Science.gov

Sample records for preconditioning prevents postischemic

  1. Dexmedetomidine prevents post-ischemic LTP via presynaptic and postsynaptic mechanisms.

    PubMed

    Zhou, Li; Qin, Shou-Jun; Gao, Xin; Han, Jun-Ping; Hu, Bin; Li, Mei; Wu, Yu-Qing; Ma, Xing; Gu, Shu-Ling; Ma, Teng-Fei

    2015-10-01

    Increasing evidence indicates that dexmedetomidine (DEX), a selective ?2-adrenergic receptor agonist, has a neuroprotective effect against cerebral injury. However, it remains unknown whether and how DEX functionally prevents the pathological form of synaptic plasticity caused by ischemia in the hippocampal CA1 neurons. To address this issue, we analyzed the role of DEX using a model of brain ischemia (oxygen and glucose deprivation, OGD) referred to as post-ischemic LTP (i-LTP). We found that DEX could reduce i-LTP by selectively activating ?2 receptors. To clarify its detailed mechanisms, the presynaptic and postsynaptic roles of DEX were investigated. The activation of the ?2 receptors of DEX decreased the frequency spontaneous mEPSCs, which exerted its presynaptic mechanisms. In addition, DEX also decreased the amplitude of mEPSCs and prevented the depolarization of postsynaptic membranes during OGD treatment, which exerted its postsynaptic mechanisms. More importantly, our results indicate that postsynaptic ? receptors, not ?1 receptors, participated in i-LTP. Therefore, these results demonstrated that decreasing ? receptors activation by DEX-medicated pre- and post-synaptic ?2 receptors activation is responsible for i-LTP. Because of the NMDARs required for i-LTP, we further examined the critical roles of postsynaptic ? receptors downstream PKA regulation of NMDA receptor-mediated EPSCs (NMDA EPSC). We clarified that it is attributable to the direct effect of DEX on NMDA EPSC as mediated by PKA inactivation. These findings suggest that DEX can protect neurons from functional damage caused by a relatively mild degree of transient cerebral ischemia, and this effect is mediated by both presynaptic reduction of NE and glutamate release and postsynaptic suppression of NMDAR activation by ? receptors and downstream PKA regulation. PMID:26168895

  2. Superiority of zinc complex of acetylsalicylic acid to acetylsalicylic acid in preventing postischemic myocardial dysfunction.

    PubMed

    Korkmaz, Sevil; Atmanli, Ayhan; Li, Shiliang; Radovits, Tamás; Heged?s, Peter; Barnucz, Enik?; Hirschberg, Kristóf; Loganathan, Sivakkanan; Yoshikawa, Yutaka; Yasui, Hiroyuki; Karck, Matthias; Szabó, Gábor

    2015-09-01

    The pathophysiology of ischemic myocardial injury involves cellular events, reactive oxygen species, and an inflammatory reaction cascade. The zinc complex of acetylsalicylic acid (Zn(ASA)2) has been found to possess higher anti-inflammatory and lower ulcerogenic activities than acetylsalicylic acid (ASA). Herein, we studied the effects of both ASA and Zn(ASA)2 against acute myocardial ischemia. Rats were pretreated with ASA (75?mg/kg) or Zn(ASA)2 (100?mg/kg) orally for five consecutive days. Isoproterenol (85?mg/kg, subcutaneously [s.c.]) was applied to produce myocardial infarction. After 17-22?h, animals were anesthetized with sodium pentobarbital (60?mg/kg, intraperitoneally [i.p.]) and both electrical and mechanical parameters of cardiac function were evaluated in vivo. Myocardial histological and gene expression analyses were performed. In isoproterenol-treated rats, Zn(ASA)2 treatment normalized significantly impaired left-ventricular contractility index (Emax 2.6?±?0.7?mmHg/µL vs. 4.6?±?0.5?mmHg/µL, P?preventing electrical, mechanical, and histological changes after acute myocardial ischemia. The induction of antioxidant enzymes and the anti-inflammatory cytokine TGF-?1 may play a pivotal role in the mechanism of action of Zn(ASA)2. PMID:25670850

  3. Lipopolysaccharide preconditioning prevents acceleration of kindling epileptogenesis induced by traumatic brain injury.

    PubMed

    Eslami, Mansoureh; Sayyah, Mohammad; Soleimani, Mansoureh; Alizadeh, Leila; Hadjighassem, Mahmoudreza

    2015-12-15

    10-20% of symptomatic epilepsies are post-traumatic. We examined effect of LPS preconditioning on epileptogenesis after controlled cortical impact (CCI). LPS (0.01, 0.1 and 0.5mg/kg) was injected i.p. to rats 5days before induction of CCI to parieto-temporal cortex. Kindling started 24h after CCI by i.p. injection of 30mg/kg of pentylenetetrazole every other day until manifestation of 3 consecutive generalized seizures. CCI injury accelerated the rate of kindled seizures acquisition. LPS (0.1 and 0.5mg/kg) prevented the acceleration of kindling. LPS preconditioning significantly decreased IL-1? and TNF-? over-expression and the number of damaged neurons in the hippocampus of traumatic rats. PMID:26616884

  4. Ozone-Oxidative Preconditioning Prevents Doxorubicin-induced Cardiotoxicity in Sprague-Dawley Rats

    PubMed Central

    Delgado-Roche, Livan; Hernández-Matos, Yanet; Medina, Emilio A.; Morejón, Dalia Á.; González, Maité R.; Martínez-Sánchez, Gregorio

    2014-01-01

    Objectives: Induced dilated cardiomyopathy is the main limitation of the anti-cancer drug doxorubicin, which causes oxidative stress and cardiomyocyte death. As ozone therapy can activate the antioxidant systems, this study aimed to investigate the therapeutic efficacy of ozone-oxidative preconditioning against doxorubicin-induced cardiotoxicity. Methods: The study was carried out from September 2013 to January 2014. Sprague-Dawley rats were randomly distributed in the following treatment groups: Group 1 were treated with 2 mg/kg intraperitoneal (i.p.) of doxorubicin twice a week for 50 days; Group 2 were treated with 0.3 mg of ozone/oxygen mixture at 50 ?g/mL of ozone per 6 mL of oxygen by rectal insufflation and then treated with doxorubicin; Group 3 were treated as Group 2 but only with the oxygen, and Group 4 were treated with oxygen first, and then with sodium chloride i.p. as the control group. Results: The results showed that ozone therapy preserved left ventricle morphology which was accompanied by a reduction of serum pro-brain natriuretic peptide levels. The cardioprotective effects of ozone-oxidative preconditioning were associated with a significant increase (P <0.05) of antioxidant enzymes activities and a reduction of lipid and protein oxidation (P <0.05). Conclusion: Ozone-oxidative preconditioning prevents doxorubicin-induced dilated cardiomyopathy through an increase of antioxidant enzymes and a reduction of oxidised macromolecules. This establishes the background for future studies to determine if ozone therapy can be used as a complementary treatment for attenuating doxorubicin-induced cardiotoxicity in cancer patients. PMID:25097769

  5. Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of heme oxygenase-1

    PubMed Central

    Zuidema, Mozow Y.; Peyton, Kelly J.; Fay, William P.; Durante, William

    2011-01-01

    We recently demonstrated that preconditioning with an exogenous hydrogen sulfide donor (NaHS-PC) 24 h before ischemia and reperfusion (I/R) causes postcapillary venules to shift to an anti-inflammatory phenotype in C57BL/6J wild-type (WT) mice such that these vessels fail to support increases in postischemic leukocyte rolling (LR) and leukocyte adhesion (LA). The objective of the present study was to determine whether heme oxygenase-1 (HO-1) is a mediator of these anti-inflammatory effects noted during I/R in mice preconditioned with NaHS. Intravital fluorescence microscopy was used to visualize LR and LA in single postcapillary venules of the murine small intestine. I/R induced marked increases in LR and LA, effects that were prevented by NaHS-PC. Treatment with the HO inhibitor tin protoporphyrin IX, but not the inactive protoporphyrin CuPPIX, just before reperfusion prevented the anti-inflammatory effects of antecedent NaHS. The anti-inflammatory effects of NaHS-PC were mimicked by preconditioning with hemin, an agent that induces HO-1 expression. We then evaluated the effect of NaHS as a preconditioning stimulus in mice that were genetically deficient in HO-1 (HO-1?/? on an H129 background with appropriate WT strain controls). NaHS-PC was ineffective in HO-1?/? mice. Our work indicates that HO-1 serves as an effector of the anti-inflammatory effects of NaHS-PC during I/R 24 h later. PMID:21666111

  6. The mitochondrial origin of postischemic arrhythmias

    PubMed Central

    Akar, Fadi G.; Aon, Miguel A.; Tomaselli, Gordon F.; O’Rourke, Brian

    2005-01-01

    Recovery of the mitochondrial inner membrane potential (??m) is a key determinant of postischemic functional recovery of the heart. Mitochondrial ROS-induced ROS release causes the collapse of ??m and the destabilization of the action potential (AP) through a mechanism involving a mitochondrial inner membrane anion channel (IMAC) modulated by the mitochondrial benzodiazepine receptor (mBzR). Here, we test the hypothesis that this mechanism contributes to spatiotemporal heterogeneity of ??m during ischemia-reperfusion (IR), thereby promoting abnormal electrical activation and arrhythmias in the whole heart. High-resolution optical AP mapping was performed in perfused guinea pig hearts subjected to 30 minutes of global ischemia followed by reperfusion. Typical electrophysiological responses, including progressive AP shortening followed by membrane inexcitablity in ischemia and ventricular fibrillation upon reperfusion, were observed in control hearts. These responses were reduced or eliminated by treatment with the mBzR antagonist 4?-chlorodiazepam (4?-Cl-DZP), which blocks depolarization of ??m. When applied throughout the IR protocol, 4?-Cl-DZP blunted AP shortening and prevented reperfusion arrhythmias. Inhibition of ventricular fibrillation was also achieved by bolus infusion of 4?-Cl-DZP just before reperfusion. Conversely, treatment with an agonist of the mBzR that promotes ??m depolarization exacerbated IR-induced electrophysiological changes and failed to prevent arrhythmias. The effects of these compounds were consistent with their actions on IMAC and ??m. These findings directly link instability of ??m to the heterogeneous electrophysiological substrate of the postischemic heart and highlight the mitochondrial membrane as a new therapeutic target for arrhythmia prevention in ischemic heart disease. PMID:16284648

  7. Remote ischemic preconditioning for prevention of high-altitude diseases: fact or fiction?

    PubMed

    Berger, Marc Moritz; Macholz, Franziska; Mairbäurl, Heimo; Bärtsch, Peter

    2015-11-15

    Preconditioning refers to exposure to brief episodes of potentially adverse stimuli and protects against injury during subsequent exposures. This was first described in the heart, where episodes of ischemia/reperfusion render the myocardium resistant to subsequent ischemic injury, which is likely caused by reactive oxygen species (ROS) and proinflammatory processes. Protection of the heart was also found when preconditioning was performed in an organ different from the target, which is called remote ischemic preconditioning (RIPC). The mechanisms causing protection seem to include stimulation of nitric oxide (NO) synthase, increase in antioxidant enzymes, and downregulation of proinflammatory cytokines. These pathways are also thought to play a role in high-altitude diseases: high-altitude pulmonary edema (HAPE) is associated with decreased bioavailability of NO and increased generation of ROS, whereas mechanisms causing acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) seem to involve cytotoxic effects by ROS and inflammation. Based on these apparent similarities between ischemic damage and AMS, HACE, and HAPE, it is reasonable to assume that RIPC might be protective and improve altitude tolerance. In studies addressing high-altitude/hypoxia tolerance, RIPC has been shown to decrease pulmonary arterial systolic pressure in normobaric hypoxia (13% O2) and at high altitude (4,342 m). Our own results indicate that RIPC transiently decreases the severity of AMS at 12% O2. Thus preliminary studies show some benefit, but clearly, further experiments to establish the efficacy and potential mechanism of RIPC are needed. PMID:26089545

  8. Quercetin Improves Postischemic Recovery of Heart Function in Doxorubicin-Treated Rats and Prevents Doxorubicin-Induced Matrix Metalloproteinase-2 Activation and Apoptosis Induction

    PubMed Central

    Barteková, Monika; Šimon?íková, Petra; Fogarassyová, Mária; Ivanová, Monika; Okruhlicová, ?udmila; Tribulová, Narcisa; Dovinová, Ima; Baran?ík, Miroslav

    2015-01-01

    Quercetin (QCT) is flavonoid that possesses various biological functions including anti-oxidative and radical-scavenging activities. Moreover, QCT exerts some preventive actions in treatment of cardiovascular diseases. The aim of present study was to explore effects of prolonged administration of QCT on changes induced by repeated application of doxorubicin (DOX) in rat hearts. We focused on the ultrastructure of myocardium, matrix metalloproteinases (MMPs), biometric parameters, and apoptosis induction. Our aim was also to examine effects of QCT on ischemic tolerance in hearts exposed to chronic effects of DOX, and to determine possible mechanisms underlying effects of QCT. Our results showed that QCT prevented several negative chronic effects of DOX: (I) reversed DOX-induced blood pressure increase; (II) mediated improvement of deleterious effects of DOX on ultrastructure of left ventricle; (III) prevented DOX-induced effects on tissue MMP-2 activation; and (iv) reversed effects of DOX on apoptosis induction and superoxide dismutase inhibition. Moreover, we showed that rat hearts exposed to effects of QCT were more resistant to ischemia/reperfusion injury. Effects of QCT on modulation of ischemic tolerance were linked to Akt kinase activation and connexin-43 up-regulation. Taken together, these results demonstrate that prolonged treatment with QCT prevented negative chronic effects of DOX on blood pressure, cellular damage, MMP-2 activation, and apoptosis induction. Moreover, QCT influenced myocardial responses to acute ischemic stress. These facts bring new insights into mechanisms of QCT action on rat hearts exposed to the chronic effects of DOX. PMID:25872140

  9. Menstrual preconditioning for the prevention of major obstetrical syndromes in polycystic ovary syndrome.

    PubMed

    Brosens, Ivo; Benagiano, Giuseppe

    2015-10-01

    The presence of multiple ovarian cysts, anovulation, and endometrial progesterone resistance in the neonate seems remarkably similar to ovarian and endometrial features of the polycystic ovary syndrome (PCOS) of adolescent and adult women. In fact, in the absence of cyclic menstruations after menarche, the neonatal progesterone resistance is likely to persist and adversely affect young women with PCOS at the time of pregnancy after induction of ovulation, because any persisting defect in progesterone response can interfere with the process of decidualization and trophoblast invasion. The primigravid woman with PCOS therefore is likely to be at risk of defective deep placentation as manifested by the increased risk of major obstetric syndromes. A recent, large epidemiologic study has demonstrated that the risk of preeclampsia and preterm delivery is elevated in the 13- to 15-year old group, although it does not persist in the 16- to 17-year old group. It is proposed therefore that induction of ovulation in the infertile nulligravid woman with PCOS should be preceded by a period of progesterone withdrawal bleedings to achieve full endometrial progesterone response by the time of pregnancy. The cyclic administration of clomiphene citrate for a period to be determined by vascular response may be an appropriate tool to reduce the risk of major obstetric syndromes by menstrual preconditioning. PMID:26212182

  10. The GRONORUN 2 study: effectiveness of a preconditioning program on preventing running related injuries in novice runners. The design of a randomized controlled trial

    PubMed Central

    2010-01-01

    Background Distance running is a popular recreational exercise. It is a beneficial activity for health and well being. However, running may also cause injuries, especially of the lower extremities. In literature there is no agreement what intrinsic and extrinsic factors cause running related injuries (RRIs). In theory, most RRIs are elicited by training errors, this too much, too soon. In a preconditioning program runners can adapt more gradually to the high mechanical loads of running and will be less susceptible to RRIs. In this study the effectiveness of a 4-week preconditioning program on the incidence of RRIs in novice runners prior to a training program will be studied. Methods/Design The GRONORUN 2 (Groningen Novice Running) study is a two arm randomized controlled trial studying the effect of a 4-week preconditioning (PRECON) program in a group of novice runners. All participants wanted to train for the recreational Groningen 4-Mile running event. The PRECON group started a 4-week preconditioning program with walking and hopping exercises 4 weeks before the start of the training program. The control (CON) and PRECON group started a frequently used 9-week training program in preparation for the Groningen 4-Mile running event. During the follow up period participants registered their running exposure, other sporting activities and running related injuries in an Internet based running log. The primary outcome measure was the number of RRIs. RRI was defined as a musculoskeletal ailment or complaint of the lower extremities or back causing a restriction on running for at least three training sessions. Discussion The GRONORUN 2 study will add important information to the existing running science. The concept of preconditioning is easy to implement in existing training programs and will hopefully prevent RRIs especially in novice runners. Trial registration The Netherlands National Trial Register NTR1906. The NTR is part of the WHO Primary Registries. PMID:20809930

  11. Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heart

    PubMed Central

    Murphy, Elizabeth

    2010-01-01

    As a G protein-coupled receptor, the extracellular Ca2+-sensing receptor (CaSR) responds to changes not only in extracellular Ca2+, but also to many other ligands. CaSR has been found to be expressed in the hearts and cardiovascular system. In this study, we confirmed that CaSR is expressed in mouse cardiomyocytes and showed that it is predominantly localized in caveolae. The goal of this study was to investigate whether CaSR plays a cardioprotective role in ischemic preconditioning (IPC). Hearts from C57BL/6J mice (male, 12–16 wk) were perfused in the Langendorff mode and subjected to the following treatments: 1) control perfusion; 2) perfusion with a specific CaSR antagonist, NPS2143; 3) IPC (four cycles of 5 min of global ischemia and 5 min of reperfusion); or 4) perfusion with NPS2143 before and during IPC. Following these treatments, hearts were subjected to 20 min of no-flow global ischemia and 120 min of reperfusion. Compared with control, IPC significantly improved postischemic left ventricular functional recovery and reduced infarct size. Although NPS2143 perfusion alone did not change the hemodynamic function and did not change the extent of postischemic injury, NPS2143 treatment abolished cardioprotection of IPC. Through immunoblot analysis, it was demonstrated that IPC significantly increased the levels of phosphorylated ERK1/2, AKT, and GSK-3?, which were also prevented by NPS2143 treatment. Taken together, the distribution of CaSR in caveolae along with NPS2143-blockade of IPC-induced cardioprotective signaling suggest that the activation of CaSR during IPC is cardioprotective by a process involving caveolae. PMID:20833954

  12. Effect of ischemic preconditioning on P-selectin expression in hepatocytes of rats with cirrhotic ischemia-reperfusion injury

    PubMed Central

    Cheng, Xiang-Dong; Jiang, Xian-Chuan; Liu, Yin-Bing; Peng, Cheng-Hong; Xu, Bin; Peng, Shu-You

    2003-01-01

    AIM: To investigate the effects and mechanisms of ischemic preconditioning (IPC) on the ischemia/reperfusion (I/R) injury of liver cirrhosis in rats and the effect of IPC on P-selectin expression in hepatocytes. METHODS: Forty male SD rats with liver cirrhosis were randomly divided into sham operation group (SO group), ischemia/reperfusion group (I/R group), ischemic preconditioning group (IPC group), L-Arginine preconditioning group (APC group), L-NAME preconditioning group (NPC group), eight rats in each group. Hepatocellular viability was assessed by hepatic adenine nucleotide level and energy charge (EC) determined by HPLC, ALT, AST and LDH in serum measured by auto- biochemical analyzer and bile output. The expression of P-selectin in the liver tissue was analyzed by immunohistochemical technique. Leukocyte count in ischemic hepatic lobe was calculated. RESULTS: At 120 min after reperfusion, the level of ATP and EC in IPC and APC groups was higher than that in I/R group significantly. The increases in AST, ALT and LDH were prevented in IPC and APC groups. The livers produced more bile in IPC group than in I/R group during 120 min after reperfusion (0.101 ± 0.027 vs 0.066 ± 0.027 mL/g liver, P = 0.002). There was a significant difference between APC and I/R groups, (P = 0.001). The leukocyte count in liver tissues significantly increased in I/R group as compared with SO group (P < 0.05). The increase in the leukocyte count was prevented in IPC group. Administration of L-arginine resulted in the same effects as in IPC group. However, inhibition of NO synthesis (NPC group) held back the beneficial effects of preconditioning. Significant promotion of P-selectin expression in hepatocytes in the I/R group was observed compared with the SO group (P < 0.01). IPC or L-arginine attenuated P-selectin expression remarkably (P < 0.01). However, inhibition of NO synthesis enhanced P-selectin expression (P < 0.01). The degree of P-selectin expression was positively correlated with the leukocyte counts infiltrating in liver (r = 0.602, P = 0.000). CONCLUSION: IPC can attenuate the damage induced by I/R in cirrhotic liver and increase the ischemic tolerance of the rats with liver cirrhosis. IPC can abolish I/R induced leukocyte adhesion and infiltration by preventing post-ischemic P-selectin expression in the rats with liver cirrhosis via a NO-initiated pathway. PMID:14562395

  13. Preconditioning with glycyrrhizic, ferulic, paeoniflorin, cinnamic prevents rat hearts from ischemia/reperfusion injury via endothelial nitric oxide pathway

    PubMed Central

    Qian, Guo-Qiang; Ding, Jingjing; Zhang, Xiaozhao; Yin, Xiaofeng; Gao, Yuqin; Zhao, Guo-Ping

    2015-01-01

    Objective: The objective was to investigate the endothelial nitric oxide synthase (eNOS/NO) pathway is involved or not in the protective effects of glycyrrhizic, ferulic, paeoniflorin, cinnamic (GFPC) in myocardial ischemia-reperfusion injury Sprague-Dawley rats. Materials and Methods: Ischemia-reperfusion (I/R) model was made by ligating the left anterior descending branch of the coronary artery for 30 min and releasing for 120 min, then the left ventricular apical was fixed and sliced, morphological changes of myocardial microvascular endothelial cell (MMVEC) was observed by electron microscopy, apoptosis index of MMVEC was observed by means of TUNEL, serum NO was tested by methods of nitrate reduction, lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) was detected by automatic biochemical analyzer; Phosphorylated eNOS (PeNOS) and inducible NOS (iNOS) protein were measured by means of western blot. Results: In positive product control group, the serum levels of NO, LDH, CK-MB significantly increased (P < 0.05); MMVEC apoptosis was significantly decreased (P < 0.05); incidence of area at risk decreased significantly (P < 0.05); PeNOS protein increased (P < 0.05); iNOS protein decreased significantly (P < 0.05). Conclusion: Ischemic preconditioning of GFPC from GFPC plays a protective role in I/R heart through regulating the eNOS/NO signal pathway by increasing the PeNOS protein expression and decreasing the expression of iNOS protein. PMID:25829767

  14. A Top Pilot Tunnel Preconditioning Method for the Prevention of Extremely Intense Rockbursts in Deep Tunnels Excavated by TBMs

    NASA Astrophysics Data System (ADS)

    Zhang, Chuanqing; Feng, Xiating; Zhou, Hui; Qiu, Shili; Wu, Wenping

    2012-05-01

    The headrace tunnels at the Jinping II Hydropower Station cross the Jinping Mountain with a maximum overburden depth of 2,525 m, where 80% of the strata along the tunnels consist of marble. A number of extremely intense rockbursts occurred during the excavation of the auxiliary tunnels and the drainage tunnel. In particular, a tunnel boring machine (TBM) was destroyed by an extremely intense rockburst in a 7.2-m-diameter drainage tunnel. Two of the four subsequent 12.4-m-diameter headrace tunnels will be excavated with larger size TBMs, where a high risk of extremely intense rockbursts exists. Herein, a top pilot tunnel preconditioning method is proposed to minimize this risk, in which a drilling and blasting method is first recommended for the top pilot tunnel excavation and support, and then the TBM excavation of the main tunnel is conducted. In order to evaluate the mechanical effectiveness of this method, numerical simulation analyses using the failure approaching index, energy release rate, and excess shear stress indices are carried out. Its construction feasibility is discussed as well. Moreover, a microseismic monitoring technique is used in the experimental tunnel section for the real-time monitoring of the microseismic activities of the rock mass in TBM excavation and for assessing the effect of the top pilot tunnel excavation in reducing the risk of rockbursts. This method is applied to two tunnel sections prone to extremely intense rockbursts and leads to a reduction in the risk of rockbursts in TBM excavation.

  15. Captopril Pretreatment Produces an Additive Cardioprotection to Isoflurane Preconditioning in Attenuating Myocardial Ischemia Reperfusion Injury in Rabbits and in Humans

    PubMed Central

    Tian, Yi; Li, Haobo; Liu, Peiyu; Xu, Jun-mei; Irwin, Michael G.; Xia, Zhengyuan; Tian, Guogang

    2015-01-01

    Background. Pretreatment with the angiotensin-converting inhibitor captopril or volatile anesthetic isoflurane has, respectively, been shown to attenuate myocardial ischemia reperfusion (MI/R) injury in rodents and in patients. It is unknown whether or not captopril pretreatment and isoflurane preconditioning (Iso) may additively or synergistically attenuate MI/R injury. Methods and Results. Patients selected for heart valve replacement surgery were randomly assigned to five groups: untreated control (Control), captopril pretreatment for 3 days (Cap3d), or single dose captopril (Cap1hr, 1 hour) before surgery with or without Iso (Cap3d+Iso and Cap1hr+Iso). Rabbit MI/R model was induced by occluding coronary artery for 30?min followed by 2-hour reperfusion. Rabbits were randomized to receive sham operation (Sham), MI/R (I/R), captopril (Cap, 24 hours before MI/R), Iso, or the combination of captopril and Iso (Iso+Cap). In patients, Cap3d+Iso but not Cap1hr+Iso additively reduced postischemic myocardial injury and attenuated postischemic myocardial inflammation. In rabbits, Cap or Iso significantly reduced postischemic myocardial infarction. Iso+Cap additively reduced cellular injury that was associated with improved postischemic myocardial functional recovery and reduced myocardial apoptosis and attenuated oxidative stress. Conclusion. A joint use of 3-day captopril treatment and isoflurane preconditioning additively attenuated MI/R by reducing oxidative stress and inflammation. PMID:26273143

  16. Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of BK channels

    PubMed Central

    Zuidema, Mozow Y.; Yang, Yan; Wang, Meifang; Kalogeris, Theodore; Liu, Yajun; Meininger, Cynthia J.; Hill, Michael A.; Davis, Michael J.

    2010-01-01

    The objectives of this study were to determine the role of calcium-activated, small (SK), intermediate (IK), and large (BK) conductance potassium channels in initiating the development of an anti-inflammatory phenotype elicited by preconditioning with an exogenous hydrogen sulfide (H2S) donor, sodium hydrosulfide (NaHS). Intravital microscopy was used to visualize rolling and firmly adherent leukocytes in vessels of the small intestine of mice preconditioned with NaHS (in the absence and presence of SK, IK, and BK channel inhibitors, apamin, TRAM-34, and paxilline, respectively) or SK/IK (NS-309) or BK channel activators (NS-1619) 24 h before ischemia-reperfusion (I/R). I/R induced marked increases in leukocyte rolling and adhesion, effects that were largely abolished by preconditioning with NaHS, NS-309, or NS-1619. The postischemic anti-inflammatory effects of NaHS-induced preconditioning were mitigated by BKB channel inhibitor treatment coincident with NaHS, but not by apamin or TRAM-34, 24 h before I/R. Confocal imaging and immunohistochemistry were used to demonstrate the presence of BK? subunit staining in both endothelial and vascular smooth muscle cells of isolated, pressurized mesenteric venules. Using patch-clamp techniques, we found that BK channels in cultured endothelial cells were activated after exposure to NaHS. Bath application of the same concentration of NaHS used in preconditioning protocols led to a rapid increase in a whole cell K+ current; specifically, the component of K+ current blocked by the selective BK channel antagonist iberiotoxin. The activation of BK current by NaHS could also be demonstrated in single channel recording mode where it was independent of a change in intracellular Ca+ concentration. Our data are consistent with the concept that H2S induces the development of an anti-adhesive state in I/R in part mediated by a BK channel-dependent mechanism. PMID:20833953

  17. Pharmacologic modulation of experimental postischemic hepatic function.

    PubMed Central

    Ontell, S J; Makowka, L; Trager, J; Mazzaferro, V; Ove, P; Starzl, T E

    1989-01-01

    The present study evaluated and compared the effects of SRI 63-441, a potent platelet activating factor antagonist, superoxide dismutase (SOD), an oxygen free radical scavenger, and ibuprofen, a cyclooxygenase inhibitor on hepatic function after 90 minutes of warm ischemia. After warm ischemia, livers were harvested and underwent 90 minutes of warm, oxygenated, sanguinous perfusion on an isolated liver perfusion apparatus. Pretreatment of donor animals with 20 mg/kg intravenous (I.V.) SRI 63-441 5 minutes before induction of total hepatic ischemia resulted in significantly increased bile production, a significant decrease in transaminase release, and a higher tissue adenosine triphosphate (ATP) content when compared with ischemic nontreated controls. SOD resulted in improved bile production and decreased transaminase liberation only when present in the perfusate at the time of in vitro reperfusion. Ibuprofen did not improve postischemic hepatic function in this model. Electron microscopy revealed patchy hepatocellular vacuolization with an intact sinusoidal endothelium in all ischemic livers. However, the degree of damage was less severe in the livers from those rats pretreated with 20 mg/kg SRI 63-441. This study demonstrates that SRI 63-441 pretreatment significantly reduces hepatic warm ischemic injury, and in the present model, appears superior to two other agents that have been advanced in the treatment of ischemic injury. The use of such agents singly or in combinations have important implications as regards gaining a better understanding of the basic mechanisms in organ ischemia, and moreover, for therapeutic applications in organ ischemia and preservation. Images Fig. 3. Figs. 6A-C. Figs. 6A-C. Fig. 7. Figs. 8A-C. Figs. 8A-C. PMID:2916864

  18. Sustained postischemic cardiodepression following magnesium-diltiazem cardioplegia

    SciTech Connect

    Wallis, D.E.; Gierke, L.W.; Scanlon, P.J.; Wolfson, P.M.; Kopp, S.J.

    1986-07-01

    Magnesium-diltiazem cardioplegia was evaluated in the intact, perfused rat heart to determine whether the joint administration of these agents would adversely affect myocardial contractile and high-energy phosphate recovery following intermittent, normothermic global ischemic arrest. Sequential metabolic and functional analyses were performed on isolated perfused rat hearts during each phase of the experimental protocol: control, normoxic cardioplegia, intermittent global ischemic arrest, and normoxic postischemic control reperfusion. Four different cardioplegic solutions were evaluated: 30 mM KCl, 30 mM KCl with 2 mg diltiazem/liter, 20 mM MgCl/sub 2/, and 20 mM MgCl/sub 2/ with 2 mg diltiazem/liter. Myocardial phosphatic metabolite levels and intracellular pH were analyzed nondestructively in the intact hearts by phosphorus-31 NMR spectroscopy. Corresponding measurements of peak left intraventricular pressure, rate of peak pressure development (dP/dt), and contraction frequency were performed at the midpoint during each 5-min interval of /sup 31/P NMR signal averaging. Magnesium plus diltiazem-treated hearts were distinguished from all other groups by a marked delay in postischemic functional recovery consisting of a prolonged depression in contractility (34% of control, P < 0.01) that persisted throughout the first 50 min of postischemic reperfusion. The apparent adverse interactive effects of excess magnesium and diltiazem suggest that elective ischemic arrest with magnesium cardioplegia in combination with diltiazem may be contraindicated clinically.

  19. Enhanced Postischemic Functional Recovery in CYP2J2 Transgenic Hearts Involves Mitochondrial ATP-Sensitive K

    E-print Network

    Hammock, Bruce D.

    Enhanced Postischemic Functional Recovery in CYP2J2 Transgenic Hearts Involves Mitochondrial ATP the improved postischemic LVDP recovery in CYP2J2 Tr hearts. Perfusion with the ATP-sensitive K channel (KATP

  20. Novel cardioprotective strategy combining three different preconditioning methods to prevent ischemia/reperfusion injury in aged hearts in an improved rabbit model

    PubMed Central

    YE, JIAN-XI; CHEN, DAO-ZHONG

    2015-01-01

    The use of ischemic preconditioning (IPC) to protect the myocardium is usually not effective in elderly patients. The aim of the present study was to design new methods to achieve enhanced myocardial protection, based on the differential role of endogenous adenosine (ADO) and ADO receptors (ARs) in the effects of IPC on young and old animals. An improved New Zealand white rabbit model of ischemia/reperfusion was established based on the Langendorff model. Adult or elderly rabbit hearts, with or without exposure to IPC, were used in order to assess the roles of ADO and ARs in the different effects of IPC. Different protective methods were designed based on a combination of endogenous and exogenous interventions. Cardiac function, as well as biochemical, histopathological and apoptotic indices, were measured in the different intervention groups. The improved Langendorff model was stable, reliable and suitable for the undertaking of the experiments. The ADO levels in the aged rabbit hearts pre- and post-IPC were lower than those in the adult hearts, indicating that ADO levels may be an endogenous factor influencing IPC. A new protection strategy combining ADO-enhanced IPC, A1AR agonist 2-chloro-N(6)-cyclopentyladenosine preconditioning and cold crystalloid cardioplegia had a significant protective effect in aged hearts. The results of the present study suggested that endogenous ADO enhancement, A1AR agonist preconditioning and exogenous treatment yield an additive effect in aged rabbit hearts. The simultaneous application of these three types of intervention provided the most effective myocardial protection in the improved aged rabbit heart model. PMID:26622489

  1. Noopept reduces the postischemic functional and metabolic disorders in the brain of rats with different sensitivity to hypoxia.

    PubMed

    Zarubina, I V; Shabanov, P D

    2009-03-01

    Chronic cerebral ischemia was induced by ligation of both common carotid arteries in Wistar rats, divided by sensitivity to hypoxia into highly sensitive and low-sensitive. Noopept (peptide preparation), injected (0.5 mg/kg) during 7 days after occlusion of the carotid arteries, reduced the neurological disorders in rats with high and low sensitivity to hypoxia and improved their survival during the postischemic period. Noopept normalized behavior disordered by cerebral ischemia (according to the open field and elevated plus maze tests), prevented accumulation of LPO products and inhibition of antioxidant systems in the brain of rats with high and low sensitivity to hypoxia. Hence, noopept exhibited a neuroprotective effect in cerebral ischemia. PMID:19529857

  2. Early postischemic /sup 45/Ca accumulation in rat dentate hilus

    SciTech Connect

    Benveniste, H.; Diemer, N.H.

    1988-10-01

    Several studies have found postischemic regional accumulation of calcium to be time-dependent and coincident with the progression of ischemic cell change. In the most vulnerable cells in the hippocampus one would therefore expect to find a primary and specific early uptake of calcium after ischemia. Autoradiograms of /sup 45/Ca and /sup 3/H-inulin distribution were investigated before and 1 h after 20 min ischemia in the rat hippocampus. Two different methodological approaches were used for administration of /sup 45/Ca: (a) administration via microdialysis probes, (b) intraventricular injection. During control conditions the /sup 45/Ca autoradiograms showed variations in distribution volume in accordance with /sup 3/H-inulin determination of extracellular space size. One hour after ischemia a massive accumulation of /sup 45/Ca was found in the dentate hilus. No change in the distribution pattern of /sup 3/H-inulin could be demonstrated 1 h after ischemia. We suggest that /sup 45/Ca accumulation in dentate hilus 1 h after ischemia is a result of increased Ca/sup 2 +/ uptake before irreversible cell damage occurs and is not due to passive influx of calcium across a leaky plasma membrane.

  3. Protective effects of remote ischemic preconditioning in isolated rat hearts

    PubMed Central

    Teng, Xiao; Yuan, Xin; Tang, Yue; Shi, Jingqian

    2015-01-01

    To use Langendorff model to investigate whether remote ischemic preconditioning (RIPC) attenuates post-ischemic mechanical dysfunction on isolated rat heart and to explore possible mechanisms. SD rats were randomly divided into RIPC group, RIPC + norepinephrine (NE) depletion group, RIPC + pertussis toxin (PTX) pretreatment group, ischemia/reperfusion group without treatment (ischemia group) and time control (TC) group. RIPC was achieved through interrupted occlusion of anterior mesenteric artery. Then, Langendorff model was established using routine methods. Heart function was tested; immunohistochemistry and ELISA methods were used to detect various indices related to myocardial injury. Compared with ischemia group in which the hemodynamic parameters deteriorated significantly, heart function recovered to a certain degree among the RIPC, RIPC + NE depletion, and RIPC + PTX groups (P<0.05). More apoptotic nuclei were observed in ischemia group than in the other three groups (P<0.05); more apoptotic nuclei were detected in NE depletion and PTX groups than in RIPC group (P<0.05). While, there was no significant difference between NE depletion and PTX groups. In conclusion, RIPC protection on I/R myocardium extends to the period after hearts are isolated. NE and PTX-sensitive inhibitory G protein might have a role in the protection process. PMID:26550168

  4. Post-ischemic intra-arterial infusion of liposome-encapsulated hemoglobin can reduce ischemia reperfusion injury.

    PubMed

    Shimbo, Daisuke; Abumiya, Takeo; Shichinohe, Hideo; Nakayama, Naoki; Kazumata, Ken; Houkin, Kiyohiro

    2014-03-20

    Despite successful revascularization, reperfusion after prolonged ischemia causes ischemia reperfusion (I/R) injury. Recruitment and activation of neutrophils is thought to be a key event causing I/R injury. We examined whether post-ischemic intra-arterial infusion of liposome-encapsulated hemoglobin (LEH), an artificial oxygen carrier without neutrophils, could reduce I/R injury in a rat transient middle cerebral artery occlusion (MCAO) model. Male Sprague-Dawley rats were subjected to 2-h MCAO and then were divided into three groups: (1) LEH group (n=7) infused with LEH (Hb concentration of 6g/dl, 10ml/kg/h) through the recanalized internal carotid artery for 2h, (2) vehicle group (n=8) infused with saline (10ml/kg/h) in the same manner as the LEH group, and (3) control group (n=9) subjected to recanalization only. After 24-h reperfusion, all rats were tested for neurological score and then sacrificed to examine infarct and edema volumes, myeloperoxidase (MPO) expression, matrix metalloproteinase-9 (MMP-9) expression and activity, and reactive oxygen species (ROS) production. Compared with the control group and the vehicle group, the LEH group showed a significantly better neurological score and significantly smaller infarct and edema volumes. MPO expression, MMP-9 expression and activity, and ROS production in the LEH group were also significantly lower than those in the control and vehicle groups. The results in the present study suggest that post-ischemic intra-arterial infusion of LEH can reduce I/R injury through reducing the effect of MMP-9, most likely produced by neutrophils. This therapeutic strategy may be a promising candidate to prevent I/R injury after thrombolysis and/or thromboectomy. PMID:24486612

  5. Arterial spin labeling and dynamic susceptibility contrast CBF MRI in postischemic hyperperfusion,

    E-print Network

    Duong, Timothy Q.

    Arterial spin labeling and dynamic susceptibility contrast CBF MRI in postischemic hyperperfusion Texas Veterans Health Care System, San Antonio, Texas, USA Arterial spin labeling (ASL) and dynamic.76±0.14 seconds in normal pixels to 1.93±0.17 seconds in hyperperfusion pixels. Arterial transit time decreased

  6. Localization of Proliferating Cell Nuclear Antigen, Vimentin, c-Fos, and Clusterin in the Postischemic Kidney

    E-print Network

    Witzgall, Ralph - Naturwissenschaftliche Fakultät III

    in the Postischemic Kidney Evidence for a Heterogenous Genetic Response among Nephron Segments, and a Large Pool 02139 Abstract The mechanisms leading to the recovery of the kidney after ischemic acute renal failure - ischemia - kidney - tissue repair Introduction The pathophysiological processes responsible for cell death

  7. Orderings for conjugate gradient preconditionings

    NASA Technical Reports Server (NTRS)

    Ortega, James M.

    1991-01-01

    The effect of orderings on the rate of convergence of the conjugate gradient method with SSOR or incomplete Cholesky preconditioning is examined. Some results also are presented that help to explain why red/black ordering gives an inferior rate of convergence.

  8. Liver ischemia preconditions the heart against ischemia-reperfusion arrhythmias

    PubMed Central

    Noorbakhsh, Mohammad-Foad; Arab, Hossein-Ali; Kazerani, Hamid-Reza

    2015-01-01

    Objective(s): This study aimed to examine the hypothesis that an antiarrhythmic effect might be obtained by ischemic preconditioning of the liver, and also to characterize the potential underlying mechanisms. Materials and Methods: Male Wistar rats were anesthetized by thiopental sodium (50 mg/kg, IP) followed by IV injection of heparin (250 IU). Remote ischemic preconditioning (RIPC) was induced by 3 cycles of 5 min liver ischemia followed by 5 min of reperfusion. The hearts were excised within 5 min after the final cycle of preconditioning and perfused using Langendorff’s system. The isolated perfused hearts were subjected to 30 min global ischemia followed by 90 min reperfusion. The myocardial arrhythmias induced by ischemia- reperfusion (I/R) were determined in accordance with the guidelines of Lambeth Conventions. The potential role of KATP channels on RIPC was assessed by injection of glibenclamide (nonselective KATP blocker) or 5-hydroxydecanoate (mitochondrial KATP blocker) on rats 30 and 15 min before induction of RIPC in the liver, respectively. Results: Hepatic remote preconditioning of the heart significantly (P<0.0001) prevented the incidence of myocardial arrhythmias induced by I/R in the perfused hearts (5.33±1.54 vs. 32.33±6.44,). However, the protective effects of remote preconditioning was significantly (P<0.01) abolished by the KATP blocker, glibenclamide (25.5±4.9 vs. 5.33±1.54,). Conclusion: Hepatic RIPC may prevent the arrhythmias induced by I/R in the isolated perfused hearts via KATP channels. PMID:25810880

  9. IQGAP1 Is Involved in Post-Ischemic Neovascularization by Regulating Angiogenesis and Macrophage Infiltration

    PubMed Central

    Urao, Norifumi; Razvi, Masooma; Oshikawa, Jin; McKinney, Ronald D.; Chavda, Rupal; Bahou, Wadie F.; Fukai, Tohru; Ushio-Fukai, Masuko

    2010-01-01

    Background Neovascularization is an important repair mechanism in response to ischemic injury and is dependent on inflammation, angiogenesis and reactive oxygen species (ROS). IQGAP1, an actin-binding scaffold protein, is a key regulator for actin cytoskeleton and motility. We previously demonstrated that IQGAP1 mediates vascular endothelial growth factor (VEGF)-induced ROS production and migration of cultured endothelial cells (ECs); however, its role in post-ischemic neovascularization is unknown. Methodology/Principal Findings Ischemia was induced by left femoral artery ligation, which resulted in increased IQGAP1 expression in Mac3+ macrophages and CD31+ capillary-like ECs in ischemic legs. Mice lacking IQGAP1 exhibited a significant reduction in the post-ischemic neovascularization as evaluated by laser Doppler blood flow, capillary density and ?-actin positive arterioles. Furthermore, IQGAP1?/? mice showed a decrease in macrophage infiltration and ROS production in ischemic muscles, leading to impaired muscle regeneration and increased necrosis and fibrosis. The numbers of bone marrow (BM)-derived cells in the peripheral blood were not affected in these knockout mice. BM transplantation revealed that IQGAP1 expressed in both BM-derived cells and tissue resident cells, such as ECs, is required for post-ischemic neovascularization. Moreover, thioglycollate-induced peritoneal macrophage recruitment and ROS production were inhibited in IQGAP1?/? mice. In vitro, IQGAP1?/? BM-derived macrophages showed inhibition of migration and adhesion capacity, which may explain the defective macrophage recruitment into the ischemic tissue in IQGAP1?/? mice. Conclusions/Significance IQGAP1 plays a key role in post-ischemic neovascularization by regulating, not only, ECs-mediated angiogenesis but also macrophage infiltration as well as ROS production. Thus, IQGAP1 is a potential therapeutic target for inflammation- and angiogenesis-dependent ischemic cardiovascular diseases. PMID:20976168

  10. Myocardial stunning, hibernation, and ischemic preconditioning.

    PubMed

    Vroom, M B; van Wezel, H B

    1996-10-01

    From the present review, it may be concluded that myocardial ischemia results in far more complicated syndromes than previously realized. Although not all aspects of the issues discussed in this review are currently a clinical reality in the daily practice of cardiovascular anesthesiologists, the understanding and application of these concepts are growing rapidly. Indications for revascularization procedures will be adjusted in patients with evidence of hibernating myocardium. In the future, postoperative myocardial dysfunction may be diminished by the prevention of myocardial stunning, for instance by altering the composition of the cardioplegic solution and other interventions. Finally, additional advances may involve reduction of the extent of perioperative myocardial infarctions by application of ischemic preconditioning. PMID:8910163

  11. Molecular mechanisms of ischemic preconditioning in the kidney.

    PubMed

    Kapitsinou, Pinelopi P; Haase, Volker H

    2015-11-15

    More effective therapeutic strategies for the prevention and treatment of acute kidney injury (AKI) are needed to improve the high morbidity and mortality associated with this frequently encountered clinical condition. Ischemic and/or hypoxic preconditioning attenuates susceptibility to ischemic injury, which results from both oxygen and nutrient deprivation and accounts for most cases of AKI. While multiple signaling pathways have been implicated in renoprotection, this review will focus on oxygen-regulated cellular and molecular responses that enhance the kidney's tolerance to ischemia and promote renal repair. Central mediators of cellular adaptation to hypoxia are hypoxia-inducible factors (HIFs). HIFs play a crucial role in ischemic/hypoxic preconditioning through the reprogramming of cellular energy metabolism, and by coordinating adenosine and nitric oxide signaling with antiapoptotic, oxidative stress, and immune responses. The therapeutic potential of HIF activation for the treatment and prevention of ischemic injuries will be critically examined in this review. PMID:26311114

  12. Effect of Hypoxic Preconditioning on Stress Reaction in Rats.

    PubMed

    Naryzhnaya, N V; Maslov, L N; Vychuzhanova, E A; Sementsov, A S; Podoksyonov, Yu K; Portnichenko, A G; Lishmanov, Yu B

    2015-08-01

    In rats, immobilization stress (24 h) induced involution of the thymus and spleen, adrenal hypertrophy, and pronounced elevation (by 67%) of serum cortisol in comparison with intact animals; the mean number of stomach ulcers in rats subjected to stress was 6.9. Hypoxic preconditioning consisting of 6 sessions of 10-min hypoxia (8% O2) followed by 10-min reoxygenation with atmospheric air induced adrenal hypertrophy and spleen involution, but did not change blood cortisol level; no stomach ulcers were found in preconditioned rats. In rats subjected to both hypoxic preconditioning and immobilization, the weights of the thymus, adrenal glands, and spleen, as well as cortisol level did not differ from the corresponding parameters in rats subjected to immobilization stress alone. The number of stomach ulcers in experimental rats was 1.5-fold lower than in the stress-control ones. Thus, hypoxic preconditioning exerts a pronounced preventive anti-ulcer effect during immobilization, but it does not affect other indices of the stress reaction. PMID:26385407

  13. Remote Ischemic Preconditioning for Kidney Protection: GSK3?-Centric Insights Into the Mechanism of Action.

    PubMed

    Liu, Zhangsuo; Gong, Rujun

    2015-11-01

    Preventing acute kidney injury (AKI) in high-risk patients following medical interventions is a paramount challenge for clinical practice. Recent data from animal experiments and clinical trials indicate that remote ischemic preconditioning, represented by limb ischemic preconditioning, confers a protective action on the kidney. Ischemic preconditioning is effective in reducing the risk for AKI following cardiovascular interventions and the use of iodinated radiocontrast media. Nevertheless, the underlying mechanisms for this protective effect are elusive. A protective signal is conveyed from the remote site undergoing ischemic preconditioning, such as the limb, to target organs, such as the kidney, by multiple potential communication pathways, which may involve humoral, neuronal, and systemic mechanisms. Diverse transmitting pathways trigger a variety of signaling cascades, including the reperfusion injury salvage kinase and survivor activating factor enhancement pathways, all of which converge on glycogen synthase kinase 3? (GSK3?). Inhibition of GSK3? subsequent to ischemic preconditioning reinforces the Nrf2-mediated antioxidant defense, diminishes the nuclear factor-?B-dependent proinflammatory response, and exerts prosurvival effects ensuing from the desensitized mitochondria permeability transition. Thus, therapeutic targeting of GSK3? by ischemic preconditioning or by pharmacologic preconditioning with existing US Food and Drug Administration-approved drugs having GSK3?-inhibitory activities might represent a pragmatic and cost-effective adjuvant strategy for kidney protection and prophylaxis against AKI. PMID:26271146

  14. Exercise and Cardiac Preconditioning Against Ischemia Reperfusion Injury

    PubMed Central

    Quindry, John C; Hamilton, Karyn L

    2013-01-01

    Cardiovascular disease (CVD), including ischemia reperfusion (IR) injury, remains a major cause of morbidity and mortality in industrialized nations. Ongoing research is aimed at uncovering therapeutic interventions against IR injury. Regular exercise participation is recognized as an important lifestyle intervention in the prevention and treatment of CVD and IR injury. More recent understanding reveals that moderate intensity aerobic exercise is also an important experimental model for understanding the cellular mechanisms of cardioprotection against IR injury. An important discovery in this regard was the observation that one-to-several days of exercise will attenuate IR injury. This phenomenon has been observed in young and old hearts of both sexes. Due to the short time course of exercise induced protection, IR injury prevention must be mediated by acute biochemical alterations within the myocardium. Research over the last decade reveals that redundant mechanisms account for exercise induced cardioprotection against IR. While much is now known about exercise preconditioning against IR injury, many questions remain. Perhaps most pressing, is what mechanisms mediate cardioprotection in aged hearts and what sex-dependent differences exist. Given that that exercise preconditioning is a polygenic effect, it is likely that multiple mediators of exercise induced cardioprotection have yet to be uncovered. Also unknown, is whether post translational modifications due to exercise are responsible for IR injury prevention. This review will provide an overview the major mechanisms of IR injury and exercise preconditioning. The discussion highlights many promising avenues for further research and describes how exercise preconditioning may continue to be an important scientific paradigm in the translation of cardioprotection research to the clinic. PMID:23909636

