucleotide Sequence Database in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through the NCBI Entrez retrieval system, which integrates data from the major DNA and protein sequence databases along with taxonomy, genome, mapping, protein structure and domain information, and the biomedical journal literature via PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bi-monthly releases and daily updates of the GenBank database are available by FTP. To access GenBank and its related retrieval and analysis services, begin at the NCBI homepage: www.ncbi.nlm.nih.gov.

Thapsigargin-induced activation of Ca(2+)-CaMKII-ERK in brainstem contributes to substance P release and induction of emesis in the least shrew.

PubMed

Zhong, Weixia; Chebolu, Seetha; Darmani, Nissar A

2016-04-01

Cytoplasmic calcium (Ca(2+)) mobilization has been proposed to be an important factor in the induction of emesis. The selective sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin, is known to deplete intracellular Ca(2+) stores, which consequently evokes extracellular Ca(2+) entry through cell membrane-associated channels, accompanied by a prominent rise in cytosolic Ca(2+). A pro-drug form of thapsigargin is currently under clinical trial as a targeted cancer chemotherapeutic. We envisioned that the intracellular effects of thapsigargin could cause emesis and planned to investigate its mechanisms of emetic action. Indeed, thapsigargin did induce vomiting in the least shrew in a dose-dependent and bell-shaped manner, with maximal efficacy (100%) at 0.5 mg/kg (i.p.). Thapsigargin (0.5 mg/kg) also caused increases in c-Fos immunoreactivity in the brainstem emetic nuclei including the area postrema (AP), nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNX), as well as enhancement of substance P (SP) immunoreactivity in DMNX. In addition, thapsigargin (0.5 mg/kg, i.p.) led to vomit-associated and time-dependent increases in phosphorylation of Ca(2+)/calmodulin kinase IIα (CaMKIIα) and extracellular signal-regulated protein kinase 1/2 (ERK1/2) in the brainstem. We then explored the suppressive potential of diverse chemicals against thapsigargin-evoked emesis including antagonists of: i) neurokinin-1 receptors (netupitant), ii) the type 3 serotonin receptors (palonosetron), iii) store-operated Ca(2+) entry (YM-58483), iv) L-type Ca(2+) channels (nifedipine), and v) SER Ca(2+)-release channels inositol trisphosphate (IP3Rs) (2-APB)-, and ryanodine (RyRs) (dantrolene)-receptors. In addition, the antiemetic potential of inhibitors of CaMKII (KN93) and ERK1/2 (PD98059) were investigated. All tested antagonists/blockers attenuated emetic parameters to varying degrees except palonosetron, however a combination of non

75 FR 70262 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-17

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

75 FR 71130 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-22

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 45535 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-07-29

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 81939 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-29

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 3425 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-01-16

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 31612 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-05-29

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 64801 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-23

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 43883 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-07-22

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 33459 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-06-06

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 43824 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-07-26

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 16223 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-20

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 13877 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-03-01

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 9250 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-02-16

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 37406 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-06-21

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 49268 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-08-13

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 62301 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-10-15

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 27458 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-05-10

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank [[Page...

76 FR 75882 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-05

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 72864 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-12-06

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 3897 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-01-17

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 39729 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-07-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

75 FR 77876 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-12-14

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 23599 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-04-27

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 20635 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-04-05

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

75 FR 67969 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-04

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 41929 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-07-12

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 51726 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-08-21

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 27389 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-05-10

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 19665 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-04-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 75548 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-02

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 34385 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-06-11

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 4323 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-01-27

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 10595 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-02-25

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 68121 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-11-15

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 10899 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-02-28

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 70722 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-11-15

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 16839 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-22

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 284 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-01-04

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 76305 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-12-17

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 50689 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-08-22

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 54917 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-09-06

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 72205 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-11-22

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

77 FR 60702 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-04

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 40730 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-07-11

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 32361 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-06-06

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 81940 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-29

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

76 FR 19099 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-04-06

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

78 FR 35271 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-12

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

75 FR 7597 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-02-22

... Family Immediate Family Control Group, consisting of Harold D. Rogers, individually, and as Trustee of... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

The security concern on internet banking adoption among Malaysian banking customers.

PubMed

Sudha, Raju; Thiagarajan, A S; Seetharaman, A

2007-01-01

The existing literatures highlights that the security is the primary factor which determines the adoption of Internet banking technology. The secondary information on Internet banking development in Malaysia shows a very slow growth rate. Hence, this study aims to study the banking customers perception towards security concern and Internet banking adoption through the information collected from 150 sample respondents. The data analysis reveals that the customers have much concern about security and privacy issue in adoption of Internet banking, whether the customers are adopted Internet banking or not. Hence, it infers that to popularize Internet banking system there is a need for improvement in security and privacy issue among the banking customers.

Umbilical cord blood banks. Ethical aspects. Public versus private banks.

PubMed

Aznar Lucea, Justo

2012-01-01

The creation of umbilical cord blood (UCB) banks raises interesting medical, social, economic and ethical issues. This paper reviews the ethical problems specifically. In this respect, it evaluates: a) whether there are advantages to the use of UCB compared to bone marrow, b) whether or not it is ethical to create UCB banks, c) whether their creation is ethically acceptable in terms of their clinical usefulness or d) the use made of them for therapeutic purposes, and finally e) whether their creation is ethically justified from a cost/profitability point of view. We focus primarily on evaluating the ethical controversy between public and private banks, particularly on whether it is ethical to bank autologous blood in private UCB banks, on the basis of its limited possibilities for use by the cord blood donor. We can conclude that, from an ethical point of view, autologous blood banks have limited acceptance among specialised researchers, scientific societies and other public institutions. Therefore, we believe that it is ethically more acceptable to support the creation of public UCB banks for medical and social reasons and, above all, based on the principle of justice and human solidarity. Nevertheless, there is no definitive ethical argument why a couple, according to their autonomy and freedom, cannot bank their child's UCB in a private bank. An equally acceptable solution could be the creation of mixed banks, such as that proposed by the Virgin Health Bank or like the Spanish system where autologous samples can be stored in public banks but with the proviso that if at any time the stored sample is required by any person other than the donor, it would have to be given to them.

12 CFR 583.3 - Bank.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 5 2011-01-01 2011-01-01 false Bank. 583.3 Section 583.3 Banks and Banking... AND LOAN HOLDING COMPANIES § 583.3 Bank. The term bank means any national bank, state bank, state-chartered savings bank, cooperative bank, or industrial bank, the deposits of which are insured by the...

77 FR 32637 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-06-01

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank.... Eckles as Trustee, Blue Earth, Minnesota; to retain control of FNB Bancshares, Inc., and thereby indirectly retain control of First Bank Blue Earth, both in Blue Earth, Minnesota. Board of Governors of the...

76 FR 4896 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-01-27

... the Young Family control group; to retain control of Southeastern Bancshares, Inc., and thereby... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 33093 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-03

... Freeman family control group, to retain voting shares of Texhoma Bancshares, Inc., and thereby indirectly... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 76834 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-12-19

..., Bexley, Ohio; (collectively the Graham Family Control Group) to retain voting shares of North Valley... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

76 FR 41259 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-07-13

... Family control group; to retain control of RCB Holding Company, Inc., Claremore, Oklahoma, parent of RCB... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 60118 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-02

..., Illinois; to join the existing Kirschner Family Control Group by acquiring voting shares of Town and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 19708 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-02

... Family Control Group, to acquire voting shares of Johnson Financial Group, Inc., and thereby indirectly... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 17478 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-26

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... Russell Bauman, both of Kerkhoven, Minnesota, as individuals and members of the Bauman Family Control...

77 FR 42730 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-07-20

... members of The Hales Family Control Group; to gain control of First Trust Financial Corporation, and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 20919 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-08

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... Street, Cleveland, Ohio 44101-2566: 1. Julie Rose Akemon, individually, and the Julie Rose Akemon Control...

78 FR 25084 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-29

... existing Lubar Family Control Group and retain voting shares of Ixonia Bancshares, Inc., and thereby... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 36781 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-19

... the existing Lubar Family Control Group through the acquisition of voting shares of Ixonia Bancshares... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

76 FR 78657 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-19

... Garst Revocable Trust, Des Moines, Iowa; Sarah Garst, West Des Moines, Iowa; as a group acting in... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 75349 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-12-11

... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... Control Trust, both of Dubuque, Iowa, to acquire voting shares of, and the Kennedy Control Trust to join...

77 FR 58141 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-09-19

..., Iowa, Kate Garst Trustee; Sarah Garst, West Des Moines, Iowa), as a group acting in concert and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 22879 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-17

... in concert with a control group consisting of Mr. Reid, Jacob Reid, Lauren Reid Patton, Cathy Switzer... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

76 FR 7849 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-02-11

... individual, and by the control group including the Betty J. Bradshaw 2000 Irrevocable Trust dated 10/30/00... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 33092 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-03

... as a member of the Rowland family control group voting shares of Lead Financial Group, Inc., and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 61606 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-10

... of a family control group which consists of Clayton B. Patrick; Liz S. Patrick; Clayton M. Patrick... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 12057 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-02-28

... Hodgson, all of Charlevoix, Michigan; to join the existing Hodgson control group and to retain and acquire... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 68073 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-11-13

... member of a family control group consisting of James T. Wilson, Jr., Sarah Wilson, James Terill Wilson... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 65382 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-26

..., all of Denver, Colorado; to become members of the Sturm control group, and acquire voting shares of... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 14015 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-08

... family control group (Jason L. Crews, Cynthia Michelle Leslie Crews, Roger L. McGee, and Stacy Crews... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 23934 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-23

..., Monticello, Iowa, and Sarah Jones, Dyer, Indiana, to join the Audrey G. Savage Family Control group and... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

75 FR 71440 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-23

...-2034: 1. The House Family Control Group (which consists of Verlene H. House Revocable Trust, Verlene H... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

77 FR 65689 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-10-30

... Marguerite Fowler Trust, and as a member of a family control group which includes L. Ingles Ferry; Hubert L... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

78 FR 97 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-01-02

... Marguerite Fowler Trust, and as a member of a family control group which includes, David L. Ferry, Joseph D... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C...

75 FR 62132 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-10-07

... Simmons, San Benito, Texas; and Leonard P. Simmons and Mary Beth Simmons, San Benito, Texas, Delores M... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank.... 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or...

e-EVN radio detection of Aql X-1 in outburst

NASA Astrophysics Data System (ADS)

Tudose, V.; Paragi, Z.; Yang, J.; Miller-Jones, J. C. A.; Fender, R.; Garrett, M.; Rushton, A.; Spencer, R.

2013-06-01

The neutron star X-ray binary Aql X-1 is currently in outburst (ATel #5114, #5117, #5129, #5136, #5148). Using the European VLBI Network (e-EVN) we observed Aql X-1 at 5 GHz in two time-slots: 2013 June 18 between 19:48 - 20:36 UT (MJD 56461.825 - 56461.858), and 2013 June 19 between 02:53 - 05:54 UT (MJD 56462.120 - 56462.246). The two datasets were combined together and then calibrated. The participating radio telescopes were: Effelsberg (Germany), Jodrell Bank Mk2 (UK), Medicina (Italy), Noto (Italy), Onsala 25m (Sweden), Torun (Poland), Yebes (Spain), Westerbork Synthesis Radio Telescope (Netherlands), Shanghai (China), Hartebeesthoek (South Africa).

5 CFR 630.1003 - Establishing leave banks and leave bank boards.

Code of Federal Regulations, 2013 CFR

2013-01-01

... boards. 630.1003 Section 630.1003 Administrative Personnel OFFICE OF PERSONNEL MANAGEMENT CIVIL SERVICE REGULATIONS ABSENCE AND LEAVE Voluntary Leave Bank Program § 630.1003 Establishing leave banks and leave bank boards. (a) Each agency that participates in the voluntary leave bank program shall, in accordance with...

5 CFR 630.1003 - Establishing leave banks and leave bank boards.

Code of Federal Regulations, 2011 CFR

2011-01-01

... boards. 630.1003 Section 630.1003 Administrative Personnel OFFICE OF PERSONNEL MANAGEMENT CIVIL SERVICE REGULATIONS ABSENCE AND LEAVE Voluntary Leave Bank Program § 630.1003 Establishing leave banks and leave bank boards. (a) Each agency that participates in the voluntary leave bank program shall, in accordance with...

5 CFR 630.1003 - Establishing leave banks and leave bank boards.

Code of Federal Regulations, 2014 CFR

2014-01-01

... boards. 630.1003 Section 630.1003 Administrative Personnel OFFICE OF PERSONNEL MANAGEMENT CIVIL SERVICE REGULATIONS ABSENCE AND LEAVE Voluntary Leave Bank Program § 630.1003 Establishing leave banks and leave bank boards. (a) Each agency that participates in the voluntary leave bank program shall, in accordance with...

5 CFR 630.1003 - Establishing leave banks and leave bank boards.

Code of Federal Regulations, 2012 CFR

2012-01-01

... boards. 630.1003 Section 630.1003 Administrative Personnel OFFICE OF PERSONNEL MANAGEMENT CIVIL SERVICE REGULATIONS ABSENCE AND LEAVE Voluntary Leave Bank Program § 630.1003 Establishing leave banks and leave bank boards. (a) Each agency that participates in the voluntary leave bank program shall, in accordance with...

An analysis of river bank slope and unsaturated flow effects on bank storage.

PubMed

Doble, Rebecca; Brunner, Philip; McCallum, James; Cook, Peter G

2012-01-01

Recognizing the underlying mechanisms of bank storage and return flow is important for understanding streamflow hydrographs. Analytical models have been widely used to estimate the impacts of bank storage, but are often based on assumptions of conditions that are rarely found in the field, such as vertical river banks and saturated flow. Numerical simulations of bank storage and return flow in river-aquifer cross sections with vertical and sloping banks were undertaken using a fully-coupled, surface-subsurface flow model. Sloping river banks were found to increase the bank infiltration rates by 98% and storage volume by 40% for a bank slope of 3.4° from horizontal, and for a slope of 8.5°, delay bank return flow by more than four times compared with vertical river banks and saturated flow. The results suggested that conventional analytical approximations cannot adequately be used to quantify bank storage when bank slope is less than 60° from horizontal. Additionally, in the unconfined aquifers modeled, the analytical solutions did not accurately model bank storage and return flow even in rivers with vertical banks due to a violation of the dupuit assumption. Bank storage and return flow were also modeled for more realistic cross sections and river hydrograph from the Fitzroy River, Western Australia, to indicate the importance of accurately modeling sloping river banks at a field scale. Following a single wet season flood event of 12 m, results showed that it may take over 3.5 years for 50% of the bank storage volume to return to the river. © 2011, The Author(s). Ground Water © 2011, National Ground Water Association.