  15. Preconditioning Provides Neuroprotection in Models of CNS Disease: Paradigms and Clinical Significance

    PubMed Central

    Stetler, R. Anne; Leak, Rehana K.; Gan, Yu; Li, Peiying; Hu, Xiaoming; Jing, Zheng; Chen, Jun; Zigmond, Michael J.; Gao, Yanqin

    2014-01-01

    Preconditioning is a phenomenon in which brief episodes of a sublethal insult induce robust protection against subsequent lethal injuries. Preconditioning has been observed in multiple organisms and can occur in the brain as well as other tissues. Extensive animal studies suggest that the brain can be preconditioned to resist acute injuries, such as ischemic stroke, neonatal hypoxia/ischemia, trauma, and agents that are used in models of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Effective preconditioning stimuli are numerous and diverse, ranging from transient ischemia, hypoxia, hyperbaric oxygen, hypothermia and hyperthermia, to exposure to neurotoxins and pharmacological agents. The phenomenon of “cross-tolerance,” in which a sublethal stress protects against a different type of injury, suggests that different preconditioning stimuli may confer protection against a wide range of injuries. Research conducted over the past few decades indicates that brain preconditioning is complex, involving multiple effectors such as metabolic inhibition, activation of extra- and intracellular defense mechanisms, a shift in the neuronal excitatory/inhibitory balance, and reduction in inflammatory sequelae. An improved understanding of brain preconditioning should help us identify innovative therapeutic strategies that prevent or at least reduce neuronal damage in susceptible patients. In this review, we focus on the experimental evidence of preconditioning in the brain and systematically survey the models used to develop paradigms for neuroprotection, and then discuss the clinical potential of brain preconditioning. In a subsequent components of this two-part series, we will discuss the cellular and molecular events that are likely to underlie these phenomena. PMID:24389580

  16. Management of Preconditioned Calves and Impacts of Preconditioning.

    PubMed

    Hilton, W Mark

    2015-07-01

    When studying the practice of preconditioning (PC) calves, many factors need to be examined to determine if cow-calf producers should make this investment. Factors such as average daily gain, feed efficiency, available labor, length of the PC period, genetics, and marketing options must be analyzed. The health sales price advantage is an additional benefit in producing and selling PC calves but not the sole determinant of PC's financially feasibility. Studies show that a substantial advantage of PC is the selling of additional pounds at a cost of gain well below the marginal return of producing those additional pounds. PMID:26139187

  17. Combination treatment with ethyl pyruvate and aspirin enhances neuroprotection in the postischemic brain.

    PubMed

    Kim, Seung-Woo; Jeong, Ji-Young; Kim, Hyun Ji; Seo, Ji-Seon; Han, Pyung-Lim; Yoon, Sung-Hwa; Lee, Ja-Kyeong

    2010-01-01

    Ethyl pyruvate (EP), a simple aliphatic ester of pyruvic acid, has been shown to act as an anti-inflammatory molecule in various pathological conditions, which include sepsis or hemorrhagic shock. Recently, we showed that ethyl pyruvate has a neuroprotective effect in the postischemic brain and also in KA-induced pathogenesis in the brain. In this study, we examined whether aspirin augments neuroprotective effect of ethyl pyruvate in transient focal ischemia model by complementing the neuroprotective effects of ethyl pyruvate. Although, most of neuroprotective effect of aspirin has been attributed to the anti-platelet action, aspirin also has direct neuroprotective effects, including NF-kappaB inhibition. Ethyl pyruvate dose-dependently suppressed infarct formation in the postischemic brain, wherein intravenous administration of 5 mg/kg ethyl pyruvate 30 min after the occlusion reduced infarct volume to 34.5 +/- 15.5% (n = 6, P < 0.01) of that of the untreated control. In combination with aspirin (5 mg/kg, i.v.), the neuroprotective effect was enhanced, resulting in 16.0 +/- 5.9% (n = 6, P < 0.01) infarct volume. The time window for synergistic neuroprotection by ethyl pyruvate and aspirin extended to 9 h post-MCAO. The synergistic reduction in infarct volume was accompanied by suppression of the clinical manifestations associated with cerebral ischemia including motor impairment and neurological deficits. Inflammatory processes including microglial activation and proinflammatory cytokine expression were notably suppressed by the combination treatment in the postischemic brain and in primary microglia cultures, wherein ethyl pyruvate and aspirin modulate NF-kappaB signaling differentially. Aspirin interferes with IkappaB phosphorylation and degradation in the cytoplasm, possibly by specifically inhibiting IkappaB kinase-beta, whereas, the effect of ethyl pyruvate seems to occur in the nucleus, where it may interfere with the binding of NF-kappaB to responsive promoter elements in the target genes. Similar enhancement in neuroprotective effect was also observed in primary cortical cultures after NMDA or Zn(2+) treatment or oxygen-glucose deprivation. Together, these results indicate that combination treatment of ethyl pyruvate and aspirin affords synergistic neuroprotection in the postischemic brain with a wide therapeutic window, in part via differential modulation of the NF-kappaB signaling pathway. PMID:19636661

  18. Direct Evidence that Myocardial Insulin Resistance following Myocardial Ischemia Contributes to Post-Ischemic Heart Failure

    PubMed Central

    Fu, Feng; Zhao, Kun; Li, Jia; Xu, Jie; Zhang, Yuan; Liu, Chengfeng; Yang, Weidong; Gao, Chao; Li, Jun; Zhang, Haifeng; Li, Yan; Cui, Qin; Wang, Haichang; Tao, Ling; Wang, Jing; Quon, Michael J; Gao, Feng

    2015-01-01

    A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its association with HF are inadequately investigated. This study aims to determine the role of myocardial insulin resistance in ischemic HF and its underlying mechanisms. Male Sprague-Dawley rats subjected to myocardial infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk post-MI. Of note, myocardial insulin sensitivity was decreased as early as 1 wk after MI, which was accompanied by increased production of myocardial TNF-?. Overexpression of TNF-? in heart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI. Treatment of rats with a specific TNF-? inhibitor improved myocardial insulin signaling post-MI. Insulin treatment given immediately following MI suppressed myocardial TNF-? production and improved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling. Moreover, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with controls. In conclusion, MI induces myocardial insulin resistance (without systemic insulin resistance) mediated partly by ischemia-induced myocardial TNF-? overproduction and promotes the development of HF. Our findings underscore the direct and essential role of myocardial insulin signaling in protection against post-ischemic HF. PMID:26659007

  19. Stress-induced fever after postischemic rectal temperature measurements in the gerbil.

    PubMed

    Clark, Darren L; DeBow, Suzanne B; Iseke, Melanie D; Colbourne, Frederick

    2003-09-01

    Postischemic temperature, which modulates brain injury, is commonly determined via a rectal temperature (Trec) probe. This procedure causes a stress-induced fever (SIF) in rodents that may aggravate injury or diminish the efficacy of a neuroprotectant. We continually measured core temperature (Tcore) via an implanted telemetry probe and made 16 Trec measurements over 4 days in sham and ischemic gerbils (5 min bilateral carotid artery occlusion). Controls did not have Trec sampled, but Tcore was measured. Rectal temperature measurements predicted Tcore in sham and ischemic gerbils. The Trec measurements caused a SIF (1 degrees C peak) in shams that did not habituate, whereas the SIF was initially absent and then increased over days in ischemic gerbils. Ischemic groups had similar CA1 injury (approximately 32% remaining), presumably because Trec measurements only resulted in a significant SIF starting on day 2 postischemia, when cell death is less sensitive to hyperthermia. Caution is warranted with Trec measurements, since the resultant SIF occurs to different extents in normal and ischemic rodents. Furthermore, the SIF could vary according to many other factors, such as the type and severity of insult, the time and frequency of measurement, and drug treatment. Accordingly, postischemic Trec measurements should be replaced with telemetry probes. PMID:14614524

  20. Prevention

    Cancer.gov

    NCI’s prevention research has a broad focus, from identifying environmental and lifestyle factors that influence cancer risk to studying the biology of how cancer develops and studying ways to disseminate prevention interventions.

  1. Preconditioning in H(div) and Applications

    E-print Network

    the eigenvalues of Jh by (Jh), since the spectral condition number (Jh) := max |(Jh)| min |(Jh)| of the operator Jh is O(h-2 ), we will clearly need to precondition any standard iterative scheme if we want

  2. 40 CFR 1065.518 - Engine preconditioning.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...Specified Duty Cycles § 1065.518 Engine preconditioning. (a) This section applies for engines where measured emissions are affected by prior operation, such as with a diesel engine that relies on urea-based...

  3. Adverse effects of free fatty acid associated with increased oxidative stress in postischemic isolated rat hearts.

    PubMed

    Gambert, Ségolène; Vergely, Catherine; Filomenko, Rodolphe; Moreau, Daniel; Bettaieb, Ali; Opie, Lionel H; Rochette, Luc

    2006-02-01

    The mechanisms of the adverse effects of free fatty acids on the ischemic-reperfused myocardium are not fully understood. Long-chain fatty acids, including palmitate, uncouple oxidative phosphorylation and should therefore promote the formation of oxygen-derived free radicals, with consequent adverse effects. Conversely, the antianginal agent trimetazidine (TMZ), known to inhibit cardiac fatty acid oxidation, could hypothetically lessen the formation of reactive oxygen species (ROS) and thus improve reperfusion mechanical function. Isolated perfused rat hearts underwent 30 min of total global ischemia followed by 30 min of reperfusion. Hearts were perfused with glucose 5.5 mmol/l or palmitate 1.5 mmol/l with or without TMZ (100 micromol/l). Ascorbyl free radical (AFR) release during perfusion periods was measured by electron spin resonance as a marker of oxidative stress. Post-ischemic recovery in the palmitate group of heart was lower than in the glucose group with a marked rise in diastolic tension and reduction in left ventricular developed pressure (Glucose: 85 +/- 11 mmHg; Palmitate: 10 +/- 6 mmHg; p < 0.001). TMZ decreased diastolic tension in both glucose- and in palmitate-perfused hearts. Release of AFR within the first minute of reperfusion was greater in palmitate-perfused hearts and in hearts perfused with either substrate, this marker of oxidative stress was decreased by TMZ (expressed in arbitrary units/ml; respectively: 8.49 +/- 1.24 vs. 1.06 +/- 0.70 p < 0.05; 12.47 +/- 2.49 vs. 3.37 +/- 1.29 p < 0.05). Palmitate increased the formation of ROS and reperfusion contracture. TMZ, a potential inhibitor of palmitate-induced mitochondrial uncoupling, decreased the formation of free radicals and improved postischemic mechanical dysfunction. The novel conclusion is that adverse effects of fatty acids on ischemic-reperfusion injury may be mediated, at least in part, by oxygen-derived free radicals. PMID:16444597

  4. Depression of action potential characteristics and a decreased space constant are present in postischemic, reperfused myocardium.

    PubMed Central

    Levine, J H; Moore, E N; Weisman, H F; Kadish, A H; Becker, L C; Spear, J F

    1987-01-01

    Brief periods of ischemia and reperfusion may lead to arrhythmias and delayed epicardial activation. To determine the nature of the electrophysiologic substrate and to gain insight into potential mechanisms underlying the electrophysiologic and hemodynamic abnormalities that develop in this setting, standard microelectrode techniques were used to measure action potential characteristics, conduction velocity, and space constants in canine isolated epicardial preparations removed after a 15-min anterior descending artery occlusion and 20-min reflow period in vivo. Our results demonstrate a significant reduction in conduction velocity (0.78 +/- 0.38 vs. 0.31 +/- 0.12 m/s, P less than 0.001), space constant (1.05 +/- 0.42 vs. 0.45 +/- 0.12 mm, P = 0.004), resting membrane potential (81.3 +/- 2.5 vs. 61.7 +/- 7.8 mV, P less than 0.001), action potential amplitude (94.1 +/- 4.2 vs. 64.1 +/- 1.5 mV, P less than 0.001), and dV/dT (164.7 +/- 37.3 vs. 52.6 +/- 19.7 V/s, P less than 0.001) in postischemic reperfused myocardium. The space constant and dV/dT each correlated with conduction velocity; in addition, the space constant was an independent predictor of conduction velocity in these tissues. These electrophysiologic abnormalities may play a role in the arrhythmias and abnormalities of contraction present in postischemic, reperfused myocardium. Images PMID:3793920

  5. Prevention

    MedlinePLUS

    ... Symptoms Transmission Prevention Treatment 2003 U.S. Outbreak African Rodent Importation Ban For Clinicians Clinical Recognition Specimen Collection ... Veterinarians Transmission Examining Animals with Suspected Monkeypox African Rodent Importation ... Resources Related Links Poxvirus Molluscum Contagiosum ...

  6. Hypoxic preconditioning decreases nuclear factor ?B activity via Disrupted in Schizophrenia-1.

    PubMed

    Liu, Jia-Ren; Liu, Qian; Khoury, Joseph; Li, Yue-Jin; Han, Xiao-Hui; Li, Jing; Ibla, Juan C

    2016-01-01

    Nuclear factor ?B is a key mediator of inflammation during conditions of hypoxia. Here, we used models of hypoxic pre-conditioning as mechanism to decrease nuclear factor ?B activity induced by hypoxia. Our initial studies suggested that Disrupted in Schizophrenia-1 may be induced by hypoxic pre-conditioning and possibly involved in the regulation of nuclear factor ?B. In this study we used Disrupted in Schizophrenia-1 exogenous over-expression and knock-down to determine its effect on ataxia telangiectasia mutated - nuclear factor ?B activation cascade. Our results demonstrated that hypoxic pre-conditioning significantly increased the expression of Disrupted in Schizophrenia-1 at mRNA and protein levels both in vitro and in vivo. Over-expression of Disrupted in Schizophrenia-1 significantly attenuated the hypoxia-mediated ataxia telangiectasia mutated phosphorylation and prevented its cytoplasm translocation where it functions to activate nuclear factor ?B. We further determined that Disrupted in Schizophrenia-1 activated the protein phosphatase 2A, preventing the phosphorylation of ataxia telangiectasia mutated serine-1981, the main regulatory site of ataxia telangiectasia mutated activity. Cellular levels of Disrupted in Schizophrenia-1 protein significantly decreased nuclear factor ?B activation profiles and pro-inflammatory gene expression. Taken together, these results demonstrate that hypoxic pre-conditioning decreases the activation of nuclear factor ?B through the transcriptional induction of Disrupted in Schizophrenia-1. PMID:26615762

  7. Support graph preconditioning for elliptic finite element problems 

    E-print Network

    Wang, Meiqiu

    2009-05-15

    A relatively new preconditioning technique called support graph preconditioning has many merits over the traditional incomplete factorization based methods. A major limitation of this technique is that it is applicable to ...

  8. Postischemic cardiac recovery in heme oxygenase-1 transgenic ischemic/reperfused mouse myocardium

    PubMed Central

    Juhasz, Bela; Varga, Balazs; Czompa, Attila; Bak, Istvan; Lekli, Istvan; Gesztelyi, Rudolf; Zsuga, Judit; Kemeny-Beke, Adam; Antal, Miklos; Szendrei, Levente; Tosaki, Arpad

    2011-01-01

    Abstract Heme oxygenase-1 (HO-1) transgenic mice (Tg) were created using a rat HO-1 genomic transgene. Transgene expression was detected by RT-PCR and Western blots in the left ventricle (LV), right ventricle (RV) and septum (S) in mouse hearts, and its function was demonstrated by the elevated HO enzyme activity. Tg and non-transgenic (NTg) mouse hearts were isolated and subjected to ischemia/reperfusion. Significant post-ischemic recovery in coronary flow (CF), aortic flow (AF), aortic pressure (AOP) and first derivative of AOP (AOPdp/dt) were detected in the HO-1 Tg group compared to the NTg values. In HO-1 Tg hearts treated with 50 ?mol/kg of tin protoporphyrin IX (SnPPIX), an HO enzyme inhibitor, abolished the post-ischemic cardiac recovery. HO-1 related carbon monoxide (CO) production was detected in NTg, HO-1 Tg and HO-1 Tg + SnPPIX treated groups, and a substantial increase in CO production was observed in the HO-1 Tg hearts subjected to ischemia/reperfusion. Moreover, in ischemia/reperfusion-induced tissue Na+ and Ca2+ gains were reduced in HO-1 Tg group in comparison with the NTg and HO-1 Tg + SnPPIX treated groups; furthermore K+ loss was reduced in the HO-1 Tg group. The infarct size was markedly reduced from its NTg control value of 37 ± 4% to 20 ± 6% (P < 0.05) in the HO-1 Tg group, and was increased to 47 ± 5% (P < 0.05) in the HO-1 knockout (KO) hearts. Parallel to the infarct size reduction, the incidence of total and sustained ventricular fibrillation were also reduced from their NTg control values of 92% and 83% to 25% (P < 0.05) and 8% (P < 0.05) in the HO-1 Tg group, and were increased to 100% and 100% in HO-1 KO?/? hearts. Immunohistochemical staining of HO-1 was intensified in HO-1 Tg compared to the NTg myocardium. Thus, the HO-1 Tg mouse model suggests a valuable therapeutic approach in the treatment of ischemic myocardium. PMID:20716121

  9. Ischemic preconditioning enhances integrity of coronary endothelial tight junctions

    SciTech Connect

    Li, Zhao; Jin, Zhu-Qiu

    2012-08-31

    Highlights: Black-Right-Pointing-Pointer Cardiac tight junctions are present between coronary endothelial cells. Black-Right-Pointing-Pointer Ischemic preconditioning preserves the structural and functional integrity of tight junctions. Black-Right-Pointing-Pointer Myocardial edema is prevented in hearts subjected to ischemic preconditioning. Black-Right-Pointing-Pointer Ischemic preconditioning enhances translocation of ZO-2 from cytosol to cytoskeleton. -- Abstract: Ischemic preconditioning (IPC) is one of the most effective procedures known to protect hearts against ischemia/reperfusion (IR) injury. Tight junction (TJ) barriers occur between coronary endothelial cells. TJs provide barrier function to maintain the homeostasis of the inner environment of tissues. However, the effect of IPC on the structure and function of cardiac TJs remains unknown. We tested the hypothesis that myocardial IR injury ruptures the structure of TJs and impairs endothelial permeability whereas IPC preserves the structural and functional integrity of TJs in the blood-heart barrier. Langendorff hearts from C57BL/6J mice were prepared and perfused with Krebs-Henseleit buffer. Cardiac function, creatine kinase release, and myocardial edema were measured. Cardiac TJ function was evaluated by measuring Evans blue-conjugated albumin (EBA) content in the extravascular compartment of hearts. Expression and translocation of zonula occludens (ZO)-2 in IR and IPC hearts were detected with Western blot. A subset of hearts was processed for the observation of ultra-structure of cardiac TJs with transmission electron microscopy. There were clear TJs between coronary endothelial cells of mouse hearts. IR caused the collapse of TJs whereas IPC sustained the structure of TJs. IR increased extravascular EBA content in the heart and myocardial edema but decreased the expression of ZO-2 in the cytoskeleton. IPC maintained the structure of TJs. Cardiac EBA content and edema were reduced in IPC hearts. IPC enhanced the translocation of ZO-2 from cytosol to cytoskeleton. In conclusion, TJs occur in normal mouse heart. IPC preserves the integrity of TJ structure and function that are vulnerable to IR injury.

  10. Sound preconditioning therapy inhibits ototoxic hearing loss in mice.

    PubMed

    Roy, Soumen; Ryals, Matthew M; Van den Bruele, Astrid Botty; Fitzgerald, Tracy S; Cunningham, Lisa L

    2013-11-01

    Therapeutic drugs with ototoxic side effects cause significant hearing loss for thousands of patients annually. Two major classes of ototoxic drugs are cisplatin and the aminoglycoside antibiotics, both of which are toxic to mechanosensory hair cells, the receptor cells of the inner ear. A critical need exists for therapies that protect the inner ear without inhibiting the therapeutic efficacy of these drugs. The induction of heat shock proteins (HSPs) inhibits both aminoglycoside- and cisplatin-induced hair cell death and hearing loss. We hypothesized that exposure to sound that is titrated to stress the inner ear without causing permanent damage would induce HSPs in the cochlea and inhibit ototoxic drug–induced hearing loss. We developed a sound exposure protocol that induces HSPs without causing permanent hearing loss. We used this protocol in conjunction with a newly developed mouse model of cisplatin ototoxicity and found that preconditioning mouse inner ears with sound has a robust protective effect against cisplatin-induced hearing loss and hair cell death. Sound therapy also provided protection against aminoglycoside-induced hearing loss. These data indicate that sound preconditioning protects against both classes of ototoxic drugs, and they suggest that sound therapy holds promise for preventing hearing loss in patients receiving these drugs. PMID:24216513

  11. AIF depletion provides neuroprotection through a preconditioning effect.

    PubMed

    Öxler, Eva-Maria; Dolga, Amalia; Culmsee, C

    2012-10-01

    Previous studies established a major role for apoptosis inducing factor (AIF) in neuronal cell death after acute brain injury. For example, AIF translocation from mitochondria to the nucleus determined delayed neuronal death, whereas reduced AIF expression provided neuroprotective effects in models of cerebral ischemia or brain trauma. The question remains, however, why reduced AIF levels are sufficient to mediate neuroprotection, since only very little AIF translocation to the nucleus is required for induction of cell death. Thus, the present study addresses the question, whether AIF gene silencing affects intrinsic death pathways upstream of nuclear translocation at the level of the mitochondria. Using MTT assays and real-time cell impedance measurements we confirmed the protective effect of AIF siRNA against glutamate toxicity in immortalized mouse hippocampal HT-22 neurons. Further, AIF siRNA prevented glutamate-induced mitochondrial fragmentation and loss of mitochondrial membrane potential. The protection of mitochondrial integrity was associated with preserved ATP levels, attenuated increases in lipid peroxidation and reduced complex I expression levels. Notably, low concentrations of the complex I inhibitor rotenone (20 nM), provided similar protective effects against glutamate toxicity at the mitochondrial level. These results expose a preconditioning effect as a mechanism for neuroprotection mediated by AIF depletion. In particular, they point out an association between mitochondrial complex I and AIF, which regulate each other's stability in mitochondria. Overall, these findings postulate that AIF depletion mediates a preconditioning effect protecting neuronal cells from subsequent glutamate toxicity through reduced levels of complex I protein. PMID:22865232

  12. Backleak, tight junctions, and cell- cell adhesion in postischemic injury to the renal allograft.

    PubMed Central

    Kwon, O; Nelson, W J; Sibley, R; Huie, P; Scandling, J D; Dafoe, D; Alfrey, E; Myers, B D

    1998-01-01

    Postischemic injury in recipients of 3-7-d-old renal allografts was classified into sustained (n = 19) or recovering (n = 20) acute renal failure (ARF) according to the prevailing inulin clearance. Recipients of optimally functioning, long-standing allografts and living donors undergoing nephrectomy served as functional (n = 14) and structural controls (n = 10), respectively. Marked elevation above control of fractional clearance of dextrans of graded size was consistent with transtubular backleak of 57% of filtrate (inulin) in sustained ARF. No backleak was detected in recovering ARF. To explore a structural basis for backleak, allograft biopsies were taken intraoperatively, 1 h after reperfusion in all recipients, and again on day 7 after transplant in a subset (n = 10). Electron microscopy revealed disruption of both apical and basolateral membranes of proximal tubule cells in both sustained and recovering ARF, but cell exfoliation and tubule basement membrane denudation were negligible. Histochemical analysis of membrane-associated adhesion complexes confirmed an abnormality of proximal but not distal tubule cells, marked in sustained ARF but not in recovering ARF. Staining for the zonula occludens complex (ZO-1) and adherens complex (alpha, beta, and gamma catenins) revealed diminished intensity and redistribution of each cytoskeletal protein from the apico-lateral membrane boundary. We conclude that impaired integrity of tight junctions and cell-cell adhesion in the proximal tubule provides a paracellular pathway through which filtrate leaks back in sustained allograft ARF. PMID:9593761

  13. Temporal assessment of vascular reactivity and functionality using MRI during postischemic proangiogenenic vascular remodeling.

    PubMed

    Huang, Chien-Hsiang; Shih, Yen-Yu Ian; Siow, Tiing-Yee; Hsu, Yi-Hua; Chen, Chiao-Chi V; Lin, Teng-Nan; Jaw, Fu-Shan; Chang, Chen

    2015-09-01

    Postischemic angiogenesis is an important recovery mechanism. Both arteries and veins are upregulated during angiogenesis, but eventually there are more angiogenic veins than arteries in terms of number and length. It is critical to understand how the veins are modulated after ischemia and then transitioned into angiogenic vessels during the proangiogenic stage to finally serve as a restorative strength to the injured area. Using a rat model of transient focal cerebral ischemia, the hypercapnic blood oxygen level-dependent (BOLD) response was used to evaluate vascular reactivity, while the hyperoxic BOLD and tissue oxygen level-dependent (TOLD) responses were used to evaluate the vascular functionality at 1, 3, and 7days after ischemia. Vessel-like venous signals appeared on R2* maps on days 3 and 7, but not on day 1. The large hypercapnic BOLD responses on days 3 and 7 indicated that these areas have high vascular reactivity. The temporal correlation between vascular reactivity and the immunoreactivity to desmin and VEGF further indicates that the integrity of vascular reactivity is associated with the pericyte coverage as regulated by the VEGF level. Vascular functionality remained low on days 1, 3, and 7, as reflected by the small hyperoxic BOLD and large hyperoxic TOLD responses, indicating the low oxygen consumption of the ischemic tissues. These functional changes in proangiogenic veins may be critical for angiogenesis. PMID:25944092

  14. Ischemic and postischemic conditioning of the myocardium in clinical practice: challenges, expectations and obstacles.

    PubMed

    Iliodromitis, Efstathios K; Andreadou, Ioanna; Iliodromitis, Konstantinos; Dagres, Nikolaos

    2014-01-01

    Conditioning refers to endogenous mechanisms rendering the myocardium more tolerant against reperfusion injury. Application of brief ischemia-reperfusion cycles prior to the index ischemia has a beneficial effect and limits the infarct size. This is called preconditioning and is mainly mediated by activation of adenosine, bradykinin, opioid and other receptors, with subsequent activation of intracellular mediators leading to mitochondrial protection. A clinical equivalent of preconditioning is preinfarction angina. Benefits for the ischemic and reperfused myocardium are also provided by repetitive short-lived cycles of ischemia-reperfusion applied after the index ischemia. This is termed postconditioning, shares a common pathway with preconditioning, and is more useful and relevant in clinical practice. Finally, benefits are also derived from remote conditioning, i.e. ischemia applied in a remote vascular territory parallel with or immediately after the index myocardial ischemia. Several pharmacological interventions may interfere with these mechanisms leading to enhanced protection of the myocardium and limitation of the infarct size. Despite the huge interest and the great body of evidence that verify the effectiveness of conditioning, clinical application has remained limited due to controversies over the appropriate intervention protocol, but also interference of medication, comorbidities and other factors that may enhance or blur the protective effect. PMID:25227478

  15. 40 CFR 1065.518 - Engine preconditioning.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ..., such as with a diesel engine that relies on urea-based selective catalytic reduction. Note that § 1065... cycle specified in 40 CFR 1039.505(b)(1), the second half of the cycle consists of modes three through... 40 Protection of Environment 33 2014-07-01 2014-07-01 false Engine preconditioning....

  16. Revealing Preconditions for Trustful Collaboration in CSCL

    ERIC Educational Resources Information Center

    Gerdes, Anne

    2010-01-01

    This paper analyses preconditions for trust in virtual learning environments. The concept of trust is discussed with reference to cases reporting trust in cyberspace and through a philosophical clarification holding that trust in the form of self-surrender is a common characteristic of all human co-existence. In virtual learning environments,…

  17. Effects of Postconditioning, Preconditioning and Perfusion of L-carnitine During Whole Period of Ischemia/ Reperfusion on Cardiac Hemodynamic Functions and Myocardial Infarction Size in Isolated Rat Heart

    PubMed Central

    Najafi, Moslem

    2013-01-01

    Objective(s): In the present work, the effects of L-carnitine (LC) on postischemic cardiac hemodynamic functions and infarction size were studied in isolated rat heart. Materials and Methods: The hearts were subjected to 30 min regional ischemia followed by 120 min reperfusion. Then they were perfused by a drug-free or LC-enriched Krebs–Henseleit (K/H) solution during ischemia/ reperfusion (I/R) (Protocol 1), 10 min before ischemia induction (Protocol 2; preconditioning group) or the first 10 min of reperfusion (Protocol 3; postconditioning group). Results: The perfusion of LC in protocol 1 significantly reduced left ventricular end diastolic pressure (LVEDP) (P<0.05), and increased left ventricular developed pressure (LVDP) (P<0.05), rate pressure product (RPP) (P<0.01) and coronary flow rate (CFR) (P<0.05). The short-term preischemic administration of LC in protocol 2 improved RPP, CFR and decreased the extent of LVEDP elevation. However, protective effects of LC in this protocol were low compared to the whole period perfusion. In protocol 3, LC preserved postischemic cardiac functions not as much as the other protocols. In addition, infarct size significantly decreased by LC in all protocols as opposed to the control group (P<0.001). Conclusion: The results of the present work showed that LC produced protective effects against I/R injury. These protective actions were reversed by concomitant use of etomoxir (a CPT-I inhibitor), suggesting that the efficacy of LC could be due to its mitochondrial action, probably related to the raise in glucose oxidation of the reperfused hearts. PMID:24250943

  18. Effects of Postconditioning, Preconditioning and Perfusion of L-carnitine During Whole Period of Ischemia/ Reperfusion on Cardiac Hemodynamic Functions and Myocardial Infarction Size in Isolated Rat Heart

    PubMed Central

    Najafi, Moslem

    2013-01-01

    Objective(s): In the present work, the effects of L-carnitine (LC) on postischemic cardiac hemodynamic functions and infarction size were studied in isolated rat heart. Materials and Methods: The hearts were subjected to 30 min regional ischemia followed by 120 min reperfusion. Then they were perfused by a drug-free or LC-enriched Krebs–Henseleit (K/H) solution during ischemia/ reperfusion (I/R) (Protocol 1), 10 min before ischemia induction (Protocol 2; preconditioning group) or the first 10 min of reperfusion (Protocol 3; postconditioning group). Results: The perfusion of LC in protocol 1 significantly reduced left ventricular end diastolic pressure (LVEDP) (P<0.05), and increased left ventricular developed pressure (LVDP) (P<0.05), rate pressure product (RPP) (P<0.01) and coronary flow rate (CFR) (P<0.05). The short-term preischemic administration of LC in protocol 2 improved RPP, CFR and decreased the extent of LVEDP elevation. However, protective effects of LC in this protocol were low compared to the whole period perfusion. In protocol 3, LC preserved postischemic cardiac functions not as much as the other protocols. In addition, infarct size significantly decreased by LC in all protocols as opposed to the control group (P<0.001). Conclusion: The results of the present work showed that LC produced protective effects against I/R injury. These protective actions were reversed by concomitant use of etomoxir (a CPT-I inhibitor), suggesting that the efficacy of LC could be due to its mitochondrial action, probably related to the raise in glucose oxidation of the reperfused hearts. PMID:24250945

  19. Does intraperitoneal medical ozone preconditioning and treatment ameliorate the methotrexate induced nephrotoxicity in rats?

    PubMed Central

    Aslaner, Arif; Çak?r, Tu?rul; Çelik, Betül; Do?an, U?ur; Mayir, Burhan; Akyüz, Cebrail; Polat, Cemal; Ba?türk, Ahmet; Soyer, Vural; Koç, Süleyman; ?ehirli, Ahmet Özer

    2015-01-01

    Methotrexate is a chemotherapeutic agent used for many cancer treatments. It leads to toxicity with its oxidative injury. The purpose of our study is investigating the medical ozone preconditioning and treatment has any effect on the methotrexate-induced kidneys by activating antioxidant enzymes in rats. Eighteen rats were divided into three equal groups; control, Mtx without and with medical ozone. Nephrotoxicity was performed with a single dose of 20 mg/kg Mtx intraperitoneally at the fifteenth day of experiment on groups 2 and 3. Medical ozone preconditioning was performed at a dose of 25 mcg/ml (5 ml) intraperitoneally everyday in the group 3 and treated with medical ozone for five more days while group 2 was received only 5 ml of saline everyday for twenty days. All rats were sacrificed at the end of third week and the blood and kidney tissue samples were obtained to measure the levels of TNF-?, IL-1?, malondialdehyde, glutathione and myeloperoxidase. Kidney injury score was evaluated histolopatologically. Medical ozone preconditioning and treatment ameliorated the biochemical parameters and kidney injury induced by Mtx. There was significant increase in tissue MDA, MPO activity, TNF-? and IL-1? (P<0.05) and significant decrease in tissue GSH and histopathology (P<0.05) after Mtx administration. The preconditioning and treatment with medical ozone ameliorated the nephrotoxicity induced by Mtx in rats by activating antioxidant enzymes and prevented renal tissue. PMID:26550330

  20. Anti-inflammatory effects of OBA-09, a salicylic acid/pyruvate ester, in the postischemic brain.

    PubMed

    Lee, Hye-Kyung; Kim, Seung-Woo; Jin, Yinchuan; Kim, Il-Doo; Park, Ju-Young; Yoon, Sung-Hwa; Lee, Ja-Kyeong

    2013-08-28

    Cerebral ischemia leads to brain injury via a complex series of pathophysiological events, and therefore, multi-drug treatments or multi-targeting drug treatments provide attractive options with respect to limiting brain damage. Previously, we reported that a novel multi-functional compound oxopropanoyloxy benzoic acid (OBA-09, a simple ester of pyruvate and salicylic acid) affords robust neuroprotective effects in the postischemic rat brain. OBA-09 exhibited anti-oxidative effects that appeared to be executed by OBA-09 and by the salicylic acid afforded by hydrolysis. Here, we report the anti-inflammatory effects of OBA-09. Microglial activation observed at 2 days post-middle cerebral artery occlusion (MCAO, 90 min) and at 1 day after a LPS injection (0.5 mg/kg, intravenously) in the brains of Sprague-Dawley rats were markedly suppressed by the administration of OBA-09 (10 mg/kg). Inductions of proinflammatory markers (TNF-?, IL-1?, iNOS, and COX-2) were also suppressed by OBA-09 in both the LPS and MCAO models. Moreover, the anti-inflammatory effect of OBA-09 was accompanied by the suppression of infarct formation in the postischemic brain, but appeared to be independent of neuroprotection in LPS-treated rats. The inductions of proinflammatory markers were also inhibited by OBA-09 in LPS-treated BV2 cells (a microglia cell line) and in LPS-treated-primary neutrophils, possibly due to the suppression of NF-?B activity. Interestingly, the anti-inflammatory effect of OBA-09 was greater than that of equivalent co-treatment with pyruvate and salicylic acid. Together these results indicate that OBA-09 is a potent multi-modal neuroprotectant in the postischemic brain, and that its anti-inflammatory effect contributes to its neuroprotective function. PMID:23850644

  1. Recovery of postischemic contractile function is depressed by antegrade warm continuous blood cardioplegia.

    PubMed

    Misare, B D; Krukenkamp, I B; Lazer, Z P; Levitsky, S

    1993-01-01

    To assess the effectiveness of warm antegrade continuous blood cardioplegia in the setting of an acute coronary arterial occlusion, we instrumented 19 Yorkshire swine to quantitate left ventricular global, systolic, diastolic, and regional mechanics. Data were acquired before and after 10 minutes of mid-left anterior descending coronary artery occlusion followed by 60 minutes of aortic crossclamping. Cardiac arrest was induced by the antegrade infusion of 20 ml/kg of warm (37 degrees C) or cold (4 degrees C) oxygenated blood cardioplegic solution followed by either continuous warm (75 ml/min, n = 9) or intermittent cold (10 ml/kg every 20 minutes, n = 10) cardioplegic reinfusions. Left anterior descending coronary artery occlusion was released 20 minutes after aortic crossclamping and resulted in warm-arrested hearts developing a 139% increase in global oxygen consumption compared with values obtained with the left anterior descending coronary artery occluded (p < 0.02). Recovery of global left ventricle contractility, quantitated by the linear preload recruitable stroke-work relationship, was significantly worse after warm cardioplegia (52.4% +/- 5.1% versus 68.0% +/- 5.9%, warm versus cold, p < 0.05). Similarly, left anterior descending coronary artery regional ischemic zone contractility recovered 34.5% +/- 7.3% of control function with cold cardioplegia, whereas warm cardioplegia resulted in -11.36% +/- 7.46% functional recovery indicative of dyssynchronous contraction (p < 0.05). Diastolic compliance, calculated with an exponential end-diastolic pressure-versus-volume relationship, was not changed postischemically in either group. These data suggest that warm antegrade blood cardioplegia may potentiate acute ischemic injury and provide inadequate myocardial protection. PMID:8419707

  2. Preserving Symmetry in Preconditioned Krylov Subspace Methods

    NASA Technical Reports Server (NTRS)

    Chan, Tony F.; Chow, E.; Saad, Y.; Yeung, M. C.

    1996-01-01

    We consider the problem of solving a linear system Ax = b when A is nearly symmetric and when the system is preconditioned by a symmetric positive definite matrix M. In the symmetric case, one can recover symmetry by using M-inner products in the conjugate gradient (CG) algorithm. This idea can also be used in the nonsymmetric case, and near symmetry can be preserved similarly. Like CG, the new algorithms are mathematically equivalent to split preconditioning, but do not require M to be factored. Better robustness in a specific sense can also be observed. When combined with truncated versions of iterative methods, tests show that this is more effective than the common practice of forfeiting near-symmetry altogether.

  3. Regeneration through autologous hypoxia preconditioned plasma

    PubMed Central

    Hadjipanayi, Ektoras; Schilling, Arndt F

    2014-01-01

    Cellular hypoxic preconditioning is being employed to obtain complex, yet physiological, secretomes rich is angiogenic factors. We previously proposed exposing peripheral blood cells (PBCs) to hypoxic stress stimulation, and demonstrated that controlled release of PBC-derived factor mixtures induces directional microvessel growth in vitro. Hypoxia therefore provides a useful tool for enhancing the angiogenic potential of blood plasma, by generating compositions based on PBCs' natural responses to a wound-like microenvironment. Here, we discuss various methods for preparing and delivering Hypoxia Preconditioned Plasma (HPP), i.e., plasma derived after extracorporeal conditioning of anticoagulated blood under physiological temperature and hypoxia. Special emphasis is given to those approaches that will likely facilitate the clinical translation of HPP-based therapies. We finally draw a comparison between HPP and other, currently available blood-based products, and present the case that its arrival paves the way for developing next-generation autologous therapies toward angiogenesis-supported tissue repair and regeneration. PMID:24831225

  4. M-step preconditioned conjugate gradient methods

    NASA Technical Reports Server (NTRS)

    Adams, L.

    1983-01-01

    Preconditioned conjugate gradient methods for solving sparse symmetric and positive finite systems of linear equations are described. Necessary and sufficient conditions are given for when these preconditioners can be used and an analysis of their effectiveness is given. Efficient computer implementations of these methods are discussed and results on the CYBER 203 and the Finite Element Machine under construction at NASA Langley Research Center are included.

  5. On polynomial preconditioning for indefinite Hermitian matrices

    NASA Technical Reports Server (NTRS)

    Freund, Roland W.

    1989-01-01

    The minimal residual method is studied combined with polynomial preconditioning for solving large linear systems (Ax = b) with indefinite Hermitian coefficient matrices (A). The standard approach for choosing the polynomial preconditioners leads to preconditioned systems which are positive definite. Here, a different strategy is studied which leaves the preconditioned coefficient matrix indefinite. More precisely, the polynomial preconditioner is designed to cluster the positive, resp. negative eigenvalues of A around 1, resp. around some negative constant. In particular, it is shown that such indefinite polynomial preconditioners can be obtained as the optimal solutions of a certain two parameter family of Chebyshev approximation problems. Some basic results are established for these approximation problems and a Remez type algorithm is sketched for their numerical solution. The problem of selecting the parameters such that the resulting indefinite polynomial preconditioners speeds up the convergence of minimal residual method optimally is also addressed. An approach is proposed based on the concept of asymptotic convergence factors. Finally, some numerical examples of indefinite polynomial preconditioners are given.

  6. Preconditioning and the limit to the incompressible flow equations

    NASA Technical Reports Server (NTRS)

    Turkel, E.; Fiterman, A.; Vanleer, B.

    1993-01-01

    The use of preconditioning methods to accelerate the convergence to a steady state for both the incompressible and compressible fluid dynamic equations are considered. The relation between them for both the continuous problem and the finite difference approximation is also considered. The analysis relies on the inviscid equations. The preconditioning consists of a matrix multiplying the time derivatives. Hence, the steady state of the preconditioned system is the same as the steady state of the original system. For finite difference methods the preconditioning can change and improve the steady state solutions. An application to flow around an airfoil is presented.

  7. Forbidding Preconditions and Ordered Abstraction Hierarchies Eugene Fink \\Lambda

    E-print Network

    Fink, Eugene

    Forbidding Preconditions and Ordered Abstraction Hierarchies Eugene Fink \\Lambda School of Computer Science Carnegie Mellon University Pittsbugrh, PA 15213 eugene@cs.cmu.edu Qiang Yang \\Lambda Department

  8. Approximate polynomial preconditioning applied to biharmonic equations on vector supercomputers

    NASA Technical Reports Server (NTRS)

    Wong, Yau Shu; Jiang, Hong

    1987-01-01

    Applying a finite difference approximation to a biharmonic equation results in a very ill-conditioned system of equations. This paper examines the conjugate gradient method used in conjunction with the generalized and approximate polynomial preconditionings for solving such linear systems. An approximate polynomial preconditioning is introduced, and is shown to be more efficient than the generalized polynomial preconditionings. This new technique provides a simple but effective preconditioning polynomial, which is based on another coefficient matrix rather than the original matrix operator as commonly used.

  9. Neuroprotection by biodegradable PAMAM ester (e-PAM-R)-mediated HMGB1 siRNA delivery in primary cortical cultures and in the postischemic brain

    E-print Network

    Park, Jong-Sang

    cortical cultures and in the postischemic brain Il-Doo Kim a,1 , Chae-Moon Lim a,1 , Jung-Bin Kim a , Hye Yeong Nam b , Kihoon Nam b , Seung-Woo Kim a , Jong-Sang Park b , Ja-Kyeong Lee a, a Department

  10. H(curl) Auxiliary Mesh Preconditioning

    SciTech Connect

    Kolev, T V; Pasciak, J E; Vassilevski, P S

    2006-08-31

    This paper analyzes a two-level preconditioning scheme for H(curl) bilinear forms. The scheme utilizes an auxiliary problem on a related mesh that is more amenable for constructing optimal order multigrid methods. More specifically, we analyze the case when the auxiliary mesh only approximately covers the original domain. The latter assumption is important since it allows for easy construction of nested multilevel spaces on regular auxiliary meshes. Numerical experiments in both two and three space dimensions illustrate the optimal performance of the method.

  11. 40 CFR 86.132-00 - Vehicle preconditioning.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 18 2011-07-01 2011-07-01 false Vehicle preconditioning. 86.132-00 Section 86.132-00 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS... manufacturer has concerns about fuel effects on adaptive memory systems, a manufacturer may precondition a...

  12. [STRESS AND INFARCT LIMITING EFFECTS OF EARLY HYPOXIC PRECONDITIONING].

    PubMed

    Lishmanov, Yu B; Maslov, L N; Sementsov, A S; Naryzhnaya, N V; Tsibulnikov, S Yu

    2015-09-01

    It was established that early hypoxic preconditioning is an adaptive state different from eustress and distress. Hypoxic preconditioning has the cross effects, increasing the tolerance of the heart to ischemia-reperfusion and providing antiulcerogenic effect during immobilization stress. PMID:26672158

  13. A preconditioned formulation of the Cauchy-Riemann equations

    NASA Technical Reports Server (NTRS)

    Phillips, T. N.

    1983-01-01

    A preconditioning of the Cauchy-Riemann equations which results in a second-order system is described. This system is shown to have a unique solution if the boundary conditions are chosen carefully. This choice of boundary condition enables the solution of the first-order system to be retrieved. A numerical solution of the preconditioned equations is obtained by the multigrid method.

  14. Pharmacological Preconditioning by Adenosine A2a Receptor Stimulation: Features of the Protected Liver Cell Phenotype

    PubMed Central

    Alchera, Elisa; Imarisio, Chiara; Mandili, Giorgia; Merlin, Simone; Chandrashekar, Bangalore R.; Novelli, Francesco; Follenzi, Antonia; Carini, Rita

    2015-01-01

    Ischemic preconditioning (IP) of the liver by a brief interruption of the blood flow protects the damage induced by a subsequent ischemia/reperfusion (I/R) preventing parenchymal and nonparenchymal liver cell damage. The discovery of IP has shown the existence of intrinsic systems of cytoprotection whose activation can stave off the progression of irreversible tissue damage. Deciphering the molecular mediators that underlie the cytoprotective effects of preconditioning can pave the way to important therapeutic possibilities. Pharmacological activation of critical mediators of IP would be expected to emulate or even to intensify its salubrious effects. In vitro and in vivo studies have demonstrated the role of the adenosine A2a receptor (A2aR) as a trigger of liver IP. This review will provide insight into the phenotypic changes that underline the resistance to death of liver cells preconditioned by pharmacological activation of A2aR and their implications to develop innovative strategies against liver IR damage. PMID:26539478

  15. Pre-Conditioning with Low-Level Laser (Light) Therapy: Light Before the Storm

    PubMed Central

    Agrawal, Tanupriya; Gupta, Gaurav K.; Rai, Vikrant; Carroll, James D.; Hamblin, Michael R.

    2014-01-01

    Pre-conditioning by ischemia, hyperthermia, hypothermia, hyperbaric oxygen (and numerous other modalities) is a rapidly growing area of investigation that is used in pathological conditions where tissue damage may be expected. The damage caused by surgery, heart attack, or stroke can be mitigated by pre-treating the local or distant tissue with low levels of a stress-inducing stimulus, that can induce a protective response against subsequent major damage. Low-level laser (light) therapy (LLLT) has been used for nearly 50 years to enhance tissue healing and to relieve pain, inflammation and swelling. The photons are absorbed in cytochrome(c) oxidase (unit four in the mitochondrial respiratory chain), and this enzyme activation increases electron transport, respiration, oxygen consumption and ATP production. A complex signaling cascade is initiated leading to activation of transcription factors and up- and down-regulation of numerous genes. Recently it has become apparent that LLLT can also be effective if delivered to normal cells or tissue before the actual insult or trauma, in a pre-conditioning mode. Muscles are protected, nerves feel less pain, and LLLT can protect against a subsequent heart attack. These examples point the way to wider use of LLLT as a pre-conditioning modality to prevent pain and increase healing after surgical/medical procedures and possibly to increase athletic performance. PMID:25552961

  16. Mechanisms of filtration failure during postischemic injury of the human kidney. A study of the reperfused renal allograft.

    PubMed Central

    Alejandro, V; Scandling, J D; Sibley, R K; Dafoe, D; Alfrey, E; Deen, W; Myers, B D

    1995-01-01

    Postischemic filtration failure in experimental animals results primarily from depression of the transcapillary hydraulic pressure difference (delta P), a quantity that cannot be determined in humans. To circumvent this limitation we determined the GFR and each of its remaining determinants in transplanted kidneys. Findings in 12 allografts that exhibited subsequent normofiltration (group 1) were compared with those in 11 allografts that exhibited persistent hypofiltration (group 2). Determinations were made intraoperatively in the exposed graft after 1-3 h of reperfusion. GFR (6 +/- 2 vs 29 +/- 5 ml/min) and renal plasma flow by Doppler flow meter (140 +/- 30 vs 315 +/- 49 ml/min) were significantly lower in group 2 than group 1. Morphometric analysis of glomeruli obtained by biopsy and a structural hydrodynamic model of viscous flow revealed the glomerular ultrafiltration coefficient to be similar, averaging 3.5 +/- 0.6 and 3.1 +/- 0.2 ml/(min.mmHg) in group 2 vs 1, respectively. Corresponding values for plasma oncotic pressure were also similar, averaging 19 +/- 1 vs 21 +/- 1 mmHg. We next used a mathematical model of glomerular ultrafiltration and a sensitivity analysis to calculate the prevailing range for delta P from the foregoing measured quantities. This revealed delta P to vary from only 20-21 mmHg in group 2 vs 34-45 mmHg in group 1 (P < 0.001). Further morphometric analysis revealed the diameters of Bowman's space and tubular lumens, as well as the percentage of tubular cells that were necrotic or devoid of brush border, to be similar in the two groups. We thus conclude (a) that delta P depression is the predominant cause of hypofiltration in this form of postischemic injury; and (b) that afferent vasoconstriction rather than tubular obstruction is the proximate cause of the delta P depression. Images PMID:7860766

  17. Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.