75 FR 67731 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-03

... South LaSalle Street, Chicago, Illinois 60690-1414: 1. Robert John Dentel, Victor, Iowa, and Mary P...; First State Bank of Colfax, Colfax, Iowa; Maxwell State Bank, Maxwell, Iowa; Pocahontas State Bank...

12 CFR 1270.17 - Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks.

Code of Federal Regulations, 2014 CFR

2014-01-01

... 12 Banks and Banking 10 2014-01-01 2014-01-01 false Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks. 1270.17 Section 1270.17 Banks and Banking FEDERAL HOUSING FINANCE AGENCY... of Banks, FHFA, Office of Finance and Federal Reserve Banks. The Banks, FHFA, the Director, the...

12 CFR 1270.17 - Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks.

Code of Federal Regulations, 2013 CFR

2013-01-01

... 12 Banks and Banking 9 2013-01-01 2013-01-01 false Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks. 1270.17 Section 1270.17 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL... Banks, FHFA, Office of Finance and Federal Reserve Banks. The Banks, FHFA, the Director, the Office of...

12 CFR 1270.17 - Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks.

Code of Federal Regulations, 2012 CFR

2012-01-01

... 12 Banks and Banking 9 2012-01-01 2012-01-01 false Liability of Banks, FHFA, Office of Finance and Federal Reserve Banks. 1270.17 Section 1270.17 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL... Banks, FHFA, Office of Finance and Federal Reserve Banks. The Banks, FHFA, the Director, the Office of...

12 CFR 7.1003 - Money lent at banking offices or at other than banking offices.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Money lent at banking offices or at other than banking offices. 7.1003 Section 7.1003 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Powers § 7.1003 Money lent at banking offices or at other than...

Reduction of SR Ca2+ leak and arrhythmogenic cellular correlates by SMP-114, a novel CaMKII inhibitor with oral bioavailability.

PubMed

Neef, Stefan; Mann, Christian; Zwenger, Anne; Dybkova, Nataliya; Maier, Lars S

2017-07-01

Sarcoplasmic reticulum (SR) Ca 2+ leak induced by Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) is centrally involved in atrial and ventricular arrhythmogenesis as well as heart failure remodeling. Consequently, treating SR Ca 2+ leak has been proposed as a novel therapeutic paradigm, but compounds for use in humans are lacking. SMP-114 ("Rimacalib") is a novel, orally available CaMKII inhibitor developed for human use that has already entered clinical phase II trials to treat rheumatoid arthritis. We speculated that SMP-114 might also be useful to treat cardiac SR Ca 2+ leak. SMP-114 significantly reduces SR Ca 2+ leak (as assessed by Ca 2+ sparks) in human atrial (0.72 ± 0.33 sparks/100 µm/s vs. control 3.02 ± 0.91 sparks/100 µm/s) and failing left ventricular (0.78 ± 0.23 vs. 1.69 ± 0.27 sparks/100 µm/s) as well as in murine ventricular cardiomyocytes (0.30 ± 0.07 vs. 1.50 ± 0.28 sparks/100 µm/s). Associated with lower SR Ca 2+ leak, we found that SMP-114 suppressed the occurrence of spontaneous arrhythmogenic spontaneous Ca 2+ release (0.356 ± 0.109 vs. 0.927 ± 0.216 events per 30 s stimulation cessation). In consequence, post-rest potentiation of Ca 2+ -transient amplitude (measured using Fura-2) during the 30 s pause was improved by SMP-114 (52 ± 5 vs. 37 ± 4%). Noteworthy, SMP-114 has these beneficial effects without negatively impairing global excitation-contraction coupling: neither systolic Ca 2+ release nor single cell contractility was compromised, and also SR Ca 2+ reuptake, in line with resulting cardiomyocyte relaxation, was not impaired by SMP-114 in our assays. SMP-114 demonstrated potential to treat SR Ca 2+ leak and consequently proarrhythmogenic events in rodent as well as in human atrial cardiomyocytes and cardiomyocytes from patients with heart failure. Further research is necessary towards clinical use in cardiac disease.

12 CFR 583.3 - Bank.

Code of Federal Regulations, 2010 CFR

2010-01-01

... OFFICE OF THRIFT SUPERVISION, DEPARTMENT OF THE TREASURY DEFINITIONS FOR REGULATIONS AFFECTING SAVINGS AND LOAN HOLDING COMPANIES § 583.3 Bank. The term bank means any national bank, state bank, state-chartered savings bank, cooperative bank, or industrial bank, the deposits of which are insured by the...

Using GenBank.

PubMed

Wheeler, David

2007-01-01

GenBank(R) is a comprehensive database of publicly available DNA sequences for more than 205,000 named organisms and for more than 60,000 within the embryophyta, obtained through submissions from individual laboratories and batch submissions from large-scale sequencing projects. Daily data exchange with the European Molecular Biology Laboratory (EMBL) in Europe and the DNA Data Bank of Japan ensures worldwide coverage. GenBank is accessible through the National Center for Biotechnology Information (NCBI) retrieval system, Entrez, which integrates data from the major DNA and protein sequence databases with taxonomy, genome, mapping, protein structure, and domain information and the biomedical journal literature through PubMed. BLAST provides sequence similarity searches of GenBank and other sequence databases. Complete bimonthly releases and daily updates of the GenBank database are available through FTP. GenBank usage scenarios ranging from local analyses of the data available through FTP to online analyses supported by the NCBI Web-based tools are discussed. To access GenBank and its related retrieval and analysis services, go to the NCBI Homepage at http://www.ncbi.nlm.nih.gov.

12 CFR 209.2 - Banks desiring to become member banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... opens for business. In the case of a mutual savings bank not authorized to purchase Reserve Bank shares... new national bank organized by the Federal Deposit Insurance Corporation under § 11(n) of the Federal.... Upon authorization to commence business by the Comptroller of the Currency in the case of a national...

78 FR 37222 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-06-20

... Livingston, Tennessee; to join the currently approved control, group of The Jack Windle Irrevocable Life... Livingston, Tennessee. Collectively, the new control group controls 100 percent of the outstanding stock of... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

75 FR 69444 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2010-11-12

... South LaSalle Street, Chicago, Illinois 60690-1414: 1. Robert John Dentel, Victor, Iowa, and Mary P. Howell, Ames, Iowa, individually; and the Robert John Dentel Family (Robert J. Dentel, Patricia A. Dentel... Bank, Corydon, Iowa; First State Bank of Colfax, Colfax, Iowa; Maxwell State Bank, Maxwell, Iowa...

76 FR 2688 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-01-14

... 442, St. Louis, Missouri 63166-2034: 1. The Coffey Family Control Group, which consists of Avery..., Minnesota, and both as members of The Wilcox Family Control Group; to acquire control of Wilcox Bancshares... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

77 FR 48983 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-08-15

... Family Control Group which consists of Eric A. Gillett Revocable Trust, and Denise E. Gillett Revocable..., Troy, Ohio; and The James A. Gorrell Family Control Group which consist of James A. Gorrell, Tiffin... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

78 FR 19268 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-03-29

... Street, Dallas, Texas 75201-2272: 1. Larry Alton Jobe, Dallas, Texas; Leland A. Jobe, Dallas, Texas; Jennifer M. Jobe, Dallas, Texas; Lezlie MacElroy, Pilot Point, Texas; and Lorrie J. Fry, Austin, Texas... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

32 CFR 643.113 - Banks.

Code of Federal Regulations, 2010 CFR

2010-07-01

... Authority of Commanders § 643.113 Banks. (a) The establishment of banks, branch banks, and banking... banking facility is self-sustaining and notifies the Commander, U.S. Army Finance and Accounting Center. (c) Banking facilities which are not self-sustaining will be furnished space, utilities and custodial...

77 FR 19287 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-03-30

... thereby indirectly retain control of Northstar Bank, both in Bad Axe, Michigan, and Seaway Community Bank... Bad Axe, Michigan, and certain of their minor children as a group acting in concert, to retain voting... in Bad Axe, Michigan, and Seaway Community Bank, St. Clair, Michigan. In addition, Lynette Drake, as...

76 FR 76412 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-07

..., both of Des Moines, Iowa; to acquire control of Exchange Financial, Inc., and thereby indirectly... City, New Jersey; to become part of the group acting in concert to acquire control of First Federal of... FEDERAL RESERVE SYSTEM Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank...

EVN observations of eleven GHz-Peaked-Spectrum radio sources at 2.3/8.4 GHz

NASA Astrophysics Data System (ADS)

Xiang, L.; Dallacasa, D.; Cassaro, P.; Jiang, D.; Reynolds, C.

2005-04-01

We present results of EVN observations of eleven GHz-Peaked-Spectrum (GPS) radio sources at 2.3/8.4 GHz. These sources are from the classical "bright" GPS source samples with peak flux densities > 0.2 Jy and spectral indices α < -0.2 (S ∝ ν-α) in the optically thick regime of their convex spectra. Most of the target sources did not have VLBI images at the time this project started. The aim of the work is to find Compact Symmetric Object (CSO) candidates from the "bright" GPS samples. These CSOs play a key role in understanding the very early stage of the evolution of individual radio galaxies. The reason for investigating GPS source samples is that CSO candidates are more frequently found among this class of radio sources. In fact both classes, GPS and CSO, represent a small fraction of the flux limited and flat-spectrum samples like PR+CJ1 (PR: Pearson-Readhead survey, CJ1: the first Caltech-Jodrell Bank survey) and CJF (the Caltech-Jodrell Bank flat spectrum source survey) with a single digit percentage progressively decreasing with decreasing flux density limit. Our results, with at least 3, but possibly more CSO sources detected among a sample of 11, underline the effectiveness of our approach. The three confirmed CSO sources (1133+432, 1824+271, and 2121-014) are characterized by a symmetric pair of resolved components, each with steep spectral indices. Five further sources (0144+209, 0554-026, 0904+039, 0914+114 and 2322-040) can be considered likely CSO candidates. The remaining three sources (0159+839, 0602+780 and 0802+212) are either of core-jet type or dominated by a single component at both frequencies.

12 CFR 225.14 - Expedited action for certain bank acquisitions by well-run bank holding companies.

Code of Federal Regulations, 2012 CFR

2012-01-01

... 12 Banks and Banking 3 2012-01-01 2012-01-01 false Expedited action for certain bank acquisitions by well-run bank holding companies. 225.14 Section 225.14 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM BANK HOLDING COMPANIES AND CHANGE IN BANK CONTROL (REGULATION Y) Regulations Acquisition...

12 CFR 225.14 - Expedited action for certain bank acquisitions by well-run bank holding companies.

Code of Federal Regulations, 2014 CFR

2014-01-01

... 12 Banks and Banking 3 2014-01-01 2014-01-01 false Expedited action for certain bank acquisitions by well-run bank holding companies. 225.14 Section 225.14 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM (CONTINUED) BANK HOLDING COMPANIES AND CHANGE IN BANK CONTROL (REGULATION Y) Regulations...

12 CFR 225.14 - Expedited action for certain bank acquisitions by well-run bank holding companies.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Expedited action for certain bank acquisitions by well-run bank holding companies. 225.14 Section 225.14 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM BANK HOLDING COMPANIES AND CHANGE IN BANK CONTROL (REGULATION Y) Regulations Acquisition...

12 CFR 917.10 - Bank bylaws.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Bank bylaws. 917.10 Section 917.10 Banks and Banking FEDERAL HOUSING FINANCE BOARD GOVERNANCE AND MANAGEMENT OF THE FEDERAL HOME LOAN BANKS POWERS AND RESPONSIBILITIES OF BANK BOARDS OF DIRECTORS AND SENIOR MANAGEMENT § 917.10 Bank bylaws. A Bank's board of...

12 CFR 917.10 - Bank bylaws.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Bank bylaws. 917.10 Section 917.10 Banks and Banking FEDERAL HOUSING FINANCE BOARD GOVERNANCE AND MANAGEMENT OF THE FEDERAL HOME LOAN BANKS POWERS AND RESPONSIBILITIES OF BANK BOARDS OF DIRECTORS AND SENIOR MANAGEMENT § 917.10 Bank bylaws. A Bank's board of...

Very low density lipoprotein receptor regulates dendritic spine formation in a RasGRF1/CaMKII dependent manner

PubMed Central

DiBattista, Amanda Marie; Dumanis, Sonya B.; Song, Jung Min; Bu, Guojun; Weeber, Edwin; Rebeck, G. William; Hoe, Hyang-Sook

2015-01-01

Very Low Density Lipoprotein Receptor (VLDLR) is an apolipoprotein E receptor involved in synaptic plasticity, learning, and memory. However, it is unknown how VLDLR can regulate synaptic and cognitive function. In the present study, we found that VLDLR is present at the synapse both pre- and post-synaptically. Overexpression of VLDLR significantly increases, while knockdown of VLDLR decreases, dendritic spine number in primary hippocampal cultures. Additionally, knockdown of VLDLR significantly decreases synaptophysin puncta number while differentially regulating cell surface and total levels of glutamate receptor subunits. To identify the mechanism by which VLDLR induces these synaptic effects, we investigated whether VLDLR affects dendritic spine formation through the Ras signaling pathway, which is involved in spinogenesis and neurodegeneration. Interestingly, we found that VLDLR interacts with RasGRF1, a Ras effector, and knockdown of RasGRF1 blocks the effect of VLDLR on spinogenesis. Moreover, we found that VLDLR did not rescue the deficits induced by the absence of Ras signaling proteins CaMKIIα or CaMKIIβ. Taken together, our results suggest that VLDLR requires RasGRF1/CaMKII to alter dendritic spine formation. PMID:25644714

12 CFR Appendix D to Part 229 - Indorsement, Reconverting Bank Identification, and Truncating Bank Identification Standards

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Indorsement, Reconverting Bank Identification, and Truncating Bank Identification Standards D Appendix D to Part 229 Banks and Banking FEDERAL... COLLECTION OF CHECKS (REGULATION CC) Pt. 229, App. D Appendix D to Part 229—Indorsement, Reconverting Bank...

Radio Non-Detections of SN 2010cu and PSN J13203538+3408222 in IC 883

NASA Astrophysics Data System (ADS)

Romero-Canizales, Cristina; Perez-Torres, Miguel A.; Alberdi, Antxon; Kankare, Erkki; Ryder, Stuart D.; Mattila, Seppo

2011-04-01

We report 5 GHz eEVN observations of the luminous infrared galaxy IC 883 intended as a radio follow-up of SN 2010cu (CBET # 2213 and 2286) and PSN J13203538+3408222 (ATel # 3245) that were recently discovered within the nuclear regions of IC 883 by near-IR adaptive-optics observations. The observations were carried out on 23rd March 2011 between 0200UT and 0400UT (total time on source ~1.3 hours) and included the following antennae (diameter, location): Effelsberg (100m, Germany), Jodrell Bank (25m, UK), Medicina (32 m, Italy), Onsala (25 m, Sweden), Torun (32 m, Poland), Westerbork array (14x25 m, NL) and Yebes (40 m, Spain).

The role of bank collapse on tidal creek ontogeny: A novel process-based model for bank retreat

NASA Astrophysics Data System (ADS)

Gong, Zheng; Zhao, Kun; Zhang, Changkuan; Dai, Weiqi; Coco, Giovanni; Zhou, Zeng

2018-06-01

Bank retreat in coastal tidal flats plays a primary role on the planimetric shape of tidal creeks and is commonly driven by both flow-induced bank erosion and gravity-induced bank collapse. However, existing modelling studies largely focus on bank erosion and overlook bank collapse. We build a bank retreat model coupling hydrodynamics, bank erosion and bank collapse. To simulate the process of bank collapse, a stress-deformation model is utilized to calculate the stress variation of bank soil after bank erosion, and the Mohr-Coulomb failure criterion is then applied to evaluate the stability of the tidal creek bank. Results show that the bank failure process can be categorized into three stages, i.e., shear failure at the bank toe (stage I), tensile failure on the bank top (stage II), and sectional cracking from the bank top to the toe (stage III). With only bank erosion, the planimetric shapes of tidal creeks are funneled due to the gradually seaward increasing discharge. In contrast to bank erosion, bank collapse is discontinuous, and the contribution of bank collapse to bank retreat can reach 85%, highlighting that the expansion of tidal creeks can be dominated by bank collapse process. The planimetric shapes of tidal creeks are funneled with a much faster expansion rate when bank collapse is considered. Overall, this study makes a further step toward more physical and realistic simulation of bank retreat in estuarine and coastal settings and the developed bank collapse module can be readily included in other morphodynamic models.

12 CFR 987.7 - Liability of Banks, Finance Board, Office of Finance and Federal Reserve Banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Liability of Banks, Finance Board, Office of Finance and Federal Reserve Banks. 987.7 Section 987.7 Banks and Banking FEDERAL HOUSING FINANCE BOARD OFFICE OF FINANCE BOOK-ENTRY PROCEDURE FOR CONSOLIDATED OBLIGATIONS § 987.7 Liability of Banks, Finance...

77 FR 74482 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-12-14

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or bank... the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the Federal...

12 CFR 7.1003 - Money lent at banking offices or at other than banking offices.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Money lent at banking offices or at other than banking offices. 7.1003 Section 7.1003 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE... without violating 12 U.S.C. 36, 12 U.S.C. 81 and 12 CFR 5.30, provided that a third party is used to...

12 CFR 996.2 - Bank employees.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Bank employees. 996.2 Section 996.2 Banks and Banking FEDERAL HOUSING FINANCE BOARD NON-BANK SYSTEM ENTITIES AUTHORITY FOR BANK ASSISTANCE OF THE RESOLUTION FUNDING CORPORATION § 996.2 Bank employees. Upon the request of the Directorate of the Resolution...

12 CFR 987.7 - Liability of Banks, Finance Board, Office of Finance and Federal Reserve Banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Liability of Banks, Finance Board, Office of Finance and Federal Reserve Banks. 987.7 Section 987.7 Banks and Banking FEDERAL HOUSING FINANCE BOARD OFFICE OF FINANCE BOOK-ENTRY PROCEDURE FOR CONSOLIDATED OBLIGATIONS § 987.7 Liability of Banks, Finance Board, Office of Finance and Federal Reserve...

12 CFR 2.5 - Bank compensation.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Bank compensation. 2.5 Section 2.5 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY SALES OF CREDIT LIFE INSURANCE § 2.5 Bank compensation. (a) Nothing contained in this part prohibits a bank employee, officer, director, or principal...

12 CFR 2.5 - Bank compensation.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Bank compensation. 2.5 Section 2.5 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY SALES OF CREDIT LIFE INSURANCE § 2.5 Bank compensation. (a) Nothing contained in this part prohibits a bank employee, officer, director, or principal...

An experimental comparison of conventional two-bank and novel four-bank dynamic MLC tracking.

PubMed

Davies, G A; Clowes, P; McQuaid, D; Evans, P M; Webb, S; Poludniowski, G

2013-03-07

The AccuLeaf mMLC featuring four multileaf-collimator (MLC) banks has been used for the first time for an experimental comparison of conventional two-bank with novel four-bank dynamic MLC tracking of a two-dimensional sinusoidal respiratory motion. This comparison was performed for a square aperture, and for three conformal treatment apertures from clinical radiotherapy lung cancer patients. The system latency of this prototype tracking system was evaluated and found to be 1.0 s and the frequency at which MLC positions could be updated, 1 Hz, and therefore accurate MLC tracking of irregular patient motion would be difficult with the system in its current form. The MLC leaf velocity required for two-bank-MLC and four-bank-MLC tracking was evaluated for the apertures studied and a substantial decrease was found in the maximum MLC velocity required when four-banks were used for tracking rather than two. A dosimetric comparison of the two techniques was also performed and minimal difference was found between two-bank-MLC and four-bank-MLC tracking. The use of four MLC banks for dynamic MLC tracking is shown to be potentially advantageous for increasing the delivery efficiency compared with two-bank-MLC tracking where difficulties are encountered if large leaf shifts are required to track motion perpendicular to the direction of leaf travel.

77 FR 42312 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-07-18

... shares of Rising Sun Bancorp, and thereby indirectly acquire voting shares of NBRS Financial Bank, both in Rising Sun, Maryland. B. Federal Reserve Bank of San Francisco (Kenneth Binning, Vice President...

Using Banks: Teaching Banking Skills to Low-Income Consumers.

ERIC Educational Resources Information Center

Shurtz, Mary Ann; LeFlore, Ann Becker

This module, one of six on teaching consumer matters to low-income adults, discusses banking skills. Topics include banking services (savings accounts, safety deposit boxes, Christmas clubs, loans, etc.), checking accounts (deposits, checkwriting, check registers, opening an account), how to use the check register (cancelled checks, deposits),…

12 CFR 204.121 - Bankers' banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Bankers' banks. 204.121 Section 204.121 Banks... REQUIREMENTS OF DEPOSITORY INSTITUTIONS (REGULATION D) Interpretations § 204.121 Bankers' banks. (a)(1) The...' banks. (2) In its application of these requirements to specific institutions, the Board will use the...

Bank Record Processing

NASA Technical Reports Server (NTRS)

1982-01-01

Barnett Banks of Florida, Inc. operates 150 banking offices in 80 Florida cities. Banking offices have computerized systems for processing deposits or withdrawals in checking/savings accounts, and for handling commercial and installment loan transactions. In developing a network engineering design for the terminals used in record processing, an affiliate, Barnett Computing Company, used COSMIC's STATCOM program. This program provided a reliable network design tool and avoided the cost of developing new software.

78 FR 61352 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-10-03

... shares of FirstSecure Bank and Trust Company, Palos Hill, IL. B. Federal Reserve Bank of Minneapolis..., Julie Jennings, Lone Tree, Colorado, and R. Will Isham, Gordon, Nebraska, in their individual capacities...

12 CFR 1261.14 - Vacant Bank directorships.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Vacant Bank directorships. 1261.14 Section 1261.14 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS FEDERAL HOME LOAN BANK DIRECTORS Federal Home Loan Bank Boards of Directors: Eligibility and Elections § 1261.14 Vacant Bank...

12 CFR 1261.13 - Ineligible Bank directors.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Ineligible Bank directors. 1261.13 Section 1261.13 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS FEDERAL HOME LOAN BANK DIRECTORS Federal Home Loan Bank Boards of Directors: Eligibility and Elections § 1261.13 Ineligible Bank...

12 CFR 1261.14 - Vacant Bank directorships.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Vacant Bank directorships. 1261.14 Section 1261.14 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS FEDERAL HOME LOAN BANK DIRECTORS Federal Home Loan Bank Boards of Directors: Eligibility and Elections § 1261.14 Vacant Bank...

12 CFR 1261.13 - Ineligible Bank directors.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Ineligible Bank directors. 1261.13 Section 1261.13 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS FEDERAL HOME LOAN BANK DIRECTORS Federal Home Loan Bank Boards of Directors: Eligibility and Elections § 1261.13 Ineligible Bank...

Improving Soil Seed Bank Management.

PubMed

Haring, Steven C; Flessner, Michael L

2018-05-08

Problems associated with simplified weed management motivate efforts for diversification. Integrated weed management uses fundamentals of weed biology and applied ecology to provide a framework for diversified weed management programs; the soil seed bank comprises a necessary part of this framework. By targeting seeds, growers can inhibit the propagule pressure on which annual weeds depend for agricultural invasion. Some current management practices affect weed seed banks, such as crop rotation and tillage, but these tools are often used without specific intention to manage weed seeds. Difficulties quantifying the weed seed bank, understanding seed bank phenology, and linking seed banks to emerged weed communities challenge existing soil seed bank management practices. Improved seed bank quantification methods could include DNA profiling of the soil seed bank, mark and recapture, or 3D LIDAR mapping. Successful and sustainable soil seed bank management must constrain functionally diverse and changing weed communities. Harvest weed seed controls represent a step forward, but over-reliance on this singular technique could make it short-lived. Researchers must explore tools inspired by other pest management disciplines, such as gene drives or habitat modification for predatory organisms. Future weed seed bank management will combine multiple complementary practices that enhance diverse agroecosystems. This article is protected by copyright. All rights reserved.

12 CFR 996.2 - Bank employees.

Code of Federal Regulations, 2010 CFR

2010-01-01

... RESOLUTION FUNDING CORPORATION § 996.2 Bank employees. Upon the request of the Directorate of the Resolution..., employees, or agents of the Banks are authorized to act for and on behalf of the Resolution Funding... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Bank employees. 996.2 Section 996.2 Banks and...

BONE BANKS.

PubMed

de Alencar, Paulo Gilberto Cimbalista; Vieira, Inácio Facó Ventura

2010-01-01

Bone banks are necessary for providing biological material for a series of orthopedic procedures. The growing need for musculoskeletal tissues for transplantation has been due to the development of new surgical techniques, and this has led to a situation in which a variety of hospital services have been willing to have their own source of tissue for transplantation. To increase the safety of transplanted tissues, standards for bone bank operation have been imposed by the government, which has limited the number of authorized institutions. The good performance in a bone bank depends on strict control over all stages, including: formation of well-trained harvesting teams; donor selection; conducting various tests on the tissues obtained; and strict control over the processing techniques used. Combination of these factors enables greater scope of use and numbers of recipient patients, while the incidence of tissue contamination becomes statistically insignificant, and there is traceability between donors and recipients. This paper describes technical considerations relating to how a bone bank functions, the use of grafts and orthopedic applications, the ethical issues and the main obstacles encountered.

Tissue banking in australia.

PubMed

Ireland, Lynette; McKelvie, Helen

2003-01-01

The legal structure for the regulation of tissue banking has existed for many years. In Australia, the donation of human tissue is regulated by legislation in each of the eight States and Territories. These substantially uniform Acts were passed in the late 1970's and early 1980's, based on model legislation and underpinned by the concept of consensual giving. However, it was not until the early 1990's that tissue banking came under the notice of regulatory authorities. Since then the Australian Government has moved quickly to oversee the tissue banking sector in Australia. Banked human tissue has been deemed to be a therapeutic good under the Therapeutic Goods Act 1989, and tissue banks are required to be licensed by the Therapeutic Goods Administration and are audited for compliance with the Code of Good Manufacturing Practice- Human Blood and Tissues. In addition, tissue banks must comply with a myriad of other standards, guidelines and recommendations.

GluN2B/CaMKII mediates CFA-induced hyperalgesia via HDAC4-modified spinal COX2 transcription.

PubMed

Lai, Cheng-Yuan; Hsieh, Ming-Chun; Ho, Yu-Cheng; Chen, Gin-Den; Chou, Dylan; Ruan, Ting; Lee, An-Sheng; Wang, Hsueh-Hsiao; Chau, Yat-Pang; Peng, Hsien-Yu; Lai, Cheng-Hung

2018-06-01

Histone deacetylase 4 (HDAC4), which actively shuttles between the nucleus and cytoplasm, is an attractive candidate for a repressor mechanism in epigenetic modification. However, the potential role of HDAC4-dependent epigenetics in the neural plasticity underlying the development of inflammatory pain has not been well established. By injecting complete Freund's adjuvant (CFA) into the hind-paw of Sprague-Dawley rats (200-250 g), we found animals displayed behavioral hyperalgesia was accompanied with HDAC4 phosphorylation and cytoplasmic redistribution in the dorsal horn neurons. Cytoplasmic HDAC4 retention led to its uncoupling with the COX2 promoter, hence prompting spinal COX2 transcription and expression in the dorsal horn. Moreover, the GluN2B-bearing N-methyl-d-aspartate receptor (GluN2B-NMDAR)/calmodulin-dependent protein kinase II (CaMKII) acted as an upstream cascade to facilitate HDAC4 phosphorylation/redistribution-associated spinal COX2 expression after inflammatory insults. The results of this pilot study demonstrated that the development and/or maintenance of inflammatory pain involved the spinal HDAC4-dependent epigenetic mechanisms. Our findings open up a new avenue for the development of a novel medical strategy for the relief of inflammatory pain. Copyright © 2018 Elsevier Ltd. All rights reserved.

iBank

ERIC Educational Resources Information Center

Bermundo, Cesar B.; Bermundo, Alex B.; Ballester, Rex C.

2012-01-01

iBank is a project that utilizes a software to create an item Bank that store quality questions, generate test and print exam. The items are from analyze teacher-constructed test questions that provides the basis for discussing test results, by determining why a test item is or not discriminating between the better and poorer students, and by…

12 CFR 619.9020 - Agricultural credit banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Agricultural credit banks. 619.9020 Section 619.9020 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9020 Agricultural credit banks. Agricultural credit banks are those banks created by the merger of a Farm Credit...