    PubMed

    Doeppner, T R; Kaltwasser, B; Schlechter, J; Jaschke, J; Kilic, E; Bähr, M; Hermann, D M; Weise, J

    2015-01-01

    Although cellular prion protein (PrP(c)) has been suggested to have physiological roles in neurogenesis and angiogenesis, the pathophysiological relevance of both processes remain unknown. To elucidate the role of PrP(c) in post-ischemic brain remodeling, we herein exposed PrP(c) wild type (WT), PrP(c) knockout (PrP-/-) and PrP(c) overexpressing (PrP+/+) mice to focal cerebral ischemia followed by up to 28 days reperfusion. Improved neurological recovery and sustained neuroprotection lasting over the observation period of 4 weeks were observed in ischemic PrP+/+ mice compared with WT mice. This observation was associated with increased neurogenesis and angiogenesis, whereas increased neurological deficits and brain injury were noted in ischemic PrP-/- mice. Proteasome activity and oxidative stress were increased in ischemic brain tissue of PrP-/- mice. Pharmacological proteasome inhibition reversed the exacerbation of brain injury induced by PrP-/-, indicating that proteasome inhibition mediates the neuroprotective effects of PrP(c). Notably, reduced proteasome activity and oxidative stress in ischemic brain tissue of PrP+/+ mice were associated with an increased abundance of hypoxia-inducible factor 1? and PACAP-38, which are known stimulants of neural progenitor cell (NPC) migration and trafficking. To elucidate effects of PrP(c) on intracerebral NPC homing, we intravenously infused GFP(+) NPCs in ischemic WT, PrP-/- and PrP+/+ mice, showing that brain accumulation of GFP(+) NPCs was greatly reduced in PrP-/- mice, but increased in PrP+/+ animals. Our results suggest that PrP(c) induces post-ischemic long-term neuroprotection, neurogenesis and angiogenesis in the ischemic brain by inhibiting proteasome activity. PMID:26673668

  18. Mechanisms of filtration failure during postischemic injury of the human kidney. A study of the reperfused renal allograft.

    PubMed

    Alejandro, V; Scandling, J D; Sibley, R K; Dafoe, D; Alfrey, E; Deen, W; Myers, B D

    1995-02-01

    Postischemic filtration failure in experimental animals results primarily from depression of the transcapillary hydraulic pressure difference (delta P), a quantity that cannot be determined in humans. To circumvent this limitation we determined the GFR and each of its remaining determinants in transplanted kidneys. Findings in 12 allografts that exhibited subsequent normofiltration (group 1) were compared with those in 11 allografts that exhibited persistent hypofiltration (group 2). Determinations were made intraoperatively in the exposed graft after 1-3 h of reperfusion. GFR (6 +/- 2 vs 29 +/- 5 ml/min) and renal plasma flow by Doppler flow meter (140 +/- 30 vs 315 +/- 49 ml/min) were significantly lower in group 2 than group 1. Morphometric analysis of glomeruli obtained by biopsy and a structural hydrodynamic model of viscous flow revealed the glomerular ultrafiltration coefficient to be similar, averaging 3.5 +/- 0.6 and 3.1 +/- 0.2 ml/(min.mmHg) in group 2 vs 1, respectively. Corresponding values for plasma oncotic pressure were also similar, averaging 19 +/- 1 vs 21 +/- 1 mmHg. We next used a mathematical model of glomerular ultrafiltration and a sensitivity analysis to calculate the prevailing range for delta P from the foregoing measured quantities. This revealed delta P to vary from only 20-21 mmHg in group 2 vs 34-45 mmHg in group 1 (P < 0.001). Further morphometric analysis revealed the diameters of Bowman's space and tubular lumens, as well as the percentage of tubular cells that were necrotic or devoid of brush border, to be similar in the two groups. We thus conclude (a) that delta P depression is the predominant cause of hypofiltration in this form of postischemic injury; and (b) that afferent vasoconstriction rather than tubular obstruction is the proximate cause of the delta P depression. PMID:7860766

  19. Meclizine Preconditioning Protects the Kidney Against Ischemia–Reperfusion Injury

    PubMed Central

    Kishi, Seiji; Campanholle, Gabriela; Gohil, Vishal M.; Perocchi, Fabiana; Brooks, Craig R.; Morizane, Ryuji; Sabbisetti, Venkata; Ichimura, Takaharu; Mootha, Vamsi K.; Bonventre, Joseph V.

    2015-01-01

    Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a ‘nutrient-sensitized’ chemical screen. Pretreatment with 100 mg/kg of meclizine, 17 h prior to ischemia protected mice from IRI. Serum creatinine levels at 24 h after IRI were 0.13 ± 0.06 mg/dl (sham, n = 3), 1.59 ± 0.10 mg/dl (vehicle, n = 8) and 0.89 ± 0.11 mg/dl (meclizine, n = 8). Kidney injury was significantly decreased in meclizine treated mice compared with vehicle group (p < 0.001). Protection was also seen when meclizine was administered 24 h prior to ischemia. Meclizine reduced inflammation, mitochondrial oxygen consumption, oxidative stress, mitochondrial fragmentation, and tubular injury. Meclizine preconditioned kidney tubular epithelial cells, exposed to blockade of glycolytic and oxidative metabolism with 2-deoxyglucose and NaCN, had reduced LDH and cytochrome c release. Meclizine upregulated glycolysis in glucose-containing media and reduced cellular ATP levels in galactose-containing media. Meclizine inhibited the Kennedy pathway and caused rapid accumulation of phosphoethanolamine. Phosphoethanolamine recapitulated meclizine-induced protection both in vitro and in vivo. PMID:26501107

  20. Meclizine Preconditioning Protects the Kidney Against Ischemia-Reperfusion Injury.

    PubMed

    Kishi, Seiji; Campanholle, Gabriela; Gohil, Vishal M; Perocchi, Fabiana; Brooks, Craig R; Morizane, Ryuji; Sabbisetti, Venkata; Ichimura, Takaharu; Mootha, Vamsi K; Bonventre, Joseph V

    2015-09-01

    Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a 'nutrient-sensitized' chemical screen. Pretreatment with 100 mg/kg of meclizine, 17 h prior to ischemia protected mice from IRI. Serum creatinine levels at 24 h after IRI were 0.13 ± 0.06 mg/dl (sham, n = 3), 1.59 ± 0.10 mg/dl (vehicle, n = 8) and 0.89 ± 0.11 mg/dl (meclizine, n = 8). Kidney injury was significantly decreased in meclizine treated mice compared with vehicle group (p < 0.001). Protection was also seen when meclizine was administered 24 h prior to ischemia. Meclizine reduced inflammation, mitochondrial oxygen consumption, oxidative stress, mitochondrial fragmentation, and tubular injury. Meclizine preconditioned kidney tubular epithelial cells, exposed to blockade of glycolytic and oxidative metabolism with 2-deoxyglucose and NaCN, had reduced LDH and cytochrome c release. Meclizine upregulated glycolysis in glucose-containing media and reduced cellular ATP levels in galactose-containing media. Meclizine inhibited the Kennedy pathway and caused rapid accumulation of phosphoethanolamine. Phosphoethanolamine recapitulated meclizine-induced protection both in vitro and in vivo. PMID:26501107

  1. Hepatic Branch Vagus Nerve Plays a Critical Role in the Recovery of Post-Ischemic Glucose Intolerance and Mediates a Neuroprotective Effect by Hypothalamic Orexin-A

    PubMed Central

    Harada, Shinichi; Yamazaki, Yui; Koda, Shuichi; Tokuyama, Shogo

    2014-01-01

    Orexin-A (a neuropeptide in the hypothalamus) plays an important role in many physiological functions, including the regulation of glucose metabolism. We have previously found that the development of post-ischemic glucose intolerance is one of the triggers of ischemic neuronal damage, which is suppressed by hypothalamic orexin-A. Other reports have shown that the communication system between brain and peripheral tissues through the autonomic nervous system (sympathetic, parasympathetic and vagus nerve) is important for maintaining glucose and energy metabolism. The aim of this study was to determine the involvement of the hepatic vagus nerve on hypothalamic orexin-A-mediated suppression of post-ischemic glucose intolerance development and ischemic neuronal damage. Male ddY mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Intrahypothalamic orexin-A (5 pmol/mouse) administration significantly suppressed the development of post-ischemic glucose intolerance and neuronal damage on day 1 and 3, respectively after MCAO. MCAO-induced decrease of hepatic insulin receptors and increase of hepatic gluconeogenic enzymes on day 1 after was reversed to control levels by orexin-A. This effect was reversed by intramedullary administration of the orexin-1 receptor antagonist, SB334867, or hepatic vagotomy. In the medulla oblongata, orexin-A induced the co-localization of cholin acetyltransferase (cholinergic neuronal marker used for the vagus nerve) with orexin-1 receptor and c-Fos (activated neural cells marker). These results suggest that the hepatic branch vagus nerve projecting from the medulla oblongata plays an important role in the recovery of post-ischemic glucose intolerance and mediates a neuroprotective effect by hypothalamic orexin-A. PMID:24759941

  2. Remote ischaemic preconditioning for coronary artery bypass grafting

    PubMed Central

    Benstoem, Carina; Stoppe, Christian; Liakopoulos, Oliver J; Meybohm, Patrick; Clayton, Tim C; Yellon, Derek M; Hausenloy, Derek J; Goetzenich, Andreas

    2015-01-01

    This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the benefits and harms of remote ischaemic preconditioning in patients undergoing coronary artery bypass grafting, with or without valve surgery.

  3. Preconditioning methods for improved convergence rates in iterative reconstructions

    SciTech Connect

    Clinthorne, N.H.; Chiao, Pingchun; Rogers, W.L. . Div. of Nuclear Medicine); Pan, T.S. . Dept. of Nuclear Medicine); Stamos, J.A. . Dept. of Nuclear Engineering)

    1993-03-01

    Because of the characteristics of the tomographic inversion problem, iterative reconstruction techniques often suffer from poor convergence rates--especially at high spatial frequencies. By using preconditioning methods, the convergence properties of most iterative methods can be greatly enhanced without changing their ultimate solution. To increase reconstruction speed, the authors have applied spatially-invariant preconditioning filters that can be designed using the tomographic system response and implemented using 2-D frequency-domain filtering techniques. In a sample application, the authors performed reconstructions from noiseless, simulated projection data, using preconditioned and conventional steepest-descent algorithms. The preconditioned methods demonstrated residuals that were up to a factor of 30 lower than the unassisted algorithms at the same iteration. Applications of these methods to regularized reconstructions from projection data containing Poisson noise showed similar, although not as dramatic, behavior.

  4. 40 CFR 1065.516 - Sample system decontamination and preconditioning.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...PROCEDURES Performing an Emission Test Over Specified Duty Cycles § 1065.516 Sample system decontamination and preconditioning...measure hydrocarbon and PM emissions by sampling purified air or nitrogen. (3) When calculating zero emission levels, apply...

  5. Preconditioning Outside Air: Cooling Loads from Building Ventilation 

    E-print Network

    Kosar, D.

    1998-01-01

    of the standard. To mitigate or nullify these additional weather loads, outdoor air preconditioning technologies are being promoted in combination with conventional HVAC operations downstream as a means to deliver the required fresh air and control humidity...

  6. PRECONDITIONING FOR THE MIXED FORMULATION OF LINEAR PLANE A Dissertation

    E-print Network

    Wang, Yanqiu

    as to style and content by: Joseph E. Pasciak (Chair of Committee) James H. Bramble (Member) Raytcho Lazarov thank Dr. James H. Bramble for his inspiring lectures on finite element methods and preconditioning

  7. A SUBSPACE PRECONDITIONING ALGORITHM FOR EIGENVECTOR/EIGENVALUE COMPUTATION

    E-print Network

    Pasciak, Joseph

    A SUBSPACE PRECONDITIONING ALGORITHM FOR EIGENVECTOR/EIGENVALUE COMPUTATION James H. Bramble, Cornell University. Typeset by A M S­T E X 1 #12; 2 BRAMBLE, ET. AL. We consider the case where the first

  8. Effective matrix-free preconditioning for the augmented immersed ...

    E-print Network

    2015-09-05

    Sep 5, 2015 ... The immersed interface method can then be applied conveniently with a fast. Poisson solver .... Thus, the preconditioning cost is negligible as compared with the matrix- ...... and an external forcing term, respectively. There is a ...

  9. THE PERIVASCULAR POOL OF AQUAPORIN-4 MEDIATES THE EFFECT OF OSMOTHERAPY IN POST-ISCHEMIC CEREBRAL EDEMA

    PubMed Central

    Zeynalov, Emil; Chen, Chih-Hung; Froehner, Stanley C.; Adams, Marvin E.; Ottersen, Ole Petter; Amiry-Moghaddam, Mahmood; Bhardwaj, Anish

    2009-01-01

    Objective Osmotherapy with hypertonic saline (HS) ameliorates cerebral edema associated with experimental ischemic stroke. We tested the hypothesis that HS exerts its anti-edema effect by promoting an efflux of water from brain via the perivascular aquaporin-4 (AQP4) pool. We utilized mice with targeted disruption of the gene encoding ?-syntrophin (?-Syn?/?) that lack the perivascular AQP4 pool but retain the endothelial pool of this protein. Design Prospective laboratory animal study. Setting Research laboratory in a university teaching hospital. Measurements and Main Results Halothane-anesthetized adult male wildtype (WT) C57B/6 and ?-Syn?/? mice were subjected to 90 min of transient middle cerebral artery occlusion (MCAO) and treated with either a continuous intravenous infusion of 0.9% saline (NS) or 3% HS (1.5 mL/Kg/hr) for 48 hr. In the first series of experiments (n = 59), brain water content analyzed by wet-to-dry ratios in the ischemic hemisphere of WT mice was attenuated after HS (79.9 ± 0.5%mean ± SEM) but not after NS (82.3 ± 1.0%) treatment. In contrast in ?-Syn?/? mice, HS had no effect on the postischemic edema (HS: 80.3 ± 0.7% NS: 80.3 ± 0.4%). In the second series of experiments (n = 31), treatment with HS attenuated post-ischemic BBB disruption at 48 hr in WT mice but not in ?-Syn?/? mice; ?-Syn deletion alone had no effect on BBB integrity. In the third series of experiments (n=34), ?-Syn?/? mice treated with either HS or NS had smaller infarct volume as compared with their WT counterparts. Conclusions These data demonstrate that: 1) osmotherapy with HS exerts anti-edema effects via the perivascular pool of AQP4 2) HS attenuates BBB disruption depending on the presence of perivascular AQP4, and 3) deletion of the perivascular pool of AQP4 alleviates tissue damage following stroke, in mice subjected to osmotherapy as well as in non-treated mice. PMID:18679106

  10. Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina

    SciTech Connect

    Camici, P.; Araujo, L.I.; Spinks, T.; Lammertsma, A.A.; Kaski, J.C.; Shea, M.J.; Selwyn, A.P.; Jones, T.; Maseri, A.

    1986-07-01

    Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography. In patients at rest, the myocardial uptake of /sup 82/Rb and FDG did not differ significantly from that measured in normal subjects. The exercise test performed within the positron camera in eight patients produced typical chest pain and ischemic electrocardiographic changes in all. In each of the eight patients a region of reduced cation uptake was demonstrated in the /sup 82/Rb scan recorded at peak exercise, after which uptake of /sup 82/Rb returned to the control value 5 to 14 min after the end of the exercise. In these patients, FDG was injected in the recovery phase when all the variables that were altered during exercise, including regional myocardial /sup 82/Rb uptake, had returned to control values. In all but one patient, FDG accumulation in the regions of reduced /sup 82/Rb uptake during exercise was significantly higher than that in the nonischemic regions, i.e., the ones with a normal increment of /sup 82/Rb uptake on exercise. In the nonischemic areas, FDG uptake was not significantly different from that found in normal subjects after exercise. In conclusion, myocardial glucose transport and phosphorylation seem to be enhanced in the postischemic myocardium of patients with exercise-induced ischemia.

  11. Fetal asphyctic preconditioning alters the transcriptional response to perinatal asphyxia

    PubMed Central

    2014-01-01

    Background Genomic reprogramming is thought to be, at least in part, responsible for the protective effect of brain preconditioning. Unraveling mechanisms of this endogenous neuroprotection, activated by preconditioning, is an important step towards new clinical strategies for treating asphyctic neonates. Therefore, we investigated whole-genome transcriptional changes in the brain of rats which underwent perinatal asphyxia (PA), and rats where PA was preceded by fetal asphyctic preconditioning (FAPA). Offspring were sacrificed 6 h and 96 h after birth, and whole-genome transcription was investigated using the Affymetrix Gene1.0ST chip. Microarray data were analyzed with the Bioconductor Limma package. In addition to univariate analysis, we performed Gene Set Enrichment Analysis (GSEA) in order to derive results with maximum biological relevance. Results We observed minimal, 25% or less, overlap of differentially regulated transcripts across different experimental groups which leads us to conclude that the transcriptional phenotype of these groups is largely unique. In both the PA and FAPA group we observe an upregulation of transcripts involved in cellular stress. Contrastingly, transcripts with a function in the cell nucleus were mostly downregulated in PA animals, while we see considerable upregulation in the FAPA group. Furthermore, we observed that histone deacetylases (HDACs) are exclusively regulated in FAPA animals. Conclusions This study is the first to investigate whole-genome transcription in the neonatal brain after PA alone, and after perinatal asphyxia preceded by preconditioning (FAPA). We describe several genes/pathways, such as ubiquitination and proteolysis, which were not previously linked to preconditioning-induced neuroprotection. Furthermore, we observed that the majority of upregulated genes in preconditioned animals have a function in the cell nucleus, including several epigenetic players such as HDACs, which suggests that epigenetic mechanisms are likely to play a role in preconditioning-induced neuroprotection. PMID:24885038

  12. Transplantation of hypoxia preconditioned bone marrow mesenchymal stem cells enhances angiogenesis and neurogenesis after cerebral ischemia in rats

    E-print Network

    Hayar, Abdallah

    Transplantation of hypoxia preconditioned bone marrow mesenchymal stem cells enhances angiogenesis online 9 March 2012 Keywords: Hypoxic preconditioning Bone marrow mesenchymal stem cell Transplantation that hypoxic preconditioning of bone marrow mesenchymal stem cells (BMSCs) could not only enhance

  13. Nanoparticle Pre-Conditioning for Enhanced Thermal Therapies in Cancer

    PubMed Central

    Shenoi, Mithun M.; Shah, Neha B.; Griffin, Robert J.; Vercellotti, Gregory M.; Bischof, John C.

    2011-01-01

    Nanoparticles show tremendous promise in the safe and effective delivery of molecular adjuvants to enhance local cancer therapy. One important form of local cancer treatment that suffers from local recurrence and distant metastases is thermal therapy. Here we review a new concept involving the use of nanoparticle delivered adjuvants to “pre-condition” or alter the vascular and immunological biology of the tumor to enhance its susceptibility to thermal therapy. To this end, a number of opportunities to combine nanoparticles with vascular and immunologically active agents are reviewed. One specific example of pre-conditioning involves a gold nanoparticle tagged with a vascular targeting agent (i.e. TNF-?). This nanoparticle embodiment demonstrates pre-conditioning through a dramatic reduction in tumor blood flow and induction of vascular damage which recruits a strong and sustained inflammatory infiltrate in the tumor. The ability of this nanoparticle pre-conditioning to enhance subsequent heat or cold thermal therapy in a variety of tumor models is reviewed. Finally, the potential for future clinical imaging to judge the extent of pre-conditioning and thus the optimal timing and extent of combinatorial thermal therapy is discussed. PMID:21542691

  14. Implementation of Preconditioned Dual-Time Procedures in OVERFLOW

    NASA Technical Reports Server (NTRS)

    Pandya, Shishir A.; Venkateswaran, Sankaran; Pulliam, Thomas H.; Kwak, Dochan (Technical Monitor)

    2003-01-01

    Preconditioning methods have become the method of choice for the solution of flowfields involving the simultaneous presence of low Mach and transonic regions. It is well known that these methods are important for insuring accurate numerical discretization as well as convergence efficiency over various operating conditions such as low Mach number, low Reynolds number and high Strouhal numbers. For unsteady problems, the preconditioning is introduced within a dual-time framework wherein the physical time-derivatives are used to march the unsteady equations and the preconditioned time-derivatives are used for purposes of numerical discretization and iterative solution. In this paper, we describe the implementation of the preconditioned dual-time methodology in the OVERFLOW code. To demonstrate the performance of the method, we employ both simple and practical unsteady flowfields, including vortex propagation in a low Mach number flow, flowfield of an impulsively started plate (Stokes' first problem) arid a cylindrical jet in a low Mach number crossflow with ground effect. All the results demonstrate that the preconditioning algorithm is responsible for improvements to both numerical accuracy and convergence efficiency and, thereby, enables low Mach number unsteady computations to be performed at a fraction of the cost of traditional time-marching methods.

  15. Operator-Based Preconditioning of Stiff Hyperbolic Systems

    SciTech Connect

    Reynolds, Daniel R.; Samtaney, Ravi; Woodward, Carol S.

    2009-02-09

    We introduce an operator-based scheme for preconditioning stiff components encoun- tered in implicit methods for hyperbolic systems of partial differential equations posed on regular grids. The method is based on a directional splitting of the implicit operator, followed by a char- acteristic decomposition of the resulting directional parts. This approach allows for solution to any number of characteristic components, from the entire system to only the fastest, stiffness-inducing waves. We apply the preconditioning method to stiff hyperbolic systems arising in magnetohydro- dynamics and gas dynamics. We then present numerical results showing that this preconditioning scheme works well on problems where the underlying stiffness results from the interaction of fast transient waves with slowly-evolving dynamics, scales well to large problem sizes and numbers of processors, and allows for additional customization based on the specific problems under study.

  16. Liquid hydrogen turbopump rapid start program. [thermal preconditioning using coatings

    NASA Technical Reports Server (NTRS)

    Wong, G. S.

    1973-01-01

    This program was to analyze, test, and evaluate methods of achieving rapid-start of a liquid hydrogen feed system (inlet duct and turbopump) using a minimum of thermal preconditioning time and propellant. The program was divided into four tasks. Task 1 includes analytical studies of the testing conducted in the other three tasks. Task 2 describes the results from laboratory testing of coating samples and the successful adherence of a KX-635 coating to the internal surfaces of the feed system tested in Task 4. Task 3 presents results of testing an uncoated feed system. Tank pressure was varied to determine the effect of flowrate on preconditioning. The discharge volume and the discharge pressure which initiates opening of the discharge valve were varied to determine the effect on deadhead (no through-flow) start transients. Task 4 describes results of testing a similar, internally coated feed system and illustrates the savings in preconditioning time and propellant resulting from the coatings.

  17. On adaptive weighted polynomial preconditioning for Hermitian positive definite matrices

    NASA Technical Reports Server (NTRS)

    Fischer, Bernd; Freund, Roland W.

    1992-01-01

    The conjugate gradient algorithm for solving Hermitian positive definite linear systems is usually combined with preconditioning in order to speed up convergence. In recent years, there has been a revival of polynomial preconditioning, motivated by the attractive features of the method on modern architectures. Standard techniques for choosing the preconditioning polynomial are based only on bounds for the extreme eigenvalues. Here a different approach is proposed, which aims at adapting the preconditioner to the eigenvalue distribution of the coefficient matrix. The technique is based on the observation that good estimates for the eigenvalue distribution can be derived after only a few steps of the Lanczos process. This information is then used to construct a weight function for a suitable Chebyshev approximation problem. The solution of this problem yields the polynomial preconditioner. In particular, we investigate the use of Bernstein-Szego weights.

  18. 40 CFR 85.2219 - Idle test with loaded preconditioning-EPA 91.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 2013-07-01 2013-07-01 false Idle test with loaded preconditioning-EPA 91. 85.2219...Emission Control System Performance Warranty Short Tests § 85.2219 Idle test with loaded preconditioning—EPA 91. (a)...

  19. 40 CFR 92.125 - Pre-test procedures and preconditioning.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ...2013-07-01 2013-07-01 false Pre-test procedures and preconditioning. 92.125 Section...POLLUTION FROM LOCOMOTIVES AND LOCOMOTIVE ENGINES Test Procedures § 92.125 Pre-test procedures and preconditioning. (a)...

  20. 40 CFR 85.2218 - Preconditioned idle test-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 2012-07-01 false Preconditioned idle test-EPA 91. 85.2218 Section 85.2218 ...Emission Control System Performance Warranty Short Tests § 85.2218 Preconditioned idle test—EPA 91. (a) General requirements...

  1. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...and canister preconditioning; refueling test. 86.153-98 Section 86.153-98...Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister...

  2. 40 CFR 85.2219 - Idle test with loaded preconditioning-EPA 91.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 2011-07-01 2011-07-01 false Idle test with loaded preconditioning-EPA 91. 85.2219...Emission Control System Performance Warranty Short Tests § 85.2219 Idle test with loaded preconditioning—EPA 91. (a)...

  3. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ...and canister preconditioning; refueling test. 86.153-98 Section 86.153-98...Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister...

  4. 40 CFR 85.2219 - Idle test with loaded preconditioning-EPA 91.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 2010-07-01 2010-07-01 false Idle test with loaded preconditioning-EPA 91. 85.2219...Emission Control System Performance Warranty Short Tests § 85.2219 Idle test with loaded preconditioning—EPA 91. (a)...

  5. 40 CFR 85.2218 - Preconditioned idle test-EPA 91.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 2011-07-01 false Preconditioned idle test-EPA 91. 85.2218 Section 85.2218 ...Emission Control System Performance Warranty Short Tests § 85.2218 Preconditioned idle test—EPA 91. (a) General requirements...

  6. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ...and canister preconditioning; refueling test. 86.153-98 Section 86.153-98...Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister...

  7. 40 CFR 85.2219 - Idle test with loaded preconditioning-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 2012-07-01 2012-07-01 false Idle test with loaded preconditioning-EPA 91. 85.2219...Emission Control System Performance Warranty Short Tests § 85.2219 Idle test with loaded preconditioning—EPA 91. (a)...

  8. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...and canister preconditioning; refueling test. 86.153-98 Section 86.153-98...Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister...

  9. 40 CFR 85.2218 - Preconditioned idle test-EPA 91.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 2010-07-01 false Preconditioned idle test-EPA 91. 85.2218 Section 85.2218 ...Emission Control System Performance Warranty Short Tests § 85.2218 Preconditioned idle test—EPA 91. (a) General requirements...

  10. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ...and canister preconditioning; refueling test. 86.153-98 Section 86.153-98...Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister...

  11. 40 CFR 85.2218 - Preconditioned idle test-EPA 91.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 2013-07-01 false Preconditioned idle test-EPA 91. 85.2218 Section 85.2218 ...Emission Control System Performance Warranty Short Tests § 85.2218 Preconditioned idle test—EPA 91. (a) General requirements...

  12. Scalable Preconditioned Eigenvalue Solver in Hypre Merico Argentati and Andrew Knyazev (speaker)

    E-print Network

    Knyazev, Andrew

    Scalable Preconditioned Eigenvalue Solver in Hypre Merico Argentati and Andrew Knyazev (speaker of a symmetric matrix using preconditioning directly, without using the shift-and-invert scheme and inner

  13. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... false PM sampling media (e.g., filters) preconditioning and tare weighing...590 PM sampling media (e.g., filters) preconditioning and tare weighing...to prepare PM sampling media (e.g., filters) and equipment for PM...

  14. AdipoRon, the first orally active adiponectin receptor activator, attenuates postischemic myocardial apoptosis through both AMPK-mediated and AMPK-independent signalings.

    PubMed

    Zhang, Yanqing; Zhao, Jianli; Li, Rui; Lau, Wayne Bond; Yuan, Yue-Xing; Liang, Bin; Li, Rong; Gao, Er-He; Koch, Walter J; Ma, Xin-Liang; Wang, Ya-Jing

    2015-08-01

    Adiponectin (APN) is a cardioprotective molecule. Its reduction in diabetes exacerbates myocardial ischemia/reperfusion (MI/R) injury. Although APN administration in animals attenuates MI/R injury, multiple factors limit its clinical application. The current study investigated whether AdipoRon, the first orally active molecule that binds APN receptors, may protect the heart against MI/R injury, and if so, to delineate the involved mechanisms. Wild-type (WT), APN knockout (APN-KO), and cardiomyocyte specific-AMPK dominant negative (AMPK-DN) mice were treated with vehicle or AdipoRon (50 mg/kg, 10 min prior to MI) and subjected to MI/R (30 min/3-24 h). Compared with vehicle, oral administration of AdipoRon to WT mice significantly improved cardiac function and attenuated postischemic cardiomyocyte apoptosis, determined by DNA ladder formation, TUNEL staining, and caspase-3 activation (all P < 0.01). MI/R-induced apoptotic cell death was significantly enhanced in mice deficient in either APN (APN-KO) or AMPK (AMPK-DN). In APN-KO mice, AdipoRon attenuated MI/R injury to the same degree as observed in WT mice. In AMPK-DN mice, AdipoRon's antiapoptotic action was partially inhibited but not lost. Finally, AdipoRon significantly attenuated postischemic oxidative stress, as evidenced by reduced NADPH oxidase expression and superoxide production. Collectively, these results demonstrate for the first time that AdipoRon, an orally active APN receptor activator, effectively attenuated postischemic cardiac injury, supporting APN receptor agonists as a promising novel therapeutic approach treating cardiovascular complications caused by obesity-related disorders such as type 2 diabetes. PMID:26037251

  15. Fourier analysis of finite element preconditioned collocation schemes

    NASA Technical Reports Server (NTRS)

    Deville, Michel O.; Mund, Ernest H.

    1990-01-01

    The spectrum of the iteration operator of some finite element preconditioned Fourier collocation schemes is investigated. The first part of the paper analyses one-dimensional elliptic and hyperbolic model problems and the advection-diffusion equation. Analytical expressions of the eigenvalues are obtained with use of symbolic computation. The second part of the paper considers the set of one-dimensional differential equations resulting from Fourier analysis (in the tranverse direction) of the 2-D Stokes problem. All results agree with previous conclusions on the numerical efficiency of finite element preconditioning schemes.

  16. A subspace preconditioning algorithm for eigenvector/eigenvalue computation

    SciTech Connect

    Bramble, J.H.; Knyazev, A.V.; Pasciak, J.E.

    1996-12-31

    We consider the problem of computing a modest number of the smallest eigenvalues along with orthogonal bases for the corresponding eigen-spaces of a symmetric positive definite matrix. In our applications, the dimension of a matrix is large and the cost of its inverting is prohibitive. In this paper, we shall develop an effective parallelizable technique for computing these eigenvalues and eigenvectors utilizing subspace iteration and preconditioning. Estimates will be provided which show that the preconditioned method converges linearly and uniformly in the matrix dimension when used with a uniform preconditioner under the assumption that the approximating subspace is close enough to the span of desired eigenvectors.

  17. FTY720 Reduces Post-Ischemic Brain Lymphocyte Influx but Does Not Improve Outcome in Permanent Murine Cerebral Ischemia

    PubMed Central

    Liesz, Arthur; Sun, Li; Zhou, Wei; Schwarting, Sönke; Mracsko, Eva; Zorn, Markus; Bauer, Henrike; Sommer, Clemens; Veltkamp, Roland

    2011-01-01

    Background The contribution of neuroinflammation and specifically brain lymphocyte invasion is increasingly recognised as a substantial pathophysiological mechanism after stroke. FTY720 is a potent treatment for primary neuroinflammatory diseases by inhibiting lymphocyte circulation and brain immigration. Previous studies using transient focal ischemia models showed a protective effect of FTY720 but did only partially characterize the involved pathways. We tested the neuroprotective properties of FTY720 in permanent and transient cortical ischemia and analyzed the underlying neuroimmunological mechanisms. Methodology/Principal Findings FTY720 treatment resulted in substantial reduction of circulating lymphocytes while blood monocyte counts were significantly increased. The number of histologically and flow cytometrically analyzed brain invading T- and B lymphocytes was significantly reduced in FTY720 treated mice. However, despite testing a variety of treatment protocols, infarct volume and behavioural dysfunction were not reduced 7d after permanent occlusion of the distal middle cerebral artery (MCAO). Additionally, we did not measure a significant reduction in infarct volume at 24h after 60 min filament-induced MCAO, and did not see differences in brain edema between PBS and FTY720 treatment. Analysis of brain cytokine expression revealed complex effects of FTY720 on postischemic neuroinflammation comprising a substantial reduction of delayed proinflammatory cytokine expression at 3d but an early increase of IL-1? and IFN-? at 24 h after MCAO. Also, serum cytokine levels of IL-6 and TNF-? were increased in FTY720 treated animals compared to controls. Conclusions/Significance In the present study we were able to detect a reduction of lymphocyte brain invasion by FTY720 but could not achieve a significant reduction of infarct volumes and behavioural dysfunction. This lack of neuroprotection despite effective lymphopenia might be attributed to a divergent impact of FTY720 on cytokine expression and possible activation of innate immune cells after brain ischemia. PMID:21701599

  18. Thermal Preconditioning and Heat-Shock Protein 72 Preserve Synaptic Transmission during Thermal Stress

    E-print Network

    Robertson, Meldrum

    Thermal Preconditioning and Heat-Shock Protein 72 Preserve Synaptic Transmission during Thermal, exposing the mammalian CNS to nonle- thal heat stress (i.e., thermal preconditioning) increases levels that generates respiratory rhythm (the pre- Bo¨ tzinger complex), we show that thermal preconditioning has

  19. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 18 2010-07-01 2010-07-01 false Vehicle and canister preconditioning... New Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister preconditioning. Vehicles and vapor storage...

  20. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 18 2011-07-01 2011-07-01 false Vehicle and canister preconditioning... New Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister preconditioning. Vehicles and vapor storage...

  1. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 19 2012-07-01 2012-07-01 false Vehicle and canister preconditioning... New Otto-Cycle Complete Heavy-Duty Vehicles; Test Procedures § 86.153-98 Vehicle and canister preconditioning; refueling test. (a) Vehicle and canister preconditioning. Vehicles and vapor storage...

  2. Poly(ADP-Ribose)Polymerase 1 (PARP-1) Activation and Ca(2+) Permeable ?-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionic Acid (AMPA) Channels in Post-Ischemic Brain Damage: New Therapeutic Opportunities?

    PubMed

    Gerace, Elisabetta; Pellegrini-Giampietro, Domenico E; Moroni, Flavio; Mannaioni, Guido

    2015-01-01

    A significant number of laboratories observed that poly (ADP-ribose) polymerase (PARP) inhibitors, administered a few hours after ischemic or traumatic brain injury, may drastically reduce the subsequent neurological damage. It has also been shown that PARP inhibitors, administered for 24 hours to rats with permanent middle cerebral artery occlusion (MCAO), may reduce the number of dying neurons for a long period after surgery, thus suggesting that these agents could reduce the delayed brain damage and the neurological and cognitive impairment (dementia) frequently observed a few months after a stroke. In organotypic hippocampal slices exposed to N-methyl-N'-nitro-N'-nitrosoguanidine (MNNG), an alkylating agent able to activate PARP, a selective and delayed degeneration of the CA1 pyramidal cells which was anatomically similar to that observed after a short period of oxygen and glucose deprivation (OGD) has been described. Biochemical and electrophysiological approaches showed that MNNG exposure caused an increased expression and function of the calcium permeable ?-amino- 3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) channels in the CA1 but not in the CA3 hippocampal region. PARP inhibitors prevented this increase and reduced CA1 cell death. The AMPA receptor antagonist 2,3-dihydroxy-6- nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione or the selective Ca(2+) permeable AMPA channel blocker 1-Naphthyl acetyl spermine (NASPM), also reduced the MNNG-induced CA1 pyramidal cell death. Since activation of PARP-1 facilitate the expression of Ca(2+) permeable channels and the subsequent delayed cell death, PARP inhibitors administered a few hours after a stroke may not only reduce the early post-ischemic brain damage but also the late neuronal death frequently occurring after severe stroke. PMID:25924998

  3. Ischemic preconditioning protects hippocampal pyramidal neurons from transient ischemic injury via the attenuation of oxidative damage through upregulating heme oxygenase-1.

    PubMed

    Lee, Jae-Chul; Kim, In Hye; Park, Joon Ha; Ahn, Ji Hyeon; Cho, Jeong-Hwi; Cho, Geum-Sil; Tae, Hyun-Jin; Chen, Bai Hui; Yan, Bing Chun; Yoo, Ki-Yeon; Choi, Jung Hoon; Lee, Choong Hyun; Hwang, In Koo; Cho, Jun Hwi; Kwon, Young-Guen; Kim, Young-Myeong; Won, Moo-Ho

    2015-02-01

    Ischemic preconditioning (IPC) provides neuroprotection against subsequent severe ischemic injury by activating specific mechanisms. In this study, we tested the hypothesis that IPC attenuates postischemic neuronal death via heme oxygenase-1 (HO-1). Animals used in this study were randomly assigned to 4 groups; sham-operated group, ischemia-operated group, IPC plus (+) sham-operated group and IPC+ischemia-operated group. IPC was induced by subjecting gerbils to 2min of ischemia followed by 1 day of recovery. A significant loss of neurons was observed in pyramidal neurons of the hippocampal CA1 region (CA1) in the ischemia-operated groups at 5 days postischemia. In the IPC+ischemia-operated groups, CA1 pyramidal neurons were well protected. The level of HO-1 protein and its activity increased significantly in the CA1 of the IPC+sham-operated group, and the level and activity was maintained in all the time after ischemia-reperfusion compared with the ischemia-operated groups. HO-1 immunoreactivity was induced in the CA1 pyramidal neurons in both IPC+sham-operated- and IPC+ischemia-operated groups. We also found that levels or immunoreactivities of superoxide anion, 8-hydroxy-2'-deoxyguanosine and 4-hydroxy-2-nonenal were significantly decreased in the CA1 of both IPC+sham-operated- and IPC+ischemia-operated groups. Whereas, treatment with zinc protoporphyrin IX (a HO-1 inhibitor) into the IPC+ischemia-operated groups did not preserve the IPC-mediated increase of HO-1 and lost beneficial effects of IPC by inhibiting ischemia-induced DNA damage and lipid peroxidation. In brief, IPC protects CA1 pyramidal neurons from ischemic injury by upregulating HO-1, and we suggest that the enhancement of HO-1 expression by IPC may be a legitimate strategy for a therapeutic intervention of cerebral ischemic damage. PMID:25483558

  4. Finding Chemical Reaction Paths with a Multilevel Preconditioning Seyit Kale,,

    E-print Network

    Dinner, Aaron

    Finding Chemical Reaction Paths with a Multilevel Preconditioning Protocol Seyit Kale,, Olaseni for chemical reactions can be computationally costly owing to the level of quantum- chemical theory needed for the reaction path iteratively. These methods have yielded important insights in quantum chemical contexts9

  5. 33 CFR 183.220 - Preconditioning for tests.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... (CONTINUED) BOATING SAFETY BOATS AND ASSOCIATED EQUIPMENT Flotation Requirements for Outboard Boats Rated for Engines of More Than 2 Horsepower General § 183.220 Preconditioning for tests. A boat must meet the... boat. (b) The boat must be loaded with a quantity of weight that, when submerged, is equal to the...

  6. 40 CFR 1065.516 - Sample system decontamination and preconditioning.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 33 2014-07-01 2014-07-01 false Sample system decontamination and preconditioning. 1065.516 Section 1065.516 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR POLLUTION CONTROLS ENGINE-TESTING PROCEDURES Performing an Emission Test Over Specified Duty Cycles § 1065.516 Sample...

  7. Behavioral/Systems/Cognitive Octopamine Mediates Thermal Preconditioning of the

    E-print Network

    Robertson, Meldrum

    with a high (45°C) and prolonged (3 h) exposure to heat followed by a 1 h recovery [heat shock treatment (HS generation. However, OA treatment by bath applications (10 4 M OA) or by injections into the hemocoel (2 g/10 l OA) mimicked heat shock preconditioning and improved the thermotolerance of the motor pattern

  8. 40 CFR 86.132-00 - Vehicle preconditioning.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ...highway, US06 or SC03 test cycles. (ii) [Reserved] (iii) If a manufacturer has concerns about fuel effects on adaptive memory systems, a manufacturer may precondition a test vehicle on test fuel and the US06 cycle. Upon request from a...

  9. PRECONDITIONED ITERATIVE METHODS FOR SOLVING LINEAR LEAST SQUARES PROBLEMS

    E-print Network

    Tùma, Miroslav

    ´IN, JOS´E MAS AND MIROSLAV T°UMA Abstract. New preconditioning strategies for solving m × n overdetermined´arenskou vez´i 2, 182 07 Prague 8, Czech Republic, (tuma@cs.cas.cz). 1 #12;equations and a factorization

  10. 40 CFR 86.132-00 - Vehicle preconditioning.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 19 2013-07-01 2013-07-01 false Vehicle preconditioning. 86.132-00 Section 86.132-00 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF EMISSIONS FROM NEW AND IN-USE HIGHWAY VEHICLES AND ENGINES Emission Regulations for 1977 and Later Model Year New...

  11. 40 CFR 86.132-00 - Vehicle preconditioning.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...Emission Regulations for 1977 and Later Model Year New Light-Duty Vehicles and New Light-Duty Trucks and New Otto-Cycle Complete Heavy-Duty...subsequent test shall begin with the preconditioning drive specified in § 86.132-96(c)(1). The...

  12. On preconditioning strategies for geotechnics C.E. Augarde

    E-print Network

    Augarde, Charles

    On preconditioning strategies for geotechnics C.E. Augarde School of Engineering, University in geotechnics is overwhelmingly dominated by the use of finite element (FE) methods. They have proved" to model the majority of geotechnical problems, although this was a decision based on the capabilities

  13. Preconditioned Multigrid Simulation of an Axisymmetric Laminar Diffusion Flame \\Lambda

    E-print Network

    Zhang, Jun

    the growth of the Krylov iterations. Key words ­ laminar diffusion flame, vorticity­velocity formulationPreconditioned Multigrid Simulation of an Axisymmetric Laminar Diffusion Flame \\Lambda Samir Karaa of an elliptic flame sheet problem. By selecting the generalized minimum residual method as the linear smoother

  14. PRECONDITIONING BY APPROXIMATE SCHUR COMPLEMENTS ON HIERARCHICAL GRIDS

    E-print Network

    PRECONDITIONING BY APPROXIMATE SCHUR COMPLEMENTS ON HIERARCHICAL GRIDS C. BRAND AND J. KRAUS], [8] and [5]. A specific ordering of the unknowns, introduced by Brand [4], improved the asymptotic and Eijkhout investigated in their work [1] also W­cycles realized by employment of second order matrix

  15. Numerical simulation of cavitating flows based on preconditioning technique

    NASA Astrophysics Data System (ADS)

    Goncalvès, E.

    2013-10-01

    A preconditioned numerical method for gas-liquid two-phase flows is applied to solve cavitating flow. The mass transfer between phases is modelled through a void ratio transport equation. Two-dimensional turbulent Venturi flows are computed. Comparisons with a 3-equation model and experimental data are provided and discussed.

  16. 40 CFR 86.132-00 - Vehicle preconditioning.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 18 2010-07-01 2010-07-01 false Vehicle preconditioning. 86.132-00 Section 86.132-00 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF EMISSIONS FROM NEW AND IN-USE HIGHWAY VEHICLES AND ENGINES Emission Regulations for 1977 and Later Model Year New...

  17. Universitat Regensburg Preconditioning for Allen-Cahn variational

    E-print Network

    Blank, Luise - Naturwissenschaftliche Fakultät I

    -local constraints Luise Blank, Lavinia Sarbu and Martin Stoll Preprint Nr. 11/2010 #12;PRECONDITIONING FOR ALLEN-CAHN VARIATIONAL INEQUALITIES WITH NON-LOCAL CONSTRAINTS LUISE BLANK§, LAVINIA SARBUAND MARTIN STOLL Abstract. AMS subject classifications. Primary 65F10, 65N22, 65F50 Secondary 76D07 Key words. PDE

  18. 40 CFR 86.232-94 - Vehicle preconditioning.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ...Medium-Duty Passenger Vehicles; Cold Temperature Test Procedures § 86.232-94 ...fuel fill. The test fuel shall be at a temperature less than or equal to 60 °F. For...certification testing, precondition vehicles at temperatures above 20 °F (?7 °C) and with...

  19. 40 CFR 86.232-94 - Vehicle preconditioning.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...Medium-Duty Passenger Vehicles; Cold Temperature Test Procedures § 86.232-94 ...fuel fill. The test fuel shall be at a temperature less than or equal to 60 °F. For...certification testing, precondition vehicles at temperatures above 20 °F (?7 °C) and with...

  20. 40 CFR 86.232-94 - Vehicle preconditioning.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ...Medium-Duty Passenger Vehicles; Cold Temperature Test Procedures § 86.232-94 ...fuel fill. The test fuel shall be at a temperature less than or equal to 60 °F. For...certification testing, precondition vehicles at temperatures above 20 °F (?7 °C) and with...

  1. 40 CFR 86.232-94 - Vehicle preconditioning.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ...Medium-Duty Passenger Vehicles; Cold Temperature Test Procedures § 86.232-94 ...fuel fill. The test fuel shall be at a temperature less than or equal to 60 °F. For...certification testing, precondition vehicles at temperatures above 20 °F (?7 °C) and with...

  2. Thrombin Preconditioning in Surgical Brain Injury in Rats.

    PubMed

    Benggon, Michael; Chen, Hank; Applegate, Richard L; Zhang, John

    2016-01-01

    The surgical brain injury model replicates neurosurgical brain parenchymal damage. Postsurgical brain edema correlates with postoperative neurological dysfunction. Intranasal administration is a proven method of delivering therapies to brain tissue. Thrombin preconditioning decreased brain edema and improved neurological outcomes in models of ischemic brain injury. We hypothesized thrombin preconditioning in surgical brain injury may improve postoperative brain edema and neurological outcomes. Adult male Sprague-Dawley rats (n?=?78) weighing 285-355 g were randomly assigned to sham or pre-injury treatment: one-time pretreatment 1 day prior, one-time pretreatment 5 days prior, and daily preconditioning for 5 days prior. Treatment arms were divided into vehicle or thrombin therapies, and subdivided into intranasal (thrombin 5 units/50 ?L 0.9 % saline) or intracerebral ventricular (thrombin 0.1 unit/10 ?L 0.9 % saline) administration. Blinded observers performed neurological testing 24 h after brain injury followed immediately by measurement of brain water content. There was a significant difference in ipsilateral brain water content and neurological outcomes between all treatment groups and the sham group. However, there was no change in brain water content or neurological outcomes between thrombin- and vehicle-treated animals. Thrombin preconditioning did not significantly improve brain edema or neurological function in surgical brain injury in rats. PMID:26463965

  3. AN INVERSE FREE PRECONDITIONED KRYLOV SUBSPACE METHOD FOR

    E-print Network

    Kentucky, University of

    AN INVERSE FREE PRECONDITIONED KRYLOV SUBSPACE METHOD FOR SYMMETRIC GENERALIZED EIGENVALUE PROBLEMS Gene H. Golub #3; Qiang Ye y ABSTRACT In this paper, we present an inverse free Krylov subspace method, Stanford University, Stanford, CA 94305. E-mail : golub@sccm.stanford.edu. Research supported in part

  4. [Transfer of Preventive Interventions into Health Care Provision].

    PubMed

    Finck, S; Nöcker, G; Wildner, M; Walter, U

    2015-09-01

    Successful transfer of evidence based prevention programs and interventions in health care is a precondition for improvement of public health. The BMBF research focus on prevention contained substantial transfer experiences that have been analysed. As a result, a set up of a new research focus including specific methodology was recommended. The paper summarizes the KNP transfer results. PMID:24288257

  5. Inhibition of CXCL12 signaling attenuates the postischemic immune response and improves functional recovery after stroke.

    PubMed

    Ruscher, Karsten; Kuric, Enida; Liu, Yawei; Walter, Helene L; Issazadeh-Navikas, Shohreh; Englund, Elisabet; Wieloch, Tadeusz

    2013-08-01

    After stroke, brain inflammation in the ischemic hemisphere hampers brain tissue reorganization and functional recovery. Housing rats in an enriched environment (EE) dramatically improves recovery of lost neurologic functions after experimental stroke. We show here that rats housed in EE after stroke induced by permanent occlusion of the middle cerebral artery (pMCAO), showed attenuated levels of proinflammatory cytokines in the ischemic core and the surrounding peri-infarct area, including a significant reduction in the stroke-induced chemokine receptor CXCR4 and its natural ligand stromal cell-derived factor-1 (CXCL12). To mimic beneficial effects of EE, we studied the impact of inhibiting CXCL12 action on functional recovery after transient MCAO (tMCAO). Rats treated with the specific CXCL12 receptor antagonist 1-[4-(1,4,8,11-tetrazacyclotetradec-1-ylmethyl)phenyl]methyl]-1,4,8,11-tetrazacyclo-tetradecan (AMD3100) showed improved recovery compared with saline-treated rats after tMCAO, without a concomitant reduction in infarct size. This was accompanied by a reduction of infiltrating immune cells in the ischemic hemisphere, particularly cluster of differentiation 3-positive (CD3(+)) and CD3(+)/CD4(+) T cells. Spleen atrophy and delayed death of splenocytes, induced by tMCAO, was prevented by AMD3100 treatment. We conclude that immoderate excessive activation of the CXCL12 pathway after stroke contributes to depression of neurologic function after stroke and that CXCR4 antagonism is beneficial for the recovery after stroke. PMID:23632969

  6. Remote ischemic preconditioning and renoprotection: from myth to a novel therapeutic option?

    PubMed

    Gassanov, Natig; Nia, Amir M; Caglayan, Evren; Er, Fikret

    2014-02-01

    There is currently no effective prophylactic regimen available to prevent contrast-induced AKI (CI-AKI), a frequent and life-threatening complication after cardiac catheterization. Therefore, novel treatment strategies are required to decrease CI-AKI incidence and to improve clinical outcomes in these patients. Remote ischemic preconditioning (rIPC), defined as transient brief episodes of ischemia at a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects against ischemic and reperfusion insult. Indeed, several studies demonstrated the tissue-protective effects of rIPC in various target organs, including the kidneys. In this regard, rIPC may offer a novel noninvasive and virtually cost-free treatment strategy for decreasing CI-AKI incidence. This review evaluates the current experimental and clinical evidence for rIPC as a potential renoprotective strategy, and discusses the underlying mechanisms and key areas for future research. PMID:24309187

  7. Activation of cerebral sodium-glucose transporter type 1 function mediated by post-ischemic hyperglycemia exacerbates the development of cerebral ischemia.