12 CFR 619.9020 - Agricultural credit banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Agricultural credit banks. 619.9020 Section 619.9020 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9020 Agricultural credit banks. Agricultural credit banks are those banks created by the merger of a Farm Credit...

Constraints facing Arab banks

DOE Office of Scientific and Technical Information (OSTI.GOV)

Khadra, F.

1980-04-01

Development projects in the Arab world have enormous investment requirements that Arab banks at present can only partially handle due to: (1) the low level of personal savings in a number of Arab countries as a result of low income levels; (2) the low capitalization of most Arab banks relative to the volume of lending activity required; (3) the reluctance of oil surplus countries to deposit any sizeable part of their funds with their own banks instead of foreign banks. Funds available in the currencies of the oil surplus countries are very limited compared to the volume of funds requiredmore » for projects. It is necessary therefore that the majority of loans be made in foreign currencies, making it necessary for Arab banks to have high international credit status. Arab banking practices and laws, which vary from country to country, are not compatible with the requirements of international lending or the establishment of well-developed financial markets. Some of the banks' organizational structures and internal practices may have become so entrenched as to make any transition not feasible. In some cases it may be more practical to establish a new financial institution with different orientations and activities than to transform the existing one. Another major constraint of the Arab banking environment is the lack of a permanent intermediary, acceptable to both the surplus countries' banks and to the borrowers. The final constraint discussed, the political environment, has prompted many Arab countries to enact legislation to guarantee a politically stable environment to safeguard risk against expropriation, nationalization, or freezing of assets. (SAC)« less

Commercial Banking Industry Survey.

ERIC Educational Resources Information Center

Bright Horizons Children's Centers, Cambridge, MA.

Work and family programs are becoming increasingly important in the commercial banking industry. The objective of this survey was to collect information and prepare a commercial banking industry profile on work and family programs. Fifty-nine top American commercial banks from the Fortune 500 list were invited to participate. Twenty-two…

Methodological bias in the seed bank flora holds significant implications for understanding seed bank community functions.

PubMed

Plue, J; Colas, F; Auffret, A G; Cousins, S A O

2017-03-01

Persistent seed banks are a key plant regeneration strategy, buffering environmental variation to allow population and species persistence. Understanding seed bank functioning within herb layer dynamics is therefore important. However, rather than assessing emergence from the seed bank in herb layer gaps, most studies evaluate the seed bank functioning via a greenhouse census. We hypothesise that greenhouse data may not reflect seed bank-driven emergence in disturbance gaps due to methodological differences. Failure in detecting (specialist) species may then introduce methodological bias into the ecological interpretation of seed bank functions using greenhouse data. The persistent seed bank was surveyed in 40 semi-natural grassland plots across a fragmented landscape, quantifying seedling emergence in both the greenhouse and in disturbance gaps. Given the suspected interpretational bias, we tested whether each census uncovers similar seed bank responses to fragmentation. Seed bank characteristics were similar between censuses. Census type affected seed bank composition, with >25% of species retrieved better by either census type, dependent on functional traits including seed longevity, production and size. Habitat specialists emerged more in disturbance gaps than in the greenhouse, while the opposite was true for ruderal species. Both censuses uncovered fragmentation-induced seed bank patterns. Low surface area sampling, larger depth of sampling and germination conditions cause underrepresentation of the habitat-specialised part of the persistent seed bank flora during greenhouse censuses. Methodological bias introduced in the recorded seed bank data may consequently have significant implications for the ecological interpretation of seed bank community functions based on greenhouse data. © 2016 German Botanical Society and The Royal Botanical Society of the Netherlands.

12 CFR 619.9145 - Farm Credit Bank.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Farm Credit Bank. 619.9145 Section 619.9145 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9145 Farm Credit Bank. The term Farm Credit Bank refers to a bank resulting from the mandatory merger of the Federal land...

12 CFR 619.9145 - Farm Credit Bank.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Farm Credit Bank. 619.9145 Section 619.9145 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9145 Farm Credit Bank. The term Farm Credit Bank refers to a bank resulting from the mandatory merger of the Federal land...

12 CFR 619.9060 - Bank for cooperatives.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Bank for cooperatives. 619.9060 Section 619.9060 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9060 Bank for cooperatives. A bank for cooperatives is a bank that is operating under section 3.0 of the Act. [61 FR 67188...

12 CFR 583.4 - Bank holding company.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 5 2011-01-01 2011-01-01 false Bank holding company. 583.4 Section 583.4 Banks... AFFECTING SAVINGS AND LOAN HOLDING COMPANIES § 583.4 Bank holding company. The term bank holding company means any company which has control over any bank or over any company that is or becomes a bank holding...

12 CFR 619.9060 - Bank for cooperatives.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Bank for cooperatives. 619.9060 Section 619.9060 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM DEFINITIONS § 619.9060 Bank for cooperatives. A bank for cooperatives is a bank that is operating under section 3.0 of the Act. [61 FR 67188...

26 CFR 1.581-2 - Mutual savings banks, building and loan associations, and cooperative banks.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 7 2011-04-01 2009-04-01 true Mutual savings banks, building and loan associations, and cooperative banks. 1.581-2 Section 1.581-2 Internal Revenue INTERNAL REVENUE SERVICE... § 1.581-2 Mutual savings banks, building and loan associations, and cooperative banks. (a) While the...

Banking on the Internet.

ERIC Educational Resources Information Center

Internet Research, 1996

1996-01-01

Electronic ground was broken in 1995 with the development of the completely Internet-based bank Security First Network Bank. This article discusses the need for developing online services, outlines the reasons for the formation of an Internet-based bank and argues that to remain competitive financial services providers must provide easier customer…

Metric-wave and decimetric-wave aperture synthesis systems (review)

NASA Astrophysics Data System (ADS)

Ilyasov, Y. P.

1984-09-01

Aperture synthesis systems using metric or decimetric waves are adequate and promising for astrophysical study of extragalactic radioemission sources, operation with metric waves being characterized by destabilizing effects of the ionosphere and thus requiring special methods of data processing. Methods of closure phase and closure amplitude were proposed and then successfully implemented in very-large-baseline radiotelescope and multi-element interferometers, respectively. Several radiotelescopes were developed which operate in the supersynthesis mode, with rotation of the Earth used for filling the space-frequency plane. Further achievements include the Swarup system (Uti/INDIA) with phase-stable interferometer, the Jodrell Bank system (Manchester/UK), the Palmer Merlin multielement system (UK) with CLEAN procedure and CORTEL telescope correction algorithm, the VLA system (USA), and the international giant equatorial radiotelescope.

12 CFR 614.4540 - Other financing institution access to Farm Credit Banks and agricultural credit banks for funding...

Code of Federal Regulations, 2010 CFR

2010-01-01

...) Otherwise expose the Farm Credit Bank or agricultural credit bank to safety and soundness risks. (e) Notice... Credit Banks and agricultural credit banks for funding, discount, and other similar financial assistance. 614.4540 Section 614.4540 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN...

12 CFR 1281.23 - Bank data integrity.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Bank data integrity. 1281.23 Section 1281.23 Banks and Banking FEDERAL HOUSING FINANCE AGENCY HOUSING GOALS AND MISSION FEDERAL HOME LOAN BANK HOUSING GOALS Reporting Requirements § 1281.23 Bank data integrity. (a) Certification. (1) The senior...

12 CFR 34.84 - Future bank expansion.

Code of Federal Regulations, 2010 CFR

2010-01-01

..., the bank shall state, by resolution of the board of directors or an appropriately authorized bank... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Future bank expansion. 34.84 Section 34.84 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY REAL ESTATE LENDING AND...

12 CFR 583.4 - Bank holding company.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 5 2010-01-01 2010-01-01 false Bank holding company. 583.4 Section 583.4 Banks and Banking OFFICE OF THRIFT SUPERVISION, DEPARTMENT OF THE TREASURY DEFINITIONS FOR REGULATIONS AFFECTING SAVINGS AND LOAN HOLDING COMPANIES § 583.4 Bank holding company. The term bank holding company...

12 CFR 614.4355 - Banks for cooperatives.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Banks for cooperatives. 614.4355 Section 614.4355 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4355 Banks for cooperatives. No bank for cooperatives may make a loan if...

12 CFR 34.84 - Future bank expansion.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Future bank expansion. 34.84 Section 34.84 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY REAL ESTATE LENDING AND APPRAISALS Other Real Estate Owned § 34.84 Future bank expansion. A national bank normally should use real...

12 CFR 614.4355 - Banks for cooperatives.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Banks for cooperatives. 614.4355 Section 614.4355 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4355 Banks for cooperatives. No bank for cooperatives may make a loan if...

78 FR 19267 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-03-29

... indirectly retain voting shares of First-Citizens Bank & Trust Company, both in Raleigh, North Carolina. B... Byrd Street, Richmond, Virginia 23261-4528: 1. Olivia Britton Holding, Raleigh, North Carolina; to... First-Citizens Bank & Trust Company, both in Raleigh, North Carolina. 2. Frank Brown Holding, Jr...

Information technology for brain banking.

PubMed

Schmitz, Peer

2018-01-01

Implementing and maintaining the information technology (IT) infrastructure of a brain bank can be a daunting task for any brain bank coordinator, particularly when access to both funds and IT professionals is limited. Many questions arise when attempting to determine which IT products are most suitable for a brain bank. The requirements of each brain bank must be assessed carefully to ensure that the chosen IT infrastructure will be able to meet those requirements successfully and will be able to expand and adapt as the size of the brain bank increases. This chapter provides some valuable insights to be considered when implementing the IT infrastructure for a brain bank and discusses the pros and cons of various approaches and products. Copyright © 2018 Elsevier B.V. All rights reserved.

12 CFR 7.3000 - Bank hours and closings.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Bank hours and closings. 7.3000 Section 7.3000 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Operations § 7.3000 Bank hours and closings. (a) Bank hours. A national bank's board of directors...

12 CFR 7.3000 - Bank hours and closings.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Bank hours and closings. 7.3000 Section 7.3000 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Operations § 7.3000 Bank hours and closings. (a) Bank hours. A national bank's board of directors...

75 FR 55582 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-09-13

... Holding Companies The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... company. The factors that are considered in acting on the notices are set forth in paragraph 7 of the Act... Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1 Memorial Drive, Kansas City...

75 FR 12240 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-03-15

.... Michael Montgomery, Dallas, Texas; to acquire voting shares of Casey Bancorp., Inc., and thereby.... 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank... the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the Federal...

75 FR 47596 - Change in Bank Control Notices; Acquisition of Shares of Bank or Bank Holding Companies

Federal Register 2010, 2011, 2012, 2013, 2014

2010-08-06

... Benito, Texas; Delores M. Simmons, San Benito, Texas; Ricardo Leal, Harlingen, Texas; Audrey Simmons...; and Jennifer Stone and Tyler Stone, both of Dallas, Texas, together as a group acting in concert, to.... 1817(j)) and Sec. [thinsp]225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire a bank or bank...

31 CFR 1010.652 - Special measures against Myanmar Mayflower Bank and Asia Wealth Bank.

Code of Federal Regulations, 2012 CFR

2012-07-01

... 31 Money and Finance:Treasury 3 2012-07-01 2012-07-01 false Special measures against Myanmar... Special measures against Myanmar Mayflower Bank and Asia Wealth Bank. (a) Definitions. For purposes of... Exchange Commission pursuant to that Act. (4) Myanmar Mayflower Bank means all headquarters, branches, and...

31 CFR 1010.652 - Special measures against Myanmar Mayflower Bank and Asia Wealth Bank.

Code of Federal Regulations, 2011 CFR

2011-07-01

... 31 Money and Finance:Treasury 3 2011-07-01 2011-07-01 false Special measures against Myanmar... Special measures against Myanmar Mayflower Bank and Asia Wealth Bank. (a) Definitions. For purposes of... Exchange Commission pursuant to that Act. (4) Myanmar Mayflower Bank means all headquarters, branches, and...

12 CFR 220.108 - International Bank Securities.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false International Bank Securities. 220.108 Section 220.108 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM CREDIT BY BROKERS AND DEALERS (REGULATION T) Interpretations § 220.108 International Bank...

12 CFR 220.108 - International Bank Securities.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false International Bank Securities. 220.108 Section 220.108 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM CREDIT BY BROKERS AND DEALERS (REGULATION T) Interpretations § 220.108 International Bank...

12 CFR 7.4002 - National bank charges.

Code of Federal Regulations, 2010 CFR

2010-01-01

... judgment and safe and sound banking principles. A national bank establishes non-interest charges and fees in accordance with safe and sound banking principles if the bank employs a decision-making process... of the competitive position of the bank in accordance with the bank's business plan and marketing...

12 CFR 614.4000 - Farm Credit Banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... institutions. (3) Farm Credit Banks, in their capacity as certified agricultural mortgage marketing facilities... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Farm Credit Banks. 614.4000 Section 614.4000 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending...

12 CFR 614.4010 - Agricultural credit banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Agricultural credit banks. 614.4010 Section 614.4010 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending Authorities § 614.4010 Agricultural credit banks. (a) Long-term real estate lending. Except to the...

12 CFR 208.61 - Bank security procedures.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Bank security procedures. 208.61 Section 208.61 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM MEMBERSHIP OF STATE BANKING INSTITUTIONS IN THE FEDERAL RESERVE SYSTEM (REGULATION H) Miscellaneous Requirements § 208...

12 CFR 614.4010 - Agricultural credit banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Agricultural credit banks. 614.4010 Section 614.4010 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending Authorities § 614.4010 Agricultural credit banks. (a) Long-term real estate lending. Except to the...

12 CFR 811.1 - Authority of Reserve Banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Authority of Reserve Banks. 811.1 Section 811.1 Banks and Banking FEDERAL FINANCING BANK BOOK-ENTRY PROCEDURE FOR FEDERAL FINANCING BANK SECURITIES § 811.1 Authority of Reserve Banks. Each Reserve Bank is hereby authorized, in accordance with the...

12 CFR 811.1 - Authority of Reserve Banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Authority of Reserve Banks. 811.1 Section 811.1 Banks and Banking FEDERAL FINANCING BANK BOOK-ENTRY PROCEDURE FOR FEDERAL FINANCING BANK SECURITIES § 811.1 Authority of Reserve Banks. Each Reserve Bank is hereby authorized, in accordance with the...