    PubMed

    Yamazaki, Y; Ogihara, S; Harada, S; Tokuyama, S

    2015-12-01

    The regulation of post-ischemic hyperglycemia plays an important role in suppressing neuronal damage in therapeutic strategies for cerebral ischemia. We previously reported that the cerebral sodium-glucose transporter (SGLT) was involved in the post-ischemic hyperglycemia-induced exacerbation of cerebral ischemic neuronal damage. Cortical SGLT-1, one of the cerebral SGLT isoforms, is dramatically increased by focal cerebral ischemia. In this study, we focused on the involvement of cerebral SGLT-1 in the development of cerebral ischemic neuronal damage. It was previously reported that activation of 5'-adenosine monophosphate-activated protein kinase (AMPK) increases SGLT-1 expression. Moreover, ischemic stress-induced activation of AMPK exacerbates cerebral ischemic neuronal damage. Therefore, we directly confirmed the relationship between cerebral SGLT-1 and cerebral AMPK activation using in vitro primary culture of mouse cortical neurons. An in vivo mouse model of focal cerebral ischemia was generated using a middle cerebral artery occlusion (MCAO). The development of infarct volume and behavioral abnormalities on day 3 after MCAO were ameliorated in cerebral SGLT-1 knock down mice. Cortical and striatal SGLT-1 expression levels were significantly increased at 12h after MCAO. Immunofluorescence revealed that SGLT-1 and the neuronal nuclear antigen (NeuN) were co-localized in the cortex and striatum of MCAO mice. In the in vitro study, primary cortical neurons were cultured for five days before each treatment with reagents. Concomitant treatment with hydrogen peroxide and glucose induced the elevation of SGLT-1 and phosphorylated AMPK/AMPK ratio, and this elevation was suppressed by compound C, an AMPK inhibitor in primary cortical neurons. Moreover, compound C suppressed neuronal cell death induced by concomitant hydrogen peroxide/glucose treatment in primary cortical neurons. Therefore, we concluded that enhanced cerebral SGLT-1 function mediated by post-ischemic hyperglycemia exacerbates the development of cerebral ischemic neuronal damage. One of the mechanisms of cerebral SGLT-1 up-regulation may be involved in the AMPK activation after cerebral ischemia. PMID:26454021

  8. Shape reanalysis and sensitivities utilizing preconditioned iterative boundary solvers

    NASA Technical Reports Server (NTRS)

    Guru Prasad, K.; Kane, J. H.

    1992-01-01

    The computational advantages associated with the utilization of preconditined iterative equation solvers are quantified for the reanalysis of perturbed shapes using continuum structural boundary element analysis (BEA). Both single- and multi-zone three-dimensional problems are examined. Significant reductions in computer time are obtained by making use of previously computed solution vectors and preconditioners in subsequent analyses. The effectiveness of this technique is demonstrated for the computation of shape response sensitivities required in shape optimization. Computer times and accuracies achieved using the preconditioned iterative solvers are compared with those obtained via direct solvers and implicit differentiation of the boundary integral equations. It is concluded that this approach employing preconditioned iterative equation solvers in reanalysis and sensitivity analysis can be competitive with if not superior to those involving direct solvers.

  9. Parallel Domain Decomposition Preconditioning for Computational Fluid Dynamics

    NASA Technical Reports Server (NTRS)

    Barth, Timothy J.; Chan, Tony F.; Tang, Wei-Pai; Kutler, Paul (Technical Monitor)

    1998-01-01

    This viewgraph presentation gives an overview of the parallel domain decomposition preconditioning for computational fluid dynamics. Details are given on some difficult fluid flow problems, stabilized spatial discretizations, and Newton's method for solving the discretized flow equations. Schur complement domain decomposition is described through basic formulation, simplifying strategies (including iterative subdomain and Schur complement solves, matrix element dropping, localized Schur complement computation, and supersparse computations), and performance evaluation.

  10. Preconditioned solenoidal basis method for incompressible fluid flows 

    E-print Network

    Wang, Xue

    2006-04-12

    and content by: Vivek Sarin (Chair of Committee) Andreas Klappenecker (Member) Hamn-Ching Chen (Member) Valerie E. Taylor (Head of Department) December 2004 Major Subject: Computer Science iii ABSTRACT Preconditioned Solenoidal Basis Method for Incompressible... of this research and thesis. This thesis would not have been completed without his help. I would also like to thank my committee members Dr. Hamn-Ching Chen and Dr. Andreas Klappenecker for their help, support and valuable suggestions. A special thank...

  11. Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9

    PubMed Central

    Wei, Xuan; Wu, Bing; Zhao, Jing; Zeng, Zhi; Xuan, Wanling; Cao, Shiping; Huang, Xiaobo; Asakura, Masanori; Xu, Dingli; Bin, Jianping; Kitakaze, Masafumi

    2015-01-01

    Background— Transient preceding brief ischemia provides potent cardioprotection against subsequent long ischemia, termed ischemic preconditioning. Here, we hypothesized that transient short-term hypertrophic stimulation would induce the expression of hypertrophy regression genes and render the heart resistant to subsequent hypertrophic stress, and slow the progression to heart failure, as well. Methods and Results— Cardiomyocyte hypertrophy was induced in mice by either transverse aortic constriction or an infusion of phenylephrine, and in neonatal rat ventricular cardiomyocytes by norepinephrine exposures. In the preconditioning groups, hypertrophic stimulation was provided for 1 to 7 days and then withdrawn for several days by either aortic debanding or discontinuing phenylephrine or norepinephrine treatment, followed by subsequent reexposure to the hypertrophic stimulus for the same period as in the control group. One or 6 weeks after transverse aortic constriction, the heart weight/body weight ratio was lower in the preconditioning group than in the control group, whereas the lung weight/body weight ratio was significantly decreased 6 weeks after transverse aortic constriction. Similar results were obtained in mice receiving phenylephrine infusion and neonatal rat ventricular cardiomyocytes stimulated with norepinephrine. Both mRNA and protein expression of S100A8 and S100A9 showed significant upregulation after the removal of hypertrophic stimulation and persisted for 6 weeks in response to reimposition of transverse aortic constriction. The treatment with recombinant S100A8/A9 inhibited norepinephrine-induced myocyte hypertrophy and reduced the expression of calcineurin and NFATc3, but the silencing of S100A8/A9 prevented such changes. Conclusions— Preconditioning with prohypertrophic factors exerts an antihypertrophic effect and slows the progression of heart failure, indicating the existence of the phenomenon for hypertrophic preconditioning. PMID:25820336

  12. The evolving concept of physiological ischemia training vs. ischemia preconditioning.

    PubMed

    Ni, Jun; Lu, Hongjian; Lu, Xiao; Jiang, Minghui; Peng, Qingyun; Ren, Caili; Xiang, Jie; Mei, Chengyao; Li, Jianan

    2015-11-01

    Ischemic heart diseases are the leading cause of death with increasing numbers of patients worldwide. Despite advances in revascularization techniques, angiogenic therapies remain highly attractive. Physiological ischemia training, which is first proposed in our laboratory, refers to reversible ischemia training of normal skeletal muscles by using a tourniquet or isometric contraction to cause physiologic ischemia for about 4 weeks for the sake of triggering molecular and cellular mechanisms to promote angiogenesis and formation of collateral vessels and protect remote ischemia areas. Physiological ischemia training therapy augments angiogenesis in the ischemic myocardium by inducing differential expression of proteins involved in energy metabolism, cell migration, protein folding, and generation. It upregulates the expressions of vascular endothelial growth factor, and induces angiogenesis, protects the myocardium when infarction occurs by increasing circulating endothelial progenitor cells and enhancing their migration, which is in accordance with physical training in heart disease rehabilitation. These findings may lead to a new approach of therapeutic angiogenesis for patients with ischemic heart diseases. On the basis of the promising results in animal studies, studies were also conducted in patients with coronary artery disease without any adverse effect in vivo, indicating that physiological ischemia training therapy is a safe, effective and non-invasive angiogenic approach for cardiovascular rehabilitation. Preconditioning is considered to be the most protective intervention against myocardial ischemia-reperfusion injury to date. Physiological ischemia training is different from preconditioning. This review summarizes the preclinical and clinical data of physiological ischemia training and its difference from preconditioning. PMID:26664354

  13. The evolving concept of physiological ischemia training vs. ischemia preconditioning

    PubMed Central

    Ni, Jun; Lu, Hongjian; Lu, Xiao; Jiang, Minghui; Peng, Qingyun; Ren, Caili; Xiang, Jie; Mei, Chengyao; Li, Jianan

    2015-01-01

    Abstract Ischemic heart diseases are the leading cause of death with increasing numbers of patients worldwide. Despite advances in revascularization techniques, angiogenic therapies remain highly attractive. Physiological ischemia training, which is first proposed in our laboratory, refers to reversible ischemia training of normal skeletal muscles by using a tourniquet or isometric contraction to cause physiologic ischemia for about 4 weeks for the sake of triggering molecular and cellular mechanisms to promote angiogenesis and formation of collateral vessels and protect remote ischemia areas. Physiological ischemia training therapy augments angiogenesis in the ischemic myocardium by inducing differential expression of proteins involved in energy metabolism, cell migration, protein folding, and generation. It upregulates the expressions of vascular endothelial growth factor, and induces angiogenesis, protects the myocardium when infarction occurs by increasing circulating endothelial progenitor cells and enhancing their migration, which is in accordance with physical training in heart disease rehabilitation. These findings may lead to a new approach of therapeutic angiogenesis for patients with ischemic heart diseases. On the basis of the promising results in animal studies, studies were also conducted in patients with coronary artery disease without any adverse effect in vivo, indicating that physiological ischemia training therapy is a safe, effective and non-invasive angiogenic approach for cardiovascular rehabilitation. Preconditioning is considered to be the most protective intervention against myocardial ischemia-reperfusion injury to date. Physiological ischemia training is different from preconditioning. This review summarizes the preclinical and clinical data of physiological ischemia training and its difference from preconditioning.

  14. Islet preconditioning via multimodal microfluidic modulation of intermittent hypoxia.

    PubMed

    Lo, Joe F; Wang, Yong; Blake, Alexander; Yu, Gene; Harvat, Tricia A; Jeon, Hyojin; Oberholzer, Jose; Eddington, David T

    2012-02-21

    Simultaneous stimulation of ex vivo pancreatic islets with dynamic oxygen and glucose is a critical technique for studying how hypoxia alters glucose-stimulated response, especially in transplant environments. Standard techniques using a hypoxic chamber cannot provide both oxygen and glucose modulations, while monitoring stimulus-secretion coupling factors in real-time. Using novel microfluidic device with integrated glucose and oxygen modulations, we quantified hypoxic impairment of islet response by calcium influx, mitochondrial potentials, and insulin secretion. Glucose-induced calcium response magnitude and phase were suppressed by hypoxia, while mitochondrial hyperpolarization and insulin secretion decreased in coordination. More importantly, hypoxic response was improved by preconditioning islets to intermittent hypoxia (IH, 1 min/1 min 5-21% cycling for 1 h), translating to improved insulin secretion. Moreover, blocking mitochondrial K(ATP) channels removed preconditioning benefits of IH, similar to mechanisms in preconditioned cardiomyocytes. Additionally, the multimodal device can be applied to a variety of dynamic oxygen-metabolic studies in other ex vivo tissues. PMID:22296179

  15. Preconditioning the bidomain model with almost linear complexity

    NASA Astrophysics Data System (ADS)

    Pierre, Charles

    2012-01-01

    The bidomain model is widely used in electro-cardiology to simulate spreading of excitation in the myocardium and electrocardiograms. It consists of a system of two parabolic reaction diffusion equations coupled with an ODE system. Its discretisation displays an ill-conditioned system matrix to be inverted at each time step: simulations based on the bidomain model therefore are associated with high computational costs. In this paper we propose a preconditioning for the bidomain model either for an isolated heart or in an extended framework including a coupling with the surrounding tissues (the torso). The preconditioning is based on a formulation of the discrete problem that is shown to be symmetric positive semi-definite. A block LU decomposition of the system together with a heuristic approximation (referred to as the monodomain approximation) are the key ingredients for the preconditioning definition. Numerical results are provided for two test cases: a 2D test case on a realistic slice of the thorax based on a segmented heart medical image geometry, a 3D test case involving a small cubic slab of tissue with orthotropic anisotropy. The analysis of the resulting computational cost (both in terms of CPU time and of iteration number) shows an almost linear complexity with the problem size, i.e. of type nlog ?( n) (for some constant ?) which is optimal complexity for such problems.

  16. Resveratrol preconditioning increases methionine sulfoxide reductases A expression and enhances resistance of human neuroblastoma cells to neurotoxins.

    PubMed

    Wu, Peng-Fei; Xie, Na; Zhang, Juan-Juan; Guan, Xin-Lei; Zhou, Jun; Long, Li-Hong; Li, Yuan-Long; Xiong, Qiu-Ju; Zeng, Jian-Hua; Wang, Fang; Chen, Jian-Guo

    2013-06-01

    Methionine sulfoxide reductases A (MsrA) has been postulated to act as a catalytic antioxidant system involved in the protection of oxidative stress-induced cell injury. Recently, attention has turned to MsrA in coupling with the pathology of Parkinson's disease, which is closely related to neurotoxins that cause dopaminergic neuron degeneration. Here, we firstly provided evidence that pretreatment with a natural polyphenol resveratrol (RSV) up-regulated the expression of MsrA in human neuroblastoma SH-SY5Y cells. It was also observed that the expression and nuclear translocation of forkhead box group O 3a (FOXO3a), a transcription factor that activates the human MsrA promoter, increased after RSV pretreatment. Nicotinamide , an inhibitor of silent information regulator 1 (SIRT1), prevented RSV-induced elevation of FOXO3a and MsrA expression, indicating that the effect of RSV was mediated by a SIRT1-dependent pathway. RSV preconditioning increased methionine sulfoxide(MetO)-reducing activity in SH-SY5Y cells and enhanced their resistance to neurotoxins, including chloramine-T and 1-methyl-4-phenyl-pyridinium. In addition, the enhancement of cell resistance to neurotoxins caused by RSV preconditioning can be largely prevented by MsrA inhibitor dimethyl sulfoxide. Our findings suggest that treatment with polyphenols such as RSV can be used as a potential regulatory strategy for MsrA expression and function. PMID:23022493

  17. AdVEGF-All6A+ Preconditioning of Murine Ischemic Skin Flaps Is Comparable to Surgical Delay

    PubMed Central

    Gersch, Robert P.; Fourman, Mitchell S.; Phillips, Brett T.; Nasser, Ahmed; McClain, Steve A.; Khan, Sami U.; Dagum, Alexander B.

    2015-01-01

    Background: Surgical flap delay is commonly used in preconditioning reconstructive flaps to prevent necrosis. However, staged procedures are not ideal. Pharmacologic up-regulation of angiogenic and arteriogenic factors before flap elevation poses a nonsurgical approach to improve flap survival. Methods: Male Sprague Dawley rats were divided into control (n = 16), surgical delay (Delay), AdNull, AdEgr-1, and AdVEGF (n ? 9/group) groups. Delay rats had a 9 cm × 3 cm cranial based pedicle skin flap incised 10 days prior to elevation. Adenoviral groups received 28 intradermal injections (109 pu/animal total) throughout the distal two thirds of the flap 1 week prior to elevation. At postoperative day (POD) 0 flaps were elevated and silicone sheeting was placed between flap and wound bed. Perfusion analysis in arbitrary perfusion units of the ischemic middle third of the flap using laser Doppler imaging was conducted preoperatively and on POD 0, 3, and 7. Clinical and histopathologic assessments of the skin flaps were performed on POD 7. Results: AdVEGF (50.8 ± 10.9 APU) and AdEgr-1 (39.3 ± 10.6 APU) perfusion levels were significantly higher than controls (16.5 ± 4.2 APU) on POD 7. Delay models were equivalent to controls (25.9 ± 6.8 APU). AdVEGF and Delay animals showed significantly more viable surface area on POD 7 (14.4 ± 1.3 cm2, P < 0.01 and 12.4 ± 1.2 cm2, P < 0.05, respectively) compared with Controls (8.7 ± 0.7 cm2). Conclusions: AdVEGF preconditioning resulted in flap survival comparable to surgical delay. Adenoviral preconditioning maintained perfusion levels postoperatively while surgical delay did not. PMID:26495207

  18. Roles of thioredoxin in nitric oxide-dependent preconditioning-induced tolerance against MPTP neurotoxin

    SciTech Connect

    Chiueh, C.C. . E-mail: chiueh@tmu.edu.tw; Andoh, Tsugunobu; Chock, P. Boon

    2005-09-01

    Hormesis, a stress tolerance, can be induced by ischemic preconditioning stress. In addition to preconditioning, it may be induced by other means, such as gas anesthetics. Preconditioning mechanisms, which may be mediated by reprogramming survival genes and proteins, are obscure. A known neurotoxicant, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), causes less neurotoxicity in the mice that are preconditioned. Pharmacological evidences suggest that the signaling pathway of {center_dot}NO-cGMP-PKG (protein kinase G) may mediate preconditioning phenomenon. We developed a human SH-SY5Y cell model for investigating {sup {center_dot}}NO-mediated signaling pathway, gene regulation, and protein expression following a sublethal preconditioning stress caused by a brief 2-h serum deprivation. Preconditioned human SH-SY5Y cells are more resistant against severe oxidative stress and apoptosis caused by lethal serum deprivation and 1-mehtyl-4-phenylpyridinium (MPP{sup +}). Both sublethal and lethal oxidative stress caused by serum withdrawal increased neuronal nitric oxide synthase (nNOS/NOS1) expression and {sup {center_dot}}NO levels to a similar extent. In addition to free radical scavengers, inhibition of nNOS, guanylyl cyclase, and PKG blocks hormesis induced by preconditioning. S-nitrosothiols and 6-Br-cGMP produce a cytoprotection mimicking the action of preconditioning tolerance. There are two distinct cGMP-mediated survival pathways: (i) the up-regulation of a redox protein thioredoxin (Trx) for elevating mitochondrial levels of antioxidant protein Mn superoxide dismutase (MnSOD) and antiapoptotic protein Bcl-2, and (ii) the activation of mitochondrial ATP-sensitive potassium channels [K(ATP)]. Preconditioning induction of Trx increased tolerance against MPP{sup +}, which was blocked by Trx mRNA antisense oligonucleotide and Trx reductase inhibitor. It is concluded that Trx plays a pivotal role in {sup {center_dot}}NO-dependent preconditioning hormesis against MPTP/MPP{sup +}.

  19. Weighted graph based ordering techniques for preconditioned conjugate gradient methods

    NASA Technical Reports Server (NTRS)

    Clift, Simon S.; Tang, Wei-Pai

    1994-01-01

    We describe the basis of a matrix ordering heuristic for improving the incomplete factorization used in preconditioned conjugate gradient techniques applied to anisotropic PDE's. Several new matrix ordering techniques, derived from well-known algorithms in combinatorial graph theory, which attempt to implement this heuristic, are described. These ordering techniques are tested against a number of matrices arising from linear anisotropic PDE's, and compared with other matrix ordering techniques. A variation of RCM is shown to generally improve the quality of incomplete factorization preconditioners.

  20. Preconditioning methods for ideal and multiphase fluid flows

    NASA Astrophysics Data System (ADS)

    Gupta, Ashish

    The objective of this study is to develop a preconditioning method for ideal and multiphase multispecies compressible fluid flow solver using homogeneous equilibrium mixture model. The mathematical model for fluid flow going through phase change uses density and temperature in the formulation, where the density represents the multiphase mixture density. The change of phase of the fluid is then explicitly determined using the equation of state of the fluid, which only requires temperature and mixture density. The method developed is based on a finite-volume framework in which the numerical fluxes are computed using Roe's approximate Riemann solver and the modified Harten, Lax and Van-leer scheme (HLLC). All speed Roe and HLLC flux based schemes have been developed either by using preconditioning or by directly modifying dissipation to reduce the effect of acoustic speed in its numerical dissipation when Mach number decreases. Preconditioning proposed by Briley, Taylor and Whitfield, Eriksson and Turkel are studied in this research, where as low dissipation schemes proposed by Rieper and Thornber, Mosedale, Drikakis, Youngs and Williams are also considered. Various preconditioners are evaluated in terms of development, performance, accuracy and limitations in simulations at various Mach numbers. A generalized preconditioner is derived which possesses well conditioned eigensystem for multiphase multispecies flow simulations. Validation and verification of the solution procedure are carried out on several small model problems with comparison to experimental, theoretical, and other numerical results. Preconditioning methods are evaluated using three basic geometries; 1) bump in a channel 2) flow over a NACA0012 airfoil and 3) flow over a cylinder, which are then compared with theoretical and numerical results. Multiphase capabilities of the solver are evaluated in cryogenic and non-cryogenic conditions. For cryogenic conditions the solver is evaluated by predicting cavitation on two basic geometries for which experimental data are available, that is, flow over simple foil and a quarter caliber hydrofoil in a tunnel using liquid nitrogen as a fluid. For non-cryogenic conditions, water near boiling conditions is used to predict cavitation on two simple geometries, that is, flow over simple foil in a tunnel and flow over a one caliber ogive. Cavitation predictions in both cryogenic and non-cryogenic cases are shows to agree well with available experimental data.

  1. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ...2011-07-01 false Preconditioned two speed idle test-EPA 91. 85.2220 Section 85.2220...Emission Control System Performance Warranty Short Tests § 85.2220 Preconditioned two speed idle test—EPA 91. (a) General requirements...

  2. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ...2013-07-01 false Preconditioned two speed idle test-EPA 91. 85.2220 Section 85.2220...Emission Control System Performance Warranty Short Tests § 85.2220 Preconditioned two speed idle test—EPA 91. (a) General requirements...

  3. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...2010-07-01 false Preconditioned two speed idle test-EPA 91. 85.2220 Section 85.2220...Emission Control System Performance Warranty Short Tests § 85.2220 Preconditioned two speed idle test—EPA 91. (a) General requirements...

  4. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ...2012-07-01 false Preconditioned two speed idle test-EPA 91. 85.2220 Section 85.2220...Emission Control System Performance Warranty Short Tests § 85.2220 Preconditioned two speed idle test—EPA 91. (a) General requirements...

  5. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 2012-07-01 false PM sampling media (e.g., filters) preconditioning and...Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and...the following steps to prepare PM sampling media (e.g., filters) and equipment...

  6. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 2011-07-01 false PM sampling media (e.g., filters) preconditioning and...Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and...the following steps to prepare PM sampling media (e.g., filters) and equipment...

  7. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 2013-07-01 false PM sampling media (e.g., filters) preconditioning and...Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and...the following steps to prepare PM sampling media (e.g., filters) and equipment...

  8. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 2014-07-01 false PM sampling media (e.g., filters) preconditioning and...Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and...the following steps to prepare PM sampling media (e.g., filters) and equipment...

  9. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 18 2010-07-01 2010-07-01 false Preconditioned two speed idle test-EPA... Warranty Short Tests § 85.2220 Preconditioned two speed idle test—EPA 91. (a) General requirements—(1...-speed mode followed immediately by a first-chance idle mode. (ii) The second-chance test as...

  10. Waveform Preconditioning for Clutter Rejection in Multipath for Sparse Distributed Apertures

    E-print Network

    Yazici, Birsen

    Waveform Preconditioning for Clutter Rejection in Multipath for Sparse Distributed Apertures T preconditioning, distributed aperture, sparse aperture, waveform design, imaging. 1. INTRODUCTION In this paper we transmission. The work applies to systems with an arbitrary number of transmit- and receive-antenna elements

  11. Sensory Preconditioning in Newborn Rabbits: From Common to Distinct Odor Memories

    ERIC Educational Resources Information Center

    Coureaud, Gerard; Tourat, Audrey; Ferreira, Guillaume

    2013-01-01

    This study evaluated whether olfactory preconditioning is functional in newborn rabbits and based on joined or independent memory of odorants. First, after exposure to odorants A+B, the conditioning of A led to high responsiveness to odorant B. Second, responsiveness to B persisted after amnesia of A. Third, preconditioning was also functional…

  12. Sevoflurane Preconditioning Confers Neuroprotection via Anti-apoptosis Effects.

    PubMed

    Wang, Hailian; Shi, Hong; Yu, Qiong; Chen, Jun; Zhang, Feng; Gao, Yanqin

    2016-01-01

    Neuroprotection against cerebral ischemia afforded by volatile anesthetic preconditioning (APC) has been demonstrated both in vivo and in vitro, yet the underlying mechanism is poorly understood. We previously reported that repeated sevoflurane APC reduced infarct size in rats after focal ischemia. In this study, we investigated whether inhibition of apoptotic signaling cascades contributes to sevoflurane APC-induced neuroprotection. Male Sprague-Dawley rats were exposed to ambient air or 2.4 % sevoflurane for 30 min per day for 4 consecutive days and then subjected to occlusion of the middle cerebral artery (MCAO) for 60 min at 24 h after the last sevoflurane intervention. APC with sevoflurane markedly decreased apoptotic cell death in rat brains, which was accompanied by decreased caspase-3 cleavage and cytochrome c release. The apoptotic suppression was associated with increased ratios of anti-apoptotic Bcl-2 family proteins over pro-apoptotic proteins and with decreased activation of JNK and p53 pathways. Thus, our data suggest that suppression of apoptotic cell death contributes to the neuroprotection against ischemic brain injury conferred by sevoflurane preconditioning. PMID:26463923

  13. Low diffusion E-CUSP scheme with high order WENO scheme for preconditioned Navier-Stokes equations

    E-print Network

    Zha, Gecheng

    Low diffusion E-CUSP scheme with high order WENO scheme for preconditioned Navier-Stokes equations-Seidel relaxation scheme for time integration, the LDE scheme with high-order WENO reconstruction is used is to develop a preconditioned low diffusion E-CUSP scheme with high order WENO scheme for preconditioned Navier

  14. Hypobaric Preconditioning Modifies Group I mGluRs Signaling in Brain Cortex.

    PubMed

    Semenov, Dmitry G; Belyakov, Alexandr V; Glushchenko, Tatjana S; Samoilov, Mikhail O; Salinska, Elzbieta; Lazarewicz, Jerzy W

    2015-11-01

    The study assessed involvement of Ca(2+) signaling mediated by the metabotropic glutamate receptors mGluR1/5 in brain tolerance induced by hypoxic preconditioning. Acute slices of rat piriform cortex were tested 1 day after exposure of adult rats to mild hypobaric hypoxia for 2 h at a pressure of 480 hPa once a day for three consecutive days. We detected 44.1 ± 11.6 % suppression of in vitro anoxia-induced increases of intracellular Ca(2+) levels and a fivefold increase in Ca(2+) transients evoked by selective mGluR1/5 agonist, DHPG. Western blot analysis of cortical homogenates demonstrated a 11 ± 4 % decrease in mGluR1 immunoreactivity (IR), and in the nuclei-enriched fraction a 12 ± 3 % increase in IR of phospholipase C?1 (PLC?1), which is a major mediator of mGluR1/5 signaling. Immunocytochemical analysis of the cortex revealed increase in the mGluR1/5 and PLC?1 IR in perikarya, and a decrease in IR of the neuronal inositol trisphosphate receptors (IP3Rs). We suggest that enhanced expression of mGluR5 and PLC?1 and potentiation of Ca(2+) signaling may represent pro-survival upregulation of Ca(2+)-dependent genomic processes, while decrease in mGluR1 and IP3R IR may be attributed to a feedback mechanism preventing excessive intracellular Ca(2+) release. PMID:26318863

  15. Effect of Preconditioning and Soldering on Failures of Chip Tantalum Capacitors

    NASA Technical Reports Server (NTRS)

    Teverovsky, Alexander A.

    2014-01-01

    Soldering of molded case tantalum capacitors can result in damage to Ta205 dielectric and first turn-on failures due to thermo-mechanical stresses caused by CTE mismatch between materials used in the capacitors. It is also known that presence of moisture might cause damage to plastic cases due to the pop-corning effect. However, there are only scarce literature data on the effect of moisture content on the probability of post-soldering electrical failures. In this work, that is based on a case history, different groups of similar types of CWR tantalum capacitors from two lots were prepared for soldering by bake, moisture saturation, and longterm storage at room conditions. Results of the testing showed that both factors: initial quality of the lot, and preconditioning affect the probability of failures. Baking before soldering was shown to be effective to prevent failures even in lots susceptible to pop-corning damage. Mechanism of failures is discussed and recommendations for pre-soldering bake are suggested based on analysis of moisture characteristics of materials used in the capacitors' design.

  16. Impact of ischemic preconditioning on ischemia-reperfusion injury of the rat sciatic nerve

    PubMed Central

    Dong, Shuanghai; Cao, Yun; Li, Haoqing; Tian, Jiwei; Yi, Chengqing; Sang, Weilin

    2015-01-01

    The aim of this study was to assess the preventive effects of ischemic preconditioning (IPC) on ischemia-reperfusion (IR) injury in the sciatic nerve of the rat hind limb. This study included two experiments. For Experiment 1, 40 Sprague-Dawley (SD) rats were randomly divided into 4 equal groups that received different IPC treatments prior to IR. Serum concentrations of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) were assessed following reperfusion. Furthermore, we tested the electrophysiological response and ultrastructural changes in the ipsilateral sciatic nerve after IR. After determining the best IPC protocol for protection, we performed a second experiment with 30 SD rats randomly divided into 3 equal groups. Each group underwent 1, 2, or 3 IPC cycles before prolonged ischemia and reperfusion. The same analyses as in Experiment 1 were performed. In Experiment 1, the AST, LDH, and MDA concentrations were decreased in all IPC groups compared with the control group. Concentration of these enzymes showed decreases with increasing IPC cycle number in Experiment 2; however, the difference between 2 and 3 cycles of IPC did not reach significance. Conversely, SOD activity increased in the rapid and delayed groups, and with increasing cycles of IPC. The electrophysiological test showed a decrease in amplitude and increase in conduction velocity with increasing IPC cycles. Moreover, ultrastructural damage decreased with increasing IPC cycles. IPC protected against IR injury in the peripheral nerves. This effect was positively correlated with the number of IPC cycles. PMID:26629140

  17. Ozone oxidative preconditioning: a protection against cellular damage by free radicals.

    PubMed

    León, O S; Menéndez, S; Merino, N; Castillo, R; Sam, S; Pérez, L; Cruz, E; Bocci, V

    1998-01-01

    There is some anecdotal evidence that oxygen-ozone therapy may be beneficial in some human diseases. However so far only a few biochemical and pharmacodynamic mechanisms have been elucidated. On the basis of preliminary data we postulated that controlled ozone administration would promote an oxidative preconditioning preventing the hepatocellular damage mediated by free radicals. Six groups of rats were classified as follows: (1) negative control, using intraperitoneal sunflower oil; (2) positive control using carbon tetrachloride (CCl4) as an oxidative challenge; (3) oxygen-ozone, pretreatment via rectal insufflation (15 sessions) and after it, CCl4; (4) oxygen, as group 3 but using oxygen only; (5) control oxygen-ozone, as group 3, but without CCl4; group (6) control oxygen, as group 5, but using oxygen only. We have evaluated critical biochemical parameters such as levels of transaminase, cholinesterase, superoxide dismutase, catalase, phospholipase A, calcium dependent ATPase, reduced glutathione, glucose 6 phosphate dehydrogenase and lipid peroxidation. Interestingly, in spite of CCl4 administration, group 3 did not differ from group 1, while groups 2 and 4 showed significant differences from groups 1 and 3 and displayed hepatic damage. To our knowledge these are the first experimental results showing that repeated administration of ozone in atoxic doses is able to induce an adaptation to oxidative stress thus enabling the animals to maintain hepatocellular integrity after CCl4 poisoning. PMID:9792340

  18. Provisional Matrix Deposition in Hemostasis and Venous Insufficiency: Tissue Preconditioning for Nonhealing Venous Ulcers

    PubMed Central

    Parker, Tony J.; Broadbent, James A.; McGovern, Jacqui A.; Broszczak, Daniel A.; Parker, Christina N.; Upton, Zee

    2015-01-01

    Significance: Chronic wounds represent a major burden on global healthcare systems and reduce the quality of life of those affected. Significant advances have been made in our understanding of the biochemistry of wound healing progression. However, knowledge regarding the specific molecular processes influencing chronic wound formation and persistence remains limited. Recent Advances: Generally, healing of acute wounds begins with hemostasis and the deposition of a plasma-derived provisional matrix into the wound. The deposition of plasma matrix proteins is known to occur around the microvasculature of the lower limb as a result of venous insufficiency. This appears to alter limb cutaneous tissue physiology and consequently drives the tissue into a ‘preconditioned’ state that negatively influences the response to wounding. Critical Issues: Processes, such as oxygen and nutrient suppression, edema, inflammatory cell trapping/extravasation, diffuse inflammation, and tissue necrosis are thought to contribute to the advent of a chronic wound. Healing of the wound then becomes difficult in the context of an internally injured limb. Thus, interventions and therapies for promoting healing of the limb is a growing area of interest. For venous ulcers, treatment using compression bandaging encourages venous return and improves healing processes within the limb, critically however, once treatment concludes ulcers often reoccur. Future Directions: Improved understanding of the composition and role of pericapillary matrix deposits in facilitating internal limb injury and subsequent development of chronic wounds will be critical for informing and enhancing current best practice therapies and preventative action in the wound care field. PMID:25785239

  19. The Effect of Hypoxic Preconditioning on Induced Schwann Cells under Hypoxic Conditions

    PubMed Central

    Chen, Ou; Wu, Miaomiao; Jiang, Liangfu

    2015-01-01

    Object Our objective was to explore the protective effects of hypoxic preconditioning on induced Schwann cells exposed to an environment with low concentrations of oxygen. It has been observed that hypoxic preconditioning of induced Schwann cells can promote axonal regeneration under low oxygen conditions. Method Rat bone marrow mesenchymal stem cells (MSCs) were differentiated into Schwann cells and divided into a normal oxygen control group, a hypoxia-preconditioning group and a hypoxia group. The ultrastructure of each of these groups of cells was observed by electron microscopy. In addition, flow cytometry was used to measure changes in mitochondrial membrane potential. Annexin V-FITC/PI staining was used to detect apoptosis, and Western blots were used to detect the expression of Bcl-2/Bax. Fluorescence microscopic observations of axonal growth in NG-108 cells under hypoxic conditions were also performed. Results The hypoxia-preconditioning group maintained mitochondrial cell membrane and crista integrity, and these cells exhibited less edema than the hypoxia group. In addition, the cells in the hypoxia-preconditioning group were found to be in early stages of apoptosis, whereas cells from the hypoxia group were in the later stages of apoptosis. The hypoxia-preconditioning group also had higher levels of Bcl-2/Bax expression and longer NG-108 cell axons than were observed in the hypoxia group. Conclusion Hypoxic preconditioning can improve the physiological state of Schwann cells in a severe hypoxia environment and improve the ability to promote neurite outgrowth. PMID:26509259

  20. A frequency dependent preconditioned wavelet method for atmospheric tomography

    NASA Astrophysics Data System (ADS)

    Yudytskiy, Mykhaylo; Helin, Tapio; Ramlau, Ronny

    2013-12-01

    Atmospheric tomography, i.e. the reconstruction of the turbulence in the atmosphere, is a main task for the adaptive optics systems of the next generation telescopes. For extremely large telescopes, such as the European Extremely Large Telescope, this problem becomes overly complex and an efficient algorithm is needed to reduce numerical costs. Recently, a conjugate gradient method based on wavelet parametrization of turbulence layers was introduced [5]. An iterative algorithm can only be numerically efficient when the number of iterations required for a sufficient reconstruction is low. A way to achieve this is to design an efficient preconditioner. In this paper we propose a new frequency-dependent preconditioner for the wavelet method. In the context of a multi conjugate adaptive optics (MCAO) system simulated on the official end-to-end simulation tool OCTOPUS of the European Southern Observatory we demonstrate robustness and speed of the preconditioned algorithm. We show that three iterations are sufficient for a good reconstruction.

  1. Entanglement as precondition for secure quantum key distribution

    E-print Network

    Marcos Curty; Maciej Lewenstein; Norbert Lütkenhaus

    2003-07-21

    We demonstrate that a necessary precondition for unconditionally secure quantum key distribution is that sender and receiver can use the available measurement results to prove the presence of entanglement in a quantum state that is effectively distributed between them. One can thus systematically search for entanglement using the class of entanglement witness operators that can be constructed from the observed data. We apply such analysis to two well-known quantum key distribution protocols, namely the 4-state protocol and the 6-state protocol. As a special case, we show that, for some asymmetric error patterns, the presence of entanglement can be proven even for error rates above 25% (4-state protocol) and 33% (6-state protocol).

  2. Two New Gradient Precondition Schemes for Full Waveform Inversion

    E-print Network

    Huang, Guanghui; Ren, Haoran

    2014-01-01

    We propose two preconditioned gradient direction for full waveform inversion (FWI). The first one is using time integral wavefields. The Least square problem is formulated as the time integral residual wavefields, which can partially resolve the effect of high-passed filter in the traditional gradient formula; the convergence rate is greatly accelerated. The other one is localized offset Hessian inspired by the generalized imaging condition, which provides another redundancy in the Hessian. We compare the traditional conjugate gradient scaled by the shot illumination and localized offset Hessian (actually, only diagonal part is considered here), and contrast their performance for waveform inversion. The results demonstrate the localized offset Hessian (diagonal part) can provide much more information in the subsurface, and is preferred to the layer-strip inversion.

  3. Preconditioned Mixed Spectral Element Methods for Elasticity and Stokes Problems

    NASA Technical Reports Server (NTRS)

    Pavarino, Luca F.

    1996-01-01

    Preconditioned iterative methods for the indefinite systems obtained by discretizing the linear elasticity and Stokes problems with mixed spectral elements in three dimensions are introduced and analyzed. The resulting stiffness matrices have the structure of saddle point problems with a penalty term, which is associated with the Poisson ratio for elasticity problems or with stabilization techniques for Stokes problems. The main results of this paper show that the convergence rate of the resulting algorithms is independent of the penalty parameter, the number of spectral elements Nu and mildly dependent on the spectral degree eta via the inf-sup constant. The preconditioners proposed for the whole indefinite system are block-diagonal and block-triangular. Numerical experiments presented in the final section show that these algorithms are a practical and efficient strategy for the iterative solution of the indefinite problems arising from mixed spectral element discretizations of elliptic systems.

  4. Exercise and Cyclic Light Preconditioning Protect Against Light-Induced Retinal Degeneration and Evoke Similar Gene Expression Patterns.

    PubMed

    Chrenek, Micah A; Sellers, Jana T; Lawson, Eric C; Cunha, Priscila P; Johnson, Jessica L; Girardot, Preston E; Kendall, Cristina; Han, Moon K; Hanif, Adam; Ciavatta, Vincent T; Gogniat, Marissa A; Nickerson, John M; Pardue, Machelle T; Boatright, Jeffrey H

    2016-01-01

    To compare patterns of gene expression following preconditioning cyclic light rearing versus preconditioning aerobic exercise. BALB/C mice were preconditioned either by rearing in 800 lx 12:12 h cyclic light for 8 days or by running on treadmills for 9 days, exposed to toxic levels of light to cause light-induced retinal degeneration (LIRD), then sacrificed and retinal tissue harvested. Subsets of mice were maintained for an additional 2 weeks and for assessment of retinal function by electroretinogram (ERG). Both preconditioning protocols partially but significantly preserved retinal function and morphology and induced similar leukemia inhibitory factor (LIF) gene expression pattern. The data demonstrate that exercise preconditioning and cyclic light preconditioning protect photoreceptors against LIRD and evoke a similar pattern of retinal LIF gene expression. It may be that similar stress response pathways mediate the protection provided by the two preconditioning modalities. PMID:26427444

  5. Eigenmode Analysis of Boundary Conditions for One-Dimensional Preconditioned Euler Equations

    NASA Technical Reports Server (NTRS)

    Darmofal, David L.

    1998-01-01

    An analysis of the effect of local preconditioning on boundary conditions for the subsonic, one-dimensional Euler equations is presented. Decay rates for the eigenmodes of the initial boundary value problem are determined for different boundary conditions. Riemann invariant boundary conditions based on the unpreconditioned Euler equations are shown to be reflective with preconditioning, and, at low Mach numbers, disturbances do not decay. Other boundary conditions are investigated which are non-reflective with preconditioning and numerical results are presented confirming the analysis.

  6. Preventing stroke

    MedlinePLUS

    Stroke - prevention; CVA - prevention; cerebral vascular accident - prevention; TIA - prevention, transient ischemic attack - prevention ... Biology; Council on Hypertension. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from ...

  7. Analysis of a Lipid/Polymer Membrane for Bitterness Sensing with a Preconditioning Process.

    PubMed

    Yatabe, Rui; Noda, Junpei; Tahara, Yusuke; Naito, Yoshinobu; Ikezaki, Hidekazu; Toko, Kiyoshi

    2015-01-01

    It is possible to evaluate the taste of foods or medicines using a taste sensor. The taste sensor converts information on taste into an electrical signal using several lipid/polymer membranes. A lipid/polymer membrane for bitterness sensing can evaluate aftertaste after immersion in monosodium glutamate (MSG), which is called "preconditioning". However, we have not yet analyzed the change in the surface structure of the membrane as a result of preconditioning. Thus, we analyzed the change in the surface by performing contact angle and surface zeta potential measurements, Fourier transform infrared spectroscopy (FTIR), X-ray photon spectroscopy (XPS) and gas cluster ion beam time-of-flight secondary ion mass spectrometry (GCIB-TOF-SIMS). After preconditioning, the concentrations of MSG and tetradodecylammonium bromide (TDAB), contained in the lipid membrane were found to be higher in the surface region than in the bulk region. The effect of preconditioning was revealed by the above analysis methods. PMID:26404301

  8. Analysis of a Lipid/Polymer Membrane for Bitterness Sensing with a Preconditioning Process

    PubMed Central

    Yatabe, Rui; Noda, Junpei; Tahara, Yusuke; Naito, Yoshinobu; Ikezaki, Hidekazu; Toko, Kiyoshi

    2015-01-01

    It is possible to evaluate the taste of foods or medicines using a taste sensor. The taste sensor converts information on taste into an electrical signal using several lipid/polymer membranes. A lipid/polymer membrane for bitterness sensing can evaluate aftertaste after immersion in monosodium glutamate (MSG), which is called “preconditioning”. However, we have not yet analyzed the change in the surface structure of the membrane as a result of preconditioning. Thus, we analyzed the change in the surface by performing contact angle and surface zeta potential measurements, Fourier transform infrared spectroscopy (FTIR), X-ray photon spectroscopy (XPS) and gas cluster ion beam time-of-flight secondary ion mass spectrometry (GCIB-TOF-SIMS). After preconditioning, the concentrations of MSG and tetradodecylammonium bromide (TDAB), contained in the lipid membrane were found to be higher in the surface region than in the bulk region. The effect of preconditioning was revealed by the above analysis methods. PMID:26404301

  9. Hybrid preconditioning for iterative diagonalization of ill-conditioned generalized eigenvalue problems in electronic structure calculations

    SciTech Connect

    Cai, Yunfeng; Department of Computer Science, University of California, Davis 95616 ; Bai, Zhaojun; Pask, John E.; Sukumar, N.

    2013-12-15

    The iterative diagonalization of a sequence of large ill-conditioned generalized eigenvalue problems is a computational bottleneck in quantum mechanical methods employing a nonorthogonal basis for ab initio electronic structure calculations. We propose a hybrid preconditioning scheme to effectively combine global and locally accelerated preconditioners for rapid iterative diagonalization of such eigenvalue problems. In partition-of-unity finite-element (PUFE) pseudopotential density-functional calculations, employing a nonorthogonal basis, we show that the hybrid preconditioned block steepest descent method is a cost-effective eigensolver, outperforming current state-of-the-art global preconditioning schemes, and comparably efficient for the ill-conditioned generalized eigenvalue problems produced by PUFE as the locally optimal block preconditioned conjugate-gradient method for the well-conditioned standard eigenvalue problems produced by planewave methods.

  10. Preconditioning for Numerical Simulation of Low Mach Number Three-Dimensional Viscous Turbomachinery Flows

    NASA Technical Reports Server (NTRS)

    Tweedt, Daniel L.; Chima, Rodrick V.; Turkel, Eli

    1997-01-01

    A preconditioning scheme has been implemented into a three-dimensional viscous computational fluid dynamics code for turbomachine blade rows. The preconditioning allows the code, originally developed for simulating compressible flow fields, to be applied to nearly-incompressible, low Mach number flows. A brief description is given of the compressible Navier-Stokes equations for a rotating coordinate system, along with the preconditioning method employed. Details about the conservative formulation of artificial dissipation are provided, and different artificial dissipation schemes are discussed and compared. The preconditioned code was applied to a well-documented case involving the NASA large low-speed centrifugal compressor for which detailed experimental data are available for comparison. Performance and flow field data are compared for the near-design operating point of the compressor, with generally good agreement between computation and experiment. Further, significant differences between computational results for the different numerical implementations, revealing different levels of solution accuracy, are discussed.

  11. Inhalational anesthetics as neuroprotectants or chemical preconditioning agents in ischemic brain

    PubMed Central

    Kitano, Hideto; Kirsch, Jeffrey R; Hurn, Patricia D; Murphy, Stephanie J

    2008-01-01

    This review will focus on inhalational anesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury. The limitations and challenges of past and current research in this area will be addressed before reviewing experimental and clinical studies evaluating the effects of inhalational anesthetics before and during cerebral ischemia. Mechanisms underlying volatile anesthetic neuroprotection and preconditioning will also be examined. Lastly, future directions for inhalational anesthetics and ischemic brain injury will be briefly discussed. PMID:17047683

  12. Atorvastatin preconditioning improves the forward blood flow in the no-reflow rats.

    PubMed

    Shao, Liang; Zhang, Yong; Ma, Aiqun; Zhang, Ping; Wu, Dayin; Li, Wenzhu; Wang, Jue; Liu, Kun; Wang, Zhaohui

    2014-02-01

    Atorvastatin is not only an antilipemic but also used as an anti-inflammatory medicine in heart disease. Our working hypothesis was that atorvastatin preconditioning could improve the forward blood flow in the no-reflow rats associated with inflammation. We investigated that two doses of atorvastatin preconditioning (20 and 5 mg/kg/day) could alleviate deterioration of early cardiac diastolic function in rats with inflammation detected by echocardiography and haemodynamics. This benefit was obtained from the effect of atorvastatin preconditioning on improving forward blood flow and preserving the infarct cardiomyocytes, which was estimated by Thioflavin S and TTC staining in rats with myocardial ischemia/reperfusion. Subsequently, the improving of forward blood flow was ascribed to reduction of microthrombus in microvascular and myocardial fibrosis observed by MSB and Masson's trichrome staining with atorvastatin preconditioning. Ultimately, we found that atorvastatin preconditioning could reduce inflammation factor, such as tumor necrosis factor-? and fibrinogen-like protein 2, both in myocardial and in mononuclear cells, which probably attribute to microcirculation dysfunction in no-reflow rats detected by immunohistochemistry staining, western blot, and ELISA detection, respectively. In conclusion, atorvastatin preconditioning could alleviate deterioration of early cardiac diastolic function and improve the forward blood flow in the no-reflow rats attributing to reduction of TNF-? and fgl-2 expression. PMID:22985249

  13. Convergence Acceleration of the Navier-Stokes Equations Through Time-Derivative Preconditioning

    NASA Technical Reports Server (NTRS)

    Merkle, Charles L.; Venkateswaran, Sankaran; Deshpande, Manish

    1996-01-01

    Chorin's method of artificial compressibility is extended to both compressible and incompressible fluids by using physical arguments to define artificial fluid properties that make up a local preconditioning matrix. In particular, perturbation expansions are used to provide appropriate temporal derivatives for the equations of motion at both low speeds and low Reynolds numbers. These limiting forms are then combined into a single function that smoothly merges into the physical time derivatives at high speeds so that the equations are left unchanged at transonic, high Reynolds number conditions. The effectiveness of the resulting preconditioning procedures for the Navier-Stokes equations is demonstrated for a wide speed and Reynolds number ranges by means of stability results and computational solutions. Nevertheless, the preconditioned equations sometimes fail to provide a solution for applications for which the non-preconditioned equations converge. Often this is because the reduced dissipation in the preconditioned equations results in an unsteady solution while the more dissipative non-preconditioned equations result in a steady state. Problems of this type represent a computational challenge; it is important to distinguish between non-convergence of algorithms, and the non-existence of steady state solutions.

  14. Mesenchymal stem cells preconditioned with trimetazidine promote neovascularization of hearts under hypoxia/reoxygenation injury

    PubMed Central

    Hu, Xiaowu; Yang, Junjie; Wang, Ying; Zhang, You; Ii, Masaaki; Shen, Zhenya; Hui, Jie

    2015-01-01

    Background: Cell-based angiogenesis is a promising treatment for ischemic diseases; however, survival of implanted cells is impaired by the ischemic microenvironment. In this study, mesenchymal stem cells (MSCs) for cell transplantation were preconditioned with trimetazidine (TMZ). We hypothesized that TMZ enhances the survival rate of MSCs under hypoxic stimuli through up-regulation of HIF1-?. Methods and results: Bone marrow-derived rat mesenchymal stem cells were preconditioned with 10 ?M TMZ for 6 h. TMZ preconditioning of MSCs remarkably increased cell viability and the expression of HIF1-? and Bcl-2, when cells were under hypoxia/reoxygenation (H/R) stimuli. But the protective effects of TMZ were abolished after knocking down of HIF-1?. Three days after implantation of the cells into the peri-ischemic zone of rat myocardial ischemia-reperfusion (I/R) injury model, survival of the TMZ-preconditioned MSCs was high. Furthermore, capillary density and cardiac function were significantly better in the rats implanted with TMZ-preconditioned MSCs 28 days after cell injection. Conclusions: TMZ preconditioning increased the survival rate of MSCs, through up-regulation of HIF1-?, thus contributing to neovascularization and improved cardiac function of rats subjected to myocardial I/R injury.

  15. Enhanced nucleotide excision repair capacity in lung cancer cells by preconditioning with DNA-damaging agents

    PubMed Central

    Choi, Ji Ye; Park, Jeong-Min; Yi, Joo Mi; Leem, Sun-Hee; Kang, Tae-Hong

    2015-01-01

    The capacity of tumor cells for nucleotide excision repair (NER) is a major determinant of the efficacy of and resistance to DNA-damaging chemotherapeutics, such as cisplatin. Here, we demonstrate that using lesion-specific monoclonal antibodies, NER capacity is enhanced in human lung cancer cells after preconditioning with DNA-damaging agents. Preconditioning of cells with a nonlethal dose of UV radiation facilitated the kinetics of subsequent cisplatin repair and vice versa. Dual-incision assay confirmed that the enhanced NER capacity was sustained for 2 days. Checkpoint activation by ATR kinase and expression of NER factors were not altered significantly by the preconditioning, whereas association of XPA, the rate-limiting factor in NER, with chromatin was accelerated. In preconditioned cells, SIRT1 expression was increased, and this resulted in a decrease in acetylated XPA. Inhibition of SIRT1 abrogated the preconditioning-induced predominant XPA binding to DNA lesions. Taking these data together, we conclude that upregulated NER capacity in preconditioned lung cancer cells is caused partly by an increased level of SIRT1, which modulates XPA sensitivity to DNA damage. This study provides some insights into the molecular mechanism of chemoresistance through acquisition of enhanced DNA repair capacity in cancer cells. PMID:26317794

  16. Effects of Thermal Preconditioning on Tissue Susceptibility to Histotripsy.

    PubMed

    Vlaisavljevich, Eli; Xu, Zhen; Arvidson, Alexa; Jin, Lifang; Roberts, William; Cain, Charles

    2015-11-01

    Histotripsy is a non-invasive ablation method that mechanically fractionates tissue by controlling acoustic cavitation. Previous work has revealed that tissue mechanical properties play a significant role in the histotripsy process, with stiffer tissues being more resistant to histotripsy-induced tissue damage. In this study, we propose a thermal pretreatment strategy to precondition tissues before histotripsy. We hypothesize that a thermal pretreatment can be used to alter tissue stiffness by modulating collagen composition, thus changing tissue susceptibility to histotripsy. More specifically, we hypothesize that tissues will soften and become more susceptible to histotripsy when preheated at ?60°C because of collagen denaturation, but that tissues will rapidly stiffen and become less susceptible to histotripsy when preheated at ?90°C because of collagen contraction. To test this hypothesis, a controlled temperature water bath was used to heat various ex vivo bovine tissues (tongue, artery, liver, kidney medulla, tendon and urethra). After heating, the Young's modulus of each tissue sample was measured using a tissue elastometer, and changes in tissue composition (i.e., collagen structure/density) were analyzed histologically. The susceptibility of tissues to histotripsy was investigated by treating the samples using a 750-kHz histotripsy transducer. Results revealed a decrease in stiffness and an increase in susceptibility to histotripsy for tissues (except urethra) preheated to 58°C. In contrast, preheating to 90°C increased tissue stiffness and reduced susceptibility to histotripsy for all tissues except tendon, which was significantly softened due to collagen hydrolysis into gelatin. On the basis of these results, a final set of experiments were conducted to determine the feasibility of using high-intensity focused ultrasound to provide the thermal pretreatment. Overall, the results of this study indicate the initial feasibility of a thermal pretreatment strategy to precondition tissue mechanical properties and alter tissue susceptibility to histotripsy. Future work will aim to optimize this thermal pretreatment strategy to determine if this approach is practical for specific clinical applications in vivo without causing unwanted damage to surrounding or overlying tissue. PMID:26318560

  17. HIF-regulated HO-1 gene transfer improves the post-ischemic limb recovery and diminishes TLR-triggered immune responses - Effects modified by concomitant VEGF overexpression.

    PubMed

    Jazwa, Agnieszka; Stoszko, Mateusz; Tomczyk, Mateusz; Bukowska-Strakova, Karolina; Pichon, Chantal; Jozkowicz, Alicja; Dulak, Jozef

    2015-08-01

    Heme oxygenase-1 (HO-1) mitigates cellular injury by antioxidant, anti-apoptotic, anti-inflammatory and proangiogenic effects. Vascular endothelial growth factor (VEGF) is a critical regulator of blood vessel growth. Their coordinated action was analyzed in a model of femoral artery ligation (FAL) in mice lacking HO-1 gene (HO-1 KO). Gastrocnemius skeletal muscles of HO-1 KO mice were preemptively injected with plasmids containing hypoxia-response element (HRE) driving the expression of only HO-1 (pHRE-HO1) or both HO-1 and VEGF (pHRE-HO1-VEGF). At day 14th the pHRE-HO1 vector increased an impaired post-ischemic blood flow recovery in HO-1 KO mice to the level observed in wild-type (WT) mice subjected to FAL and pHRE-HO1-VEGF restored it already at day 7. The pHRE-HO1 gene therapy diminished, when compared to control pHRE-empty-treated HO-1 KO mice, the expression of toll-like receptors (TLR4 and TLR9) and inflammatory cytokines (IL-1?, IL-6 and TNF?) at day 3, whereas opposite effects were observed following concomitant HO-1 and VEGF gene transfer. Moreover, HO-1 diminished ischemia-induced expression of MyoD involved in satellite cell differentiation in HO-1 KO mice. Our results confirm the therapeutic potential of HO-1 and VEGF against critical limb ischemia although, their concomitant delivery may have contradictory actions on the resolution of inflammation. PMID:25869523

  18. Grafts Enriched with Subamnion-Cord-Lining Mesenchymal Stem Cell Angiogenic Spheroids Induce Post-Ischemic Myocardial Revascularization and Preserve Cardiac Function in Failing Rat Hearts

    PubMed Central

    Vu, Duc-Thang; Wang, Jing; Lilyanna, Shera; Ling, Lieng H.; Gan, Shu U.; Tan, Ai Li; Phan, Thang T.; Lee, Chuen N.; Kofidis, Theo

    2013-01-01

    A crucial question in post-ischemic cell therapy refers to the ideal method of cell delivery to the heart. We hypothesized that epicardial implantation of subamnion-cord-lining mesenchymal stem cells (CL-MSC) angiogenic spheroids embedded within fibrin grafts (SASG) facilitates donor cell survival and enhances cardiac function in failing rat hearts. Furthermore, we compared the efficacy of this approach applied through two delivery methods. Spheroids made of 1.5×104 human CL-MSC coated with 2×103 human umbilical vein endothelial cells were self-assembled in hanging drops. SASG were constructed by embedding 150 spheroids in fibrin matrix. Except for untreated rats (MI, n=8), grafts were implanted 2 weeks after myocardial infarction upon confirmation of ensued heart failure through thoracotomy: SASG (n=8) and fibrin graft (FG, n=8); or video-assisted thoracoscopic surgery (VATS): SASG-VATS (n=8) and FG-VATS (n=7). In vivo CL-MSC survival was comparable between both SASG-treated groups throughout the study. SASG and SASG-VATS animals had decreased left ventricular end-diastolic pressure relative to untreated animals, and increased fractional shortening compared to MI and FG controls, 4 weeks after treatment. A 14.1% and 6.2% enhancement in ejection fraction from week 2 to 6 after injury was observed in SASG/SASG-VATS, paralleled by improvement in cardiac output. Treated hearts had smaller scar size, and more blood vessels than MI, while donor CL-MSC contributed to arteriogenesis within the graft and infarct areas. Taken together, our data suggest that SASG treatment has the potential to restore failing hearts by preserving cardiac function and inducing myocardial revascularization, while attenuating cardiac fibrosis. Furthermore, we introduce a method for minimally invasive in situ graft assembly. PMID:23869939

  19. Cerenkov luminescence tomography based on preconditioning orthogonal matching pursuit

    NASA Astrophysics Data System (ADS)

    Liu, Haixiao; Hu, Zhenhua; Wang, Kun; Tian, Jie; Yang, Xin

    2015-03-01

    Cerenkov luminescence imaging (CLI) is a novel optical imaging method and has been proved to be a potential substitute of the traditional radionuclide imaging such as positron emission tomography (PET) and single-photon emission computed tomography (SPECT). This imaging method inherits the high sensitivity of nuclear medicine and low cost of optical molecular imaging. To obtain the depth information of the radioactive isotope, Cerenkov luminescence tomography (CLT) is established and the 3D distribution of the isotope is reconstructed. However, because of the strong absorption and scatter, the reconstruction of the CLT sources is always converted to an ill-posed linear system which is hard to be solved. In this work, the sparse nature of the light source was taken into account and the preconditioning orthogonal matching pursuit (POMP) method was established to effectively reduce the ill-posedness and obtain better reconstruction accuracy. To prove the accuracy and speed of this algorithm, a heterogeneous numerical phantom experiment and an in vivo mouse experiment were conducted. Both the simulation result and the mouse experiment showed that our reconstruction method can provide more accurate reconstruction result compared with the traditional Tikhonov regularization method and the ordinary orthogonal matching pursuit (OMP) method. Our reconstruction method will provide technical support for the biological application for Cerenkov luminescence.

  20. Concepts of hypoxic NO signaling in remote ischemic preconditioning

    PubMed Central

    Totzeck, Matthias; Hendgen-Cotta, Ulrike; Rassaf, Tienush

    2015-01-01

    Acute coronary syndromes remain a leading single cause of death worldwide. Therapeutic strategies to treat cardiomyocyte threatening ischemia/reperfusion injury are urgently needed. Remote ischemic preconditioning (rIPC) applied by brief ischemic episodes to heart-distant organs has been tested in several clinical studies, and the major body of evidence points to beneficial effects of rIPC for patients. The underlying signaling, however, remains incompletely understood. This relates particularly to the mechanism by which the protective signal is transferred from the remote site to the target organ. Many pathways have been forwarded but none can explain the protective effects completely. In light of recent experimental studies, we here outline the current knowledge relating to the generation of the protective signal in the remote organ, the signal transfer to the target organ and the transduction of the transferred signal into cardioprotection. The majority of studies favors a humoral factor that activates cardiomyocyte downstream signaling - receptor-dependent and independently. Cellular targets include deleterious calcium (Ca2+) signaling, reactive oxygen species, mitochondrial function and structure, and cellular apoptosis and necrosis. Following an outline of the existing evidence, we will furthermore characterize the existing knowledge and discuss future perspectives with particular emphasis on the interaction between the recently discovered hypoxic nitrite-nitric oxide signaling in rIPC. This refers to the protective role of nitrite, which can be activated endogenously using rIPC and which then contributes to cardioprotection by rIPC. PMID:26516418

  1. Preconditioning Doses of NMDA Promote Neuroprotection by Enhancing Neuronal Excitability

    PubMed Central

    Soriano, Francesc X.; Papadia, Sofia; Hofmann, Frank; Hardingham, Neil R.; Bading, Hilmar; Hardingham, Giles E.

    2008-01-01

    Neuroprotection can be induced by low doses of NMDA, which activate both synaptic and extrasynaptic NMDA receptors. This is in apparent contradiction with our recent findings that extrasynaptic NMDA receptor signaling exerts a dominant inhibitory effect on prosurvival signaling from synaptic NMDA receptors. Here we report that exposure to low preconditioning doses of NMDA results in preferential activation of synaptic NMDA receptors because of a dramatic increase in action potential firing. Both acute and long-lasting phases of neuroprotection in the face of apoptotic or excitotoxic insults are dependent on this firing enhancement. Key mediators of synaptic NMDA receptor-dependent neuroprotection, phosphatidylinositol 3 kinase-Akt (PI3 kinase-Akt) signaling to Forkhead box subgroup O (FOXO) export and glycogen synthase kinase 3? (GSK3?) inhibition and cAMP response element-binding protein-dependent (CREB-dependent) activation of brain-derived neurotrophic factor (BDNF), can be induced only by low doses of NMDA via this action potential-dependent route. In contrast, NMDA doses on the other side of the toxicity threshold do not favor synaptic NMDA receptor activation because they strongly suppress firing rates below baseline. The classic bell-shaped curve depicting neuronal fate in response to NMDA dose can be viewed as the net effect of two antagonizing (synaptic vs extrasynaptic) curves: via increased firing the synaptic signaling dominates at low doses, whereas firing becomes suppressed and extrasynaptic signaling dominates as the toxicity threshold is crossed. PMID:16641230

  2. Remote ischemic preconditioning delays fatigue development during handgrip exercise.

    PubMed

    Barbosa, T C; Machado, A C; Braz, I D; Fernandes, I A; Vianna, L C; Nobrega, A C L; Silva, B M

    2015-06-01

    Ischemic preconditioning (IPC) of one or two limbs improves performance of exercise that recruits the same limb(s). However, it is unclear whether IPC application to another limb than that in exercise is also effective and which mechanisms are involved. We investigated the effect of remote IPC (RIPC) on muscle fatigue, time to task failure, forearm hemodynamics, and deoxygenation during handgrip exercise. Thirteen men underwent RIPC in the lower limbs or a control intervention (CON), in random order, and then performed a constant load rhythmic handgrip protocol until task failure. Rates of contraction and relaxation (?Force/?Time) were used as indices of fatigue. Brachial artery blood flow and conductance, besides forearm microvascular deoxygenation, were assessed during exercise. RIPC attenuated the slowing of contraction and relaxation throughout exercise (P??0.05). In conclusion, RIPC applied to the lower limbs delayed the development of fatigue during handgrip exercise, prolonged time to task failure, but was not accompanied by changes in forearm hemodynamics and deoxygenation. PMID:24731023

  3. What Happened if Various Kinds of Postconditioning Working on the Preconditioned Ischemic Skin Flaps

    PubMed Central

    Huang, Lin

    2013-01-01

    Objective: Ischemic pre-conditioning and post-conditioning are useful manipulations to reduce the undesirable effects of ischemia-reperfusion skin flap each. But the impact of post-conditioning on the pre-conditioning skin flap is not manifested. Here we investigated the influence of ischemic post-conditioning in a preconditioned axial pattern skin flap model. Method: We used the skin flap in 40 rabbits and divided them into 5 groups randomly. At first we induced the ischemic pre-conditioning of the flap which was applied by 2 periods of 15 minutes of ischemia/15 minutes of reperfusion cycle. Next post-conditioning was performed by 6 cycles of 10 seconds of repeated ischemia/reperfusion periods at different times of just after the reperfusion,5 minutes after the reperfusion,10 minutes after the reperfusion. The animals were allocated into 5 groups: group 1 (Ischemia Group); group 2: (Pre-conditioning Group); group 3: (Pre-conditioning+ Post-conditioning Group); group 4 (Pre-conditioning+ Post-conditioning 5 minutes later Group); group5 (Pre-conditioning+ Post-conditioning 10 minutes later). The neutrophil count was assessed with histologic analysis before the dissection of the skin flap. Flap viability was assessed 1 week after the operation, and surviving flap area was recorded as a percentage of the whole flap area. LSD test was used for statistical analysis among different groups to evaluate the effects of ischemic pre-conditioning against ischemia. Result: Among the varying groups, the neutrophil count varied: Group 1 was50.12±5.91; Group 2, 30.00±2.00, and Group 3, 18.87±3; Group 4, 22.50±1.92; Group 5, 30.12±1.88.The mean± SD surviving areas of the flaps for groups 1, 2, 3, 4 and 5 were 31.76±4.59, 51.26±3.24,82.18±5.28,66.85±3.87 and 51.13±2.90 respectively. Spearman correlation analysis shows an increase relation between neutrophil count and flap survival rate in the different groups (P <0.05). Conclusion: Ischemic post-conditioning has protective effect on ischemic preconditioned skin flaps, but the post-conditioning should be performed within 5 minutes after the end of ischemia. PMID:24147150

  4. Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning

    PubMed Central

    Jiang, Shuxia; Streeter, Jennifer; Schickling, Brandon M.; Zimmerman, Kathy; Weiss, Robert M.; Miller, Francis J.

    2014-01-01

    Aims Ischaemic preconditioning (IPC) is an adaptive mechanism that renders the myocardium resistant to injury from subsequent hypoxia. Although reactive oxygen species (ROS) contribute to both the early and late phases of IPC, their enzymatic source and associated signalling events have not yet been understood completely. Our objective was to investigate the role of the Nox1 NADPH oxidase in cardioprotection provided by IPC. Methods and results Wild-type (WT) and Nox1-deficient mice were treated with three cycles of brief coronary occlusion and reperfusion, followed by prolonged occlusion either immediately (early IPC) or after 24 h (late IPC). Nox1 deficiency had no impact on the cardioprotection afforded by early IPC. In contrast, deficiency of Nox1 during late IPC resulted in a larger infarct size, cardiac remodelling, and increased myocardial apoptosis compared with WT hearts. Furthermore, expression of Nox1 in WT hearts increased in response to late IPC. Deficiency of Nox1 abrogated late IPC-mediated activation of cardiac nuclear factor-?B (NF-?B) and induction of tumour necrosis factor-? (TNF-?) in the heart and circulation. Finally, knockdown of Nox1 in cultured cardiomyocytes prevented TNF-? induction of NF-?B and the protective effect of IPC on hypoxia-induced apoptosis. Conclusions Our data identify a critical role for Nox1 in late IPC and define a previously unrecognized link between TNF-? and NF-?B in mediating tolerance to myocardial injury. These findings have clinical significance considering the emergence of Nox1 inhibitors for the treatment of cardiovascular disease. PMID:24501329

  5. Effects of ischemia and omeprazole preconditioning on functional recovery of isolated rat heart

    PubMed Central

    Jeremic, Nevena; Petkovic, Anica; Srejovic, Ivan; Zivkovic, Vladimir; Djuric, Dragan; Jakovljevic, Vladimir

    2015-01-01

    Objective The aim of this study was to compare protective effects of ischemic and potential protective effects of pharmacological preconditioning with omeprazole on isolated rat heart subjected to ischemia/reperfusion. Methods The hearts of male Wistar albino rats were excised and perfused on a Langendorff apparatus. In control group (CG) after stabilization period, hearts were subjected to global ischemia (perfusion was totally stopped) for 20 minutes and 30 minutes of reperfusion. Hearts of group II (IPC) were submitted to ischemic preconditioning lasting 5 minutes before 20 minutes of ischemia and 30 minutes of reperfusion. In third group (OPC) hearts first underwent preconditioning lasting 5 minutes with 100?M omeprazole, and then submitted 20 minutes of ischemia and 30 minutes of reperfusion. Results Administration of omeprazole before ischemia induction had protective effect on myocardium function recovery especially regarding to values of systolic left ventricular pressure and dp/dt max. Also our findings are that values of coronary flow did not change between OPC and IPC groups in last point of reperfusion. Conclusion Based on our results it seems that ischemic preconditioning could be used as first window of protection after ischemic injury especially because all investigated parameters showed continuous trend of recovery of myocardial function. On the other hand, preconditioning with omeprazole induced sudden trend of recovery with positive myocardium protection, although less effective than results obtained with ischemic preconditioning not withstand, we must consider that omeprazole may be used in many clinical circumstances where direct coronary clamping for ischemic preconditioning is not possible. PMID:26107460

  6. Diazoxide preconditioning of endothelial progenitor cells improves their ability to repair the infarcted myocardium.

    PubMed

    Mehmood, Azra; Ali, Muhammad; Khan, Shaheen N; Riazuddin, Sheikh

    2015-11-01

    Reduced survival and homing of the transplanted cells in the oxidative stressed ischemic environment limits the potential outcome of cell therapies for myocardial ischemia. Diazoxide (DZ), a highly selective mitochondrial ATP sensitive K(+) channel opener, is known to improve the survival and therapeutic ability of mesenchymal stem cells and skeletal myoblasts for the repair of heart failure. The current study explored the effect of DZ preconditioning in improving the ability of endothelial progenitor cells (EPCs) to counteract, in vitro oxidative stress, and to repair the infarcted myocardium. The EPCs were preconditioned by 30?min incubation with 200??M DZ followed by exposure to 200??M hydrogen peroxide (H2 O2 ) for 2?h. Non-preconditioned EPCs with and without exposure to H2 O2 were used as control. DZ preconditioning of EPCs resulted in significantly reduced cell injury as shown by reduced lactate dehydrogenase release and expression of annexin V-PE in comparison to untreated EPCs. Furthermore, DZ preconditioned EPCs exhibited upregulated expression of prosurvival genes (VEGF, SDF-1?, PCNA, and Bcl2 ), improved chemokines release (VEGF, IGF, and SDF-1?), viability, Akt phosphorylation and tube formation. In vivo experiments involved transplantation of DZ preconditioned and untreated EPCs in the left ventricle after permanent ligation of left anterior descending coronary artery in rats. The results demonstrated that DZ EPCs transplanted group showed significant reduction in infarct size along with robust cell proliferation, angiogenesis and improvement in cardiac function. The current study demonstrates that DZ preconditioning enhances EPCs survival under oxidative stress in vitro and their ability to treat myocardial infarction. PMID:26032287

  7. Glaciations in response to climate variations preconditioned by evolving topography.

    PubMed

    Pedersen, Vivi Kathrine; Egholm, David Lundbek

    2013-01-10

    Landscapes modified by glacial erosion show a distinct distribution of surface area with elevation (hypsometry). In particular, the height of these regions is influenced by climatic gradients controlling the altitude where glacial and periglacial processes are the most active, and as a result, surface area is focused just below the snowline altitude. Yet the effect of this distinct glacial hypsometric signature on glacial extent and therefore on continued glacial erosion has not previously been examined. Here we show how this topographic configuration influences the climatic sensitivity of Alpine glaciers, and how the development of a glacial hypsometric distribution influences the intensity of glaciations on timescales of more than a few glacial cycles. We find that the relationship between variations in climate and the resulting variation in areal extent of glaciation changes drastically with the degree of glacial modification in the landscape. First, in landscapes with novel glaciations, a nearly linear relationship between climate and glacial area exists. Second, in previously glaciated landscapes with extensive area at a similar elevation, highly nonlinear and rapid glacial expansions occur with minimal climate forcing, once the snowline reaches the hypsometric maximum. Our results also show that erosion associated with glaciations before the mid-Pleistocene transition at around 950,000 years ago probably preconditioned the landscape--producing glacial landforms and hypsometric maxima--such that ongoing cooling led to a significant change in glacial extent and erosion, resulting in more extensive glaciations and valley deepening in the late Pleistocene epoch. We thus provide a mechanism that explains previous observations from exposure dating and low-temperature thermochronology in the European Alps, and suggest that there is a strong topographic control on the most recent Quaternary period glaciations. PMID:23302860

  8. Super-low Dose Endotoxin Pre-conditioning Exacerbates Sepsis Mortality

    PubMed Central

    Chen, Keqiang; Geng, Shuo; Yuan, Ruoxi; Diao, Na; Upchurch, Zachary; Li, Liwu

    2015-01-01

    Sepsis mortality varies dramatically in individuals of variable immune conditions, with poorly defined mechanisms. This phenomenon complements the hypothesis that innate immunity may adopt rudimentary memory, as demonstrated in vitro with endotoxin priming and tolerance in cultured monocytes. However, previous in vivo studies only examined the protective effect of endotoxin tolerance in the context of sepsis. In sharp contrast, we report herein that pre-conditioning with super-low or low dose endotoxin lipopolysaccharide (LPS) cause strikingly opposite survival outcomes. Mice pre-conditioned with super-low dose LPS experienced severe tissue damage, inflammation, increased bacterial load in circulation, and elevated mortality when they were subjected to cecal-ligation and puncture (CLP). This is in contrast to the well-reported protective phenomenon with CLP mice pre-conditioned with low dose LPS. Mechanistically, we demonstrated that super-low and low dose LPS differentially modulate the formation of neutrophil extracellular trap (NET) in neutrophils. Instead of increased ERK activation and NET formation in neutrophils pre-conditioned with low dose LPS, we observed significantly reduced ERK activation and compromised NET generation in neutrophils pre-conditioned with super-low dose LPS. Collectively, our findings reveal a mechanism potentially responsible for the dynamic programming of innate immunity in vivo as it relates to sepsis risks. PMID:26029736

  9. Enhanced cell volume regulation: a key mechanism in local and remote ischemic preconditioning.

    PubMed

    Diaz, Roberto J; Harvey, Kordan; Boloorchi, Azadeh; Hossain, Taneya; Hinek, Alina; Backx, Peter H; Wilson, Gregory J

    2014-06-15

    We have previously shown that ischemic preconditioning (IPC) protection against necrosis in whole hearts and in both fresh and cultured cardiomyocytes, as well as the improved regulatory volume decrease to hypoosmotic swelling in cardiomyocytes, is abrogated through Cl(-) channel blockade, pointing to a role for enhanced cell volume regulation in IPC. To further define this cardioprotective mechanism, cultured rabbit ventricular cardiomyocytes were preconditioned either by 10-min simulated ischemia (SI) followed by 10-min simulated reperfusion (SR), by 10-min exposure/10-min washout of remote IPC (rIPC) plasma dialysate (from rabbits subjected to repetitive limb ischemia), or by adenoviral transfection with the constitutively active PKC-? gene. These interventions were done before cardiomyocytes were subjected to either 60- or 75-min SI/60-min SR to assess cell necrosis (by trypan blue staining), 30-min SI to assess ischemic cell swelling, or 30-min hypoosmotic (200 mosM) stress to assess cell volume regulation. Necrosis after SI/SR and both SI- and hypoosmotic stress-induced swelling was reduced in preconditioned cardiomyocytes compared with control cardiomyocytes (neither preconditioned nor transfected). These effects on necrosis and cell swelling were blocked by either Cl(-) channel blockade or dominant negative knockdown of inwardly rectifying K(+) channels with adenoviruses, suggesting that Cl(-) and K(+) movements across the sarcolemma are critical for cell volume regulation and, thereby, cell survival under hypoxic/ischemic conditions. Our results define enhanced cell volume regulation as a key common mechanism of cardioprotection by preconditioning in cardiomyocytes. PMID:24760980

  10. Catestatin Increases the Expression of Anti-Apoptotic and Pro-Angiogenetic Factors in the Post-Ischemic Hypertrophied Heart of SHR

    PubMed Central

    Penna, Claudia; Pasqua, Teresa; Amelio, Daniela; Perrelli, Maria-Giulia; Angotti, Carmelina; Tullio, Francesca; Mahata, Sushil K.; Tota, Bruno; Pagliaro, Pasquale; Cerra, Maria C.; Angelone, Tommaso

    2014-01-01

    Background In the presence of comorbidities the effectiveness of many cardioprotective strategies is blunted. The goal of this study was to assess in a hypertensive rat model if the early reperfusion with anti-hypertensive and pro-angiogenic Chromogranin A-derived peptide, Catestatin (CST:hCgA352–372; CST-Post), protects the heart via Reperfusion-Injury-Salvage-Kinases (RISK)-pathway activation, limiting infarct-size and apoptosis, and promoting angiogenetic factors (e.g., hypoxia inducible factor, HIF-1?, and endothelial nitric oxide synthase, eNOS, expression). Methods and Results The effects of CST-Post on infarct-size, apoptosis and pro-angiogenetic factors were studied in isolated hearts of spontaneously hypertensive rats (SHR), which underwent the following protocols: (a) 30-min ischemia and 120-min reperfusion (I/R); (b) 30-min ischemia and 20-min reperfusion (I/R-short), both with and without CST-Post (75 nM for 20-min at the beginning of reperfusion). In unprotected Wistar-Kyoto hearts, used as normal counterpart, infarct-size resulted smaller than in SHR. CST-Post reduced significantly infarct-size and improved post-ischemic cardiac function in both strains. After 20-min reperfusion, CST-Post induced S-nitrosylation of calcium channels and phosphorylation of RISK-pathway in WKY and SHR hearts. Yet specific inhibitors of the RISK pathway blocked the CST-Post protective effects against infarct in the 120-min reperfusion groups. Moreover, apoptosis (evaluated by TUNEL, ARC and cleaved caspase) was reduced by CST-Post. Importantly, CST-Post increased expression of pro-angiogenetic factors (i.e., HIF-1? and eNOS expression) after two-hour reperfusion. Conclusions CST-Post limits reperfusion damages and reverses the hypertension-induced increase of I/R susceptibility. Moreover, CST-Post triggers antiapoptotic and pro-angiogenetic factors suggesting that CST-Post can be used as an anti-maladaptive remodeling treatment. PMID:25099124

  11. Preconditioning Strategies for Kidney Ischemia Reperfusion Injury: Implications of the “Time-Window” in Remote Ischemic Preconditioning

    PubMed Central

    Yoon, Young Eun; Lee, Kwang Suk; Choi, Kyung Hwa; Kim, Kwang Hyun; Yang, Seung Choul; Han, Woong Kyu

    2015-01-01

    Remote ischemic preconditioning (IP) is a potential renoprotective strategy. However, there has been no demonstrated result in large animals and the role of time window in remote IP remains to be defined. Using a single-kidney porcine model, we evaluated organ protective function of remote IP in renal ischemia reperfusion injury. Fifteen Yorkshire pigs, 20 weeks old and weighing 35–38 kg were used. One week after left nephrectomy, we performed remote IP (clamping right external iliac artery, 2 cycles of 10 minutes) and right renal artery clamping (warm ischemia; 90 minutes). The animals were randomly divided into three groups: control group, warm ischemia without IP; group 1 (remote IP with early window [IP-E]), IP followed by warm ischemia with a 10-minute time window; and group 2 (remote IP with late window [IP-L]), IP followed by warm ischemia after a 24-hour time window. There were no differences in serum creatinine changes between groups. The IP-L group had lower urinary neutrophil gelatinase-associated lipocalin than control and IP-E at 72 hours post-ischemia. At 72 hours post-ischemia, the urinary kidney injury molecule-1 (KIM-1) was lower in the IP-L group than in the control and IP-E groups, and the IP-L group KIM-1 was near pre-ischemic levels, whereas the control and IP-E group KIM-1 levels were rising. Microalbumin also tended to be lower in the IP-L group. Taken together, remote IP showed a significant reduction in renal injury biomarkers from ischemia reperfusion injury. To effectively provide kidney protection, remote IP might require a considerable, rather than short, time window of ischemia. PMID:25879855

  12. Peri-operative anaesthetic myocardial preconditioning and protection – cellular mechanisms and clinical relevance in cardiac anaesthesia

    PubMed Central

    Kunst, G; Klein, A A

    2015-01-01

    Preconditioning has been shown to reduce myocardial damage caused by ischaemia–reperfusion injury peri-operatively. Volatile anaesthetic agents have the potential to provide myocardial protection by anaesthetic preconditioning and, in addition, they also mediate renal and cerebral protection. A number of proof-of-concept trials have confirmed that the experimental evidence can be translated into clinical practice with regard to postoperative markers of myocardial injury; however, this effect has not been ubiquitous. The clinical trials published to date have also been too small to investigate clinical outcome and mortality. Data from recent meta-analyses in cardiac anaesthesia are also not conclusive regarding intra-operative volatile anaesthesia. These inconclusive clinical results have led to great variability currently in the type of anaesthetic agent used during cardiac surgery. This review summarises experimentally proposed mechanisms of anaesthetic preconditioning, and assesses randomised controlled clinical trials in cardiac anaesthesia that have been aimed at translating experimental results into the clinical setting. PMID:25764404

  13. Efficient Multi-Stage Time Marching for Viscous Flows via Local Preconditioning

    NASA Technical Reports Server (NTRS)

    Kleb, William L.; Wood, William A.; vanLeer, Bram

    1999-01-01

    A new method has been developed to accelerate the convergence of explicit time-marching, laminar, Navier-Stokes codes through the combination of local preconditioning and multi-stage time marching optimization. Local preconditioning is a technique to modify the time-dependent equations so that all information moves or decays at nearly the same rate, thus relieving the stiffness for a system of equations. Multi-stage time marching can be optimized by modifying its coefficients to account for the presence of viscous terms, allowing larger time steps. We show it is possible to optimize the time marching scheme for a wide range of cell Reynolds numbers for the scalar advection-diffusion equation, and local preconditioning allows this optimization to be applied to the Navier-Stokes equations. Convergence acceleration of the new method is demonstrated through numerical experiments with circular advection and laminar boundary-layer flow over a flat plate.

  14. Preconditioning for the Navier-Stokes equations with finite-rate chemistry

    NASA Technical Reports Server (NTRS)

    Godfrey, Andrew G.; Walters, Robert W.; Van Leer, Bram

    1993-01-01

    The preconditioning procedure for generalized finite-rate chemistry and the proper preconditioning for the one-dimensional Navier-Stokes equations are presented. Eigenvalue stiffness is resolved and convergence-rate acceleration is demonstrated over the entire Mach-number range from the incompressible to the hypersonic. Specific benefits are realized at low and transonic flow speeds. The extended preconditioning matrix accounts for thermal and chemical non-equilibrium and its implementation is explained for both explicit and implicit time marching. The effect of higher-order spatial accuracy and various flux splittings is investigated. Numerical analysis reveals the possible theoretical improvements from using proconditioning at all Mach numbers. Numerical results confirm the expectations from the numerical analysis. Representative test cases include flows with previously troublesome embedded high-condition-number regions.

  15. Novel Genes Critical for Hypoxic Preconditioning in Zebrafish Are Regulators of Insulin and Glucose Metabolism

    PubMed Central

    Manchenkov, Tania; Pasillas, Martina P.; Haddad, Gabriel G.; Imam, Farhad B.

    2015-01-01

    Severe hypoxia is a common cause of major brain, heart, and kidney injury in adults, children, and newborns. However, mild hypoxia can be protective against later, more severe hypoxia exposure via “hypoxic preconditioning,” a phenomenon that is not yet fully understood. Accordingly, we have established and optimized an embryonic zebrafish model to study hypoxic preconditioning. Using a functional genomic approach, we used this zebrafish model to identify and validate five novel hypoxia-protective genes, including irs2, crtc3, and camk2g2, which have been previously implicated in metabolic regulation. These results extend our understanding of the mechanisms of hypoxic preconditioning and affirm the discovery potential of this novel vertebrate hypoxic stress model. PMID:25840431

  16. Wide-field fluorescence molecular tomography with compressive sensing based preconditioning

    PubMed Central

    Yao, Ruoyang; Pian, Qi; Intes, Xavier

    2015-01-01

    Wide-field optical tomography based on structured light illumination and detection strategies enables efficient tomographic imaging of large tissues at very fast acquisition speeds. However, the optical inverse problem based on such instrumental approach is still ill-conditioned. Herein, we investigate the benefit of employing compressive sensing-based preconditioning to wide-field structured illumination and detection approaches. We assess the performances of Fluorescence Molecular Tomography (FMT) when using such preconditioning methods both in silico and with experimental data. Additionally, we demonstrate that such methodology could be used to select the subset of patterns that provides optimal reconstruction performances. Lastly, we compare preconditioning data collected using a normal base that offers good experimental SNR against that directly acquired with optimal designed base. An experimental phantom study is provided to validate the proposed technique. PMID:26713202

  17. A robust locally preconditioned semi-coarsening multigrid algorithm for the 2-D Navier-Stokes equations 

    E-print Network

    Cain, Michael D

    1999-01-01

    preconditioning for an upwind discrimination of the Navier-stokes equations. A block Jacobi iterative scheme is used because of its high frequency error mode damping ability. At low Mach numbers, the performance of a flux preconditioned is investigated. The flux...

  18. Preconditioning electromyographic data for an upper extremity model using neural networks

    NASA Technical Reports Server (NTRS)

    Roberson, D. J.; Fernjallah, M.; Barr, R. E.; Gonzalez, R. V.

    1994-01-01

    A back propagation neural network has been employed to precondition the electromyographic signal (EMG) that drives a computational model of the human upper extremity. This model is used to determine the complex relationship between EMG and muscle activation, and generates an optimal muscle activation scheme that simulates the actual activation. While the experimental and model predicted results of the ballistic muscle movement are very similar, the activation function between the start and the finish is not. This neural network preconditions the signal in an attempt to more closely model the actual activation function over the entire course of the muscle movement.

  19. Solving nonlinear heat conduction problems with multigrid preconditioned Newton-Krylov methods

    SciTech Connect

    Rider, W.J.; Knoll, D.A.

    1997-09-01

    Our objective is to investigate the utility of employing multigrid preconditioned Newton-Krylov methods for solving initial value problems. Multigrid based method promise better performance from the linear scaling associated with them. Our model problem is nonlinear heat conduction which can model idealized Marshak waves. Here we will investigate the efficiency of using a linear multigrid method to precondition a Krylov subspace method. In effect we will show that a fixed point nonlinear iterative method provides an effective preconditioner for the nonlinear problem.

  20. Propulsion-related flowfields using the preconditioned Navier-Stokes equations

    NASA Technical Reports Server (NTRS)

    Venkateswaran, S.; Weiss, J. M.; Merkle, C. L.; Choi, Y.-H.

    1992-01-01

    A previous time-derivative preconditioning procedure for solving the Navier-Stokes is extended to the chemical species equations. The scheme is implemented using both the implicit ADI and the explicit Runge-Kutta algorithms. A new definition for time-step is proposed to enable grid-independent convergence. Several examples of both reacting and non-reacting propulsion-related flowfields are considered. In all cases, convergence that is superior to conventional methods is demonstrated. Accuracy is verified using the example of a backward facing step. These results demonstrate that preconditioning can enhance the capability of density-based methods over a wide range of Mach and Reynolds numbers.

  1. Preconditioning for the Navier-Stokes equations with finite-rate chemistry

    NASA Technical Reports Server (NTRS)

    Godfrey, Andrew G.

    1993-01-01

    The extension of Van Leer's preconditioning procedure to generalized finite-rate chemistry is discussed. Application to viscous flow is begun with the proper preconditioning matrix for the one-dimensional Navier-Stokes equations. Eigenvalue stiffness is resolved and convergence-rate acceleration is demonstrated over the entire Mach-number range from nearly stagnant flow to hypersonic. Specific benefits are realized at the low and transonic flow speeds typical of complete propulsion-system simulations. The extended preconditioning matrix necessarily accounts for both thermal and chemical nonequilibrium. Numerical analysis reveals the possible theoretical improvements from using a preconditioner for all Mach number regimes. Numerical results confirm the expectations from the numerical analysis. Representative test cases include flows with previously troublesome embedded high-condition-number areas. Van Leer, Lee, and Roe recently developed an optimal, analytic preconditioning technique to reduce eigenvalue stiffness over the full Mach-number range. By multiplying the flux-balance residual with the preconditioning matrix, the acoustic wave speeds are scaled so that all waves propagate at the same rate, an essential property to eliminate inherent eigenvalue stiffness. This session discusses a synthesis of the thermochemical nonequilibrium flux-splitting developed by Grossman and Cinnella and the characteristic wave preconditioning of Van Leer into a powerful tool for implicitly solving two and three-dimensional flows with generalized finite-rate chemistry. For finite-rate chemistry, the state vector of unknowns is variable in length. Therefore, the preconditioning matrix extended to generalized finite-rate chemistry must accommodate a flexible system of moving waves. Fortunately, no new kind of wave appears in the system. The only existing waves are entropy and vorticity waves, which move with the fluid, and acoustic waves, which propagate in Mach number dependent directions. The nonequilibrium vibrational energies and species densities in the unknown state vector act strictly as convective waves. The essential concept for extending the preconditioning to generalized chemistry models is determining the differential variables which symmetrize the flux Jacobians. The extension is then straight-forward. This algorithm research effort will be released in a future version of the production level computational code coined the General Aerodynamic Simulation Program (GASP), developed by Walters, Slack, and McGrory.

  2. A load of mice to hypergravity causes AMPK? repression with liver injury, which is overcome by preconditioning loads via Nrf2

    PubMed Central

    Lee, Sang Gil; Lee, Chan Gyu; Wu, Hong Min; Oh, Choong Sik; Chung, So Won; Kim, Sang Geon

    2015-01-01

    An understanding of the effects of hypergravity on energy homeostasis is necessary in managing proper physiological countermeasures for aerospace missions. This study investigated whether a single or multiple load(s) of mice to hypergravity has an effect on molecules associated with energy metabolism. In the liver, AMPK? level and its signaling were repressed 6?h after a load to +9?Gz hypergravity for 1?h, and then gradually returned toward normal. AMPK? level was restored after 3 loads to +9?Gz, suggestive of preconditioning adaptation. In cDNA microarray analyses, 221 genes were differentially expressed by +9?Gz, and the down-regulated genes included Nrf2 targets. Nrf2 gene knockout abrogated the recovery of AMPK? elicited by 3 loads to +9?Gz, indicating that Nrf2 plays a role in the adaptive increase of AMPK?. In addition, +9?Gz stress decreased STAT3, FOXO1/3 and CREB levels, which was attenuated during the resting time. Similarly, apoptotic markers were enhanced in the liver, indicating that the liver may be vulnerable to hypergravity stress. Preconditioning loads prevented hepatocyte apoptosis. Overall, a load of mice to +9?Gz hypergravity causes AMPK? repression with liver injury, which may be overcome by multiple loads to hypergravity as mediated by Nrf2. PMID:26493041

  3. 40 CFR 86.1232-96 - Vehicle preconditioning.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... awaiting testing, to prevent unusual loading of the canisters. During this time care must be taken to... to paragraph (h) of this section. The time of initiation and completion of the canister loading shall... several minutes. Warning: If at any time the concentration of hydrocarbons, of methanol, or of...

  4. 40 CFR 86.1232-96 - Vehicle preconditioning.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... awaiting testing, to prevent unusual loading of the canisters. During this time care must be taken to... to paragraph (h) of this section. The time of initiation and completion of the canister loading shall... several minutes. Warning: If at any time the concentration of hydrocarbons, of methanol, or of...

  5. 40 CFR 86.1232-96 - Vehicle preconditioning.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... awaiting testing, to prevent unusual loading of the canisters. During this time care must be taken to... to paragraph (h) of this section. The time of initiation and completion of the canister loading shall... several minutes. Warning: If at any time the concentration of hydrocarbons, of methanol, or of...

  6. 40 CFR 86.1232-96 - Vehicle preconditioning.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... awaiting testing, to prevent unusual loading of the canisters. During this time care must be taken to... to paragraph (h) of this section. The time of initiation and completion of the canister loading shall... several minutes. Warning: If at any time the concentration of hydrocarbons, of methanol, or of...

  7. An M-step preconditioned conjugate gradient method for parallel computation

    NASA Technical Reports Server (NTRS)

    Adams, L.

    1983-01-01

    This paper describes a preconditioned conjugate gradient method that can be effectively implemented on both vector machines and parallel arrays to solve sparse symmetric and positive definite systems of linear equations. The implementation on the CYBER 203/205 and on the Finite Element Machine is discussed and results obtained using the method on these machines are given.

  8. Professors' and Trainees' Perceptions of Educational Quality as Related to Preconditions of Deep Learning in "Musikdidaktik"

    ERIC Educational Resources Information Center

    Ferm, Cecilia; Johansen, Geir

    2008-01-01

    Interview-based case studies, involving two institutions, four professors and 11 music teacher trainees were conducted in order to investigate the preconditions for deep learning in the subject of higher music education called "musikdidaktik". Analysis was based on the "didaktiktriangle" which is a theoretical model that…

  9. Progress Toward a Stabilization and Preconditioning Protocol for Polycrystalline Thin-Film Photovoltaic Modules

    SciTech Connect

    del Cueto, J. A.; Deline, C. A.; Rummel, S. R.; Anderberg, A.

    2010-08-01

    Cadmium telluride (CdTe) and copper indium gallium diselenide (CIGS) thin-film photovoltaic (PV) modules can exhibit substantial variation in measured performance depending on prior exposure history. This study examines the metastable performance changes in these PV modules with the goal of establishing standard preconditioning or stabilization exposure procedures to mitigate measured variations prior to current-voltage (IV) measurements.

  10. An anisotropic preconditioning for the Wilson fermion matrix on the lattice

    SciTech Connect

    Balint Joo, Robert G. Edwards, Michael J. Peardon

    2010-01-01

    A preconditioning for the Wilson fermion matrix on the lattice is defined which is particularly suited to the case when the temporal lattice spacing is much smaller than the spatial one. Details on the implementation of the scheme are given. The method is tested in numerical studies of QCD on anisotropic lattices.

  11. 40 CFR 92.125 - Pre-test procedures and preconditioning.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... required. Couple the engine to the dynamometer or locomotive alternator/generator. (4) Start cooling system... test is aborted, the converter must pass the efficiency check described in § 92.121 prior to starting... preconditioning. 92.125 Section 92.125 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED)...

  12. 40 CFR 92.125 - Pre-test procedures and preconditioning.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... required. Couple the engine to the dynamometer or locomotive alternator/generator. (4) Start cooling system... test is aborted, the converter must pass the efficiency check described in § 92.121 prior to starting... preconditioning. 92.125 Section 92.125 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED)...

  13. Evaluation of High-intensity and Low-intensity Preconditioning Systems 

    E-print Network

    Orsak, Andrew Nathan

    2012-02-14

    Steer calves n = 345 (year 1 n = 183; 253 ± 35 kg, year 2 n = 162; 241 ± 36 kg initial BW) were used to evaluate 56-d preconditioning systems in each of two years. Angus- and Charolais-sired calves out of crossbred dams ...

  14. Dynamic Inference of Likely Data Preconditions over Predicates by Tree Learning

    E-print Network

    Chauduri, Swarat

    Sankaranarayanan NEC Laboratories America. srirams@nec-labs.com Swarat Chaudhuri Penn. State University swarat@cse.psu.edu Franjo Ivanci´c NEC Laboratories America. ivancic@nec-labs.com Aarti Gupta NEC Laboratories America. agupta@nec-labs.com ABSTRACT We present a technique to infer likely data preconditions for procedures

  15. 40 CFR 86.153-98 - Vehicle and canister preconditioning; refueling test.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 19 2014-07-01 2014-07-01 false Vehicle and canister preconditioning; refueling test. 86.153-98 Section 86.153-98 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF EMISSIONS FROM NEW AND IN-USE HIGHWAY VEHICLES AND ENGINES Emission Regulations for 1977 and...

  16. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 34 2012-07-01 2012-07-01 false PM sampling media (e.g., filters... Specified Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and tare weighing. Before an emission test, take the following steps to prepare PM sampling media (e.g., filters) and...

  17. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 32 2010-07-01 2010-07-01 false PM sampling media (e.g., filters... Specified Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and tare weighing. Before an emission test, take the following steps to prepare PM sampling media (e.g., filters) and...

  18. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 33 2014-07-01 2014-07-01 false PM sampling media (e.g., filters... Specified Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and tare weighing. Before an emission test, take the following steps to prepare PM sampling media (e.g., filters) and...

  19. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 33 2011-07-01 2011-07-01 false PM sampling media (e.g., filters... Specified Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and tare weighing. Before an emission test, take the following steps to prepare PM sampling media (e.g., filters) and...

  20. 40 CFR 1065.590 - PM sampling media (e.g., filters) preconditioning and tare weighing.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 34 2013-07-01 2013-07-01 false PM sampling media (e.g., filters... Specified Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and tare weighing. Before an emission test, take the following steps to prepare PM sampling media (e.g., filters) and...

  1. 40 CFR 85.2218 - Preconditioned idle test-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 19 2012-07-01 2012-07-01 false Preconditioned idle test-EPA 91. 85.2218 Section 85.2218 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF AIR POLLUTION FROM MOBILE SOURCES Emission Control System Performance Warranty...

  2. 40 CFR 85.2219 - Idle test with loaded preconditioning-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 19 2012-07-01 2012-07-01 false Idle test with loaded preconditioning-EPA 91. 85.2219 Section 85.2219 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF AIR POLLUTION FROM MOBILE SOURCES Emission Control...

  3. 40 CFR 85.2220 - Preconditioned two speed idle test-EPA 91.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 19 2012-07-01 2012-07-01 false Preconditioned two speed idle test-EPA 91. 85.2220 Section 85.2220 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) AIR PROGRAMS (CONTINUED) CONTROL OF AIR POLLUTION FROM MOBILE SOURCES Emission Control System...