31 CFR 103.187 - Special measures against Myanmar Mayflower Bank and Asia Wealth Bank.

Code of Federal Regulations, 2010 CFR

2010-07-01

... Anti-Money Laundering Programs Law Enforcement Access to Foreign Bank Records § 103.187 Special... 31 Money and Finance: Treasury 1 2010-07-01 2010-07-01 false Special measures against Myanmar Mayflower Bank and Asia Wealth Bank. 103.187 Section 103.187 Money and Finance: Treasury Regulations...

Bank Terminals

NASA Technical Reports Server (NTRS)

1978-01-01

In the photo, employees of the UAB Bank, Knoxville, Tennessee, are using Teller Transaction Terminals manufactured by SCI Systems, Inc., Huntsville, Alabama, an electronics firm which has worked on a number of space projects under contract with NASA. The terminals are part of an advanced, computerized financial transaction system that offers high efficiency in bank operations. The key to the system's efficiency is a "multiplexing" technique developed for NASA's Space Shuttle. Multiplexing is simultaneous transmission of large amounts of data over a single transmission link at very high rates of speed. In the banking application, a small multiplex "data bus" interconnects all the terminals and a central computer which stores information on clients' accounts. The data bus replaces the maze-of wiring that would be needed to connect each terminal separately and it affords greater speed in recording transactions. The SCI system offers banks real-time data management through constant updating of the central computer. For example, a check is immediately cancelled at the teller's terminal and the computer is simultaneously advised of the transaction; under other methods, the check would be cancelled and the transaction recorded at the close of business. Teller checkout at the end of the day, conventionally a time-consuming matter of processing paper, can be accomplished in minutes by calling up a summary of the day's transactions. SCI manufactures other types of terminals for use in the system, such as an administrative terminal that provides an immediate printout of a client's account, and another for printing and recording savings account deposits and withdrawals. SCI systems have been installed in several banks in Tennessee, Arizona, and Oregon and additional installations are scheduled this year.

12 CFR 614.4000 - Farm Credit Banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Farm Credit Banks. 614.4000 Section 614.4000 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending Authorities § 614.4000 Farm Credit Banks. (a) Long-term real estate lending. Except to the extent such...

12 CFR 208.61 - Bank security procedures.

Code of Federal Regulations, 2010 CFR

2010-01-01

...; the cost of the security devices; other security measures in effect at the banking office; and the... 12 Banks and Banking 2 2010-01-01 2010-01-01 false Bank security procedures. 208.61 Section 208.61....61 Bank security procedures. (a) Authority, purpose, and scope. Pursuant to section 3 of the Bank...

Rapid development of tissue bank achieved by International Atomic Energy Agency (IAEA) Tissue Banking Programme in China.

PubMed

Zhang, Yu-Min; Wang, Jian-Ru; Zhang, Nai-Li; Liu, Xiao-Ming; Zhou, Mo; Ma, Shao-Ying; Yang, Ting; Li, Bao-Xing

2014-09-01

Before 1986, the development of tissue banking in China has been slow and relatively uncoordinated. Under the support of International Atomic Energy Agency (IAEA), Tissue Banking in China experienced rapid development. In this period, China Institute for Radiation Protection tissue bank mastered systematic and modern tissue banking technique by IAEA training course and gradually developed the first regional tissue bank (Shanxi Provincial Tissue Bank, SPTB) to provide tissue allograft. Benefit from training course, SPTB promoted the development of tissue transplantation by ways of training, brochure, advertisement and meeting. Tissue allograft transplantation acquired recognition from clinic and supervision and administration from government. Quality system gradually is developing and perfecting. Tissue allograft transplantation and tissue bank are developing rapidly and healthy.

76 FR 53900 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-08-30

... Mark Jones and April Jones, individually, all of Key West, Florida; to acquire additional voting shares of First State Bank of the Florida Keys Holding Company, and thereby indirectly acquire additional voting shares of First State Bank of the Florida Keys, both in Key West, Florida. Board of Governors of...

Application of DFT Filter Banks and Cosine Modulated Filter Banks in Filtering

NASA Technical Reports Server (NTRS)

Lin, Yuan-Pei; Vaidyanathan, P. P.

1994-01-01

None given. This is a proposal for a paper to be presented at APCCAS '94 in Taipei, Taiwan. (From outline): This work is organized as follows: Sec. II is devoted to the construction of the new 2m channel under-decimated DFT filter bank. Implementation and complexity of this DFT filter bank are discussed therein. IN a similar manner, the new 2m channel cosine modulated filter bank is discussed in Sec. III. Design examples are given in Sec. IV.

12 CFR 229.39 - lnsolvency of bank.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false lnsolvency of bank. 229.39 Section 229.39 Banks... AVAILABILITY OF FUNDS AND COLLECTION OF CHECKS (REGULATION CC) Collection of Checks § 229.39 lnsolvency of bank..., collecting, depositary, or returning bank that suspends payment, and which is not paid, shall be returned by...

12 CFR 229.39 - lnsolvency of bank.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false lnsolvency of bank. 229.39 Section 229.39 Banks... payment without making a settlement for the check or returned check with the prior bank that is or becomes... suspends payments without making a settlement for the check with the prior bank, which is or becomes final...

12 CFR 615.5030 - Borrowings from commercial banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Borrowings from commercial banks. 615.5030 Section 615.5030 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM FUNDING AND FISCAL... commercial banks. Each System bank board, by resolution, shall authorize all commercial bank borrowings by...

12 CFR 615.5030 - Borrowings from commercial banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... commercial banks. (a) Each System bank board, by resolution, shall authorize all commercial bank borrowings... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Borrowings from commercial banks. 615.5030 Section 615.5030 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM FUNDING AND FISCAL...

12 CFR 611.1010 - Bank charter amendment procedures.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Bank charter amendment procedures. 611.1010 Section 611.1010 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM ORGANIZATION Bank Mergers, Consolidations and Charter Amendments § 611.1010 Bank charter amendment procedures. (a) A bank may recommend a...

12 CFR 917.4 - Bank Member Products Policy.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Bank Member Products Policy. 917.4 Section 917.4 Banks and Banking FEDERAL HOUSING FINANCE BOARD GOVERNANCE AND MANAGEMENT OF THE FEDERAL HOME LOAN BANKS POWERS AND RESPONSIBILITIES OF BANK BOARDS OF DIRECTORS AND SENIOR MANAGEMENT § 917.4 Bank Member...

Mitochondrial fission promotes cell migration by Ca2+ /CaMKII/ERK/FAK pathway in hepatocellular carcinoma.

PubMed

Sun, Xiacheng; Cao, Haiyan; Zhan, Lei; Yin, Chun; Wang, Gang; Liang, Ping; Li, Jibin; Wang, Zhe; Liu, Bingrong; Huang, Qichao; Xing, Jinliang

2018-07-01

Mitochondrial dynamics of fission and fusion plays critical roles in a diverse range of important cellular functions, and its deregulation has been increasingly implicated in human diseases. Previous studies have shown that increased mitochondrial fission significantly promoted the proliferation of hepatocellular carcinoma (HCC) cells. However, how they influence the migration of tumour cells remained largely unknown. In the present study, we further investigated the effect of mitochondrial fission on the migration and metastasis of hepatocellular carcinoma cells. Moreover, the underlying molecular mechanisms and therapeutic application were explored. Our data showed that dynamin-1-like protein expression was strongly increased in distant metastasis of hepatocellular carcinoma when compared to primary hepatocellular carcinoma. In contrast, the mitochondrial fusion protein mitofusin 1 showed an opposite trend. Moreover, the expression of dynamin-1-like protein and mitofusin 1 was significantly associated with the disease-free survival of hepatocellular carcinoma patients. In addition, our data further showed that mitochondrial fission significantly promoted the reprogramming of focal-adhesion dynamics and lamellipodia formation in hepatocellular carcinoma cells mainly by activating typical Ca 2+ /CaMKII/ERK/FAK pathway. Importantly, treatment with mitochondrial division inhibitor-1 significantly decreased calcium signalling in hepatocellular carcinoma cells and had a potential treatment effect for hepatocellular carcinoma metastasis in vivo. Taken together, our findings demonstrate that mitochondrial fission plays a critical role in the regulation of hepatocellular carcinoma cell migration, which provides strong evidence for this process as a drug target in hepatocellular carcinoma metastasis treatment. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Banking: shop and compare.

PubMed

O'Brien, Jennifer A; DeJarnette, Sherry

2014-01-01

There are many reasons to take a critical look at the practice's banking relationship(s)--technology advancements, security measures, improvements in available services, recent banking enhancements designed specifically for medical practices, the impact of the financial crisis on bank ratings and stability, changing practice needs, opportunities for operational automation at the practice--and it is just simply smart to periodically evaluate and compare the features, pricing, and potential savings offered by vendors.

12 CFR 1265.2 - Mission of the Banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Mission of the Banks. 1265.2 Section 1265.2 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS CORE MISSION ACTIVITIES § 1265.2 Mission of the Banks. The mission of the Banks is to provide to their members' and housing...

26 CFR 1.581-2 - Mutual savings banks, building and loan associations, and cooperative banks.

Code of Federal Regulations, 2010 CFR

2010-04-01

... associations, and cooperative banks. 1.581-2 Section 1.581-2 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Banking Institutions...-1, relating to dividends paid by banking corporations, for special rules concerning deductions for...

76 FR 54468 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-09-01

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the.... Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1 Memorial Drive, Kansas...

76 FR 16776 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-03-25

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the..., both of Mondovi, Wisconsin. B. Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice...

12 CFR 940.2 - Mission of the Banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Mission of the Banks. 940.2 Section 940.2 Banks and Banking FEDERAL HOUSING FINANCE BOARD FEDERAL HOME LOAN BANK MISSION CORE MISSION ACTIVITIES § 940.2 Mission of the Banks. The mission of the Banks is to provide to their members' and housing...

46 CFR Sec. 2 - Bank account.

Code of Federal Regulations, 2011 CFR

2011-10-01

... 46 Shipping 8 2011-10-01 2011-10-01 false Bank account. Sec. 2 Section 2 Shipping MARITIME... TRANSACTIONS UNDER AGENCY AGREEMENTS Accounts Sec. 2 Bank account. A separate joint bank account will be... the depository or depositories, the owner will issue an order for the establishment of the joint bank...

29 CFR 1917.126 - River banks.

Code of Federal Regulations, 2011 CFR

2011-07-01

... 29 Labor 7 2011-07-01 2011-07-01 false River banks. 1917.126 Section 1917.126 Labor Regulations...) MARINE TERMINALS Terminal Facilities § 1917.126 River banks. (a) This section applies to temporary installations or temporary operations near a river bank. (b) Where working surfaces at river banks slope so...

46 CFR Sec. 2 - Bank account.

Code of Federal Regulations, 2010 CFR

2010-10-01

... 46 Shipping 8 2010-10-01 2010-10-01 false Bank account. Sec. 2 Section 2 Shipping MARITIME... TRANSACTIONS UNDER AGENCY AGREEMENTS Accounts Sec. 2 Bank account. A separate joint bank account will be... the depository or depositories, the owner will issue an order for the establishment of the joint bank...

29 CFR 1917.126 - River banks.

Code of Federal Regulations, 2010 CFR

2010-07-01

...) MARINE TERMINALS Terminal Facilities § 1917.126 River banks. (a) This section applies to temporary installations or temporary operations near a river bank. (b) Where working surfaces at river banks slope so... 29 Labor 7 2010-07-01 2010-07-01 false River banks. 1917.126 Section 1917.126 Labor Regulations...

Stream Bank Stability in Eastern Nebraska

USGS Publications Warehouse

Soenksen, Phillip J.; Turner, Mary J.; Dietsch, Benjamin J.; Simon, Andrew

2003-01-01

Dredged and straightened channels in eastern Nebraska have experienced degradation leading to channel widening by bank failure. Degradation has progressed headward and affected the drainage systems upstream from the modified reaches. This report describes a study that was undertaken to analyze bank stability at selected sites in eastern Nebraska and develop a simplified method for estimating the stability of banks at future study sites. Bank cross sections along straight reaches of channel and geotechnical data were collected at approximately 150 sites in 26 counties of eastern Nebraska. The sites were categorized into three groups based on mapped soil permeability. With increasing permeability of the soil groups, the median cohesion values decreased and the median friction angles increased. Three analytical methods were used to determine if banks were stable (should not fail even when saturated), at risk (should not fail unless saturated), or unstable (should have already failed). The Culmann and Agricultural Research Service methods were based on the Coulomb equation and planar failure; an indirect method was developed that was based on Bishop's simplified method of slices and rotational failure. The maximum angle from horizontal at which the bank would be stable for the given soil and bank height conditions also was computed with the indirect method. Because of few soil shear-strength data, all analyses were based on the assumption of homogeneous banks, which was later shown to be atypical, at least for some banks. Using the Culmann method and assuming no soil tension cracks, 67 percent of all 908 bank sections were identified as stable, 32 percent were at risk, and 1 percent were unstable; when tension cracks were assumed, the results changed to 58 percent stable, 40 percent at risk, and 1 percent unstable. Using the Agricultural Research Service method, 67 percent of all bank sections were identified as stable and 33 percent were at risk. Using the indirect

76 FR 8370 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-02-14

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... March 2, 2011. A. Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1...

76 FR 58811 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-09-22

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... October 7, 2011. A. Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1...

76 FR 80371 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-12-23

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... Albermarle, INC., SSB, both in Albermarle, North Carolina. B. Federal Reserve Bank of Kansas City (Dennis...

77 FR 29643 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-05-18

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... June 4, 2012. A. Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1...

78 FR 60873 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-10-02

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... October 16, 2013. A. Federal Reserve Bank of Kansas City (Dennis Denney, Assistant Vice President) 1...

78 FR 22263 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-04-15

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the... April 30, 2013. A. Federal Reserve Bank of St. Louis (Yvonne Sparks, Community Development Officer) P.O...

12 CFR 614.4354 - Federal land bank associations.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Federal land bank associations. 614.4354 Section 614.4354 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4354 Federal land bank associations. No Federal land bank...

12 CFR 614.4354 - Federal land bank associations.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Federal land bank associations. 614.4354 Section 614.4354 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM LOAN POLICIES AND OPERATIONS Lending and Leasing Limits § 614.4354 Federal land bank associations. No Federal land bank...