  4. The Role of Macrophage Migration Inhibitory Factor in Anesthetic-Induced Myocardial Preconditioning

    PubMed Central

    Rossaint, Rolf; Bleilevens, Christian; Dollo, Florian; Siry, Laura; Rajabi-Alampour, Setareh; Beckers, Christian; Soppert, Josefin; Lue, Hongqi; Rex, Steffen; Bernhagen, Jürgen; Stoppe, Christian

    2014-01-01

    Introduction Anesthetic-induced preconditioning (AIP) is known to elicit cardioprotective effects that are mediated at least in part by activation of the kinases AMPK and PKC? as well as by inhibition of JNK. Recent data demonstrated that the pleiotropic cytokine macrophage migration inhibitory factor (MIF) provides cardioprotection through activation and/or inhibition of kinases that are also known to mediate effects of AIP. Therefore, we hypothesized that MIF could play a key role in the AIP response. Methods Cardiomyocytes were isolated from rats and subjected to isoflurane preconditioning (4 h; 1.5 vol. %). Subsequently, MIF secretion and alterations in the activation levels of protective kinases were compared to a control group that was exposed to ambient air conditions. MIF secretion was quantified by ELISA and AIP-induced activation of protein kinases was assessed by Western blotting of cardiomyocyte lysates after isoflurane treatment. Results In cardiomyocytes, preconditioning with isoflurane resulted in a significantly elevated secretion of MIF that followed a biphasic behavior (30 min vs. baseline: p?=?0.020; 24 h vs. baseline p?=?0.000). Moreover, quantitative polymerase chain reaction demonstrated a significant increase in MIF mRNA expression 8 h after AIP. Of note, activation of AMPK and PKC? coincided with the observed peaks in MIF secretion and differed significantly from baseline. Conclusions These results suggest that the pleiotropic mediator MIF is involved in anesthetic-induced preconditioning of cardiomyocytes through stimulation of the protective kinases AMPK and PKC?. PMID:24667295

  5. WAVEFORM PRECONDITIONING FOR CLUTTER REJECTION IN MULTIPATH FOR SPARSE DISTRIBUTED APERTURES

    E-print Network

    Yazici, Birsen

    WAVEFORM PRECONDITIONING FOR CLUTTER REJECTION IN MULTIPATH FOR SPARSE DISTRIBUTED APERTURES T that is shaped in a desired manner. In our ing, distributed aperture, sparse aperture, waveform design, case to the Wefruaeteposin ofadraafom n waveforms beforetransmi ssi. then work pies topsysthe arbitrary distribution

  6. NLR-TR-2008-282 Multigrid acceleration of a preconditioned Krylov

    E-print Network

    Vuik, Kees

    sparse systems Iterative methods Algebraic multigrid Preconditioning Problem area Radar cross section report Unclassi ed Date June 2008 Knowledge area(s) Numerical Mathematics Descriptor(s) Radar RCS Large prediction methods are used to analyze the radar signature of military plat- forms when the radar signature

  7. Parallel Multistep Successive Sparse Approximate Inverse Preconditioning Strategies of General Sparse Matrices \\Lambda

    E-print Network

    a large sparse linear sytem Ax = b; (1) where A is a nonsingular general matrix of order n. A sparse approximate inverse preconditioning technique is first to find a sparse matrix M which is a good approximation of the original matrix. Thus, instead of computing a costly high ac­ curacy sparse approximate inverse

  8. Decreased effectiveness of ischemic heart preconditioning in the state of chronic inflammation.

    PubMed

    Wojciechowska, M; Zar?bi?ski, M; Pawluczuk, P; Szukiewicz, D

    2015-11-01

    There is growing evidence, that beneficial effects of ischemic heart preconditioning (IPC) may be lost or limited due to diabetes, hyperlipidemia, hypertension, atherosclerosis, heart failure and senility. It is plausible, that these conditions interfere with the biochemical pathways underlying the IPC response, but the detailed explanation is not clear. Pro-inflammatory cytokines (IL-1?, IL-6, TNF-?), monocyte chemotactic protein-1 (MCP-1), histamine and many other agents used in a single dose before prolonged ischemia mimic IPC. However prolonged exposure to preconditioning mimetics leads to tolerance (tachyphylaxis). In the state of such tolerance ischemic preconditioning is no longer protective. Studies suggest that diabetes, hyperlipidemia, hypertension, atherosclerosis, heart failure and older age are accompanied by increased plasma levels of pro-inflammatory cytokines, MCP-1 and other inflammatory mediators. Therefore, we raised the hypothesis, that the reported lack of benefits of IPC in the listed states may be due to tolerance to IPC developed during prolonged exposure of the myocardium to preconditioning mimetics. PMID:26342834

  9. Analysis of Off-Board Powered Thermal Preconditioning in Electric Drive Vehicles: Preprint

    SciTech Connect

    Barnitt, R. A.; Brooker, A. D.; Ramroth, L.; Rugh , J.; Smith, K. A.

    2010-12-01

    Following a hot or cold thermal soak, vehicle climate control systems (air conditioning or heat) are required to quickly attain a cabin temperature comfortable to the vehicle occupants. In a plug-in hybrid electric or electric vehicle (PEV) equipped with electric climate control systems, the traction battery is the sole on-board power source. Depleting the battery for immediate climate control results in reduced charge-depleting (CD) range and additional battery wear. PEV cabin and battery thermal preconditioning using off-board power supplied by the grid or a building can mitigate the impacts of climate control. This analysis shows that climate control loads can reduce CD range up to 35%. However, cabin thermal preconditioning can increase CD range up to 19% when compared to no thermal preconditioning. In addition, this analysis shows that while battery capacity loss over time is driven by ambient temperature rather than climate control loads, concurrent battery thermal preconditioning can reduce capacity loss up to 7% by reducing pack temperature in a high ambient temperature scenario.

  10. PRECONDITIONING FOR THE p-VERSION BOUNDARY ELEMENT METHOD IN THREE DIMENSIONS WITH

    E-print Network

    Guo, Benqi

    parti- tion with triangular elements is one of the most popular choices in practice, and an analysis decompositions have been developed and applied widely for the finite element methods. For boundary elementPRECONDITIONING FOR THE p-VERSION BOUNDARY ELEMENT METHOD IN THREE DIMENSIONS WITH TRIANGULAR

  11. Preconditioned iterative methods for nonselfadjoint or indefinite elliptic boundary value problems

    SciTech Connect

    Bramble, J.H.; Pasciak, J.E.

    1984-01-01

    We consider a Galerkin-Finite Element approximation to a general linear elliptic boundary value problem which may be nonselfadjoint or indefinite. We show how to precondition the equations so that the resulting systems of linear algebraic equations lead to iteration procedures whose iterative convergence rates are independent of the number of unknowns in the solution.

  12. C. Canuto, P. Gervasio, A. Quarteroni Finite-Element Preconditioning of G-NI Spectral Methods

    E-print Network

    Ceragioli, Francesca

    C. Canuto, P. Gervasio, A. Quarteroni Finite-Element Preconditioning of G-NI Spectral Methods ABSTRACT Several old and new finite-element preconditioners for nodal-based spectral discretiza- tions, Quarteroni, Zang 2006), as well as that of more general spectral-element methods in which the preconditioners

  13. TWOLEVEL DOMAIN DECOMPOSITION PRECONDITIONING FOR THE pVERSION FINITE ELEMENT METHOD

    E-print Network

    Mandel, Jan

    TWO­LEVEL DOMAIN DECOMPOSITION PRECONDITIONING FOR THE p­VERSION FINITE ELEMENT METHOD IN THREE stiffness matrices only. The method is applied to the p­version finite element method for three to the p­version finite element method for the elasticity problem, which yields a natural, discretization

  14. Protective effect of ischemic preconditioning on the jejunal graft mucosa injury during cold preservation.

    PubMed

    Jonecova, Zuzana; Toth, Stefan; Maretta, Milan; Ciccocioppo, Rachele; Varga, Jan; Rodrigo, Luis; Kruzliak, Peter

    2015-10-01

    Protection of intestinal graft mucosa during cold preservation is still an unmet need in clinical practice, thus affecting the success of transplantation. The present study investigates the ability of two ischemic preconditioning (IPC) procedures to limit cold preservation injury. Three groups of Sprague-Dawley rats were recruited (n=11 each) as follows: the short IPC (SIPC) performed through 4cycles of mesenteric ischemia of 4min each followed by 10min of reperfusion, the long IPC (LIPC) obtained by 2 ischemic cycles of 12min each followed by 10min of reperfusion, and the control group (C) without IPC. Grafts were then stored in cold histidine-tryptophan-ketoglutarate solution and samples were taken at 0, 3, 6 and 9h lasting preservation. Both IPC groups showed an advanced degree of preservation with delayed development of graft mucosa damage, mainly in the crypt region. At the beginning of preservation, the graft mucosa in both IPC groups showed lower degree of mucosal injury index (MII) by 50% in comparison with C group. Specifically, a significant improvement of MII was observed after 3h of preservation in the LIPC group (p<0.05) in comparison with untreated C grafts. Significant atrophy of the intestinal mucosa in C group was found after 3h of preservation (p<0.01), in SIPC group the progress of atrophy was delayed to 6h (p<0.001), and in LIPC group only moderate decrease in that was found. A parallel increase of laminin expression with the MII rate after 6 and 9h of preservation in comparison with the level at time 0 was observed in all grafts (p<0.001 and p<0.01, respectively). In both IPC groups the apoptotic cell (AC) rate was significantly reduced at the beginning of cold preservation (p<0.05 both). Moreover, in both the SIPC and C groups, the progressive increase in MII rate connected with AC rate decrease was due to a predominance of necrosis. By contrast in the LIPC group, after an increase of nearly 50% in the AC rate at the 3rd hour, its level remained fairly constant during the further 6h of preservation, thus probably preventing necrosis and improving graft viability. PMID:26123930

  15. Renalase contributes to the renal protection of delayed ischaemic preconditioning via the regulation of hypoxia-inducible factor-1?

    PubMed Central

    Wang, Feng; Zhang, Guangyuan; Xing, Tao; Lu, Zeyuan; Li, Junhui; Peng, Cheng; Liu, Guohua; Wang, Niansong

    2015-01-01

    Ischaemic preconditioning (IPC) attenuates acute kidney injury (AKI) from renal ischaemia reperfusion. Renalase, an amine oxidase secreted by the proximal tubule, not only degrades circulating catecholamines but also protects against renal ischaemia reperfusion injury. Here, it has been suggested that the renoprotective effect of renal IPC is partly mediated by renalase. In a model of brief intermittent renal IPC, the increased cortex renalase expression was found to last for 48 hrs. IPC significantly reduced renal tubular inflammation, necrosis and oxidative stress following renal ischaemia reperfusion injury. Such effects were attenuated by blocking renalase with an anti-renalase monoclonal antibody. We further demonstrated that renalase expression was up-regulated by hypoxia in vitro via an hypoxia-inducible factor (HIF)-1? mechanism. The IPC-induced up-regulation of renalase in vivo was also reduced by pre-treatment with an HIF-1? inhibitor, 3-(5?-Hydroxymethyl-2?-furyl)-1-benzyl indazole. In summary, the renoprotective effect of IPC is partly dependent on the renalase expression, which may be triggered by hypoxia via an HIF-1? mechanism. Endogenous renalase shows potential as a therapeutic agent for the prevention and treatment of AKI. PMID:25781495

  16. Mesenchymal stem/stromal cells precondition lung monocytes/macrophages to produce tolerance against allo- and autoimmunity in the eye.

    PubMed

    Ko, Jung Hwa; Lee, Hyun Ju; Jeong, Hyun Jeong; Kim, Mee Kum; Wee, Won Ryang; Yoon, Sun-Ok; Choi, Hosoon; Prockop, Darwin J; Oh, Joo Youn

    2016-01-01

    Intravenously administered mesenchymal stem/stromal cells (MSCs) engraft only transiently in recipients, but confer long-term therapeutic benefits in patients with immune disorders. This suggests that MSCs induce immune tolerance by long-lasting effects on the recipient immune regulatory system. Here, we demonstrate that i.v. infusion of MSCs preconditioned lung monocytes/macrophages toward an immune regulatory phenotype in a TNF-?-stimulated gene/protein (TSG)-6-dependent manner. As a result, mice were protected against subsequent immune challenge in two models of allo- and autoimmune ocular inflammation: corneal allotransplantation and experimental autoimmune uveitis (EAU). The monocytes/macrophages primed by MSCs expressed high levels of MHC class II, B220, CD11b, and IL-10, and exhibited T-cell-suppressive activities independently of FoxP3(+) regulatory T cells. Adoptive transfer of MSC-induced B220(+)CD11b(+) monocytes/macrophages prevented corneal allograft rejection and EAU. Deletion of monocytes/macrophages abrogated the MSC-induced tolerance. However, MSCs with TSG-6 knockdown did not induce MHC II(+)B220(+)CD11b(+) cells, and failed to attenuate EAU. Therefore, the results demonstrate a mechanism of the MSC-mediated immune modulation through induction of innate immune tolerance that involves monocytes/macrophages. PMID:26699483

  17. Preconditioning’ with Low Dose Lipopolysaccharide Aggravates the Organ Injury / Dysfunction Caused by Hemorrhagic Shock in Rats

    PubMed Central

    Sordi, Regina; Chiazza, Fausto; Patel, Nimesh S. A.; Doyle, Rachel A.; Collino, Massimo; Thiemermann, Christoph

    2015-01-01

    Methods Male rats were ‘pretreated’ with phosphate-buffered saline (PBS; i.p.) or LPS (1 mg/kg; i.p.) 24 h prior to HS. Mean arterial pressure (MAP) was maintained at 30 ± 2 mmHg for 90 min or until 25% of the shed blood had to be re-injected to sustain MAP. This was followed by resuscitation with the remaining shed blood. Four hours after resuscitation, parameters of organ dysfunction and systemic inflammation were assessed. Results HS resulted in renal dysfunction, and liver and muscular injury. At a first glance, LPS preconditioning attenuated organ dysfunction. However, we discovered that HS-rats that had been preconditioned with LPS (a) were not able to sustain a MAP at 30 mmHg for more than 50 min and (b) the volume of blood withdrawn in these animals was significantly less than in the PBS-control group. This effect was associated with an enhanced formation of the nitric oxide (NO) derived from inducible NO synthase (iNOS). Thus, a further control group in which all animals were resuscitated after 50 min of hemorrhage was performed. Then, LPS preconditioning aggravated both circulatory failure and organ dysfunction. Most notably, HS-rats pretreated with LPS exhibited a dramatic increase in NF-?B activation and pro-inflammatory cytokines. Conclusion In conclusion, LPS preconditioning predisposed animals to an earlier vascular decompensation, which may be mediated by an excess of NO production secondary to induction of iNOS and activation of NF-?B. Moreover, LPS preconditioning increased the formation of pro-inflammatory cytokines, which is likely to have contributed to the observed aggravation of organ injury/dysfunction caused by HS. PMID:25830444

  18. Adenosine A1 receptor activation modulates N-methyl-d-aspartate (NMDA) preconditioning phenotype in the brain.

    PubMed

    Constantino, Leandra C; Pamplona, Fabrício A; Matheus, Filipe C; Ludka, Fabiana K; Gomez-Soler, Maricel; Ciruela, Francisco; Boeck, Carina R; Prediger, Rui D; Tasca, Carla I

    2015-04-01

    N-methyl-d-aspartate (NMDA) preconditioning is induced by subtoxic doses of NMDA and it promotes a transient state of resistance against subsequent lethal insults. Interestingly, this mechanism of neuroprotection depends on adenosine A1 receptors (A1R), since blockade of A1R precludes this phenomenon. In this study we evaluated the consequences of NMDA preconditioning on the hippocampal A1R biology (i.e. expression, binding properties and functionality). Accordingly, we measured A1R expression in NMDA preconditioned mice (75mg/kg, i.p.; 24h) and showed that neither the total amount of receptor, nor the A1R levels in the synaptic fraction was altered. In addition, the A1R binding affinity to the antagonist [(3)H] DPCPX was slightly increased in total membrane extracts of hippocampus from preconditioned mice. Next, we evaluated the impact of NMDA preconditioning on A1R functioning by measuring the A1R-mediated regulation of glutamate uptake into hippocampal slices and on behavioral responses in the open field and hot plate tests. NMDA preconditioning increased glutamate uptake into hippocampal slices without altering the expression of glutamate transporter GLT-1. Interestingly, NMDA preconditioning also induced antinociception in the hot plate test and both effects were reversed by post-activation of A1R with the agonist CCPA (0.2mg/kg, i.p.). NMDA preconditioning or A1R modulation did not alter locomotor activity in the open field. Overall, the results described herein provide new evidence that post-activation of A1R modulates NMDA preconditioning-mediated responses, pointing to the importance of the cross-talk between glutamatergic and adenosinergic systems to neuroprotection. PMID:25557798

  19. Protection against acetaminophen-induced liver injury by allopurinol is dependent on aldehyde oxidase-mediated liver preconditioning

    SciTech Connect

    Williams, C. David; McGill, Mitchell R.; Lebofsky, Margitta; Bajt, Mary Lynn; Jaeschke, Hartmut

    2014-02-01

    Acetaminophen (APAP) overdose causes severe and occasionally fatal liver injury. Numerous drugs that attenuate APAP toxicity have been described. However these compounds frequently protect by cytochrome P450 inhibition, thereby preventing the initiating step of toxicity. We have previously shown that pretreatment with allopurinol can effectively protect against APAP toxicity, but the mechanism remains unclear. In the current study, C3HeB/FeJ mice were administered allopurinol 18 h or 1 h prior to an APAP overdose. Administration of allopurinol 18 h prior to APAP overdose resulted in an 88% reduction in liver injury (serum ALT) 6 h after APAP; however, 1 h pretreatment offered no protection. APAP-cysteine adducts and glutathione depletion kinetics were similar with or without allopurinol pretreatment. The phosphorylation and mitochondrial translocation of c-jun-N-terminal-kinase (JNK) have been implicated in the progression of APAP toxicity. In our study we showed equivalent early JNK activation (2 h) however late JNK activation (6 h) was attenuated in allopurinol treated mice, which suggests that later JNK activation is more critical for the toxicity. Additional mice were administered oxypurinol (primary metabolite of allopurinol) 18 h or 1 h pre-APAP, but neither treatment protected. This finding implicated an aldehyde oxidase (AO)-mediated metabolism of allopurinol, so mice were treated with hydralazine to inhibit AO prior to allopurinol/APAP administration, which eliminated the protective effects of allopurinol. We evaluated potential targets of AO-mediated preconditioning and found increased hepatic metallothionein 18 h post-allopurinol. These data show metabolism of allopurinol occurring independent of P450 isoenzymes preconditions the liver and renders the animal less susceptible to an APAP overdose. - Highlights: • 18 h allopurinol pretreatment protects against acetaminophen-induced liver injury. • 1 h allopurinol pretreatment does not protect from APAP-induced injury. • 18 h or 1 h oxypurinol pretreatment does not alter APAP-induced injury. • Inhibiting aldehyde oxidase eliminates protection from 18 h allopurinol pretreatment. • 18 h allopurinol induces metallothionein which protects the liver against APAP injury.

  20. Preconditioning Human Mesenchymal Stem Cells with a Low Concentration of BMP2 Stimulates Proliferation and Osteogenic Differentiation In Vitro

    PubMed Central

    Baatrup, Anette; Foldager, Casper Bindzus; Bünger, Cody

    2014-01-01

    Abstract Clinical trials using bone morphogenetic protein-2 (BMP2) for bone reconstruction have shown promising results. However, the relatively high concentration needed to be effective raises concerns for efficacy and safety. The aim of this study was to investigate the osteogenic effect of an alternative treatment strategy in which human bone marrow–derived mesenchymal stem cells (hMSCs) are preconditioned with low concentrations of BMP2 for a short time in vitro. hMSCs in suspension were stimulated for 15?min with 10 and 20?ng/mL of BMP2. After the BMP2 was removed, the cells were seeded and cultured in osteogenic medium. The effects of preconditioning were analyzed with regard to proliferation and expression of osteogenic markers at both gene and protein level. The results were compared to those from cultures with continuous BMP2 stimulation. A significant increase in proliferation was seen with both precondition and continuous stimulation with BMP2, with no difference between the treatments. Preconditioning with BMP2 significantly increased gene expression of RUNX2, COLI, ALP, and OC, and protein levels of COLI and ALP. This was not found with continuous stimulation. The role of preconditioning with BMP2 in osteogenesis was validated by findings of increased gene expression of SMAD1 and an increase in dual phosphorylation of ser 463 and ser 465 in the SMAD 1/5/8 pathway. We concluded that preconditioning hMSCs with BMP2 stimulates osteogenesis: proliferation with matrix secretion and matrix maturation of hMSCs. This implies that preconditioning with BMP2 might be more effective at inducing proliferation and osteogenic differentiation of hMSCs than continuous stimulation. Preconditioning with BMP2 could benefit the clinical application of BMP2 since side effects from high-dose treatments could be avoided. PMID:25469313

  1. On linearization and preconditioning for radiation diffusion coupled to material thermal conduction equations

    SciTech Connect

    Feng, Tao; Graduate School of China Academy Engineering Physics, Beijing 100083 ; An, Hengbin; Yu, Xijun; Li, Qin; Zhang, Rongpei

    2013-03-01

    Jacobian-free Newton–Krylov (JFNK) method is an effective algorithm for solving large scale nonlinear equations. One of the most important advantages of JFNK method is that there is no necessity to form and store the Jacobian matrix of the nonlinear system when JFNK method is employed. However, an approximation of the Jacobian is needed for the purpose of preconditioning. In this paper, JFNK method is employed to solve a class of non-equilibrium radiation diffusion coupled to material thermal conduction equations, and two preconditioners are designed by linearizing the equations in two methods. Numerical results show that the two preconditioning methods can improve the convergence behavior and efficiency of JFNK method.

  2. Parallelization of the preconditioned IDR solver for modern multicore computer systems

    NASA Astrophysics Data System (ADS)

    Bessonov, O. A.; Fedoseyev, A. I.

    2012-10-01

    This paper present the analysis, parallelization and optimization approach for the large sparse matrix solver CNSPACK for modern multicore microprocessors. CNSPACK is an advanced solver successfully used for coupled solution of stiff problems arising in multiphysics applications such as CFD, semiconductor transport, kinetic and quantum problems. It employs iterative IDR algorithm with ILU preconditioning (user chosen ILU preconditioning order). CNSPACK has been successfully used during last decade for solving problems in several application areas, including fluid dynamics and semiconductor device simulation. However, there was a dramatic change in processor architectures and computer system organization in recent years. Due to this, performance criteria and methods have been revisited, together with involving the parallelization of the solver and preconditioner using Open MP environment. Results of the successful implementation for efficient parallelization are presented for the most advances computer system (Intel Core i7-9xx or two-processor Xeon 55xx/56xx).

  3. Role of Circulating Immune Cells in Stroke and Preconditioning-Induced Protection.

    PubMed

    Gesuete, Raffaella; Stevens, Susan L; Stenzel-Poore, Mary P

    2016-01-01

    Stroke activates an inflammatory response that results in the infiltration of peripheral immune cells into the ischemic area, contributing to exacerbation of tissue damage. However, evidence indicates that inflammatory cell infiltration can also promote neuroprotection through regulatory immune cells that mitigate injury. These immune regulatory cells may also be important mediators of neuroprotection associated with preconditioning, a phenomenon whereby small exposure to a potential harmful stimulus is able to induce protection against a subsequent ischemic event. The elucidation of mechanisms that allow these immune cells to confer neuroprotection is critical to developing new therapeutic strategies against acute stroke. In the present review, we discuss the dual role of peripheral immune cells in stroke-related brain injury and neuroprotection. Furthermore, we report new data from our laboratory that supports the important role of peripheral cells and their interaction with the brain endothelium for the establishment of the protective phenotype in preconditioning. PMID:26463920

  4. The North Pacific High and wintertime pre-conditioning of California current productivity

    NASA Astrophysics Data System (ADS)

    Schroeder, Isaac D.; Black, Bryan A.; Sydeman, William J.; Bograd, Steven J.; Hazen, Elliott L.; Santora, Jarrod A.; Wells, Brian K.