26 CFR 1.581-1 - Banks.

Code of Federal Regulations, 2011 CFR

2011-04-01

... 26 Internal Revenue 7 2011-04-01 2009-04-01 true Banks. 1.581-1 Section 1.581-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Banking Institutions § 1.581-1 Banks. (a) In order to be a bank as defined in section 581, an...

26 CFR 1.581-1 - Banks.

Code of Federal Regulations, 2010 CFR

2010-04-01

... 26 Internal Revenue 7 2010-04-01 2010-04-01 true Banks. 1.581-1 Section 1.581-1 Internal Revenue INTERNAL REVENUE SERVICE, DEPARTMENT OF THE TREASURY (CONTINUED) INCOME TAX (CONTINUED) INCOME TAXES (CONTINUED) Banking Institutions § 1.581-1 Banks. (a) In order to be a bank as defined in section 581, an...

To See the Unseen: A History of Planetary Radar Astronomy

NASA Technical Reports Server (NTRS)

Butrica, Andrew J.

1996-01-01

This book relates the history of planetary radar astronomy from its origins in radar to the present day and secondarily to bring to light that history as a case of 'Big Equipment but not Big Science'. Chapter One sketches the emergence of radar astronomy as an ongoing scientific activity at Jodrell Bank, where radar research revealed that meteors were part of the solar system. The chief Big Science driving early radar astronomy experiments was ionospheric research. Chapter Two links the Cold War and the Space Race to the first radar experiments attempted on planetary targets, while recounting the initial achievements of planetary radar, namely, the refinement of the astronomical unit and the rotational rate and direction of Venus. Chapter Three discusses early attempts to organize radar astronomy and the efforts at MIT's Lincoln Laboratory, in conjunction with Harvard radio astronomers, to acquire antenna time unfettered by military priorities. Here, the chief Big Science influencing the development of planetary radar astronomy was radio astronomy. Chapter Four spotlights the evolution of planetary radar astronomy at the Jet Propulsion Laboratory, a NASA facility, at Cornell University's Arecibo Observatory, and at Jodrell Bank. A congeries of funding from the military, the National Science Foundation, and finally NASA marked that evolution, which culminated in planetary radar astronomy finding a single Big Science patron, NASA. Chapter Five analyzes planetary radar astronomy as a science using the theoretical framework provided by philosopher of science Thomas Kuhn. Chapter Six explores the shift in planetary radar astronomy beginning in the 1970s that resulted from its financial and institutional relationship with NASA Big Science. Chapter Seven addresses the Magellan mission and its relation to the evolution of planetary radar astronomy from a ground-based to a space-based activity. Chapters Eight and Nine discuss the research carried out at ground

Banking on cord blood stem cells.

PubMed

Sullivan, Michael J

2008-07-01

Umbilical cord blood gifted to non-profit public cord blood banks is now routinely used as an alternative source of haematopoietic stem cells for allogeneic transplantation for children and adults with cancer, bone marrow failure syndromes, haemoglobinopathies and many genetic metabolic disorders. Because of the success and outcomes of public cord banking, many companies now provide private cord banking services. However, in the absence of any published transplant evidence to support autologous and non-directed family banking, commercial cord banks currently offer a superfluous service.

31 CFR 515.320 - Domestic bank.

Code of Federal Regulations, 2011 CFR

2011-07-01

... 31 Money and Finance:Treasury 3 2011-07-01 2011-07-01 false Domestic bank. 515.320 Section 515.320... Domestic bank. The term domestic bank shall mean any branch or office within the United States of any of the following which is not a national of a designated foreign country; any bank or trust company...

31 CFR 515.320 - Domestic bank.

Code of Federal Regulations, 2010 CFR

2010-07-01

... 31 Money and Finance: Treasury 3 2010-07-01 2010-07-01 false Domestic bank. 515.320 Section 515... § 515.320 Domestic bank. The term domestic bank shall mean any branch or office within the United States of any of the following which is not a national of a designated foreign country; any bank or trust...

31 CFR 535.320 - Domestic bank.

Code of Federal Regulations, 2011 CFR

2011-07-01

... 31 Money and Finance:Treasury 3 2011-07-01 2011-07-01 false Domestic bank. 535.320 Section 535.320....320 Domestic bank. (a) The term domestic bank shall mean any branch or office within the United States of any of the following which is not Iran or an Iranian entity: any bank or trust company...

31 CFR 500.320 - Domestic bank.

Code of Federal Regulations, 2010 CFR

2010-07-01

... 31 Money and Finance: Treasury 3 2010-07-01 2010-07-01 false Domestic bank. 500.320 Section 500... § 500.320 Domestic bank. The term domestic bank shall mean any branch or office within the United States of any of the following which is not a national of any designated foreign country: Any bank or trust...

31 CFR 535.320 - Domestic bank.

Code of Federal Regulations, 2010 CFR

2010-07-01

... 31 Money and Finance: Treasury 3 2010-07-01 2010-07-01 false Domestic bank. 535.320 Section 535... § 535.320 Domestic bank. (a) The term domestic bank shall mean any branch or office within the United States of any of the following which is not Iran or an Iranian entity: any bank or trust company...

12 CFR 229.55 - Expedited recredit for banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Expedited recredit for banks. 229.55 Section 229.55 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE... Expedited recredit for banks. (a) Circumstances giving rise to a claim. A bank that has an indemnity claim...

12 CFR 229.55 - Expedited recredit for banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Expedited recredit for banks. 229.55 Section 229.55 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE... Expedited recredit for banks. (a) Circumstances giving rise to a claim. A bank that has an indemnity claim...

12 CFR 214.5 - Accounts with foreign banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 2 2010-01-01 2010-01-01 false Accounts with foreign banks. 214.5 Section 214.5 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM RELATIONS WITH FOREIGN BANKS AND BANKERS (REGULATION N) Regulations § 214.5 Accounts with foreign banks. (a...

12 CFR 214.5 - Accounts with foreign banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Accounts with foreign banks. 214.5 Section 214.5 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM RELATIONS WITH FOREIGN BANKS AND BANKERS (REGULATION N) Regulations § 214.5 Accounts with foreign banks. (a...

Quality Assurance in Stem Cell Banking: Emphasis on Embryonic and Induced Pluripotent Stem Cell Banking.

PubMed

Kallur, Therése; Blomberg, Pontus; Stenfelt, Sonya; Tryggvason, Kristian; Hovatta, Outi

2017-01-01

For quality assurance (QA) in stem cell banking, a planned system is needed to ensure that the banked products, stem cells, meet the standards required for research, clinical use, and commercial biotechnological applications. QA is process oriented, avoids, or minimizes unacceptable product defects, and particularly encompasses the management and operational systems of the bank, as well as the ethical and legal frameworks. Quality control (QC ) is product oriented and therefore ensures the stem cells of a bank are what they are expected to be. Testing is for controlling, not assuring, product quality, and is therefore a part of QC , not QA. Like QA, QC is essential for banking cells for quality research and translational application (Schwartz et al., Lancet 379:713-720, 2012). Human embryonic stem cells (hESCs), as cells derived from donated supernumerary embryos from in vitro fertilization (IVF) therapy, are different from other stem cell types in resulting from an embryo that has had two donors . This imposes important ethical and legal constraints on the utility of the cells, which, together with quite specific culture conditions, require special attention in the QA system. Importantly, although the origin and derivation of induced pluripotent stem cells (iPSCs ) differ from that of hESCs, many of the principles of QA for hESC banking are applicable to iPSC banking (Stacey et al., Cell Stem Cell 13:385-388, 2013). Furthermore, despite differences between the legal and regulatory frameworks for hESC and iPSC banking between different countries, the requirements for QA are being harmonized (Stacey et al., Cell Stem Cell 13:385-388, 2013; International Stem Cell Banking Initiative, Stem Cell Rev 5:301-314, 2009).

12 CFR 950.8 - Banks as secured creditors.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 7 2011-01-01 2011-01-01 false Banks as secured creditors. 950.8 Section 950.8 Banks and Banking FEDERAL HOUSING FINANCE BOARD FEDERAL HOME LOAN BANK ASSETS AND OFF-BALANCE SHEET ITEMS ADVANCES Advances to Out-of-District Members and Housing Associates § 950.8 Banks as secured...

12 CFR 950.8 - Banks as secured creditors.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Banks as secured creditors. 950.8 Section 950.8 Banks and Banking FEDERAL HOUSING FINANCE BOARD FEDERAL HOME LOAN BANK ASSETS AND OFF-BALANCE SHEET ITEMS ADVANCES Advances to Members § 950.8 Banks as secured creditors. (a) Except as provided in...

12 CFR 225.134 - Escrow arrangements involving bank stock resulting in a violation of the Bank Holding Company Act.

Code of Federal Regulations, 2010 CFR

2010-01-01

... resulting in a violation of the Bank Holding Company Act. 225.134 Section 225.134 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM BANK HOLDING COMPANIES AND CHANGE IN BANK CONTROL (REGULATION Y) Regulations Financial Holding Companies Interpretations § 225.134...

Calcium-calmodulin-dependent kinase II modulates Kv4.2 channel expression and upregulates neuronal A-type potassium currents.

PubMed

Varga, Andrew W; Yuan, Li-Lian; Anderson, Anne E; Schrader, Laura A; Wu, Gang-Yi; Gatchel, Jennifer R; Johnston, Daniel; Sweatt, J David

2004-04-07

Calcium-calmodulin-dependent kinase II (CaMKII) has a long history of involvement in synaptic plasticity, yet little focus has been given to potassium channels as CaMKII targets despite their importance in repolarizing EPSPs and action potentials and regulating neuronal membrane excitability. We now show that Kv4.2 acts as a substrate for CaMKII in vitro and have identified CaMKII phosphorylation sites as Ser438 and Ser459. To test whether CaMKII phosphorylation of Kv4.2 affects channel biophysics, we expressed wild-type or mutant Kv4.2 and the K(+) channel interacting protein, KChIP3, with or without a constitutively active form of CaMKII in Xenopus oocytes and measured the voltage dependence of activation and inactivation in each of these conditions. CaMKII phosphorylation had no effect on channel biophysical properties. However, we found that levels of Kv4.2 protein are increased with CaMKII phosphorylation in transfected COS cells, an effect attributable to direct channel phosphorylation based on site-directed mutagenesis studies. We also obtained corroborating physiological data showing increased surface A-type channel expression as revealed by increases in peak K(+) current amplitudes with CaMKII phosphorylation. Furthermore, endogenous A-currents in hippocampal pyramidal neurons were increased in amplitude after introduction of constitutively active CaMKII, which results in a decrease in neuronal excitability in response to current injections. Thus CaMKII can directly modulate neuronal excitability by increasing cell-surface expression of A-type K(+) channels.

Banking. Teaching Guide.

ERIC Educational Resources Information Center

Florida Univ., Gainesville. Florida Cooperative Extension Service.

One in a series of consumer education materials for teenagers, this document focuses on banking and banking services. The series is based on the philosophy that teens need the training and guidance to develop the skills needed to become competent consumers. Developed for 4-H Club members, the material is designed to acquaint students with the…

77 FR 2293 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-01-17

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the...

78 FR 61988 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2013-10-09

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the...

77 FR 71592 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2012-12-03

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the...

76 FR 45572 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-07-29

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the...

76 FR 26296 - Change in Bank Control Notices; Acquisitions of Shares of a Bank or Bank Holding Company

Federal Register 2010, 2011, 2012, 2013, 2014

2011-05-06

... Holding Company The notificants listed below have applied under the Change in Bank Control Act (12 U.S.C. 1817(j)) and Sec. 225.41 of the Board's Regulation Y (12 CFR 225.41) to acquire shares of a bank or... paragraph 7 of the Act (12 U.S.C. 1817(j)(7)). The notices are available for immediate inspection at the...

12 CFR 228.44 - Public notice by banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Public notice by banks. 228.44 Section 228.44 Banks and Banking FEDERAL RESERVE SYSTEM (CONTINUED) BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM... notice by banks. A bank shall provide in the public lobby of its main office and each of its branches the...

12 CFR 25.44 - Public notice by banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Public notice by banks. 25.44 Section 25.44 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY COMMUNITY REINVESTMENT ACT AND... Public notice by banks. A bank shall provide in the public lobby of its main office and each of its...

7 CFR 1610.5 - Minimum Bank loan.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 7 Agriculture 11 2010-01-01 2010-01-01 false Minimum Bank loan. 1610.5 Section 1610.5 Agriculture Regulations of the Department of Agriculture (Continued) RURAL TELEPHONE BANK, DEPARTMENT OF AGRICULTURE LOAN POLICIES § 1610.5 Minimum Bank loan. A Bank loan will not be made unless the applicant qualifies for a Bank...

7 CFR 1610.5 - Minimum Bank loan.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 7 Agriculture 11 2011-01-01 2011-01-01 false Minimum Bank loan. 1610.5 Section 1610.5 Agriculture Regulations of the Department of Agriculture (Continued) RURAL TELEPHONE BANK, DEPARTMENT OF AGRICULTURE LOAN POLICIES § 1610.5 Minimum Bank loan. A Bank loan will not be made unless the applicant qualifies for a Bank...

Barriers to Banking - Towards an Inclusive Banking Environment in South Africa.

PubMed

Martinson, Estelle; Martinson, Johannes

2016-01-01

A recent study in South Africa on the barriers to banking which involved customers in three disability groups namely mobility, hearing and vision has highlighted that currently banking in South Africa is not accessible. Customers with a disability are unable to independently use banking services across a wide range of channels. Exclusion from something as fundamental as managing their own financial affairs raise serious human rights concerns and requires committed action from decision-makers to address this. The fact that solutions to all of the identified barriers have been successfully implemented in banks in other parts of the world for many years emphasize that this is not a technical challenge. While some solutions require complex or expensive changes such as removing physical access barriers and ensuring that digital channels meet internationally accepted standards of accessibility, there are many simple and low-cost solutions which can be implemented immediately and would make a world of difference to these customers and their experience of banking. One key barrier which emerged in all the focus groups and surveys is attitudinal barriers - staff who are unwilling to assist, impatient, interact with the customer's assistant instead of directly with them and lack basic skills on how to interact with someone who has a disability. A comprehensive framework of banking was used to identify a wide range of barriers. The barriers were classified as attitudinal, barriers to physical access, digital access barriers, barriers to information, communication barriers and some generic concerns such as safe evacuation during emergencies and alternative authentication. Both the barriers and the solutions where ranked by participants. From a theoretical perspective, the benefit of a customer-centric approach to understanding these barriers and the innovation potential of a Universal Design approach is affirmed by this study.

Item Banking. ERIC/AE Digest.

ERIC Educational Resources Information Center

Rudner, Lawrence

This digest discusses the advantages and disadvantages of using item banks, and it provides useful information for those who are considering implementing an item banking project in their school districts. The primary advantage of item banking is in test development. Using an item response theory method, such as the Rasch model, items from multiple…

Teaching Bank Runs through Films

ERIC Educational Resources Information Center

Flynn, David T.

2009-01-01

The author advocates the use of films to supplement textbook treatments of bank runs and panics in money and banking or general banking classes. Modern students, particularly those in developed countries, tend to be unfamiliar with potential fragilities of financial systems such as a lack of deposit insurance or other safety net mechanisms. Films…

Na+ channel regulation by Ca2+/calmodulin and Ca2+/calmodulin-dependent protein kinase II in guinea-pig ventricular myocytes†

PubMed Central

Aiba, Takeshi; Hesketh, Geoffrey G.; Liu, Ting; Carlisle, Rachael; Villa-Abrille, Maria Celeste; O'Rourke, Brian; Akar, Fadi G.; Tomaselli, Gordon F.

2010-01-01

Aims Calmodulin (CaM) regulates Na+ channel gating through binding to an IQ-like motif in the C-terminus. Ca2+/CaM-dependent protein kinase II (CaMKII) regulates Ca2+ handling, and chronic overactivity of CaMKII is associated with left ventricular hypertrophy and dysfunction and lethal arrhythmias. However, the acute effects of Ca2+/CaM and CaMKII on cardiac Na+ channels are not fully understood. Methods and results Purified NaV1.5–glutathione-S-transferase fusion peptides were phosphorylated in vitro by CaMKII predominantly on the I–II linker. Whole-cell voltage-clamp was used to measure Na+ current (INa) in isolated guinea-pig ventricular myocytes in the absence or presence of CaM or CaMKII in the pipette solution. CaMKII shifted the voltage dependence of Na+ channel availability by ≈+5 mV, hastened recovery from inactivation, decreased entry into intermediate or slow inactivation, and increased persistent (late) current, but did not change INa decay. These CaMKII-induced changes of Na+ channel gating were completely abolished by a specific CaMKII inhibitor, autocamtide-2-related inhibitory peptide (AIP). Ca2+/CaM alone reproduced the CaMKII-induced changes of INa availability and the fraction of channels undergoing slow inactivation, but did not alter recovery from inactivation or the magnitude of the late current. Furthermore, the CaM-induced changes were also completely abolished by AIP. On the other hand, cAMP-dependent protein kinase A inhibitors did not abolish the CaM/CaMKII-induced alterations of INa function. Conclusion Ca2+/CaM and CaMKII have distinct effects on the inactivation phenotype of cardiac Na+ channels. The differences are consistent with CaM-independent effects of CaMKII on cardiac Na+ channel gating. PMID:19797425

From truck to optical fibre: the coming-of-age of eVLBI

NASA Astrophysics Data System (ADS)

Szomoru, A.; Biggs, A.; Garrett, M.; van Langevelde, H. J.; Olnon, F.; Paragi, Z.; Parsley, S.; Pogrebenko, S.; Reynolds, C.

Spurred by the advent of disk-based recording systems and the nearly explosive increase of internet bandwidth, eVLBI (Parsley et al. te{parsley}) has undergone a remarkable development over the past two years. From ftp-based transfers of small amounts of astronomical data, through near real-time correlation (disk-buffered at the correlator), it has culminated this spring in the first three telescope real-time correlation at JIVE (Onsala, Westerbork and Jodrell Bank). In this paper we will give a review of this development and the current state of affairs. We will also address the current limitations and the way we may improve both bandwidth and reliability and finally we will discuss the opportunities a true high-bandwidth real-time VLBI correlator will provide. (astro-ph/0412686)

Eye-bank preparation of endothelial tissue.

PubMed

Boynton, Grace E; Woodward, Maria A

2014-07-01

Eye-bank preparation of endothelial tissue for keratoplasty continues to evolve. Although eye-bank personnel have become comfortable and competent at Descemet's stripping automated endothelial keratoplasty (DSAEK), tissue preparation and tissue transport, optimization of preparation methods continues. Surgeons and eye-bank personnel should be up to date on the research in the field. As surgeons transit to Descemet's membrane endothelial keratoplasty (DMEK), eye banks have risen to the challenge of preparing tissue. Eye banks are refining their DMEK preparation and transport techniques. This article covers refinements to DSAEK tissue preparation, innovations to prepare DMEK tissue, and nuances to improve donor cornea tissue quality. As eye bank-supplied corneal tissue is the main source of tissue for many corneal surgeons, it is critical to stay informed about tissue handling and preparation. Ultimately, the surgeon is responsible for the transplantation, so involvement of clinicians in eye-banking practices and advocacy for pursuing meaningful research in this area will benefit clinical patient outcomes.

β-Adrenergic Receptor Stimulated Ncx1 Upregulation is Mediated via a CaMKII/AP-1 Signaling Pathway in Adult Cardiomyocytes

PubMed Central

Mani, Santhosh K.; Egan, Erin A.; Addy, Benjamin K.; Grimm, Michael; Kasiganesan, Harinath; Thiyagarajan, Thirumagal; Renaud, Ludivine; Brown, Joan Heller; Kern, Christine B.; Menick, Donald R.

2013-01-01

The Na+-Ca2+ exchanger gene (Ncx1) is upregulated in hypertrophy and is often found elevated in end-stage heart failure. Studies have shown that the change in its expression contributes to contractile dysfunction. β-adrenergic receptor (β-AR) signaling plays an important role in the regulation of calcium homeostasis in the cardiomyocyte but chronic activation in periods of cardiac stress contribute to heart failure by mechanisms which include Ncx1 upregulation. Here, using a Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKIIδc) null mouse, we demonstrate that β-AR-stimulated Ncx1 upregulation is dependent on CaMKII. β-AR-stimulated Ncx1 expression is mediated by activator protein 1 (AP-1) factors and is independent of cAMP-response element-binding protein (CREB) activation. The MAP kinases (ERK1/2, JNK and p38) are not required for AP-1 factor activation. Chromatin immunoprecipitation demonstrates that β-AR stimulation activates the ordered recruitment of JunB homodimers which then are replaced by c-Jun homodimers binding to the proximal AP-1 elements of the endogenous Ncx1 promoter. In conclusion, this work has provided insight into the intracellular signaling pathways and transcription factors regulating Ncx1 gene expression in a chronically β-AR-stimulated heart. PMID:19945464

Quality indicators for eye bank.

PubMed

Acharya, Manisha; Biswas, Saurabh; Das, Animesh; Mathur, Umang; Dave, Abhishek; Singh, Ashok; Dubey, Suneeta

2018-03-01

The aim of this study is to identify quality indicators of the eye bank and validate their effectivity. Adverse reaction rate, discard rate, protocol deviation rate, and compliance rate were defined as Quality Indicators of the eye bank. These were identified based on definition of quality that captures two dimensions - "result quality" and "process quality." The indicators were measured and tracked as part of quality assurance (QA) program of the eye bank. Regular audits were performed to validate alignment of standard operating procedures (SOP) with regulatory and surgeon acceptance standards and alignment of activities performed in the eye bank with the SOP. Prospective study of the indicators was performed by comparing their observed values over the period 2011-2016. Adverse reaction rate decreased more than 8-fold (from 0.61% to 0.07%), discard rate decreased and stabilized at 30%, protocol deviation rate decreased from 1.05% to 0.08%, and compliance rate reported by annual quality audits improved from 59% to 96% at the same time. In effect, adverse reaction rate, discard rate, and protocol deviation rate were leading indicators, and compliance rate was the trailing indicator. These indicators fulfill an important gap in available literature on QA in eye banking. There are two ways in which these findings can be meaningful. First, eye banks which are new to quality measurement can adopt these indicators. Second, eye banks which are already deeply engaged in quality improvement can test these indicators in their eye bank, thereby incorporating them widely and improving them over time.

12 CFR 326.8 - Bank Secrecy Act compliance.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 4 2011-01-01 2011-01-01 false Bank Secrecy Act compliance. 326.8 Section 326.8 Banks and Banking FEDERAL DEPOSIT INSURANCE CORPORATION REGULATIONS AND STATEMENTS OF GENERAL POLICY MINIMUM SECURITY DEVICES AND PROCEDURES AND BANK SECRECY ACT 1 COMPLIANCE Procedures for...

12 CFR 326.8 - Bank Secrecy Act compliance.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 4 2010-01-01 2010-01-01 false Bank Secrecy Act compliance. 326.8 Section 326.8 Banks and Banking FEDERAL DEPOSIT INSURANCE CORPORATION REGULATIONS AND STATEMENTS OF GENERAL POLICY MINIMUM SECURITY DEVICES AND PROCEDURES AND BANK SECRECY ACT 1 COMPLIANCE Procedures for...

12 CFR 345.26 - Small bank performance standards.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 4 2011-01-01 2011-01-01 false Small bank performance standards. 345.26... GENERAL POLICY COMMUNITY REINVESTMENT Standards for Assessing Performance § 345.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not intermediate small banks. The FDIC...

12 CFR 345.26 - Small bank performance standards.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 4 2010-01-01 2010-01-01 false Small bank performance standards. 345.26... GENERAL POLICY COMMUNITY REINVESTMENT Standards for Assessing Performance § 345.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not intermediate small banks. The FDIC...

12 CFR 34.24 - Nonfederally chartered commercial banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Nonfederally chartered commercial banks. 34.24 Section 34.24 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY REAL ESTATE LENDING AND APPRAISALS Adjustable-Rate Mortgages § 34.24 Nonfederally chartered commercial banks. Pursuant...

12 CFR 345.44 - Public notice by banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 4 2011-01-01 2011-01-01 false Public notice by banks. 345.44 Section 345.44 Banks and Banking FEDERAL DEPOSIT INSURANCE CORPORATION REGULATIONS AND STATEMENTS OF GENERAL POLICY COMMUNITY REINVESTMENT Records, Reporting, and Disclosure Requirements § 345.44 Public notice by banks. A...

12 CFR 225.124 - Foreign bank holding companies.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Foreign bank holding companies. 225.124 Section... SYSTEM BANK HOLDING COMPANIES AND CHANGE IN BANK CONTROL (REGULATION Y) Regulations Financial Holding Companies Interpretations § 225.124 Foreign bank holding companies. (a) Effective December 1, 1971, the...

12 CFR 7.1010 - Postal service by national bank.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Postal service by national bank. 7.1010 Section 7.1010 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Powers § 7.1010 Postal service by national bank. (a) General. A national bank may maintain...

12 CFR 7.1010 - Postal service by national bank.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Postal service by national bank. 7.1010 Section 7.1010 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Powers § 7.1010 Postal service by national bank. (a) General. A national bank may maintain...

12 CFR 225.121 - Acquisition of Edge corporation affiliate by State member banks of registered bank holding company.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Acquisition of Edge corporation affiliate by... Acquisition of Edge corporation affiliate by State member banks of registered bank holding company. (a) The... of the holding company's Edge corporation subsidiary organized under section 25(a) of the Federal...

12 CFR 210.29 - Agreement of receiving bank.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 2 2010-01-01 2010-01-01 false Agreement of receiving bank. 210.29 Section 210.29 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM COLLECTION OF CHECKS AND OTHER ITEMS BY FEDERAL RESERVE BANKS AND FUNDS TRANSFERS THROUGH FEDWIRE (REGULATION...

12 CFR 615.5335 - Bank net collateral ratio.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 6 2011-01-01 2011-01-01 false Bank net collateral ratio. 615.5335 Section 615.5335 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM FUNDING AND FISCAL AFFAIRS, LOAN POLICIES AND OPERATIONS, AND FUNDING OPERATIONS Surplus and Collateral Requirements § 615.5335 Bank net...

12 CFR 210.29 - Agreement of receiving bank.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Agreement of receiving bank. 210.29 Section 210.29 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM COLLECTION OF CHECKS AND OTHER ITEMS BY FEDERAL RESERVE BANKS AND FUNDS TRANSFERS THROUGH FEDWIRE (REGULATION...

12 CFR 615.5335 - Bank net collateral ratio.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 6 2010-01-01 2010-01-01 false Bank net collateral ratio. 615.5335 Section 615.5335 Banks and Banking FARM CREDIT ADMINISTRATION FARM CREDIT SYSTEM FUNDING AND FISCAL AFFAIRS, LOAN POLICIES AND OPERATIONS, AND FUNDING OPERATIONS Surplus and Collateral Requirements § 615.5335 Bank net...

12 CFR 215.8 - Records of member banks.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 2 2011-01-01 2011-01-01 false Records of member banks. 215.8 Section 215.8 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM LOANS TO EXECUTIVE OFFICERS, DIRECTORS, AND PRINCIPAL SHAREHOLDERS OF MEMBER BANKS (REGULATION O) § 215.8 Records of...

Human milk banking.

PubMed

O'Hare, Esther Marie; Wood, Angela; Fiske, Elizabeth

2013-01-01

Forms of human milk banking and donation have been present for more than a century worldwide, but, since 1985, the Human Milk Banking Association of North America (HM BANA) has established guidelines to make the use of donor's breast milk safe and the second best form of feeding to maternal breast milk for a neonatal intensive care unit (NICU) infant. The Indiana Mother's Human Milk Bank provides an extensive and meticulous process of selecting breast milk donors. The process begins with a phone interview with a potential donor and includes the review of the donor's medical records, blood laboratory screening, medication and dietary intake, as well as consent from the donor's pediatrician. The milk bank follows steps of collecting, storing, and receiving the breast milk in accordance with the guidelines of the HM BANA. Pasteurization is the method used to ensure the proper heating and cooling of breast milk. Despite the rigorous pasteurization method, the donor's breast milk will not lose most of the important beneficial components needed for sick or ill NICU infants. Every batch of pasteurized breast milk will be cultured for any possible contamination and shipped to NICUs after it has been cleared by laboratory testing.

Ethical considerations in umbilical cord blood banking.