    2013-02-01

    Abstract Variations in large-scale atmospheric forcing influence upwelling dynamics and ecosystem productivity in the California Current System (CCS). In this paper, we characterize interannual variability of the North Pacific High over 40 years and investigate how variation in its amplitude and position affect upwelling and biology. We develop a winter upwelling "<span class="hlt">pre-conditioning</span>" index and demonstrate its utility to understanding biological processes. Variation in the winter NPH can be well described by its areal extent and maximum pressure, which in turn is predictive of winter upwelling. Our winter <span class="hlt">pre-conditioning</span> index explained 64% of the variation in biological responses (fish and seabirds). Understanding characteristics of the NPH in winter is therefore critical to predicting biological responses in the CCS.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/989166','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/989166"><span id="translatedtitle">Microglial ablation and lipopolysaccharide <span class="hlt">preconditioning</span> affects pilocarpine-induced seizures in mice</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Mirrione, M.M.; Mirrione, M.M.; Konomosa, D.K.; Ioradanis, G.; Dewey, S.L.; Agzzid, A.; Heppnerd, F.L.; Tsirka, St.E.</p> <p>2010-04-01</p> <p>Activated microglia have been associated with neurodegeneration in patients and in animal models of Temporal Lobe Epilepsy (TLE), however their precise functions as neurotoxic or neuroprotective is a topic of significant investigation. To explore this, we examined the effects of pilocarpine-induced seizures in transgenic mice where microglia/macrophages were conditionally ablated. We found that unilateral ablation of microglia from the dorsal hippocampus did not alter acute seizure sensitivity. However, when this procedure was coupled with lipopolysaccharide (LPS) <span class="hlt">preconditioning</span> (1 mg/kg given 24 h prior to acute seizure), we observed a significant pro-convulsant phenomenon. This effect was associated with lower metabolic activation in the ipsilateral hippocampus during acute seizures, and could be attributed to activity in the mossy fiber pathway. These findings reveal that <span class="hlt">preconditioning</span> with LPS 24 h prior to seizure induction may have a protective effect which is abolished by unilateral hippocampal microglia/macrophage ablation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25743572','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25743572"><span id="translatedtitle">Effect of zinc supplements in the attenuated cardioprotective effect of ischemic <span class="hlt">preconditioning</span> in hyperlipidemic rat heart.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Kansal, Sunil Kumar; Jyoti, Uma; Sharma, Samridhi; Kaura, Arun; Deshmukh, Rahul; Goyal, Sandeep</p> <p>2015-06-01</p> <p>Hyperlipidemia is regarded as independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia-/reperfusion (I/R)-induced injury. Hyperlipidemia attenuates the cardioprotective response of ischemic <span class="hlt">preconditioning</span> (IPC). The present study investigated the effect of zinc supplements in the attenuated cardioprotective effect of ischemic <span class="hlt">preconditioning</span> in hyperlipidemic rat hearts. Hyperlipidemia was induced in rat by feeding high-fat diet (HFD) for 6 weeks then the serum lipid profile was observed. In experiment, the isolated Langendorff rat heart preparation was subjected to 4 cycles of ischemic <span class="hlt">preconditioning</span> (IPC), then 30 min of ischemia followed by 120 min of reperfusion. Myocardial infarct size was elaborated morphologically by triphenyltetrazolium chloride (TTC) staining and biochemically by lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) release from coronary effluent and left ventricular collagen content. However, the effect of zinc supplement, i.e., zinc pyrithione (10 ?M) perfused during reperfusion for 120 min, significantly abrogated the attenuated cardioprotective effect of ischemic <span class="hlt">preconditioning</span> in hyperlipidemic rat heart whereas administration of chelator of this zinc ionophore, i.e., N,N,N',N'-tetrakis(2-pyridylmethyl)ethylene diamine (TPEN; 10 ?M), perfused during reperfusion 2 min before the perfusion of zinc pyrithione abrogated the cardioprotective effect of zinc supplement during experiment in hyperlipidemic rat heart. Thus, the administration of zinc supplements limits the infarct size, LDH, and CK-MB and enhanced the collagen level which suggests that the attenuated cardioprotective effect of IPC in hyperlipidemic rat is due to zinc loss during reperfusion caused by ischemia/reperfusion. PMID:25743572</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26531833','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26531833"><span id="translatedtitle">Possible role of thromboxane A2 in remote hind limb <span class="hlt">preconditioning</span>-induced cardioprotection.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sharma, Roohani; Randhawa, Puneet Kaur; Singh, Nirmal; Jaggi, Amteshwar Singh</p> <p>2016-01-01</p> <p>Remote hind limb <span class="hlt">preconditioning</span> (RIPC) is a protective strategy in which short episodes of ischemia and reperfusion in a remote organ (hind limb) protects the target organ (heart) against sustained ischemic reperfusion injury. The present study was designed to investigate the possible role of thromboxane A2 in RIPC-induced cardioprotection in rats. Remote hind limb <span class="hlt">preconditioning</span> was performed by four episodes of 5 min of inflation and 5 min of deflation of pressure cuff. Occlusion of the hind limb with blood pressure cuff is most feasible, non-invasive, clinically relevant, and safe method for inducing RIPC. Isolated rat hearts were perfused on Langendorff apparatus and were subjected to global ischemia for 30 min followed by 120-min reperfusion. The levels of lactate dehydrogenase (LDH) and creatine kinase (CK) were measured in coronary effluent to assess the degree of myocardial injury. The extent of myocardial infarct size along with the functional parameters including left ventricular developed pressure (LVDP), dp/dtmax, and dp/dtmin were also measured. Ozagrel (thromboxane synthase inhibitor) and seratrodast (thromboxane A2 receptor antagonist) were employed as pharmacological modulators of thromboxane A2. Remote hind limb <span class="hlt">preconditioning</span> significantly attenuated ischemia/reperfusion-induced myocardial injury and produced cardioprotective effects. However, administration of ozagrel and seratrodast completely abolished the cardioprotective effects of RIPC suggesting the key role of thromboxane A2 in RIPC-induced cardioprotection. It may be concluded that brief episodes of <span class="hlt">preconditioning</span> ischemia and reperfusion activates the thromboxane synthase enzyme that produces thromboxane A2, which may elicit cardioprotection either involving humoral or neurogenic pathway. PMID:26531833</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/5458149','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/5458149"><span id="translatedtitle"><span class="hlt">Preconditioning</span> technique for indefinite systems resulting from mixed approximations of elliptic problems</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Bramble, J.H.; Pasciak, J.E.</p> <p>1988-01-01</p> <p>This paper provides a <span class="hlt">preconditioned</span> iterative technique for the solution of saddle point problems. These problems typically arise in the numerical approximation of partial differential equations by Lagrange multiplier techniques and/or mixed methods. The saddle point problem is reformulated as a symmetric positive definite system, which is then solved by conjugate gradient iteration. Applications to the equations of elasticity and Stokes are discussed and the results of numerical experiments are given.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4532962','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4532962"><span id="translatedtitle">Effects of Remifentanil <span class="hlt">Preconditioning</span> on Osteoblasts under Hypoxia-Reoxygenation Condition</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Baik, Seung-Wan; Park, Bong-Soo; Kim, Yong-Ho; Kim, Yong-Deok; Kim, Cheul-Hong; Yoon, Ji-Young; Yoon, Ji-Uk</p> <p>2015-01-01</p> <p>Background: Ischemia-reperfusion of bone occurs in a variety of clinical conditions, such as orthopedic arthroplasty, plastic gnathoplasty, spinal surgery, and amputation. Usually, cellular models of hypoxia-reoxygenation reflect in vivo models of ischemia-reperfusion. With respect to hypoxia-reoxygenation conditions, the effects of remifentanil on osteogenesis have received little attention. Therefore, we investigated the effects of remifentanil on the proliferation and differentiation of osteoblasts during hypoxic-reoxygenation. Methods: After remifentanil (0.1, 1 ng/mL) <span class="hlt">preconditioning</span> for 2 hours, human osteoblasts were cultured under 1% oxygen tension for 24 hours. Thereafter, the cells were reoxygenated for 12 hours at 37 °C. The naloxone groups were treated with naloxone for 30 minutes before remifentanil treatment. We measured cell viability via MTT assay. Osteoblast maturation was determined by assay of bone nodular mineralization. Quantitative PCR and western blot methods were used to determine BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-?1, HIF-1?, and RUNX2 expression levels. Results: Osteoblast viability and bone nodular mineralization by osteoblasts is recovered by remifentanil <span class="hlt">preconditioning</span> from hypoxia-reoxygenation insult. During hypoxic-reoxygenation condition, remifentanil <span class="hlt">preconditioning</span> induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-?1, HIF-1?, and RUNX2 in osteoblasts. Conclusions: Under hypoxia-reoxygenation conditions, remifentanil <span class="hlt">preconditioning</span> enhanced the cell viability and maturation of osteoblasts, and stimulated the expression of proteins associated with osteoblast proliferation and differentiation of the osteoblast. Our results suggest that remifentanil may help in the treatment of bone stress injuries. PMID:26283875</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/servlets/purl/197837','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/servlets/purl/197837"><span id="translatedtitle"><span class="hlt">Preconditioned</span> gradient methods for sparse linear systems for very `large structural` problems</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Abu-Shumays, I.K.; Hutula, D.N.; Haan, J.J.; Myers, G.T.</p> <p>1995-12-01</p> <p>This paper deals with background and practical experience with <span class="hlt">preconditioned</span> gradient methods for sparse linear systems for `very large` structural problems. The conjugate gradient method with diagonal <span class="hlt">preconditioning</span> (CG/D) is demonstrated to substantially increase the size of structural problems that can be analyzed, significantly reduce computer storage requirements, and cut computing cost; thus allowing for much more detailed modeling and increased engineering efficiency. For one case for a structural system with 396,087 unknowns, the conjugate gradient method with diagonal <span class="hlt">preconditioning</span> is demonstrated to be a factor of sixty faster than the direct method. For certain problems, however, the number of iterations required by the CG/D method is excessive and improved methods are needed. A stand-alone iterative solver research computer program was developed to evaluate the merits of various matrix preconditioners. A matrix preconditoner based on a shifted incomplete Cholesky factorization algorithm was demonstrated to be superior to other choices. The stand-alone program incorporates an effective data management strategy which utilizes disk and solid state auxiliary computer storage devices to make it possible to efficiently solve excessively large structural problems on state-of-the-art vector and parallel computers. The background of gradient methods, algorithms for their implementation, and practical experience in their applications to structural problems are presented.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24526448','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24526448"><span id="translatedtitle">Lrg participates in lipopolysaccharide <span class="hlt">preconditioning</span>-induced brain ischemia injury via TLR4 signaling pathway.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Gong, Gu; Bai, Shurong; Wu, Wei; Hu, Ling; Liu, Yinghai; Niu, Jie; Dai, Xuemei; Yin, Liang; Wang, Xiaowu</p> <p>2014-09-01</p> <p>Lipopolysaccharide (LPS) <span class="hlt">preconditioning</span> is a powerful neuroprotective phenomenon by which an injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. The LPS response gene (Lrg) is a recently identified gene in human dental pulp cells treated with LPS. However, the role and mechanism of Lrg in brain ischemia injury have not yet been demonstrated. Here, we sought to determine whether Lrg participates in LPS <span class="hlt">preconditioning</span>-induced brain ischemia injury. The Lrg protein accumulates in brain tissue after middle cerebral artery occlusion (MCAO). Furthermore, knockdown of Lrg by small interfering RNA (siRNA) significantly increased the infarct size of brain injury. In addition, we investigated the mechanism of Lrg in brain ischemia injury. Lrg-siRNA could regulate inflammatory cytokine expression. Moreover, interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor Kappa B (NF-?B) p65 protein levels were significantly increased by Lrg-siRNA in mice after MCAO. Conversely, interferon regulatory factor 3 (IRF3) protein level was decreased by Lrg-siRNA. Taken together, these results suggest that Lrg regulates the expression of inflammatory cytokines in LPS <span class="hlt">preconditioning</span>-induced brain ischemia injury via the toll-like receptor 4 (TLR4) signaling pathway. Lrg may therefore serve as a novel therapeutic target for brain ischemia injury. PMID:24526448</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4612942','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4612942"><span id="translatedtitle">The protective effect of intraperitoneal medical ozone <span class="hlt">preconditioning</span> and treatment on hepatotoxicity induced by methotrexate</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Aslaner, Arif; Çak?r, Tu?rul; Çelik, Betül; Do?an, U?ur; Akyüz, Cebrail; Ba?türk, Ahmet; Polat, Cemal; Gündüz, Umut; Mayir, Burhan; ?ehirli, Ahmet Özer</p> <p>2015-01-01</p> <p>The aim of this study is to determine the effects of medical ozone <span class="hlt">preconditioning</span> and treatment on the methotrexate acute induced hepatotoxicity in rats that has not reports elsewhere. Eighteen rats were randomly assigned into three equal groups; control, Mtx and Mtx with ozone. Hepatotoxicity was performed with a single dose of 20 mg/kg Mtx to group 2 and group 3 at the fifteenth day. The medical ozone <span class="hlt">preconditioning</span> was administered intraperitonealy in group 3 for fifteen days and more five days after inducing Mtx. The other rats of the group 1 and 2 received saline injection. At the twentyfirst day the blood and the liver tissue samples were obtained to measure the levels of liver enzymes ALT and AST, proinflamatory cytokines TNF-?, IL-1?, malondialdehyde, glutathione and myeloperoxidase. And the histolopatological examination was evaluated for injury score. In our study Mtx administration caused a significant increase on the liver enzymes ALT and AST, the tissue MDA and MPO activity and significant decrease in the tissue GSH. Moreover the both pro-inflammatory cytokines were significantly increased in the Mtx group. Medical ozone <span class="hlt">preconditioning</span> and treatment reversed all these biochemical parameters and histopathological changes of the hepatotoxicity induced by Mtx. We conclude that medical ozone ameliorates Mtx induced hepatotoxicity in rats. PMID:26550257</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25419789','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25419789"><span id="translatedtitle">Voluntary Exercise <span class="hlt">Preconditioning</span> Activates Multiple Antiapoptotic Mechanisms and Improves Neurological Recovery after Experimental Traumatic Brain Injury.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhao, Zaorui; Sabirzhanov, Boris; Wu, Junfang; Faden, Alan I; Stoica, Bogdan A</p> <p>2015-09-01</p> <p>Physical activity can attenuate neuronal loss, reduce neuroinflammation, and facilitate recovery after brain injury. However, little is known about the mechanisms of exercise-induced neuroprotection after traumatic brain injury (TBI) or its modulation of post-traumatic neuronal cell death. Voluntary exercise, using a running wheel, was conducted for 4 weeks immediately preceding (<span class="hlt">preconditioning</span>) moderate-level controlled cortical impact (CCI), a well-established experimental TBI model in mice. Compared to nonexercised controls, exercise <span class="hlt">preconditioning</span> (pre-exercise) improved recovery of sensorimotor performance in the beam walk task, as well as cognitive/affective functions in the Morris water maze, novel object recognition, and tail-suspension tests. Further, pre-exercise reduced lesion size, attenuated neuronal loss in the hippocampus, cortex, and thalamus, and decreased microglial activation in the cortex. In addition, exercise <span class="hlt">preconditioning</span> activated the brain-derived neurotrophic factor pathway before trauma and amplified the injury-dependent increase in heat shock protein 70 expression, thus attenuating key apoptotic pathways. The latter include reduction in CCI-induced up-regulation of proapoptotic B-cell lymphoma 2 (Bcl-2)-homology 3-only Bcl-2 family molecules (Bid, Puma), decreased mitochondria permeabilization with attenuated release of cytochrome c and apoptosis-inducing factor (AIF), reduced AIF translocation to the nucleus, and attenuated caspase activation. Given these neuroprotective actions, voluntary physical exercise may serve to limit the consequences of TBI. PMID:25419789</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2013SPIE.9067E..1ZY','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2013SPIE.9067E..1ZY"><span id="translatedtitle">Completeness set proof of <span class="hlt">precondition</span> and post-condition types of activity in any EPM</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Yu, Qian; Li, Tong; Liu, JinZhuo; Zhang, Xuan; Yu, Yong</p> <p>2013-12-01</p> <p>Software evolution process model (EPM) is created in terms of a formal evolution process meta-model (EPMM) and semi-formal approach to modeling based on EPMM [1]. In order to better manage and control the software evolution process and make the best of existing software technology, the method to transform any EPM to its execution model based logic programming has been proposed. Completeness of conversion depends on completeness of the rules, that is, all the expressions of the original model are found the correspondence in the target model. Since transformation rules are proposed based on <span class="hlt">precondition</span> or post-condition types of activities in anyone EPM, this need to prove that activity type set in anyone EPM is completeness set. To this end, the <span class="hlt">precondition</span> and post-condition of activities in EPM are classified based on analyzing all expressions in EPMs and the semantics of the activity execution. Type completeness set of activity's <span class="hlt">precondition</span> and its post-condition is presented. Lastly we prove that the activity type set in anyone EPM is completeness set by mathematical induction.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.niaid.nih.gov/topics/coronavirus/Understanding/Pages/Prevention.aspx','NIH-MEDLINEPLUS'); return false;" href="http://www.niaid.nih.gov/topics/coronavirus/Understanding/Pages/Prevention.aspx"><span id="translatedtitle">Coronavirus <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... <span class="hlt">Prevention</span> There are no vaccines available to <span class="hlt">prevent</span> human coronavirus infection. You can reduce the risk of infection by doing the following: Washing hands with soap and water Not touching your eyes, nose, or mouth Avoiding close contact with people ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://go4life.nia.nih.gov/sites/default/files/PreventingFalls.pdf','NIH-MEDLINEPLUS'); return false;" href="https://go4life.nia.nih.gov/sites/default/files/PreventingFalls.pdf"><span id="translatedtitle"><span class="hlt">Preventing</span> Falls</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... there are simple ways you can <span class="hlt">prevent</span> most falls. Stay physically active. Regular exercise makes you stronger. ... that may result from falling. Here are some fall <span class="hlt">prevention</span> tips from Go4Life : l Have your eyes ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.healthychildren.org/English/health-issues/injuries-emergencies/Pages/Drowning.aspx','NIH-MEDLINEPLUS'); return false;" href="https://www.healthychildren.org/English/health-issues/injuries-emergencies/Pages/Drowning.aspx"><span id="translatedtitle">Drowning <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Listen Español Text Size Email Print Share Drowning <span class="hlt">Prevention</span>: Information for Parents Article Body Drowning is a ... in very cold water for lengthy periods. Drowning <span class="hlt">Prevention</span>: Know the Warning Signs These signs may signal ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25473920','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25473920"><span id="translatedtitle">The natural olive constituent oleuropein induces nutritional cardioprotection in normal and cholesterol-fed rabbits: comparison with <span class="hlt">preconditioning</span>.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Andreadou, Ioanna; Benaki, Dimitra; Efentakis, Panagiotis; Bibli, Sofia-Iris; Milioni, Alkistis-Ioanna; Papachristodoulou, Anastasia; Zoga, Anastasia; Skaltsounis, Alexios-Leandros; Mikros, Emmanuel; Iliodromitis, Efstathios K</p> <p>2015-06-01</p> <p>Ischemic <span class="hlt">preconditioning</span>, which is mediated by cell signaling molecules, protects the heart from ischemia-reperfusion injury by limiting the infarct size. Oleuropein, the main polyphenolic constituent of olives, reduced the infarct size in normal and cholesterol-fed rabbits when it was administered at a nutritional dose. The aim of the present study was to compare the effects of oleuropein and <span class="hlt">preconditioning</span> in terms of the cell signaling and metabolism pathways underlying myocardial protection. Rabbits were randomly divided into six groups: the control group received 5?% dextrose for six weeks, the <span class="hlt">preconditioning</span> group was subjected to two cycles of <span class="hlt">preconditioning</span> with 5?min ischemia/10?min reperfusion, the O6 group was treated with oleuropein for six weeks, the Chol group was fed a cholesterol-enriched diet and 5?% dextrose for six weeks, and the CholO6 and CholO3 groups were treated with cholesterol and oleuropein for six and three weeks, respectively; oleuropein was dissolved in 5?% dextrose solution and was administered orally at a dose of 20?mg?×?kg(-1)?×?day(-1). All animals were subsequently subjected to 30?min myocardial ischemia followed by 10?min of reperfusion. At that time, myocardial biopsies were taken from the ischemic areas for the assessment of oxidative and nitrosative stress biomarkers (malondialdehyde and nitrotyrosine), and determination of phosphorylation of signaling molecules involved in the mechanism of <span class="hlt">preconditioning</span> (PI3K, Akt, eNOS, AMPK, STAT3). The tissue extracts NMR metabolic profile was recorded and further analyzed by multivariate statistics. Oxidative biomarkers were significantly reduced in the O6, CholO6, and CholO3 groups compared to the control, <span class="hlt">preconditioning</span>, and Chol groups. Considering the underlying signaling cascade, the phosphorylation of PI3K, Akt, eNOS, AMPK, and STAT-3 was significantly higher in the <span class="hlt">preconditioning</span> and all oleuropein-treated groups compared to the control and Chol groups. The NMR-based metabonomic study, performed through the analysis of spectroscopic data, depicted differences in the metabolome of the various groups with significant alterations in purine metabolism. In conclusion, the addition of oleuropein to a normal or hypercholesterolemic diet results in a <span class="hlt">preconditioning</span>-like intracellular effect, eliminating the deleterious consequences of ischemia and hypercholesterolemia, followed by a decrease of oxidative stress biomarkers. This effect is exerted through inducing <span class="hlt">preconditioning</span>-involved signaling transduction. Nutritional <span class="hlt">preconditioning</span> may support the low cardiovascular morbidity and mortality associated with the consumption of olive products. PMID:25473920</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24017972','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24017972"><span id="translatedtitle">Sulforaphane <span class="hlt">preconditioning</span> of the Nrf2/HO-1 defense pathway protects the cerebral vasculature against blood-brain barrier disruption and neurological deficits in stroke.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Alfieri, Alessio; Srivastava, Salil; Siow, Richard C M; Cash, Diana; Modo, Michel; Duchen, Michael R; Fraser, Paul A; Williams, Steven C R; Mann, Giovanni E</p> <p>2013-12-01</p> <p>Disruption of the blood-brain barrier (BBB) and cerebral edema are the major pathogenic mechanisms leading to neurological dysfunction and death after ischemic stroke. The brain protects itself against infarction via activation of endogenous antioxidant defense mechanisms, and we here report the first evidence that sulforaphane-mediated preactivation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream target heme oxygenase-1 (HO-1) in the cerebral vasculature protects the brain against stroke. To induce ischemic stroke, Sprague-Dawley rats were subjected to 70 min middle cerebral artery occlusion (MCAo) followed by 4, 24, or 72 h reperfusion. Nrf2 and HO-1 protein expression was upregulated in cerebral microvessels of peri-infarct regions after 4-72 h, with HO-1 preferentially associated with perivascular astrocytes rather than the cerebrovascular endothelium. In naïve rats, treatment with sulforaphane increased Nrf2 expression in cerebral microvessels after 24h. Upregulation of Nrf2 by sulforaphane treatment prior to transient MCAo (1h) was associated with increased HO-1 expression in perivascular astrocytes in peri-infarct regions and cerebral endothelium in the infarct core. BBB disruption, lesion progression, as analyzed by MRI, and neurological deficits were reduced by sulforaphane pretreatment. As sulforaphane pretreatment led to a moderate increase in peroxynitrite generation, we suggest that hormetic <span class="hlt">preconditioning</span> underlies sulforaphane-mediated protection against stroke. In conclusion, we propose that pharmacological or dietary interventions aimed to <span class="hlt">precondition</span> the brain via activation of the Nrf2 defense pathway in the cerebral microvasculature provide a novel therapeutic approach for <span class="hlt">preventing</span> BBB breakdown and neurological dysfunction in stroke. PMID:24017972</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3884906','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3884906"><span id="translatedtitle">Sevoflurane <span class="hlt">Preconditioning</span> Attenuates Myocardial Ischemia/Reperfusion Injury via Cav-3-Dependent COX-2 Inhibition</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zhao, Jianli; Zhang, Yanqing; Wang, Feng; Jiao, Liyuan; Lau, Wayne Bond; Wang, Lili; Liu, Baojiang; Gao, Erhe; Koch, Walter J.; Ma, Xin-Liang; Wang, Yajing</p> <p>2013-01-01</p> <p>Background The inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury, via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane <span class="hlt">preconditioning</span>-mediated cardioprotection, and their precise underlying mechanisms of action, remain incompletely understood. Methods and Results Sevoflurane <span class="hlt">preconditioning</span> (SF-PreCon, consisting of 3 cycles of 15 minute-exposures to 2% sevoflurane prior to 30 minutes of MI) decreased MI/R injury in WT mice (caspase-3 activity ?29.1%, infarct size ?20.2%, and LVEDP ?33.8%). In cardiac-specific AMPK?2 dominant negative overexpression (AMPK-DN) mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity ?26.7%, infarct size ?16.7%, and LVEDP ?25.9%, P<0.01). In contrast, SF-PreCon failed to significantly protect Cav3-knockout (Cav3-KO) mice against MI/R injury (P>0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in WT (?43.6%) and AMPK-DN mice (?35.5%, P<0.01), but not in Cav3-KO mice. SF-PreCon did not affect NADPH oxidase expression, but significantly inhibited COX-2 expression in WT (?38.7%) and AMPK-DN mice (?35.8%), but not in Cav-3KO mice. Conclusions We demonstrate for the first time sevoflurane <span class="hlt">preconditioning</span> mediates cardioprotection against MI/R injury via Cav-3 dependent-COX-2 inhibition and anti-oxidative effects. PMID:24030395</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_12");'>12</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li class="active"><span>14</span></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_14 --> <div id="page_15" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li class="active"><span>15</span></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="281"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26342941','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26342941"><span id="translatedtitle">Proteomic analysis of the hippocampus in naïve and ischemic-<span class="hlt">preconditioned</span> rat.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nakajima, Takayuki; Hata, Ryusuke; Kondo, Tomohiro; Takenaka, Shigeo</p> <p>2015-11-15</p> <p>The hippocampus exhibits regional differences in vulnerability to ischemia, wherein pyramidal cells in the CA1 region are vulnerable to ischemia while pyramidal cells in the CA3 region and granule cells in the dentate gyrus (DG) region are relatively ischemia resistant. However, pyramidal cells in the CA1 region reportedly exhibit ischemic tolerance following exposure to a brief non-lethal period of ischemia known as ischemic <span class="hlt">preconditioning</span>. In this study, we used proteomic analysis to examine the difference in protein expression between naïve rat CA1 and CA3/DG regions, as well as the altered protein expression in the CA1 region after 3min of ischemic <span class="hlt">preconditioning</span>. Proteomic analysis identified ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCH-L1), glutathione S-transferase ?5 (GST?5), glutamine synthetase (GS), and dynamin-1 as proteins with differential expression levels in naïve CA1 and CA3/DG regions. The difference in expression levels of GST?5 and GS between these two regions was further confirmed by western blot. Our analysis also identified aconitase2, ?-tubulin, protein-l-isoaspartate O-methiltransferase (PIMT), and voltage-dependent anion channel 1 (VDCA1) as proteins with down-regulated expression levels in the CA1 region following 3min ischemic <span class="hlt">preconditioning</span>. The decrease in the expression of aconitase2 was also confirmed by western blot and immunohistochemical staining. The present results suggest that GST?5 and GS may be associated with ischemia-resistance in the CA3/DG region and that aconitase2 may play a part in the ischemic tolerance in the CA1 region. PMID:26342941</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4556686','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4556686"><span id="translatedtitle">Ischemic <span class="hlt">Preconditioning</span> Mediates Neuroprotection against Ischemia in Mouse Hippocampal CA1 Neurons by Inducing Autophagy</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zhang, Xuebin; Huang, Huiling; Wang, Jin; Wang, Yajing; Tong, Xiaoguang; Wang, Jinhuan; Wu, Jialing</p> <p>2015-01-01</p> <p>The hippocampal CA1 region is sensitive to hypoxic and ischemic injury but can be protected by ischemic <span class="hlt">preconditioning</span> (IPC). However, the mechanism through which IPC protects hippocampal CA1 neurons is still under investigation. Additionally, the role of autophagy in determining the fate of hippocampal neurons is unclear. Here, we examined whether IPC induced autophagy to alleviate hippocampal CA1 neuronal death in vitro and in vivo with oxygen glucose deprivation (OGD) and bilateral carotid artery occlusion (BCCAO) models. Survival of hippocampal neurons increased from 51.5% ± 6.3% in the non-IPC group (55 min of OGD) to 77.3% ± 7.9% in the IPC group (15 min of OGD, followed by 55 min of OGD 24 h later). The number of hippocampal CA1 layer neurons increased from 182 ± 26 cells/mm2 in the non-IPC group (20 min of BCCAO) to 278 ± 55 cells/mm2 in the IPC group (1 min × 3 BCCAO, followed by 20 min of BCCAO 24 h later). Akt phosphorylation and microtubule-associated protein light chain 3 (LC3)-II/LC3-I expression were increased in the <span class="hlt">preconditioning</span> group. Moreover, the protective effects of IPC were abolished only by inhibiting the activity of autophagy, but not by blocking the activation of Akt in vitro. Using in vivo experiments, we found that LC3 expression was upregulated, accompanied by an increase in neuronal survival in hippocampal CA1 neurons in the <span class="hlt">preconditioning</span> group. The neuroprotective effects of IPC on hippocampal CA1 neurons were completely inhibited by treatment with 3-MA. In contrast, hippocampal CA3 neurons did not show changes in autophagic activity or beneficial effects of IPC. These data suggested that IPC may attenuate ischemic injury in hippocampal CA1 neurons through induction of Akt-independent autophagy. PMID:26325184</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2636993','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2636993"><span id="translatedtitle">Rosuvastatin induces delayed <span class="hlt">preconditioning</span> against oxygen-glucose deprivation in cultured cortical neurons</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Domoki, Ferenc; Kis, Béla; Gáspár, Tamás; Snipes, James A.; Parks, John S.; Bari, Ferenc; Busija, David W.</p> <p>2009-01-01</p> <p>We tested whether rosuvastatin (RST) protected against oxygen-glucose deprivation (OGD)-induced cell death in primary rat cortical neuronal cultures. OGD reduced neuronal viability (%naive controls, mean ± SE, n = 24–96, P < 0.05) to 44 ± 1%, but 3-day pretreatment with RST (5 ?M) increased survival to 82 ± 2% (P < 0.05). One-day RST treatment was not protective. RST-induced neuroprotection was abolished by mevalonate or geranylgeranyl pyrophosphate (GGPP), but not by cholesterol coapplication. Furthermore, RST-induced decreases in neuronal cholesterol levels were abolished by mevalonate but not by GGPP. Reactive oxygen species (ROS) levels were reduced in RST-<span class="hlt">preconditioned</span> neurons after OGD, and this effect was also reversed by both mevalonate and GGPP. These data suggested that GGPP, but not cholesterol depletion, were responsible for the induction of neuroprotection. Therefore, we tested whether 3-day treatments with perillic acid, a nonspecific inhibitor of both geranylgeranyl transferase (GGT) GGT 1 and Rab GGT, and the GGT 1-specific inhibitor GGTI-286 would reproduce the effects of RST. Perillic acid, but not GGTI-286, elicited robust neuronal <span class="hlt">preconditioning</span> against OGD. RST, GGTI-286, and perillic acid all decreased mitochondrial membrane potential and lactate dehydrogenase activity in the cultured neurons, but only RST and perillic acid reduced neuronal ATP and membrane Rab3a protein levels. In conclusion, RST <span class="hlt">preconditions</span> cultured neurons against OGD via depletion of GGPP, leading to decreased geranylgeranylation of proteins that are probably not isoprenylated by GGT 1. Reduced neuronal ATP levels and ROS production after OGD may be directly involved in the mechanism of neuroprotection. PMID:18971391</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015JCoPh.303..295X','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015JCoPh.303..295X"><span id="translatedtitle">Effective matrix-free <span class="hlt">preconditioning</span> for the augmented immersed interface method</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Xia, Jianlin; Li, Zhilin; Ye, Xin</p> <p>2015-12-01</p> <p>We present effective and efficient matrix-free <span class="hlt">preconditioning</span> techniques for the augmented immersed interface method (AIIM). AIIM has been developed recently and is shown to be very effective for interface problems and problems on irregular domains. GMRES is often used to solve for the augmented variable(s) associated with a Schur complement A in AIIM that is defined along the interface or the irregular boundary. The efficiency of AIIM relies on how quickly the system for A can be solved. For some applications, there are substantial difficulties involved, such as the slow convergence of GMRES (particularly for free boundary and moving interface problems), and the inconvenience in finding a preconditioner (due to the situation that only the products of A and vectors are available). Here, we propose matrix-free structured <span class="hlt">preconditioning</span> techniques for AIIM via adaptive randomized sampling, using only the products of A and vectors to construct a hierarchically semiseparable matrix approximation to A. Several improvements over existing schemes are shown so as to enhance the efficiency and also avoid potential instability. The significance of the preconditioners includes: (1) they do not require the entries of A or the multiplication of AT with vectors; (2) constructing the preconditioners needs only O (log ? N) matrix-vector products and O (N) storage, where N is the size of A; (3) applying the preconditioners needs only O (N) flops; (4) they are very flexible and do not require any a priori knowledge of the structure of A. The preconditioners are observed to significantly accelerate the convergence of GMRES, with heuristical justifications of the effectiveness. Comprehensive tests on several important applications are provided, such as Navier-Stokes equations on irregular domains with traction boundary conditions, interface problems in incompressible flows, mixed boundary problems, and free boundary problems. The <span class="hlt">preconditioning</span> techniques are also useful for several other problems and methods.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22215952','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22215952"><span id="translatedtitle">Augmentation of aerobic respiration and mitochondrial biogenesis in skeletal muscle by hypoxia <span class="hlt">preconditioning</span> with cobalt chloride</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Saxena, Saurabh; Shukla, Dhananjay; Bansal, Anju</p> <p>2012-11-01</p> <p>High altitude/hypoxia training is known to improve physical performance in athletes. Hypoxia induces hypoxia inducible factor-1 (HIF-1) and its downstream genes that facilitate hypoxia adaptation in muscle to increase physical performance. Cobalt chloride (CoCl{sub 2}), a hypoxia mimetic, stabilizes HIF-1, which otherwise is degraded in normoxic conditions. We studied the effects of hypoxia <span class="hlt">preconditioning</span> by CoCl{sub 2} supplementation on physical performance, glucose metabolism, and mitochondrial biogenesis using rodent model. The results showed significant increase in physical performance in cobalt supplemented rats without (two times) or with training (3.3 times) as compared to control animals. CoCl{sub 2} supplementation in rats augmented the biological activities of enzymes of TCA cycle, glycolysis and cytochrome c oxidase (COX); and increased the expression of glucose transporter-1 (Glut-1) in muscle showing increased glucose metabolism by aerobic respiration. There was also an increase in mitochondrial biogenesis in skeletal muscle observed by increased mRNA expressions of mitochondrial biogenesis markers which was further confirmed by electron microscopy. Moreover, nitric oxide production increased in skeletal muscle in cobalt supplemented rats, which seems to be the major reason for peroxisome proliferator activated receptor-gamma coactivator-1? (PGC-1?) induction and mitochondrial biogenesis. Thus, in conclusion, we state that hypoxia <span class="hlt">preconditioning</span> by CoCl{sub 2} supplementation in rats increases mitochondrial biogenesis, glucose uptake and metabolism by aerobic respiration in skeletal muscle, which leads to increased physical performance. The significance of this study lies in understanding the molecular mechanism of hypoxia adaptation and improvement of work performance in normal as well as extreme conditions like hypoxia via hypoxia <span class="hlt">preconditioning</span>. -- Highlights: ? We supplemented rats with CoCl{sub 2} for 15 days along with training. ? CoCl{sub 2} supplementation augmented endurance performance and aerobic respiration. ? It increased glucose uptake and metabolism in muscle. ? It enhanced mitochondrial biogenesis in red gastrocnemius muscle.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4567080','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4567080"><span id="translatedtitle">Simultaneous optical flow and source estimation: Space–time discretization and <span class="hlt">preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Andreev, R.; Scherzer, O.; Zulehner, W.</p> <p>2015-01-01</p> <p>We consider the simultaneous estimation of an optical flow field and an illumination source term in a movie sequence. The particular optical flow equation is obtained by assuming that the image intensity is a conserved quantity up to possible sources and sinks which represent varying illumination. We formulate this problem as an energy minimization problem and propose a space–time simultaneous discretization for the optimality system in saddle-point form. We investigate a <span class="hlt">preconditioning</span> strategy that renders the discrete system well-conditioned uniformly in the discretization resolution. Numerical experiments complement the theory. PMID:26435561</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/servlets/purl/962335','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/servlets/purl/962335"><span id="translatedtitle">Non-<span class="hlt">preconditioned</span> conjugate gradient on cell and FPCA-based hybrid supercomputer nodes</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Dubois, David H; Dubois, Andrew J; Boorman, Thomas M; Connor, Carolyn M</p> <p>2009-03-10</p> <p>This work presents a detailed implementation of a double precision, Non-<span class="hlt">Preconditioned</span>, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{trademark} in conjunction with x86 Opteron{trademark} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/servlets/purl/956510','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/servlets/purl/956510"><span id="translatedtitle">Non-<span class="hlt">preconditioned</span> conjugate gradient on cell and FPGA based hybrid supercomputer nodes</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Dubois, David H; Dubois, Andrew J; Boorman, Thomas M; Connor, Carolyn M</p> <p>2009-01-01</p> <p>This work presents a detailed implementation of a double precision, non-<span class="hlt">preconditioned</span>, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{sup TM} in conjunction with x86 Opteron{sup TM} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/19980000320','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/19980000320"><span id="translatedtitle">Graph Embedding Techniques for Bounding Condition Numbers of Incomplete Factor <span class="hlt">Preconditioning</span></span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Guattery, Stephen</p> <p>1997-01-01</p> <p>We extend graph embedding techniques for bounding the spectral condition number of <span class="hlt">preconditioned</span> systems involving symmetric, irreducibly diagonally dominant M-matrices to systems where the preconditioner is not diagonally dominant. In particular, this allows us to bound the spectral condition number when the preconditioner is based on an incomplete factorization. We provide a review of previous techniques, describe our extension, and give examples both of a bound for a model problem, and of ways in which our techniques give intuitive way of looking at incomplete factor preconditioners.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.healthychildren.org/English/safety-prevention/all-around/Pages/Poison-Prevention.aspx','NIH-MEDLINEPLUS'); return false;" href="https://www.healthychildren.org/English/safety-prevention/all-around/Pages/Poison-Prevention.aspx"><span id="translatedtitle">Poison <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... <span class="hlt">Prevention</span> Listen Español Text Size Email Print Share Poison <span class="hlt">Prevention</span> Article Body Post the Poison Help number 1-800-222-1222 on the ... or empty container of a toxic substance, call Poison Help immediately. More than a million American children ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4625514','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4625514"><span id="translatedtitle">Cerebrospinal fluid from rats given hypoxic <span class="hlt">preconditioning</span> protects neurons from oxygen-glucose deprivation-induced injury</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zhang, Yan-bo; Guo, Zheng-dong; Li, Mei-yi; Li, Si-jie; Niu, Jing-zhong; Yang, Ming-feng; Ji, Xun-ming; Lv, Guo-wei</p> <p>2015-01-01</p> <p>Hypoxic <span class="hlt">preconditioning</span> activates endogenous mechanisms that protect against cerebral ischemic and hypoxic injury. To better understand these protective mechanisms, adult rats were housed in a hypoxic environment (8% O2/92% N2) for 3 hours, and then in a normal oxygen environment for 12 hours. Their cerebrospinal fluid was obtained to culture cortical neurons from newborn rats for 1 day, and then the neurons were exposed to oxygen-glucose deprivation for 1.5 hours. The cerebrospinal fluid from rats subjected to hypoxic <span class="hlt">preconditioning</span> reduced oxygen-glucose deprivation-induced injury, increased survival rate, upregulated Bcl-2 expression and downregulated Bax expression in the cultured cortical neurons, compared with control. These results indicate that cerebrospinal fluid from rats given hypoxic <span class="hlt">preconditioning</span> protects against oxygen-glucose deprivation-induced injury by affecting apoptosis-related protein expression in neurons from newborn rats. PMID:26604909</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4188145','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4188145"><span id="translatedtitle"><span class="hlt">Preventing</span> ARDS</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Beitler, Jeremy R.; Schoenfeld, David A.</p> <p>2014-01-01</p> <p>Advances in critical care practice have led to a substantial decline in the incidence of ARDS over the past several years. Low tidal volume ventilation, timely resuscitation and antimicrobial administration, restrictive transfusion practices, and primary <span class="hlt">prevention</span> of aspiration and nosocomial pneumonia have likely contributed to this reduction. Despite decades of research, there is no proven pharmacologic treatment of ARDS, and mortality from ARDS remains high. Consequently, recent initiatives have broadened the scope of lung injury research to include targeted <span class="hlt">prevention</span> of ARDS. Prediction scores have been developed to identify patients at risk for ARDS, and clinical trials testing aspirin and inhaled budesonide/formoterol for ARDS <span class="hlt">prevention</span> are ongoing. Future trials aimed at <span class="hlt">preventing</span> ARDS face several key challenges. ARDS has not been validated as an end point for pivotal clinical trials, and caution is needed when testing toxic therapies that may <span class="hlt">prevent</span> ARDS yet potentially increase mortality. PMID:25288000</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/9782066','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/9782066"><span id="translatedtitle">Effects of WEB 2086 on the protective role of <span class="hlt">preconditioning</span> against arrhythmias in rats.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sariahmeto?lu, M; Cakici, I; Kanzik, I</p> <p>1998-09-01</p> <p>The purpose of the present study was to investigate a possible role of platelet activating factor (PAF) in ischaemic <span class="hlt">preconditioning</span> (PC). Since both PC and PAF act through protein kinase C (PKC), PAF could play a role in PC. To test this hypothesis, anaesthetized, open-chest male rats were subjected to four different protocols. Group I was subjected to 30 min of left coronary artery occlusion. In Group II, WEB 2086 (10 mg kg-1 i.v. bolus+1 mg kg-1 h-1 i.v. infusion) a selective PAF antagonist was given to non-<span class="hlt">preconditioned</span> rats 23 min before the 30-min occlusion period. In Group III and IV ischaemic PC was elicited by one cycle of 3 min occlusion and 5 min reperfusion and also in Group IV, WEB 2086 (10 mg kg-1 i.v. bolus+1 mg kg-1 h-1 i.v. infusion) was given 23 min before the 30 min occlusion period. Ventricular ectopic beats (VEB), ventricular tachycardia (VT), and ventricular fibrillation (VF) that occurred during 30 min occlusion were determined. WEB 2086 administration or PC reduced the VEBs significantly. Incidence of VT and VF were not affected by WEB 2086 compared with control values, although PC decreased the incidence of VT and VF. WEB 2086 administration did not attenuate PC-induced improvement of arrhythmia parameters. These data demonstrated that a specific PAF antagonist, WEB 2086 did not abolish PC-induced protection against arrhythmias. PMID:9782066</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4404827','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4404827"><span id="translatedtitle">Role of MicroRNAs in innate neuroprotection mechanisms due to <span class="hlt">preconditioning</span> of the brain</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Jimenez-Mateos, Eva M.</p> <p>2015-01-01</p> <p>Insults to the brain that are sub-threshold for damage activate endogenous protective pathways, which can temporarily protect the brain against a subsequent harmful episode. This mechanism has been named as tolerance and its protective effects have been shown in experimental models of ischemia and epilepsy. The <span class="hlt">preconditioning</span>-stimulus can be a short period of ischemia or mild seizures induced by low doses of convulsant drugs. Gene-array profiling has shown that both ischemic and epileptic tolerance feature large-scale gene down-regulation but the mechanism are unknown. MicroRNAs are a class of small non-coding RNAs of ~20–22 nucleotides length which regulate gene expression at a post-transcriptional level via mRNA degradation or inhibition of protein translation. MicroRNAs have been shown to be regulated after non-harmful and harmful stimuli in the brain and to contribute to neuroprotective mechanisms. This review focuses on the role of microRNAs in the development of tolerance following ischemic or epileptic <span class="hlt">preconditioning</span>. PMID:25954143</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/1237119','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/1237119"><span id="translatedtitle">Effect of exteroceptive feedback in controlling electrodermal activity in <span class="hlt">pre-conditioned</span> fears.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>McLean, P D; Milne, L G</p> <p>1975-04-01</p> <p>Ss with a strong fear of snakes were taught to increase and decrease their skin resistance during practice sessions with a continuous visual display. Ss were not aware that they were increasing or decreasing their levels of skin resistance and attempted only to influence the magnitude of the multimeter display, the polarity of which was controlled by the experimenter. The study used a within-subjects reversal design to investigate whether bidirectional control could be acquired over skin resistance level. To investigate whether this acquired control could affect the magnitude of elicited <span class="hlt">pre-conditioned</span> autonomic responses, a pre- and post-training comparison was made between the GSRs elicited during test sessions in which Ss viewed slides of snakes while attempting to influence their electrodermal activity with the assistance of the visual display. The results suggest that Ss are able to acquire voluntarily bidirectional control of their level of skin resistance with continuous visual feedback and that this control can either depress or facilitate the magnitude of <span class="hlt">pre-conditioned</span> emotional responses as a function of visual feedback. PMID:1237119</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2012CompM..50..321J','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2012CompM..50..321J"><span id="translatedtitle">Comparison of the deflated <span class="hlt">preconditioned</span> conjugate gradient method and algebraic multigrid for composite materials</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Jönsthövel, T. B.; van Gijzen, M. B.; MacLachlan, S.; Vuik, C.; Scarpas, A.</p> <p>2012-09-01</p> <p>Many applications in computational science and engineering concern composite materials, which are characterized by large discontinuities in the material properties. Such applications require fine-scale finite-element meshes, which lead to large linear systems that are challenging to solve with current direct and iterative solutions algorithms. In this paper, we consider the simulation of asphalt concrete, which is a mixture of components with large differences in material stiffness. The discontinuities in material stiffness give rise to many small eigenvalues that negatively affect the convergence of iterative solution algorithms such as the <span class="hlt">preconditioned</span> conjugate gradient (PCG) method. This paper considers the deflated <span class="hlt">preconditioned</span> conjugate gradient (DPCG) method in which the rigid body modes of sets of elements with homogeneous material properties are used as deflation vectors. As preconditioner we consider several variants of the algebraic multigrid smoothed aggregation method. We evaluate the performance of the DPCG method on a parallel computer using up to 64 processors. Our test problems are derived from real asphalt core samples, obtained using CT scans. We show that the DPCG method is an efficient and robust technique for solving these challenging linear systems.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26254913','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26254913"><span id="translatedtitle">The Protective Effect of Remote Renal <span class="hlt">Preconditioning</span> Against Hippocampal Ischemia Reperfusion Injury: Role of KATP Channels.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Mehrjerdi, Fatemeh Zare; Aboutaleb, Nahid; Pazoki-Toroudi, Hamidreza; Soleimani, Mansoureh; Ajami, Marjan; Khaksari, Mehdi; Safari, Fatemeh; Habibey, Rouhollah</p> <p>2015-12-01</p> <p>Remote ischemic <span class="hlt">preconditioning</span> (RIPC), which consists of several brief ischemia/reperfusion applied at the remote site of lethal ischemia reperfusion, can, through activating different mechanisms, increase the ability of the body's endogenous protection against prolonged ischemia/reperfusion. Recent studies have shown that RIPC has neuroprotective effects, but its mechanisms are not well elucidated. The present study aimed to determine whether activation of KATP channels in remote renal <span class="hlt">preconditioning</span> decreases hippocampus damage induced by global cerebral ischemia. RIPC was induced by ischemia of the left renal artery (IPC); 24 h later, global cerebral ischemia reperfusion (IR) was induced by common carotid arteries occlusion. 5hydroxydecanoate (5HD) and glibenclamide (Gli) were injected before of IPC. The levels of malondialdehyde (MDA) and catalase (CAT) activity were assessed in hippocampus. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was assessed to detect apoptotic cells in hippocampus. RIPC inhibited apoptosis by decreasing positive TUNEL cells (P?<?0.05). KATP channels blocking with 5HD and Gli markedly increased apoptosis in hippocampal cells in RIPC group (P?<?0.001). RIPC decreased MDA level and increased CAT activity in ischemic hippocampus (P?<?0.01). Also, 5HD and Gli inhibited the effect of RIPC on MDA level and CAT activity (P?<?0.05). The present study shows that RIPC can effectively attenuate programmed cell death, increase activity of CAT, and reduce MDA levels. Blocking of KATP channels inhibited the protective effects of RIPC. PMID:26254913</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2270833','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2270833"><span id="translatedtitle">Analysis of the retinal gene expression profile after hypoxic <span class="hlt">preconditioning</span> identifies candidate genes for neuroprotection</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Thiersch, Markus; Raffelsberger, Wolfgang; Frigg, Rico; Samardzija, Marijana; Wenzel, Andreas; Poch, Olivier; Grimm, Christian</p> <p>2008-01-01</p> <p>Background Retinal degeneration is a main cause of blindness in humans. Neuroprotective therapies may be used to rescue retinal cells and preserve vision. Hypoxic <span class="hlt">preconditioning</span> stabilizes the transcription factor HIF-1? in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. To address the molecular mechanisms of the protection, we analyzed the transcriptome of the hypoxic retina using microarrays and real-time PCR. Results Hypoxic exposure induced a marked alteration in the retinal transcriptome with significantly different expression levels of 431 genes immediately after hypoxic exposure. The normal expression profile was restored within 16 hours of reoxygenation. Among the differentially regulated genes, several candidates for neuroprotection were identified like metallothionein-1 and -2, the HIF-1 target gene adrenomedullin and the gene encoding the antioxidative and cytoprotective enzyme paraoxonase 1 which was previously not known to be a hypoxia responsive gene in the retina. The strongly upregulated cyclin dependent kinase inhibitor p21 was excluded from being essential for neuroprotection. Conclusion Our data suggest that neuroprotection after hypoxic <span class="hlt">preconditioning</span> is the result of the differential expression of a multitude of genes which may act in concert to protect visual cells against a toxic insult. PMID:18261226</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4637611','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4637611"><span id="translatedtitle">Platelet-derived microvesicles are involved in cardio-protective effects of remote <span class="hlt">preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ma, Fang; Liu, Hengchao; Shen, Yong; Zhang, Yingjie; Pan, Shaojun</p> <p>2015-01-01</p> <p>The ischemia-protective mechanism of remote <span class="hlt">precondition</span> has been a mystery for a long time. Little was known about details of the inter-organ cardio-protective. Microvesicles, also known as microparticles (MPs), are small membrane-vesicles budding from the plasma membrane of cell. Recent studies have indicated MPs to be an important messenger in various biological processes. Our research mainly examined the hypothesis that remote ischemic conditioning can attenuate heart infarction in a rat after they were subjected to 30 min ischemia and 180 min reperfusion (I/R) by MPs. MPs were extracted from three groups of rat: 1) healthy rats, 2) healthy rats that underwent hindlimb ischemia-reperfusion <span class="hlt">preconditioning</span> (RIPC) immediately, 3) healthy rats that underwent RIPC in 6 hours. Isolated MPs were transfused into rats that had undergone I/R without RIPC. The transfusion of MPs from rats that underwent RIPC immediately resulted in an increase in platelet-derived MPs in blood and reduction in infarction size, confirmed by 2-3-5-triphenyltetrazolium chloride staining. We further observed the contractile function in hearts after they were subjected to different treatments. However, no significant difference was observed in transfusion of MPs from rats that underwent RIPC in 6 hours. RIPC induces an increase in MPs, and platelet-derived MPs may confer at least part of the remote protective effect against cardiac ischemic-reperfusion injury. PMID:26617796</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4656325','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4656325"><span id="translatedtitle">Stimulation of p38 MAPK by hormal <span class="hlt">preconditioning</span> with atrial natriuretic peptide</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kiemer, Alexandra K.; Kulhanek-Heinze, Stefanie; Gerwig, Tobias; Gerbes, Alexander L.; Vollmar, Angelika M.</p> <p>2002-01-01</p> <p>AIM: Stress-activated signaling pathways responsible for hepatic ischemia reperfusion injury and their modulation by protective interventions are widely unknown. <span class="hlt">Preconditioning</span> of rat livers with Atrial Natriuretic Peptide (ANP) attenuates ischemia reperfusion injury (Gerbes et al[21] Hepatology 1998, 28:1309-1317). Since ANP has recently been shown to be a regulator of the p38 MAPK pathway in endothelial cells (Kiemer et al[25] Circ Res 2002, 90:874-881), aim of this study was to investigate activities of MAPK during ischemia and reperfusion and effects of ANP on MAPK. METHODS: Rat livers were perfused with KH-buffer in the presence or absence of ANP for 20 min, kept in cold UW solution for 24 h, and reperfused for up to 120 min. Activities of p38 MAPK and JNK was determined by in vitro phosphorylation assays using MBP and c-jun as substrates. After SDS/PAGE electrophoresis, gels were quantified by phosphorimaging. RESULTS: Activity of p38 MAPK in control organs decreased in the course of ischemia and reperfusion by 85%, whereas ANP increased p38 activity by up to 30-fold. JNK activation of control livers increased in the course of ischemia and reperfusion by up to three-fold. This increase in JNK activity was slightly elevated in ANP <span class="hlt">preconditioned</span> organs. CONCLUSION: This work represents a systematic investigation of MAPK activation during liver ischemia and reperfusion. Employing ANP, for the first time a pharmacological approach to modulate these central signal transduction molecules is presented. PMID:12174383</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_13");'>13</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li class="active"><span>15</span></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_15 --> <div id="page_16" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li class="active"><span>16</span></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="301"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24347333','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24347333"><span id="translatedtitle">Comparing various surgical delay methods with ischemic <span class="hlt">preconditioning</span> in the rat TRAM flap model.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cinpolat, Ani; Bektas, Gamze; Coskunfirat, Nesil; Rizvanovic, Zumreta; Coskunfirat, O Koray</p> <p>2014-06-01</p> <p>Both surgical delay and ischemic <span class="hlt">preconditioning</span> (IP) have been shown to be effective in improving the survival of flaps. We used a variety of flap delay methods and IP to increase the surviving area of the transverse rectus abdominis musculocutaneous (TRAM) flap in rats, and the results are compared in between. A 6-× 3-cm-sized TRAM flap in 40 Wistar rats was allocated into five groups. Group 1: TRAM flap was elevated from nondominant pedicle, and the flap was sutured to the original bed. Group 2: Left superior deep epigastric vessels (SDEV) were cut; 1 week later, TRAM flap was elevated. Group 3: Only skin incision was done; 1 week later, TRAM flap was elevated. Group 4: Skin incision was done, and the left SDEV were cut; 1 week later, TRAM flap was elevated. Group 5: TRAM flap was elevated; IP was performed using three cycles of 10 minutes of repeated ischemia/reperfusion (I/R) periods, and the flap was sutured to the original bed. The surviving area of the flap was statistically significant between the control and groups 2, 4, and 5 (p < 0.001), and groups 4 and 2 were superior to group 5. Although <span class="hlt">preconditioning</span> has been intensively studied for the last two decades and partly provided its beneficial effects in I/R injury, we determined the IP increased the surviving area of the TRAM flap but not effective as much as surgical delay method. PMID:24347333</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.nlm.nih.gov/medlineplus/magazine/issues/fall06/articles/fall06pg12.html','NIH-MEDLINEPLUS'); return false;" href="https://www.nlm.nih.gov/medlineplus/magazine/issues/fall06/articles/fall06pg12.html"><span id="translatedtitle"><span class="hlt">Preventing</span> Diabetes</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... of this page please turn Javascript on. <span class="hlt">Preventing</span> Diabetes Past Issues / Fall 2006 Table of Contents The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) suggests these ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.rorc.research.va.gov/rescue/independent-living/preventing-falls.cfm','NIH-MEDLINEPLUS'); return false;" href="http://www.rorc.research.va.gov/rescue/independent-living/preventing-falls.cfm"><span id="translatedtitle"><span class="hlt">Preventing</span> Falls</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... of falling. Exercises that improve balance, such as tai chi, are helpful. Your local health or senior center ... to <span class="hlt">prevent</span> falls. Do balance exercises, such as tai chi. These types of exercises can lower the chances ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.niaid.nih.gov/topics/tuberculosis/understanding/Pages/prevention.aspx','NIH-MEDLINEPLUS'); return false;" href="http://www.niaid.nih.gov/topics/tuberculosis/understanding/Pages/prevention.aspx"><span id="translatedtitle">Tuberculosis <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Skip Content Marketing Share this: Main Content Area Tuberculosis (TB) <span class="hlt">Prevention</span> TB is an airborne disease and ... patients. Many people who are infected with Mycobacterium tuberculosis ( Mtb ) do not get sick or spread the ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/dengue/prevention/','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/dengue/prevention/"><span id="translatedtitle">Dengue <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... <span class="hlt">Prevention</span> Dengue Branch 1324 Calle Cañada San Juan, Puerto Rico 00920-3860 800-CDC-INFO (800-232-4636) ... Publications and Related Links Dengue Branch Dengue in Puerto Rico Dengue Update Related Links CDC Traveler's Health Homepage: ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.nlm.nih.gov/medlineplus/ency/patientinstructions/000052.htm','NIH-MEDLINEPLUS'); return false;" href="https://www.nlm.nih.gov/medlineplus/ency/patientinstructions/000052.htm"><span id="translatedtitle"><span class="hlt">Preventing</span> falls</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>Gillespie LD, Robertson MC, Gillespie WJ, Lamb SE, Gates S, Cumming RG, Rowe BH. Interventions for <span class="hlt">preventing</span> falls in older people living in the community. Cochrane Database of Systematic Reviews 2009, Issue ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/Features/Shingles/','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/Features/Shingles/"><span id="translatedtitle"><span class="hlt">Prevent</span> Shingles</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... will develop chickenpox, not shingles. Disease of the Week App "Want to know more about shingles? Download CDC's mobile app now . See "Disease of the Week," highlighting disease facts and <span class="hlt">prevention</span> tips. Find "Shingles" ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4555667','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4555667"><span id="translatedtitle">Hydrogen sulfide <span class="hlt">preconditioning</span> protects against myocardial ischemia/reperfusion injury in rats through inhibition of endo/sarcoplasmic reticulum stress</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Li, Changyong; Hu, Min; Wang, Yuan; Lu, Huan; Deng, Jing; Yan, Xiaohong</p> <p>2015-01-01</p> <p>Ischemia reperfusion (I/R) injury is a major cause of myocardial damage. Hydrogen sulfide (H2S), a gaseous signal molecule, has drawn considerable attention for its role in various pathophysiological processes. Multiple lines of evidence reveal the protective effects of H2S in various models of cardiac injury, however, the exact mechanism underlying this protective effect of H2S against myocardial I/R injury is not fully understood. The present study was designed to investigate whether H2S <span class="hlt">preconditioning</span> attenuates myocardial I/R injury in rats and whether the observed protection is associated with reduced endo/sarcoplasmic reticulum (ER/SR) stress. We found that H2S <span class="hlt">preconditioning</span> significantly reduced myocardial infarct size, preserved left ventricular function, and inhibited I/R-induced cardiomyocyte apoptosis in vivo. Furthermore, H2S <span class="hlt">preconditioning</span> significantly attenuated I/R-induced ER/SR stress responses, including the increased expression of glucose-regulated protein 78, C/EBP homologous protein, and activate transcription factor in myocardium. Additionally, we demonstrate that H2S <span class="hlt">preconditioning</span> attenuates ER/SR stress and inhibits cardiomyocyte apoptosis in an in vitro model of hypoxia/reoxygenation in rat H9c2 cardiac myocytes. In conclusion, these results suggest that H2S-attenuated ER/SR stress plays an important role in its protective effects against I/R-induced myocardial injury. PMID:26339339</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4487047','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4487047"><span id="translatedtitle"><span class="hlt">Preconditioning</span> with PEP-1-SOD1 fusion protein attenuates ischemia/reperfusion-induced ventricular arrhythmia in isolated rat hearts</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>KE, ZUNPING; GAO, AIMEI; XU, PENG; WANG, JIANING; JI, LIJUAN; YANG, JIANYE</p> <p>2015-01-01</p> <p>PEP 1-Cu/Zn superoxide dismutase (PEP-1-SOD1) fusion protein <span class="hlt">preconditioning</span> has been reported to protect the myocardium from ischemia/reperfusion (I/R)-induced injury by decreasing the infarct size, reducing levels of cardiomyocyte apoptosis and reducing the release of myocardial-specific biomarkers. The aim of the present study was to examine the effects of PEP-1-SOD1 pretreatment on I/R-induced ventricular arrhythmias in Langendorff-perfused rat hearts. The isolated rat hearts were pretreated with PEP-1-SOD1 prior to I/R, and the I/R-induced hemodynamic parameters, infarct size and ventricular arrhythmias were then assessed. Compared with the unprotected hearts, PEP-1-SOD1 <span class="hlt">preconditioning</span> significantly improved the hemodynamic parameters, decreased the cardiac lactate dehydrogenase and creatine kinase-MB (CK-MB) levels, reduced the infarct size and attenuated the ventricular arrhythmia. Further investigation showed that PEP-1-SOD1 <span class="hlt">preconditioning</span> reduced both the incidence and duration of ventricular tachycardia/ventricular fibrillation. In addition, the intracellular reactive oxygen species (ROS) levels were decreased. The results of the present study suggest that PEP-1-SOD1 <span class="hlt">preconditioning</span> can protect the heart against I/R injury and attenuate I/R-induced arrhythmia by downregulating the generation of ROS. PMID:26170961</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3925051','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3925051"><span id="translatedtitle">Human Bone Marrow-Derived Mesenchymal Stem Cells Display Enhanced Clonogenicity but Impaired Differentiation With Hypoxic <span class="hlt">Preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Boyette, Lisa B.; Creasey, Olivia A.; Guzik, Lynda; Lozito, Thomas</p> <p>2014-01-01</p> <p>Stem cells are promising candidate cells for regenerative applications because they possess high proliferative capacity and the potential to differentiate into other cell types. Mesenchymal stem cells (MSCs) are easily sourced but do not retain their proliferative and multilineage differentiative capabilities after prolonged ex vivo propagation. We investigated the use of hypoxia as a <span class="hlt">preconditioning</span> agent and in differentiating cultures to enhance MSC function. Culture in 5% ambient O2 consistently enhanced clonogenic potential of primary MSCs from all donors tested. We determined that enhanced clonogenicity was attributable to increased proliferation, increased vascular endothelial growth factor secretion, and increased matrix turnover. Hypoxia did not impact the incidence of cell death. Application of hypoxia to osteogenic cultures resulted in enhanced total mineral deposition, although this effect was detected only in MSCs <span class="hlt">preconditioned</span> in normoxic conditions. Osteogenesis-associated genes were upregulated in hypoxia, and alkaline phosphatase activity was enhanced. Adipogenic differentiation was inhibited by exposure to hypoxia during differentiation. Chondrogenesis in three-dimensional pellet cultures was inhibited by <span class="hlt">preconditioning</span> with hypoxia. However, in cultures expanded under normoxia, hypoxia applied during subsequent pellet culture enhanced chondrogenesis. Whereas hypoxic <span class="hlt">preconditioning</span> appears to be an excellent way to expand a highly clonogenic progenitor pool, our findings suggest that it may blunt the differentiation potential of MSCs, compromising their utility for regenerative tissue engineering. Exposure to hypoxia during differentiation (post-normoxic expansion), however, appears to result in a greater quantity of functional osteoblasts and chondrocytes and ultimately a larger quantity of high-quality differentiated tissue. PMID:24436440</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2010-title41-vol3/pdf/CFR-2010-title41-vol3-sec102-72-68.pdf','CFR'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2010-title41-vol3/pdf/CFR-2010-title41-vol3-sec102-72-68.pdf"><span id="translatedtitle">41 CFR 102-72.68 - What <span class="hlt">preconditions</span> must be satisfied before an Executive agency may exercise the delegated...</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2010&page.go=Go">Code of Federal Regulations, 2010 CFR</a></p> <p></p> <p>2010-07-01</p> <p>..., including cost estimates, and schedule for the project, and such other information as may be reasonably... 