PubMed

Fox, Nathan S; Chervenak, Frank A; McCullough, Laurence B

2008-01-01

Pregnant patients have the option at delivery of having their cord blood collected and stored for future use. At many hospitals, they have the option of donating their cord blood to the public banking system for future use by anyone who is an appropriate match (public banking). Patients also have the option of having their cord blood stored for a fee with a commercial/private company for future use within their family (private banking). Currently, private banking is not recommended by major obstetric and pediatric professional organizations. We applied current evidence of the risks and benefits of private and public cord blood banking and accepted ethical principles to answer the following two related questions: 1) Do obstetricians have an ethical obligation to comply with a request for private banking? and 2) Do obstetricians have an ethical obligation to routinely offer private banking to women who do not request it? The only situation where there is a known benefit to private banking is when public banking is not available and the patient currently has an affected family member who may benefit from cord blood therapy. We conclude that when presented with a request for private banking, obstetricians have an ethical obligation to explain the lack of proven benefit of this procedure. If the patient still requests private banking, it would be appropriate to comply, because there is minimal or no risk to the procedure. However, obstetricians are not ethically obligated to offer private banking, even when public banking is not available, except in the limited circumstance when the patient currently has an affected family member who may benefit from cord blood therapy.

12 CFR 1261.12 - Reporting requirements for Bank directors.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 7 2010-01-01 2010-01-01 false Reporting requirements for Bank directors. 1261.12 Section 1261.12 Banks and Banking FEDERAL HOUSING FINANCE AGENCY FEDERAL HOME LOAN BANKS FEDERAL....12 Reporting requirements for Bank directors. (a) Annual reporting. Annually, each Bank shall require...

26 CFR 1.895-1 - Income derived by a foreign central bank of issue, or by Bank for International Settlements, from...

Code of Federal Regulations, 2010 CFR

2010-04-01

... issue, or by Bank for International Settlements, from obligations of the United States or from bank... foreign central bank of issue, or by Bank for International Settlements, from obligations of the United... foreign central bank of issue is a bank which is by law or government sanction the principal authority...

12 CFR 215.8 - Records of member banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... resolution of the board of directors of the bank from making an extension of credit to any company or other... 12 Banks and Banking 2 2010-01-01 2010-01-01 false Records of member banks. 215.8 Section 215.8 Banks and Banking FEDERAL RESERVE SYSTEM BOARD OF GOVERNORS OF THE FEDERAL RESERVE SYSTEM LOANS TO...

26 CFR 1.895-1 - Income derived by a foreign central bank of issue, or by Bank for International Settlements, from...

Code of Federal Regulations, 2013 CFR

2013-04-01

... issue, or by Bank for International Settlements, from obligations of the United States or from bank... by a foreign central bank of issue, or by Bank for International Settlements, from obligations of the... issue. (1) A foreign central bank of issue is a bank which is by law or government sanction the...

26 CFR 1.895-1 - Income derived by a foreign central bank of issue, or by Bank for International Settlements, from...

Code of Federal Regulations, 2012 CFR

2012-04-01

... issue, or by Bank for International Settlements, from obligations of the United States or from bank... by a foreign central bank of issue, or by Bank for International Settlements, from obligations of the... issue. (1) A foreign central bank of issue is a bank which is by law or government sanction the...

26 CFR 1.895-1 - Income derived by a foreign central bank of issue, or by Bank for International Settlements, from...

Code of Federal Regulations, 2014 CFR

2014-04-01

... issue, or by Bank for International Settlements, from obligations of the United States or from bank... by a foreign central bank of issue, or by Bank for International Settlements, from obligations of the... issue. (1) A foreign central bank of issue is a bank which is by law or government sanction the...

26 CFR 1.895-1 - Income derived by a foreign central bank of issue, or by Bank for International Settlements, from...

Code of Federal Regulations, 2011 CFR

2011-04-01

... issue, or by Bank for International Settlements, from obligations of the United States or from bank... by a foreign central bank of issue, or by Bank for International Settlements, from obligations of the... issue. (1) A foreign central bank of issue is a bank which is by law or government sanction the...

Youngest Radio Pulsar Revealed with Green Bank Telescope

NASA Astrophysics Data System (ADS)

2002-04-01

mine for years to come," noted Camilo. "We can very precisely measure how its rate of rotation changes over time, potentially inferring fundamental clues about what causes a magnetized neutron star to spin down. We also will make valuable comparisons to the X-ray data, which may help us determine exactly how these objects generate and emit radiation." The researchers also point to the fact that this discovery bodes well for the GBT being able to study additional young pulsars that have previously escaped detection. "By using this magnificent new telescope, we should be able to discover other very young pulsars that we surmise are there, but are simply too weak to detect by any other means," said Camilo. "Measuring the luminosity and spectrum of a large sample of these stars will be crucial for making an accurate census of pulsars in our Galaxy." The researchers used the new Berkeley-Caltech Pulsar Machine to process the signals from the GBT and record them for later analysis. The group led by Camilo in this investigation consists also of: Ingrid H. Stairs (NRAO Green Bank, West Virginia); Duncan R. Lorimer, Michael Kramer, Maura A. McLaughlin (University of Manchester, Jodrell Bank Observatory, Cheshire, U.K.); Donald C. Backer (University of California, Berkeley); Scott M. Ransom (McGill University, Montreal, Canada); Bernd Klein, Richard Wielebinski, Peter Muller (Max-Planck-Institut fur Radioastronomie, Bonn, Germany); and Zaven Arzoumanian (Universities Space Research Association/NASA-Goddard Space Flight Center, Greenbelt, Maryland). The GBT is the world's largest fully steerable radio telescope. It was dedicated on August 25, 2000. The National Radio Astronomy Observatory is a facility of the National Science Foundation, operated under cooperative agreement by Associated Universities, Inc.

12 CFR 7.1000 - National bank ownership of property.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false National bank ownership of property. 7.1000 Section 7.1000 Banks and Banking COMPTROLLER OF THE CURRENCY, DEPARTMENT OF THE TREASURY BANK ACTIVITIES AND OPERATIONS Bank Powers § 7.1000 National bank ownership of property. (a) Investment in real estate...

Data banks for recreation supply and participation

Treesearch

E. M. Avedon; S. L. J. Smith

1980-01-01

Data archives and data banks have become increasingly important as more researchers begin to examine trends. Characteristics of data banks, sources of bias in secondary data sources and important trends in data banks are described. The paper concludes with advice about using data banks.

The relationship between neurotrophic factors and CaMKII in the death and survival of retinal ganglion cells.

PubMed

Cooper, N G F; Laabich, A; Fan, W; Wang, X

2008-01-01

The scientific discourse relating to the causes and treatments for glaucoma are becoming reflective of the need to protect and preserve retinal neurons from degenerative changes, which result from the injurious environment associated with this disease. Knowledge, in particular, of the signal transduction pathways which affect death and survival of the retinal ganglion cells is critical to this discourse and to the development of a suitable neurotherapeutic strategy for this disease. The goal of this chapter is to review what is known of the chief suspects involved in initiating the cell death/survival pathways in these cells, and what still remains to be uncovered. The least controversial aspect of the subject relates to the potential role of neurotrophic factors in the protection of the retinal ganglion cells. On the other hand, the postulated triggers for signaling cell death in glaucoma remain controversial. Certainly, the restricted flow of neurotrophic factors has been cited as one possible trigger. However, the connections between glaucoma and other factors present in the retina, such as glutamate, long held to be a prospective culprit in retinal ganglion cell death are still being questioned. Whatever the outcome of this particular debate, it is clear that the downstream intersections between the cell death and survival pathways should provide important foci for future studies whose goal is to protect retinal neurons, situated as they are, in the stressful environment of a cell destroying disease. The evidence for CaMKII being one of these intersecting points is discussed.

12 CFR 228.44 - Public notice by banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Public notice by banks. 228.44 Section 228.44... notice by banks. A bank shall provide in the public lobby of its main office and each of its branches the appropriate public notice set forth in appendix B of this part. Only a branch of a bank having more than one...

12 CFR 25.44 - Public notice by banks.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Public notice by banks. 25.44 Section 25.44... Public notice by banks. A bank shall provide in the public lobby of its main office and each of its branches the appropriate public notice set forth in appendix B of this part. Only a branch of a bank having...

Development of tissue bank.

PubMed

Narayan, R P

2012-05-01

The history of tissue banking is as old as the use of skin grafting for resurfacing of burn wounds. Beneficial effects of tissue grafts led to wide spread use of auto and allograft for management of varied clinical conditions like skin wounds, bone defects following trauma or tumor ablation. Availability of adequate amount of tissues at the time of requirement was the biggest challenge that forced clinicians to find out techniques to preserve the living tissue for prolonged period of time for later use and thus the foundation of tissue banking was started in early twentieth century. Harvesting, processing, storage and transportation of human tissues for clinical use is the major activity of tissue banks. Low temperature storage of processed tissue is the best preservation technique at present. Tissue banking organization is a very complex system and needs high technical expertise and skilled personnel for proper functioning in a dedicated facility. A small lapse/deviation from the established protocol leads to loss of precious tissues and or harm to recipients as well as the risk of transmission of deadly diseases and tumors. Strict tissue transplant acts and stringent regulations help to streamline the whole process of tissue banking safe for recipients and to community as whole.

Educational Development in Thailand: The Role of World Bank Lending. A World Bank Operations Evaluation Study.

ERIC Educational Resources Information Center

World Bank, Washington, DC.

The World Bank's Operation Evaluation Department (OED) evaluates educational development in Thailand and assesses the cumulative impact of the Bank's projects on development in that country. From 1966 to date, the Bank supported six education projects with an estimated cost of a half billion dollars. The report covers: (1) economic and educational…

Survey of Italian human milk banks.

PubMed

De Nisi, Giuseppe; Moro, Guido E; Arslanoglu, Sertac; Ambruzzi, Amalia M; Biasini, Augusto; Profeti, Claudio; Tonetto, Paola; Bertino, Enrico

2015-05-01

At present, the Italian Association of Donor Human Milk Banks (Associazione Italiana Banche del Latte Umano Donato, AIBLUD) consists of 31 milk banks, whose management is based on Italian Guidelines. In 2013, AIBLUD performed a systematic survey to collect data on the activities of banks operating in Italy in the years previous to this date. The purpose of this survey was to evaluate the operational procedures of Italian Human Milk Banks in order to identify both areas of strength and room for improvement. A questionnaire was utilized to obtain national data from the 28 banks active in the year 2012 in order to evaluate the number of donors, volume of human milk collected, and other information relating to the period 2007 to 2012. In all, 89% of the banks (25/28) responded to the survey. Data received primarily concerned the number of donors, volume of milk collected, and average amount of milk from each donor in the period 2007 to 2012. It was evident that in 2012 human milk banks collected a higher volume of milk than in 2007. Further, the average amount of milk from each donor was higher. Most of the milk banks were following the Italian Guidelines for traceability, control of donors, bacteriological checks, method of pasteurization, storage, thawing, type of containers, and utilization of the Hazard Analysis and Critical Control Points system. This survey identified both areas of strength and room for improvement in the Italian human milk banks. © The Author(s) 2015.

Usability and trust in e-banking.

PubMed

Pravettoni, Gabriella; Leotta, Salvatore Nuccio; Lucchiari, Claudio; Misuraca, Raffaella

2007-12-01

This study assessed the role of usability in trust of e-banking services. A questionnaire was administered to 185 Italian undergraduate working students who volunteered for the experiment (M age = 30.5 yr., SD = 3.1). Participants were differentiated on computer ability (Expert, n = 104; Nonexpert, n = 81) and e-banking use (User, n = 93; Nonusers, n = 92). Analysis showed that the website usability of e-banking services did not play a very important role for the User group. Instead, institution-based trust, e.g., the trust in the security policy of the Web merchant, customers, and the overall trust of the bank were the crucial factors in the adoption of e-banking.

Wetlands Mitigation Banking Concepts

DTIC Science & Technology

1992-07-01

Naval Amphibious Bas Eslgrss Mit. Bank CA, San Diego Co. dredging & facilities Dept of the Navy SeaWorld Eelgras Mitigation Dank CA, San Diego Co...shore development, private projects SeaWorld 8 Table 2. WETLAND MITIGATION BANKS UNDER PLANNING, Institute for Water Resources Preliminary Survey Data

12 CFR 228.26 - Small bank performance standards.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 3 2011-01-01 2011-01-01 false Small bank performance standards. 228.26... RESERVE SYSTEM COMMUNITY REINVESTMENT (REGULATION BB) Standards for Assessing Performance § 228.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not intermediate small...

12 CFR 25.26 - Small bank performance standards.

Code of Federal Regulations, 2011 CFR

2011-01-01

... 12 Banks and Banking 1 2011-01-01 2011-01-01 false Small bank performance standards. 25.26 Section... REINVESTMENT ACT AND INTERSTATE DEPOSIT PRODUCTION REGULATIONS Regulations Standards for Assessing Performance § 25.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not...

12 CFR 228.26 - Small bank performance standards.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 3 2010-01-01 2010-01-01 false Small bank performance standards. 228.26... RESERVE SYSTEM COMMUNITY REINVESTMENT (REGULATION BB) Standards for Assessing Performance § 228.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not intermediate small...

12 CFR 25.26 - Small bank performance standards.

Code of Federal Regulations, 2010 CFR

2010-01-01

... 12 Banks and Banking 1 2010-01-01 2010-01-01 false Small bank performance standards. 25.26 Section... REINVESTMENT ACT AND INTERSTATE DEPOSIT PRODUCTION REGULATIONS Regulations Standards for Assessing Performance § 25.26 Small bank performance standards. (a) Performance criteria—(1) Small banks that are not...

Coral reefs and the World Bank.

PubMed

Hatziolos, M

1997-01-01

The World Bank¿s involvement in coral reef conservation is part of a larger effort to promote the sound management of coastal and marine resources. This involves three major thrusts: partnerships, investments, networks and knowledge. As an initial partner and early supporter of the International Coral Reef Initiative (ICRI), the Bank serves as the executive planning committee of ICRI. In partnership with the World Conservation Union and the Great Barrier Reef Marine Park Authority, the Bank promotes the efforts towards the establishment and maintenance of a globally representative system of marine protected areas. In addition, the Bank invested over $120 million in coral reef rehabilitation and protection programs in several countries. Furthermore, the Bank developed a ¿Knowledge Bank¿ that would market ideas and knowledge to its clients along with investment projects. This aimed to put the best global knowledge on environmentally sustainable development in the hands of its staff and clients. During the celebration of 1997, as the International Year of the Reef, the Bank planned to cosponsor an associated event that would highlight the significance of coral reefs and encourage immediate action to halt their degradation to conserve this unique ecosystem.

Cash efficiency for bank branches.