41 Public Contracts and Property Management 3 2010-07-01 2010-07-01 false What <span class="hlt">preconditions</span> must... Management Federal Property Management Regulations System (Continued) FEDERAL MANAGEMENT REGULATION...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=61821&keyword=oral+AND+surgery&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=43074142&CFTOKEN=81537834','EPA-EIMS'); return false;" href="http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=61821&keyword=oral+AND+surgery&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=43074142&CFTOKEN=81537834"><span id="translatedtitle">TARGETED DELETION OF INDUCIBLE HEAT SHOCK PROTEIN 70 ABROGATES THE LATE INFARCT-SPARING EFFECT OF MYOCARDIAL ISCHEMIC <span class="hlt">PRECONDITIONING</span></span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>Abstract submitted for 82nd annual meeting of the American Association for Thoracic Surgery, May 4-8, 2002 in Washington D.C.<br><br>Targeted Deletion of Inducible Heat Shock Protein 70 Abrogates the Late Infarct-Sparing Effect of Myocardial Ischemic <span class="hlt">Preconditioning</span><br><br>Craig...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4227258','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4227258"><span id="translatedtitle">Exercise <span class="hlt">Preconditioning</span> Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Chang, Cheng-Kuei; Chou, Willy; Lin, Hung-Jung; Huang, Yi-Ching; Tang, Ling-Yu; Lin, Mao-Tsun; Chang, Ching-Ping</p> <p>2014-01-01</p> <p>The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise <span class="hlt">preconditioning</span> in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise <span class="hlt">preconditioning</span> induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise <span class="hlt">preconditioning</span> promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise <span class="hlt">preconditioning</span> is a promising strategy for facilitating functional recovery from SCI. PMID:25334068</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2002PNAS...9913114M','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2002PNAS...9913114M"><span id="translatedtitle">Cell transplantation after oxidative hepatic <span class="hlt">preconditioning</span> with radiation and ischemia-reperfusion leads to extensive liver repopulation</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Malhi, Harmeet; Gorla, Giridhar R.; Irani, Adil N.; Annamaneni, Pallavi; Gupta, Sanjeev</p> <p>2002-10-01</p> <p>The inability of transplanted cells to proliferate in the normal liver hampers cell therapy. We considered that oxidative hepatic DNA damage would impair the survival of native cells and promote proliferation in transplanted cells. Dipeptidyl peptidase-deficient F344 rats were <span class="hlt">preconditioned</span> with whole liver radiation and warm ischemia-reperfusion followed by intrasplenic transplantation of syngeneic F344 rat hepatocytes. The <span class="hlt">preconditioning</span> was well tolerated, although serum aminotransferase levels rose transiently and hepatic injury was observed histologically, along with decreased catalase activity and 8-hydroxy adducts of guanine, indicating oxidative DNA damage. Transplanted cells did not proliferate in the liver over 3 months in control animals and animals <span class="hlt">preconditioned</span> with ischemia-reperfusion alone. Animals treated with radiation alone showed some transplanted cell proliferation. In contrast, the liver of animals <span class="hlt">preconditioned</span> with radiation plus ischemia-reperfusion was replaced virtually completely over 3 months. Transplanted cells integrated in the liver parenchyma and liver architecture were preserved normally. These findings offer a paradigm for repopulating the liver with transplanted cells. Progressive loss of cells experiencing oxidative DNA damage after radiation and ischemia-reperfusion injury could be of significance for epithelial renewal in additional organs.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.gpo.gov/fdsys/pkg/CFR-2011-title41-vol3/pdf/CFR-2011-title41-vol3-sec102-72-68.pdf','CFR2011'); return false;" href="https://www.gpo.gov/fdsys/pkg/CFR-2011-title41-vol3/pdf/CFR-2011-title41-vol3-sec102-72-68.pdf"><span id="translatedtitle">41 CFR 102-72.68 - What <span class="hlt">preconditions</span> must be satisfied before an Executive agency may exercise the delegated...</span></a></p> <p><a target="_blank" href="http://www.gpo.gov/fdsys/browse/collectionCfr.action?selectedYearFrom=2011&page.go=Go">Code of Federal Regulations, 2011 CFR</a></p> <p></p> <p>2011-01-01</p> <p>... 41 Public Contracts and Property Management 3 2011-01-01 2011-01-01 false What <span class="hlt">preconditions</span> must be satisfied before an Executive agency may exercise the delegated authority to perform an individual... satisfied before an Executive agency may exercise the delegated authority to perform an individual...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/19191501','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/19191501"><span id="translatedtitle">Combined effects of scaffold stiffening and mechanical <span class="hlt">preconditioning</span> cycles on construct biomechanics, gene expression, and tendon repair biomechanics.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Nirmalanandhan, Victor Sanjit; Juncosa-Melvin, Natalia; Shearn, Jason T; Boivin, Gregory P; Galloway, Marc T; Gooch, Cynthia; Bradica, Gino; Butler, David L</p> <p>2009-08-01</p> <p>Our group has previously reported that in vitro mechanical stimulation of tissue-engineered tendon constructs significantly increases both construct stiffness and the biomechanical properties of the repair tissue after surgery. When optimized using response surface methodology, our results indicate that a mechanical stimulus with three components (2.4% strain, 3000 cycles/day, and one cycle repetition) produced the highest in vitro linear stiffness. Such positive correlations between construct and repair stiffness after surgery suggest that enhancing structural stiffness before surgery could not only accelerate repair stiffness but also <span class="hlt">prevent</span> premature failures in culture due to poor mechanical integrity. In this study, we examined the combined effects of scaffold crosslinking and subsequent mechanical stimulation on construct mechanics and biology. Autologous tissue-engineered constructs were created by seeding mesenchymal stem cells (MSCs) from 15 New Zealand white rabbits on type I collagen sponges that had undergone additional dehydrothermal crosslinking (termed ADHT in this manuscript). Both constructs from each rabbit were mechanically stimulated for 8h/day for 12 consecutive days with half receiving 100 cycles/day and the other half receiving 3000 cycles/day. These paired MSC-collagen autologous constructs were then implanted in bilateral full-thickness, full-length defects in the central third of rabbit patellar tendons. Increasing the number of in vitro cycles/day delivered to the ADHT constructs in culture produced no differences in stiffness or gene expression and no changes in biomechanical properties or histology 12 weeks after surgery. Compared to MSC-based repairs from a previous study that received no additional treatment in culture, ADHT crosslinking of the scaffolds actually lowered the 12-week repair stiffness. Thus, while ADHT crosslinking may initially stiffen a construct in culture, this specific treatment also appears to mask any benefits of stimulation among repairs postsurgery. Our findings emphasize the importance of properly <span class="hlt">preconditioning</span> a scaffold to better control/modulate MSC differentiation in vitro and to further enhance repair outcome in vivo. PMID:19191501</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2792106','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2792106"><span id="translatedtitle">Combined Effects of Scaffold Stiffening and Mechanical <span class="hlt">Preconditioning</span> Cycles on Construct Biomechanics, Gene Expression, and Tendon Repair Biomechanics</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Juncosa-Melvin, Natalia; Shearn, Jason T.; Boivin, Gregory P.; Galloway, Marc T.; Gooch, Cynthia; Bradica, Gino; Butler, David L.</p> <p>2009-01-01</p> <p>Our group has previously reported that in vitro mechanical stimulation of tissue-engineered tendon constructs significantly increases both construct stiffness and the biomechanical properties of the repair tissue after surgery. When optimized using response surface methodology, our results indicate that a mechanical stimulus with three components (2.4% strain, 3000?cycles/day, and one cycle repetition) produced the highest in vitro linear stiffness. Such positive correlations between construct and repair stiffness after surgery suggest that enhancing structural stiffness before surgery could not only accelerate repair stiffness but also <span class="hlt">prevent</span> premature failures in culture due to poor mechanical integrity. In this study, we examined the combined effects of scaffold crosslinking and subsequent mechanical stimulation on construct mechanics and biology. Autologous tissue-engineered constructs were created by seeding mesenchymal stem cells (MSCs) from 15 New Zealand white rabbits on type I collagen sponges that had undergone additional dehydrothermal crosslinking (termed ADHT in this manuscript). Both constructs from each rabbit were mechanically stimulated for 8?h/day for 12 consecutive days with half receiving 100?cycles/day and the other half receiving 3000?cycles/day. These paired MSC–collagen autologous constructs were then implanted in bilateral full-thickness, full-length defects in the central third of rabbit patellar tendons. Increasing the number of in vitro cycles/day delivered to the ADHT constructs in culture produced no differences in stiffness or gene expression and no changes in biomechanical properties or histology 12 weeks after surgery. Compared to MSC-based repairs from a previous study that received no additional treatment in culture, ADHT crosslinking of the scaffolds actually lowered the 12-week repair stiffness. Thus, while ADHT crosslinking may initially stiffen a construct in culture, this specific treatment also appears to mask any benefits of stimulation among repairs postsurgery. Our findings emphasize the importance of properly <span class="hlt">preconditioning</span> a scaffold to better control/modulate MSC differentiation in vitro and to further enhance repair outcome in vivo. PMID:19191501</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25979673','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25979673"><span id="translatedtitle">Sevoflurane <span class="hlt">preconditioning</span> improving cerebral focal ischemia-reperfusion damage in a rat model via PI3K/Akt signaling pathway.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhang, Yan; Tian, Shou-Yuan; Li, Yan-Wei; Zhang, Ling; Yu, Jian-Bo; Li, Jing; Chen, Yi-Yang; Wang, Ya-Xin; Liang, Yu; Zhang, Xiu-Shan; Wang, Wen-Sheng; Liu, Hai-Gen</p> <p>2015-09-10</p> <p>In this study, we aimed to assess the neuroprotective effect of sevoflurane <span class="hlt">preconditioning</span> in a cerebral focal ischemia-reperfusion rat model. Sixty Sprague Dawley rats were divided into six groups: sham operated group, cerebral focal ischemia-reperfusion (CIR) group, CIR+sevoflurane <span class="hlt">preconditioning</span> (SP) (2%) group, CIR+sevoflurane <span class="hlt">preconditioning</span> (2.5%) group, CIR+sevoflurane <span class="hlt">preconditioning</span> (3%) group, and CIR+sevoflurane <span class="hlt">preconditioning</span> (3.5%) group. All subjects were euthanized 2days post-surgery and their hippocampus tissues were removed. Tissue malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH-Px) levels were measured and hippocampus tissue samples were examined histopathologically. Results showed that significant difference in antioxidant, immunity indexes, and apoptosis-related protein expression was detected in hippocampus tissue between sham-operated control and CIR groups. Sevoflurane <span class="hlt">preconditioning</span> significantly dose-dependently reduced MDA, IL-1?, IL-6, IL-10 and TNF-? levels and enhanced antioxidant enzyme activities in hippocampus tissue of CIR+SP groups compared to CIR group. In addition, sevoflurane <span class="hlt">preconditioning</span> significantly dose-dependently upregulated PI3K, p-Akt and Bcl-2 levels and downregulated caspase-3 and Bax levels in hippocampus tissue of CIR+SP groups compared to CIR group. It can be concluded that sevoflurane <span class="hlt">preconditioning</span> demonstrates a strong and ameliorative effect on cerebral I/R damage in rats. The neuroprotective mechanisms of sevoflurane <span class="hlt">preconditioning</span> are associated with its properties of anti-apoptosis and anti-oxidation as well as regulation of PI3K and p-Akt signal activation. PMID:25979673</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2014AGUFM.A34B..06A','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2014AGUFM.A34B..06A"><span id="translatedtitle">Identification of Dynamic Processes Responsible for <span class="hlt">Preconditioning</span> the Atmosphere for Severe Convective Outbreaks in Midlatitudes</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Agard, J. V.; Emanuel, K.</p> <p>2014-12-01</p> <p>Budgets of the tendency of convective available potential energy (CAPE) are calculated using reanalysis data in case studies of several North American severe weather outbreaks from the years 2012 and 2013. These budgets separate the tendency of CAPE into terms arising from diabatic heating of the subcloud boundary layer, radiative cooling of the free troposphere, and advection of air in the free troposphere relative to the motion of a parcel to be lifted. It is found that in most cases, the CAPE tendency budget is dominated by the term representing diabatic heating of the subcloud layer, which establishes high CAPE values in advance of thunderstorm development. This result suggests the relative importance of surface entropy fluxes in supporting midlatitude severe local storms through atmospheric <span class="hlt">preconditioning</span> (CAPE buildup). By extension, this result warrants further investigation into the roles of environmental land surface properties as controls on the climatology of midlatitude severe convecton, as such properties play important roles in modulating surface entropy fluxes.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22230859','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22230859"><span id="translatedtitle">Fluid <span class="hlt">preconditioning</span> for Newton–Krylov-based, fully implicit, electrostatic particle-in-cell simulations</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Chen, G.; Chacón, L.; Leibs, C.A.; Knoll, D.A.; Taitano, W.</p> <p>2014-02-01</p> <p>A recent proof-of-principle study proposes an energy- and charge-conserving, nonlinearly implicit electrostatic particle-in-cell (PIC) algorithm in one dimension [9]. The algorithm in the reference employs an unpreconditioned Jacobian-free Newton–Krylov method, which ensures nonlinear convergence at every timestep (resolving the dynamical timescale of interest). Kinetic enslavement, which is one key component of the algorithm, not only enables fully implicit PIC as a practical approach, but also allows <span class="hlt">preconditioning</span> the kinetic solver with a fluid approximation. This study proposes such a preconditioner, in which the linearized moment equations are closed with moments computed from particles. Effective acceleration of the linear GMRES solve is demonstrated, on both uniform and non-uniform meshes. The algorithm performance is largely insensitive to the electron–ion mass ratio. Numerical experiments are performed on a 1D multi-scale ion acoustic wave test problem.</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_14");'>14</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li class="active"><span>16</span></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_16 --> <div id="page_17" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li class="active"><span>17</span></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="321"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/6643317','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/6643317"><span id="translatedtitle">Lipid compositional changes during low-temperature <span class="hlt">pre-conditioning</span> against SO sub 2 in coleus</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Norman, H.A.; Krizek, D.T.; Mirecki, R.M. )</p> <p>1989-04-01</p> <p>Short periods of temperature <span class="hlt">preconditioning</span> at 13{degrees}C. were found to provide protection against SO{sub 2} injury in coleus. The present study was conducted to determine whether changes in lipid metabolism and membrane fluidity might contribute to this phytoprotection. After 5 days of hardening at 13{degrees}C, there were significant differences in polar lipid composition and free fatty acid (FA) levels between SO{sub 2}-sensitive cultivar Buckley Supreme and SO{sub 2}-insensitive Marty. Molecular species of chloroplast lipids in Marty contained increased levels of linolenic acid. Differences were also found in total FA pools. At 20{degrees}C, palmitic acid and stearic acid were the major components. After temperature hardening at 13{degrees}C, total FA levels decreased in Marty but increased in Buckley Supreme. These modifications in lipid composition suggest a possible mechanism for cultivar differences in response in SO{sub 2}.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26133420','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26133420"><span id="translatedtitle">Efficient <span class="hlt">preconditioning</span> of the electronic structure problem in large scale ab initio molecular dynamics simulations.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Schiffmann, Florian; VandeVondele, Joost</p> <p>2015-06-28</p> <p>We present an improved <span class="hlt">preconditioning</span> scheme for electronic structure calculations based on the orbital transformation method. First, a preconditioner is developed which includes information from the full Kohn-Sham matrix but avoids computationally demanding diagonalisation steps in its construction. This reduces the computational cost of its construction, eliminating a bottleneck in large scale simulations, while maintaining rapid convergence. In addition, a modified form of Hotelling's iterative inversion is introduced to replace the exact inversion of the preconditioner matrix. This method is highly effective during molecular dynamics (MD), as the solution obtained in earlier MD steps is a suitable initial guess. Filtering small elements during sparse matrix multiplication leads to linear scaling inversion, while retaining robustness, already for relatively small systems. For system sizes ranging from a few hundred to a few thousand atoms, which are typical for many practical applications, the improvements to the algorithm lead to a 2-5 fold speedup per MD step. PMID:26133420</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/doepatents/biblio/1107797','DOE-PATENT-XML'); return false;" href="http://www.osti.gov/doepatents/biblio/1107797"><span id="translatedtitle">Matrix multiplication operations with data <span class="hlt">pre-conditioning</span> in a high performance computing architecture</span></a></p> <p><a target="_blank" href="http://www.osti.gov/doepatents">DOEpatents</a></p> <p>Eichenberger, Alexandre E; Gschwind, Michael K; Gunnels, John A</p> <p>2013-11-05</p> <p>Mechanisms for performing matrix multiplication operations with data <span class="hlt">pre-conditioning</span> in a high performance computing architecture are provided. A vector load operation is performed to load a first vector operand of the matrix multiplication operation to a first target vector register. A load and splat operation is performed to load an element of a second vector operand and replicating the element to each of a plurality of elements of a second target vector register. A multiply add operation is performed on elements of the first target vector register and elements of the second target vector register to generate a partial product of the matrix multiplication operation. The partial product of the matrix multiplication operation is accumulated with other partial products of the matrix multiplication operation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015JCoPh.290...73V','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015JCoPh.290...73V"><span id="translatedtitle">A projected <span class="hlt">preconditioned</span> conjugate gradient algorithm for computing many extreme eigenpairs of a Hermitian matrix</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Vecharynski, Eugene; Yang, Chao; Pask, John E.</p> <p>2015-06-01</p> <p>We present an iterative algorithm for computing an invariant subspace associated with the algebraically smallest eigenvalues of a large sparse or structured Hermitian matrix A. We are interested in the case in which the dimension of the invariant subspace is large (e.g., over several hundreds or thousands) even though it may still be small relative to the dimension of A. These problems arise from, for example, density functional theory (DFT) based electronic structure calculations for complex materials. The key feature of our algorithm is that it performs fewer Rayleigh-Ritz calculations compared to existing algorithms such as the locally optimal block <span class="hlt">preconditioned</span> conjugate gradient or the Davidson algorithm. It is a block algorithm, and hence can take advantage of efficient BLAS3 operations and be implemented with multiple levels of concurrency. We discuss a number of practical issues that must be addressed in order to implement the algorithm efficiently on a high performance computer.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015JChPh.142x4117S','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015JChPh.142x4117S"><span id="translatedtitle">Efficient <span class="hlt">preconditioning</span> of the electronic structure problem in large scale ab initio molecular dynamics simulations</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Schiffmann, Florian; VandeVondele, Joost</p> <p>2015-06-01</p> <p>We present an improved <span class="hlt">preconditioning</span> scheme for electronic structure calculations based on the orbital transformation method. First, a preconditioner is developed which includes information from the full Kohn-Sham matrix but avoids computationally demanding diagonalisation steps in its construction. This reduces the computational cost of its construction, eliminating a bottleneck in large scale simulations, while maintaining rapid convergence. In addition, a modified form of Hotelling's iterative inversion is introduced to replace the exact inversion of the preconditioner matrix. This method is highly effective during molecular dynamics (MD), as the solution obtained in earlier MD steps is a suitable initial guess. Filtering small elements during sparse matrix multiplication leads to linear scaling inversion, while retaining robustness, already for relatively small systems. For system sizes ranging from a few hundred to a few thousand atoms, which are typical for many practical applications, the improvements to the algorithm lead to a 2-5 fold speedup per MD step.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://arxiv.org/pdf/1407.3585.pdf','EPRINT'); return false;" href="http://arxiv.org/pdf/1407.3585.pdf"><span id="translatedtitle">Conceptual <span class="hlt">preconditions</span> of overcoming of relativistic intentions in modern philosophy of science</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Kulikov, Sergey</p> <p>2014-01-01</p> <p>The paper defends the thesis that it's possible to maintain some conceptual <span class="hlt">preconditions</span> of overcoming of relativistic intentions in modern philosophy of science ("there are no any general foundations in philosophy of science"). We found two general foundations in philosophy of science as a minimum. From the first side it's realistic to reveal on the base of special understanding of time the value of time not only in natural thought (especially in theory of gravity) but also in humanitarian knowledge. That's why philosophy of science has independent position in epistemology and ontology corresponding to interpretation of time as a general category of scientific thinking. The nature of time has internally inconsistent (paradoxical) character. Time is phenomenon which existing and not existing at the same time. This phenomenon is identified with imaginary movement and also ideal (formal) process of formation of the nature. The general understanding of time is connected with its "mathematical" meaning as calcul...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25953834','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25953834"><span id="translatedtitle">A critical review of mechanisms regulating remote <span class="hlt">preconditioning</span>-induced brain protection.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Meller, Robert; Simon, Roger P</p> <p>2015-11-15</p> <p>Remote <span class="hlt">preconditioning</span> (rPC) is the phenomenon whereby brief organ ischemia evokes an endogenous response such that a different (remote) organ is protected against subsequent, normally injurious ischemia. Experiments show rPC to be effective at evoking cardioprotection against ischemic heart injury and, more recently, neuroprotection against brain ischemia. Such is the enthusiasm for rPC that human studies have been initiated. Clinical trials suggest rPC to be safe (phase II trial) and effective in reducing stroke incidence in a population with high stroke risk. However, despite the therapeutic potential of rPC, there is a large gap in knowledge regarding the effector mechanisms of rPC and how it might be orchestrated to improve outcome after stroke. Here we provide a critical review of mechanisms that are directly attributable to rPC-induced neuroprotection in preclinical trials of rPC. PMID:25953834</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2012InvPr..28e5015C','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2012InvPr..28e5015C"><span id="translatedtitle">Left and right <span class="hlt">preconditioning</span> for electrical impedance tomography with structural information</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Calvetti, Daniela; McGivney, Debra; Somersalo, Erkki</p> <p>2012-05-01</p> <p>A common problem in computational inverse problems is to find an efficient way of solving linear or nonlinear least-squares problems. For large-scale problems, iterative solvers are the method of choice for solving the associated linear systems, and for nonlinear problems, an additional effective local linearization method is required. In this paper, we discuss an efficient <span class="hlt">preconditioning</span> scheme for Krylov subspace methods, based on the Bayesian analysis of the inverse problem. The model problem to which we apply this methodology is electrical impedance tomography (EIT) augmented with prior information coming from a complementary modality, such as x-ray imaging. The particular geometry considered here models the x-ray-guided EIT for breast imaging. The interest in applying EIT concurrently with x-ray breast imaging arises from the experimental observation that the impedivity spectra of certain types of malignant and benign tissues differ significantly from each other, thus offering a possibility of diagnosis without more invasive tissue sampling. After setting up the EIT inverse problem within a Bayesian framework, we present an inner and outer iteration scheme for computing a maximum a posteriori estimate. The prior covariance provides a right preconditioner and the modeling error covariance provides a left preconditioner for the iterative method used to solve the linear least-squares problem at each outer iteration of the optimization problem. Moreover, the stopping criterion for the inner iterations is coupled with the progress of the solution of the outer iteration. Besides the <span class="hlt">preconditioning</span> scheme, the computational efficiency relies on a very efficient method to compute the Jacobian, obtained by carefully organizing the forward computation. Computed examples illustrate the robustness and computational efficiency of the proposed algorithm.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3996162','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3996162"><span id="translatedtitle">Intravenous pretreatment with emulsified isoflurane <span class="hlt">preconditioning</span> protects kidneys against ischemia/reperfusion injury in rats</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p></p> <p>2014-01-01</p> <p>Background Emulsified isoflurane (EIso) is a novel intravenous general anesthetic, which can provide rapid anesthetic induction and recovery. EIso <span class="hlt">preconditioning</span> could attenuate heart, lung and liver ischemia/reperfusion (I/R) injury. We tested the hypothesis that intravenous pretreatment with EIso would protect kidneys against I/R injury by inhibiting systemic inflammatory responses and improving renal antioxidative ability. Methods Rats were randomly divided into these six groups: sham, I/R, intralipid, 1, 2 or 4 ml/kg EIso. Rats were subjected to 45 min left renal pedicle occlusion followed by 3 h reperfusion after right nephrectomy. Rat were treated with intravenous 8% EIso with 1, 2 or 4 ml/kg, or 30% intralipid with 2 ml/kg for 30 min before ischemia, respectively. After reperfusion, renal functional parameters, serum mediator concentrations and markers of oxidative stress in kidney tissues were determined, and renal histopathological analysis were performed. Results Serum creatinine, blood urea nitrogen, cystatin c, tumor necrosis factor-?, interleukin-6, and interleukin-10 concentrations were significantly increased after renal I/R as compared to the sham group. So was renal tissue MDA content and histological scores, but renal tissue SOD activity was decreased. Additionally, severe morphological damages were observed in these study groups. In contrast, 2 or 4 ml/kg EIso reduced serum creatinine, blood urea nitrogen, cystatin c, tumor necrosis factor-?, and interleukin-6 levels, decreased renal tissue MDA content and histological scores, increased serum interleukin-10 level and tissue SOD activity as compared to the I/R, intralipid and 1 ml/kg EIso groups. Renal morphological damages were alleviated after pretreatment of 2 or 4 ml/kg EIso. Conclusions Intravenous EIso produces <span class="hlt">preconditioning</span> against renal I/R injury in rats, which might be mediated by attenuating inflammation and increasing antioxidation ability. PMID:24739487</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4120131','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4120131"><span id="translatedtitle">Cardiac <span class="hlt">preconditioning</span> with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kelly-Laubscher, Roisin F; King, Jonathan C; Hacking, Damian; Somers, Sarin; Hastie, Samantha; Stewart, Tessa; Imamdin, Aqeela; Maarman, Gerald; Pedretti, Sarah; Lecour, Sandrine</p> <p>2014-01-01</p> <p>Summary Aims Sphingosine-1-phosphate (S1P) is a cardioprotective agent. Signal transducer and activator of transcription 3 (STAT-3) is a key mediator of many cardioprotective agents. We aimed to explore whether STAT-3 is a key mediator in S1P-induced <span class="hlt">preconditioning</span>. Methods Langendorff-perfused hearts from Wistar rats and wild-type or cardiomyocyte-specific STAT-3 knockout mice were pre-treated with S1P (10 nmol/l), with or without the STAT-3 pathway inhibitor AG490, before an ischaemia–reperfusion insult. Triphenyltetrazolium chloride and Evans blue staining were used for the determination of infarct size. Western blot analysis was carried out on the S1P pre-treated hearts for detection of cytosolic, nuclear and mitochondrial phosphorylated and total STAT-3 proteins. Results Pre-treatment with S1P decreased the infarct size in isolated rat (5 ± 3% vs control 26 ± 8%, p < 0.01) and wild-type mouse hearts (13 ± 1% vs control 33 ± 3%, p < 0.05). This protective effect was abolished in the rat hearts pre-treated with AG490 (30 ± 10%, p = ns vs control) and in the hearts from STAT-3 knockout mice (35 ± 4% vs control 30 ± 3%, p = ns). Levels of phosphorylated STAT-3 were significantly increased in both the nuclear (p < 0.05 vs control) and mitochondrial (p < 0.05 vs control) fractions in the S1P pre-treated hearts, but remained unchanged in the cytosolic fraction (p = ns vs control). Conclusion These novel results demonstrate that pharmacological <span class="hlt">preconditioning</span> with S1P in the isolated heart is mediated by activation of mitochondrial and nuclear STAT-3, therefore suggesting that S1P may be a novel therapeutic target to modulate mitochondrial and nuclear function in cardiovascular disease in order to protect the heart against ischaemia–reperfusion. PMID:25000441</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/23562311','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/23562311"><span id="translatedtitle">A <span class="hlt">preconditioning</span> regimen with a PKC? activator improves islet graft function in a mouse transplant model.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Hamilton, Diana; Rugg, Caitlin; Davis, Nicolynn; Kvezereli, Manana; Tafti, Bashir Akhavan; Busque, Stephan; Fontaine, Magali</p> <p>2014-01-01</p> <p>Transplantation of islets isolated from deceased donor pancreata is an attractive method of ?-cell replacement therapy for patients with type 1 diabetes (T1D). However, the loss of islet cell viability and function during the peritransplant period is a limiting factor to long-term islet engraftment. Activation of the isoenzyme PKC? may improve islet survival and function. The current study assesses the effects of PKC? activation on islet graft function in a syngeneic streptozotocin-induced diabetic mouse model. Islets were isolated from wild-type BALB/c mice <span class="hlt">preconditioned</span> with either a PKC? activator (??RACK) or a TAT carrier control peptide. Islets were further treated with the same agents during isolation, purification, and incubation prior to transplantation. Two hundred seventy-five islet equivalents were transplanted under the kidney capsule of streptozotocin-induced diabetic BALB/c mice. Islet function was assessed by measurement of blood glucose levels every 3 days for 42 days after transplant and through an intraperitoneal glucose tolerance test (IPGTT). The time for return to euglycemia in mice transplanted with islets treated with ??RACK was improved at 14 ± 6 days versus 21 ± 6 days with TAT-treated islets. The IPGTT showed a 50% reduction in the area under the curve associated with an improved insulin response in mice transplanted with ??RACK-treated islets compared to TAT-treated islets. A <span class="hlt">preconditioning</span> regimen using PKC? agonist before pancreatic recovery and during islet isolation improves islet graft function and resistance to high glucose stress after transplantation. PMID:23562311</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=Plagiarism&pg=2&id=EJ924860','ERIC'); return false;" href="http://eric.ed.gov/?q=Plagiarism&pg=2&id=EJ924860"><span id="translatedtitle">Plagiarism <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Probett, Christine</p> <p>2011-01-01</p> <p>Plagiarism does exist at universities today. In some cases, students are naive with respect to understanding what plagiarism is and how to avoid it. In other cases, students blatantly disregard and disrespect the written work of others, claiming it as their own. Regardless, educators must be vigilant in their efforts to discourage and <span class="hlt">prevent</span>…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=summer+AND+internships&pg=2&id=EJ663430','ERIC'); return false;" href="http://eric.ed.gov/?q=summer+AND+internships&pg=2&id=EJ663430"><span id="translatedtitle"><span class="hlt">Preventing</span> Tragedy.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>One Feather, Sandra</p> <p>2003-01-01</p> <p>The Navajo supervisor in the Office of Environmental Health in New Mexico identifies diseases and their risk factors, administers an injury <span class="hlt">prevention</span> program, and ensures compliance with various health-related codes. She assists in the planning and direction of environmental health programs and public health education for local Navajo…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/2663679','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/2663679"><span id="translatedtitle">[School sports--early <span class="hlt">prevention</span> of coronary heart disease?].</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Krasemann, E O; Lewerenz, J</p> <p>1989-06-10</p> <p>In its usual form, school sports is neither calculated to motivate a lifelong pursuance of sports, nor is it particularly suitable for primary <span class="hlt">prevention</span> of coronary heart disease. In view of the multifactorial pathogenetic nature of this disease, school sports can be nothing more than an adjunctive prophylactic measure. Epidemiological studies have shown a high level of probability for the usefulness of physical exercise as a <span class="hlt">preventive</span> measure in childhood and adolescence. However, the findings of sports-medical research on endurance sports must be taken into account. In a controlled study of Hamburg children covering a period of 3 years, it was shown that pupils with high self-esteem, which was particularly encouraged, have better <span class="hlt">pre-conditions</span> for a lifelong interest in active sports. PMID:2663679</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/1848531','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/1848531"><span id="translatedtitle"><span class="hlt">Preventive</span> implantations.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Denissen, H W; Kalk, W</p> <p>1991-02-01</p> <p><span class="hlt">Preventive</span> implantology is concerned with the preservation of the alveolar ridge of the (edentulous) jaw. Maintaining the volume of the alveolar ridge is a major problem in the <span class="hlt">prevention</span> of oral disease. Loss of teeth and tooth roots leads to resorption of residual ridges. This being so, it is a logical approach to substitute artificial analogues for lost tooth roots. Hydroxyapatite implants have been studied as submerged tooth root substitutes and shown to maintain the bulk of the alveolar ridge. A drawback of the implants is that the ridge maintenance depends solely on the physical presence of the hydroxyapatite implants. No physiological influence on bone preservation can be attributed to the implants. However, long term research indicates that 75 per cent of the implants survive under full lower dentures and 100 per cent of the implants under fixed partial dentures. PMID:1848531</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://prevention.cancer.gov/sites/default/files/uploads/major_program/PREVENT_Concept_Application_0.doc','NCI'); return false;" href="https://prevention.cancer.gov/sites/default/files/uploads/major_program/PREVENT_Concept_Application_0.doc"><span id="translatedtitle"><span class="hlt">PREVENT</span> APPLICATION</span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p>For preclinical drug development projects describe the proposed development strategy, readiness of the primary assay, and any supporting secondary assays available, including structure-based, virtual, and selectivity assays. Supporting data can be included as an appendix. For new molecular entities, describe the development status of the compound and optimization strategy (for guidance, please refer to the <span class="hlt">PREVENT</span> Stage Gates). Indicate whether the compound has undergone medicinal chemistry optimization; if not, describe the proposed strategy.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4625520','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4625520"><span id="translatedtitle">Optimal concentration and time window for proliferation and differentiation of neural stem cells from embryonic cerebral cortex: 5% oxygen <span class="hlt">preconditioning</span> for 72 hours</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Yuan, Li-li; Guan, Ying-jun; Ma, Deng-dian; Du, Hong-mei</p> <p>2015-01-01</p> <p>Hypoxia promotes proliferation and differentiation of neural stem cells from embryonic day 12 rat brain tissue, but the concentration and time of hypoxic <span class="hlt">preconditioning</span> are controversial. To address this, we cultured neural stem cells isolated from embryonic day 14 rat cerebral cortex in 5% and 10% oxygen in vitro. MTT assay, neurosphere number, and immunofluorescent staining found that 5% or 10% oxygen <span class="hlt">preconditioning</span> for 72 hours improved neural stem cell viability and proliferation. With prolonged hypoxic duration (120 hours), the proportion of apoptotic cells increased. Thus, 5% oxygen <span class="hlt">preconditioning</span> for 72 hours promotes neural stem cell proliferation and neuronal differentiation. Our findings indicate that the optimal concentration and duration of hypoxic <span class="hlt">preconditioning</span> for promoting proliferation and differentiation of neural stem cells from the cerebral cortex are 5% oxygen for 72 hours.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4323815','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4323815"><span id="translatedtitle">Single Intracoronary Injection of Encapsulated Antagomir?92a Promotes Angiogenesis and <span class="hlt">Prevents</span> Adverse Infarct Remodeling</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Bellera, Neus; Barba, Ignasi; Rodriguez?Sinovas, Antonio; Ferret, Eulalia; Asín, Miguel Angel; Gonzalez?Alujas, MªTeresa; Pérez?Rodon, Jordi; Esteves, Marielle; Fonseca, Carla; Toran, Nuria; Garcia del Blanco, Bruno; Pérez, Amadeo; Garcia?Dorado, David</p> <p>2014-01-01</p> <p>Background Small and large preclinical animal models have shown that antagomir?92a?based therapy reduces early <span class="hlt">postischemic</span> loss of function, but its effect on postinfarction remodeling is not known. In addition, the reported remote miR?92a inhibition in noncardiac organs <span class="hlt">prevents</span> the translation of nonvectorized miR?targeted therapy to the clinical setting. We investigated whether a single intracoronary administration of antagomir?92a encapsulated in microspheres could <span class="hlt">prevent</span> deleterious remodeling of myocardium 1 month after acute myocardial infarction AUTHOR: Should “acute” be added before “myocardial infarction” (since abbreviation is AMI)? Also check at first mention in main text (AMI) without adverse effects. Methods and Results In a percutaneous pig model of reperfused AMI, a single intracoronary administration of antagomir?92a encapsulated in specific microspheres (9 ?m poly?d,?lactide?co?glycolide [PLGA]) inhibited miR?92a in a local, selective, and sustained manner (n=3 pigs euthanized 1, 3, and 10 days after treatment; 8×, 2×, and 5×?fold inhibition at 1, 3, and 10 days). Downregulation of miR?92a resulted in significant vessel growth (n=27 adult minipigs randomly allocated to blind receive encapsulated antagomir?92a, encapsulated placebo, or saline [n=8, 9, 9]; P=0.001), reduced regional wall?motion dysfunction (P=0.03), and <span class="hlt">prevented</span> adverse remodeling in the infarct area 1 month after injury (P=0.03). Intracoronary injection of microspheres had no significant adverse effect in downstream myocardium in healthy pigs (n=2), and fluorescein isothiocyanate albumin?PLGA microspheres were not found in myocardium outside the left anterior descending coronary artery territory (n=4) or in other organs (n=2). Conclusions Early single intracoronary administration of encapsulated antagomir?92a in an adult pig model of reperfused AMI <span class="hlt">prevents</span> left ventricular remodeling with no local or distant adverse effects, emerging as a promising therapeutic approach to translate to patients who suffer a large AMI. PMID:25240056</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4637547','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4637547"><span id="translatedtitle">Cardiac sodium/calcium exchanger <span class="hlt">preconditioning</span> promotes anti-arrhythmic and cardioprotective effects through mitochondrial calcium-activated potassium channel</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Zhang, Jian-Ying; Cheng, Kang; Lai, Dong; Kong, Ling-Heng; Shen, Min; Yi, Fu; Liu, Bing; Wu, Feng; Zhou, Jing-Jun</p> <p>2015-01-01</p> <p>Background: Reverse-mode of the Na+/Ca2+ exchanger (NCX) stimulation provides cardioprotective effects for the ischemic/reperfused heart during ischemic <span class="hlt">preconditioning</span> (IP). This study was designed to test the hypothesis that pretreatment with an inhibitor of cardiac delayed-rectifying K+ channel (IKr), E4031, increases reverse-mode of NCX activity, and triggers <span class="hlt">preconditioning</span> against infarct size (IS) and arrhythmias caused by ischemia/reperfusion injury through mitoKCa channels. Materials and methods: In the isolated perfused rat heart, myocardial ischemia/reperfusion injury was created by occlusion of the left anterior descending coronary artery for 30 min followed by 120 min reperfusion. Two cycles of coronary occlusion for 5 min and reperfusion were performed, or pretreatment with E4031 or sevoflurane (Sevo) before the 30 min occlusion with the reversed-mode of NCX inhibitor (KB-R7943) or not. Results: E4031 or Sevo <span class="hlt">preconditioning</span> not only markedly decreased IS but also reduced arrhythmias, which was significantly blunted by KB-R7943. Furthermore, these effects of E4031 <span class="hlt">preconditioning</span> on IS and arrhythmias were abolished by inhibition of the mitoKCa channels. Similarly, pretreatment with NS1619, an opener of the mitoKCa channels, for 10 min before occlusion reduced both the infarct size and arrhythmias caused by ischemia/reperfusion. However, these effects weren’t affected by blockade of the NCX with KB-R7943. Conclusion: Taken together, these preliminary results conclude that pretreatment with E4031 reduces infarct size and produces anti-arrhythmic effect via stimulating the reverse-mode NCX, and that the mitoKCa channels mediate the protective effects. PMID:26617732</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4532361','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4532361"><span id="translatedtitle">Extracellular Adenosine Formation by Ecto-5’-Nucleotidase (CD73) Is No Essential Trigger for Early Phase Ischemic <span class="hlt">Preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p></p> <p>2015-01-01</p> <p>Background Adenosine is a powerful trigger for ischemic <span class="hlt">preconditioning</span> (IPC). Myocardial ischemia induces intracellular and extracellular ATP degradation to adenosine, which then activates adenosine receptors and elicits cardioprotection. Conventionally extracellular adenosine formation by ecto-5’-nucleotidase (CD73) during ischemia was thought to be negligible compared to the massive intracellular production, but controversial reports in the past demand further evaluation. In this study we evaluated the relevance of ecto-5’-nucleotidase (CD73) for infarct size reduction by ischemic <span class="hlt">preconditioning</span> in in vitro and in vivo mouse models of myocardial infarction, comparing CD73-/- and wild type (WT) mice. Methods and Results 3x5 minutes of IPC induced equal cardioprotection in isolated saline perfused hearts of wild type (WT) and CD73-/- mice, reducing control infarct sizes after 20 minutes of ischemia and 90 minutes of reperfusion from 46 ± 6.3% (WT) and 56.1 ± 7.6% (CD73-/-) to 26.8 ± 4.7% (WT) and 25.6 ± 4.7% (CD73-/-). Coronary venous adenosine levels measured after IPC stimuli by high-pressure liquid chromatography showed no differences between WT and CD73-/- hearts. Pharmacological <span class="hlt">preconditioning</span> of WT hearts with adenosine, given at the measured venous concentration, was evenly cardioprotective as conventional IPC. In vivo, 4x5 minutes of IPC reduced control infarct sizes of 45.3 ± 8.9% (WT) and 40.5 ± 8% (CD73-/-) to 26.3 ± 8% (WT) and 22.6 ± 6.6% (CD73-/-) respectively, eliciting again equal cardioprotection. The extent of IPC-induced cardioprotection in male and female mice was identical. Conclusion The infarct size limiting effects of IPC in the mouse heart in vitro and in vivo are not significantly affected by genetic inactivation of CD73. The ecto-5’-nucleotidase derived extracellular formation of adenosine does not contribute substantially to adenosine’s well known cardioprotective effect in early phase ischemic <span class="hlt">preconditioning</span>. PMID:26261991</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_15");'>15</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li class="active"><span>17</span></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_17 --> <div id="page_18" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li class="active"><span>18</span></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="341"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2014JCoPh.276..508S','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2014JCoPh.276..508S"><span id="translatedtitle">Nonlinear <span class="hlt">preconditioning</span> for efficient and accurate interface capturing in simulation of multicomponent compressible flows</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Shukla, Ratnesh K.</p> <p>2014-11-01</p> <p>Single fluid schemes that rely on an interface function for phase identification in multicomponent compressible flows are widely used to study hydrodynamic flow phenomena in several diverse applications. Simulations based on standard numerical implementation of these schemes suffer from an artificial increase in the width of the interface function owing to the numerical dissipation introduced by an upwind discretization of the governing equations. In addition, monotonicity requirements which ensure that the sharp interface function remains bounded at all times necessitate use of low-order accurate discretization strategies. This results in a significant reduction in accuracy along with a loss of intricate flow features. In this paper we develop a nonlinear transformation based interface capturing method which achieves superior accuracy without compromising the simplicity, computational efficiency and robustness of the original flow solver. A nonlinear map from the signed distance function to the sigmoid type interface function is used to effectively couple a standard single fluid shock and interface capturing scheme with a high-order accurate constrained level set reinitialization method in a way that allows for oscillation-free transport of the sharp material interface. Imposition of a maximum principle, which ensures that the multidimensional <span class="hlt">preconditioned</span> interface capturing method does not produce new maxima or minima even in the extreme events of interface merger or breakup, allows for an explicit determination of the interface thickness in terms of the grid spacing. A narrow band method is formulated in order to localize computations pertinent to the <span class="hlt">preconditioned</span> interface capturing method. Numerical tests in one dimension reveal a significant improvement in accuracy and convergence; in stark contrast to the conventional scheme, the proposed method retains its accuracy and convergence characteristics in a shifted reference frame. Results from the test cases in two dimensions show that the nonlinear transformation based interface capturing method outperforms both the conventional method and an interface capturing method without nonlinear transformation in resolving intricate flow features such as sheet jetting in the shock-induced cavity collapse. The ability of the proposed method in accounting for the gravitational and surface tension forces besides compressibility is demonstrated through a model fully three-dimensional problem concerning droplet splash and formation of a crownlike feature.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3074007','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3074007"><span id="translatedtitle">Mitogen Activated Protein Kinase Phosphatase-1 (MKP-1) in Retinal Ischemic <span class="hlt">Preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Dreixler, John C.; Bratton, Anthony; Du, Eugenie; Shaikh, Afzhal R.; Savoie, Brian; Michael, Alexander; Marcet, Marcus; Roth, Steven</p> <p>2011-01-01</p> <p>We previously described the phenomenon of retinal ischemic <span class="hlt">preconditioning</span> (IPC) and we have shown the role of various signaling proteins in the protective pathways, including the mitogen-activated protein kinase p38. In this study we examined the role in IPC of mitogen-activated protein kinase phosphatase-1 (MKP-1), which inactivates p38. Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure in adult Wistar rats. <span class="hlt">Preconditioning</span> was produced by transient retinal ischemia for 5 min, 24 h prior to ischemia. Small interfering RNA (siRNA) to MKP-1 or a control non-silencing siRNA, was injected into the vitreous 6 h prior to IPC. Recovery was assessed by electroretinography (ERG) and histology. The a- and b-waves, and oscillatory potentials (OPs), measured before and 1 week after ischemia, were then normalized relative to pre-ischemic baseline, and corrected for diurnal variation in the normal non-ischemic eye. The P2, or post-photoreceptor component of the ERG (which reflects function of the rod bipolar cells in the inner retina), was derived using the Hood-Birch model. MKP-1 was localized in specific retinal cells using immunohistochemistry; levels of mitogen-activated protein kinases were measured using Western blotting. Injection of siRNA to MKP-1 significantly attenuated the protective effect of IPC as reflected by decreased recovery of the electroretinogram a- and b-waves and the P2 after ischemia. The injection of siRNA to MKP-1 reduced the number of cells in the retinal ganglion cell and outer nuclear layers after IPC and ischemia. Blockade of MKP-1 by siRNA also increased the activation of p38 at 24 h following IPC. MKP-1 siRNA did not alter the levels of phosphorylated jun N-terminal kinase (JNK) or extracellular signal-regulated kinase (ERK) after IPC. The results suggest the involvement of dual-specificity phosphatase MKP-1 in IPC and that MKP-1 is involved in IPC by regulating levels of activated MAPK p38. PMID:21094639</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015JaJAP..54hKG08S','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015JaJAP..54hKG08S"><span id="translatedtitle">Acceleration of potential-induced degradation by salt-mist <span class="hlt">preconditioning</span> in crystalline silicon photovoltaic modules</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Suzuki, Soh; Nishiyama, Naoki; Yoshino, Seiji; Ujiro, Takumi; Watanabe, Shin; Doi, Takuya; Masuda, Atsushi; Tanahashi, Tadanori</p> <p>2015-08-01</p> <p>We examined the sequential effects of salt-mist stress followed by high-system-voltage stress on the power loss of crystalline silicon photovoltaic (PV) modules to determine whether a crucial failure as potential-induced degradation (PID) is accelerated by material-property changes caused by the long-term effects of a less harmful stress such as salt-mist spraying. Degradation profiles confirmed in this study show that PID is accelerated by certain types of salt-mist <span class="hlt">preconditioning</span>. For the acceleration of PID, the contribution of sodium ions liberated from the front glass of the PV module seems to be excluded. Therefore, we consider that the sodium ions penetrating into the PV modules from the ambient environment may also cause degradation according to the proposed mechanisms of PID, as the sodium ions existing in the front glass cause PID. Furthermore, this type of degradation may indicate the wear-out phenomenon after a long-term exposure in the field (especially near the coast).</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26168294','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26168294"><span id="translatedtitle"><span class="hlt">Preconditioning</span> allows engraftment of mouse and human embryonic lung cells, enabling lung repair in mice.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Rosen, Chava; Shezen, Elias; Aronovich, Anna; Klionsky, Yael Zlotnikov; Yaakov, Yasmin; Assayag, Miri; Biton, Inbal Eti; Tal, Orna; Shakhar, Guy; Ben-Hur, Herzel; Shneider, David; Vaknin, Zvi; Sadan, Oscar; Evron, Shmuel; Freud, Enrique; Shoseyov, David; Wilschanski, Michael; Berkman, Neville; Fibbe, Willem E; Hagin, David; Hillel-Karniel, Carmit; Krentsis, Irit Milman; Bachar-Lustig, Esther; Reisner, Yair</p> <p>2015-08-01</p> <p>Repair of injured lungs represents a longstanding therapeutic challenge. We show that human and mouse embryonic lung tissue from the canalicular stage of development (20-22 weeks of gestation for humans, and embryonic day 15-16 (E15-E16) for mouse) are enriched with progenitors residing in distinct niches. On the basis of the marked analogy to progenitor niches in bone marrow (BM), we attempted strategies similar to BM transplantation, employing sublethal radiation to vacate lung progenitor niches and to reduce stem cell competition. Intravenous infusion of a single cell suspension of canalicular lung tissue from GFP-marked mice or human fetal donors into naphthalene-injured and irradiated syngeneic or SCID mice, respectively, induced marked long-term lung chimerism. Donor type structures or 'patches' contained epithelial, mesenchymal and endothelial cells. Transplantation of differentially labeled E16 mouse lung cells indicated that these patches were probably of clonal origin from the donor. Recipients of the single cell suspension transplant exhibited marked improvement in lung compliance and tissue damping reflecting the energy dissipation in the lung tissues. Our study provides proof of concept for lung reconstitution by canalicular-stage human lung cells after <span class="hlt">preconditioning</span> of the pulmonary niche. PMID:26168294</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015InvPr..31l5005C','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015InvPr..31l5005C"><span id="translatedtitle">A hierarchical Krylov–Bayes iterative inverse solver for MEG with physiological <span class="hlt">preconditioning</span></span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Calvetti, D.; Pascarella, A.; Pitolli, F.; Somersalo, E.; Vantaggi, B.</p> <p>2015-12-01</p> <p>The inverse problem of MEG aims at estimating electromagnetic cerebral activity from measurements of the magnetic fields outside the head. After formulating the problem within the Bayesian framework, a hierarchical conditionally Gaussian prior model is introduced, including a physiologically inspired prior model that takes into account the preferred directions of the source currents. The hyperparameter vector consists of prior variances of the dipole moments, assumed to follow a non-conjugate gamma distribution with variable scaling and shape parameters. A point estimate of both dipole moments and their variances can be computed using an iterative alternating sequential updating algorithm, which is shown to be globally convergent. The numerical solution is based on computing an approximation of the dipole moments using a Krylov subspace iterative linear solver equipped with statistically inspired <span class="hlt">preconditioning</span> and a suitable termination rule. The shape parameters of the model are shown to control the focality, and furthermore, using an empirical Bayes argument, it is shown that the scaling parameters can be naturally adjusted to provide a statistically well justified depth sensitivity scaling. The validity of this interpretation is verified through computed numerical examples. Also, a computed example showing the applicability of the algorithm to analyze realistic time series data is presented.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2002CompM..30...12C','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2002CompM..30...12C"><span id="translatedtitle">Enhancing the performance of the FETI method with <span class="hlt">preconditioning</span> techniques implemented on clusters of networked computers</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Charmpis, D. C.; Papadrakakis, M.</p> <p></p> <p>The FETI domain decomposition method for solving large-scale problems in computational structural mechanics involves the solution of an interface problem, which is handled by a <span class="hlt">Preconditioned</span> Conjugate Projected Gradient (PCPG) algorithm. Two preconditioners are widely used to accelerate the convergence of the iterative PCPG algorithm: the optimal Dirichlet preconditioner and the economical lumped preconditioner. The Dirichlet preconditioner is computationally more efficient than the lumped preconditioner for ill-conditioned problems, but needs additional storage for the stiffness matrices of the subdomains' internal degrees of freedom (d.o.f.). In this study a new set of PCPG preconditioners is presented by providing approximate expressions to the inverse iteration matrix of the PCPG algorithm. The resulting approximate Dirichlet preconditioners are obtained by using instead of the whole stiffness matrix of the internal d.o.f. in each subdomain the following alternatives: a diagonal scaling matrix, a SSOR type matrix or an incomplete Cholesky factorization matrix. The computational behavior and performance of the proposed PCPG preconditioners is evaluated using an implementation of the FETI method on a cluster of ethernet-networked PCs running the message passing software PVM. It is demonstrated that the FETI method equipped with the approximate Dirichlet preconditioners leads for a number of large-scale problems to faster and less storage demanding overall solutions than with either Dirichlet or lumped preconditioner.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2008PhRvB..78d5126A','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2008PhRvB..78d5126A"><span id="translatedtitle"><span class="hlt">Preconditioning</span> of self-consistent-field cycles in density-functional theory: The extrapolar method</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Anglade, P.-M.; Gonze, X.</p> <p>2008-07-01</p> <p>The number of self-consistent-field iterations needed for the density-functional theory treatment of metallic systems grows with the size of the unit cell, not only for basic algorithms like simple mixing, but also for more advanced schemes, in which results from several past steps are mixed. <span class="hlt">Preconditioning</span> techniques have the potential to suppress this growth, although the available methods have strong limitations: either they deliver little improvement in case of mixed systems with metallic and nonmetallic regions, or the computation of the preconditioner scales badly with the size of the system, with a large prefactor. We propose an approximate preconditioner, with tremendously reduced prefactor, that makes the number of self-consistent cycle nearly independent of the size of the system, and bears little overhead up to the one hundred atom range. The susceptibility matrix, a key ingredient in our scheme, is approximated thanks to the closure relation. Instead of using the exact formulation of the dielectric matrix, we rely on the random-phase approximation, that allows to further decrease the prefactor thanks to a very low wave vector cutoff, even for systems with both vacuum and a metallic region. We test this algorithm for systems of increasing size and demonstrate its practical usefulness.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/19665135','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/19665135"><span id="translatedtitle">Mechanical response of periodontal ligament: effects of specimen geometry, <span class="hlt">preconditioning</span> cycles and time lapse.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bergomi, Marzio; Anselm Wiskott, H W; Botsis, John; Shibata, Tatsuya; Belser, Urs C</p> <p>2009-10-16</p> <p>This study was conducted as part of research line addressing the mechanical response of periodontal ligament (PDL) to tensile-compressive sinusoidal loading. The aim of the present project was to determine the effect of three potential sources of variability: (1) specimen geometry, (2) tissue <span class="hlt">preconditioning</span> and (3) tissue structural degradation over time. For the three conditions, selected mechanical parameters were evaluated and compared. (1) Standard flat specimens (obtained by sequentially slicing portions of bone, PDL and dentin using a precision band saw) and new cylindrical specimens (extracted with a diamond-coated trephine drill) were obtained from bovine mandibular first molars and subjected to a sinusoidal load profile. (2) Specimens were loaded with up to 2000 cycles. (3) Specimens were immersed in saline and tested after 0, 30 and 60 min. From the data generated, the following was concluded: (1) specimen geometry and preparation technique do not influence the mechanical response of the PDL; (2) the mechanical response stabilizes after approximately 1000 cycles; and (3) no major structural degradation occurs when PDL is immersed in saline for a time lapse up to 60 min. PMID:19665135</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/servlets/purl/145291','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/servlets/purl/145291"><span id="translatedtitle">T2CG1, a package of <span class="hlt">preconditioned</span> conjugate gradient solvers for TOUGH2</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Moridis, G.; Pruess, K.; Antunez, E.</p> <p>1994-03-01</p> <p>Most of the computational work in the numerical simulation of fluid and heat flows in permeable media arises in the solution of large systems of linear equations. The simplest technique for solving such equations is by direct methods. However, because of large storage requirements and accumulation of roundoff errors, the application of direct solution techniques is limited, depending on matrix bandwidth, to systems of a few hundred to at most a few thousand simultaneous equations. T2CG1, a package of <span class="hlt">preconditioned</span> conjugate gradient solvers, has been added to TOUGH2 to complement its direct solver and significantly increase the size of problems tractable on PCs. T2CG1 includes three different solvers: a Bi-Conjugate Gradient (BCG) solver, a Bi-Conjugate Gradient Squared (BCGS) solver, and a Generalized Minimum Residual (GMRES) solver. Results from six test problems with up to 30,000 equations show that T2CG1 (1) is significantly (and invariably) faster and requires far less memory than the MA28 direct solver, (2) it makes possible the solution of very large three-dimensional problems on PCs, and (3) that the BCGS solver is the fastest of the three in the tested problems. Sample problems are presented related to heat and fluid flow at Yucca Mountain and WIPP, environmental remediation by the Thermal Enhanced Vapor Extraction System, and geothermal resources.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/18267484','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/18267484"><span id="translatedtitle">Conjugate-gradient <span class="hlt">preconditioning</span> methods for shift-variant PET image reconstruction.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Fessler, J A; Booth, S D</p> <p>1999-01-01</p> <p>Gradient-based iterative methods often converge slowly for tomographic image reconstruction and image restoration problems, but can be accelerated by suitable preconditioners. Diagonal preconditioners offer some improvement in convergence rate, but do not incorporate the structure of the Hessian matrices in imaging problems. Circulant preconditioners can provide remarkable acceleration for inverse problems that are approximately shift-invariant, i.e., for those with approximately block-Toeplitz or block-circulant Hessians. However, in applications with nonuniform noise variance, such as arises from Poisson statistics in emission tomography and in quantum-limited optical imaging, the Hessian of the weighted least-squares objective function is quite shift-variant, and circulant preconditioners perform poorly. Additional shift-variance is caused by edge-preserving regularization methods based on nonquadratic penalty functions. This paper describes new preconditioners that approximate more accurately the Hessian matrices of shift-variant imaging problems. Compared to diagonal or circulant <span class="hlt">preconditioning</span>, the new preconditioners lead to significantly faster convergence rates for the unconstrained conjugate-gradient (CG) iteration. We also propose a new efficient method for the line-search step required by CG methods. Applications to positron emission tomography (PET) illustrate the method. PMID:18267484</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4458764','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4458764"><span id="translatedtitle">Low G <span class="hlt">preconditioning</span> reduces liver injury induced by high +Gz exposure in rats</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Shi, Bin; Feng, Zhi-Qiang; Li, Wen-Bing; Zhang, Hong-Yi</p> <p>2015-01-01</p> <p>AIM: To investigate the effect of repeated lower +Gz exposure on liver injury induced by high +Gz exposure in rats. METHODS: Sixty male Wister rats were randomly divided into a blank control group, a low G <span class="hlt">preconditioning</span> group (LG) (exposed to +4 Gz/5 min per day for 3 d before +10 Gz/5 min exposure), and a +10 Gz/5 min group (10G) (n = 20 in each group). Blood specimens and liver tissue were harvested at 0 h and 6 h after +10 Gz/5 min exposure. Liver function was analyzed by measuring serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, and liver injury was further assessed by histopathological observation. Malondialdehyde (MDA), superoxide dismutase (SOD) and Na+-K+-ATPase were determined in hepatic tissue. RESULTS: The group LG had lower ALT, AST, and MDA values at 0 h after exposure than those in group 10G. SOD values and Na+-K+-ATPase activity in the LG group were higher than in group 10G 0 h post-exposure. Hepatocyte injury was significantly less in group LG than in group 10G on histopathological evaluation. CONCLUSION: It is suggested that repeated low +Gz exposure shows a protective effect on liver injury induced by high +Gz exposure in rats. PMID:26074692</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://kuscholarworks.ku.edu/handle/1808/16882','EPRINT'); return false;" href="http://kuscholarworks.ku.edu/handle/1808/16882"><span id="translatedtitle">Finite difference <span class="hlt">preconditioning</span> for solving orthogonal collocation equations of boundary value problems</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Sun, Weiwei; Huang, Weizhang; Russell, Robert D.</p> <p>1996-12-01</p> <p>5 3.144 32 0.326E6 3.156 8 0.753E7 3.743 i6 0.164E10 3.816 32 0.367E12 3.854 0.239E3 0.883E3 0.335E4 01743E4 0.903E1 0.i 16E6 0.182E2 0.186E7 0.364E2 013 l’0E8 0.205E4’ 0.772E10 0.188E5 0.171E13 0.162E6 K1 (T1) h (or= 1) 2.196 1.0 1.0 2.196 1.0 1....5) gives (3.6) AcoIBlto f. D ow nl oa de d 09 /1 5/ 14 to 1 29 .2 37 .4 6. 10 0. R ed ist rib ut io n su bje ct to SIA M lic en se or co py rig ht; se e h ttp ://w ww .si am .or g/j ou rna ls/ ojs a.p hp <span class="hlt">PRECONDITIONING</span> FOR COLLOCATION SYSTEMS...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://ntrs.nasa.gov/search.jsp?R=20020051027&hterms=newton+law&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D50%26Ntt%3Dnewton%2527s%2Blaw','NASA-TRS'); return false;" href="http://ntrs.nasa.gov/search.jsp?R=20020051027&hterms=newton+law&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D50%26Ntt%3Dnewton%2527s%2Blaw"><span id="translatedtitle">Discretization and <span class="hlt">Preconditioning</span> Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Barth, Timothy J.; Kutler, Paul (Technical Monitor)</p> <p>1998-01-01</p> <p>Several stabilized demoralization procedures for conservation law equations on triangulated domains will be considered. Specifically, numerical schemes based on upwind finite volume, fluctuation splitting, Galerkin least-squares, and space discontinuous Galerkin demoralization will be considered in detail. A standard energy analysis for several of these methods will be given via entropy symmetrization. Next, we will present some relatively new theoretical results concerning congruence relationships for left or right symmetrized equations. These results suggest new variants of existing FV, DG, GLS, and FS methods which are computationally more efficient while retaining the pleasant theoretical properties achieved by entropy symmetrization. In addition, the task of Jacobean linearization of these schemes for use in Newton's method is greatly simplified owing to exploitation of exact symmetries which exist in the system. The FV, FS and DG schemes also permit discrete maximum principle analysis and enforcement which greatly adds to the robustness of the methods. Discrete maximum principle theory will be presented for general finite volume approximations on unstructured meshes. Next, we consider embedding these nonlinear space discretizations into exact and inexact Newton solvers which are <span class="hlt">preconditioned</span> using a nonoverlapping (Schur complement) domain decomposition technique. Elements of nonoverlapping domain decomposition for elliptic problems will be reviewed followed by the present extension to hyperbolic and elliptic-hyperbolic problems. Other issues of practical relevance such the meshing of geometries, code implementation, turbulence modeling, global convergence, etc, will. be addressed as needed.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://ntrs.nasa.gov/search.jsp?R=20020048259&hterms=newton+law&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D60%26Ntt%3Dnewton%2527s%2Blaw','NASA-TRS'); return false;" href="http://ntrs.nasa.gov/search.jsp?R=20020048259&hterms=newton+law&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D60%26Ntt%3Dnewton%2527s%2Blaw"><span id="translatedtitle">Discretization and <span class="hlt">Preconditioning</span> Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Barth, Timothy; Chancellor, Marisa K. (Technical Monitor)</p> <p>1997-01-01</p> <p>Several stabilized discretization procedures for conservation law equations on triangulated domains will be considered. Specifically, numerical schemes based on upwind finite volume, fluctuation splitting, Galerkin least-squares, and space discontinuous Galerkin discretization will be considered in detail. A standard energy analysis for several of these methods will be given via entropy symmetrization. Next, we will present some relatively new theoretical results concerning congruence relationships for left or right symmetrized equations. These results suggest new variants of existing FV, DG, GLS and FS methods which are computationally more efficient while retaining the pleasant theoretical properties achieved by entropy symmetrization. In addition, the task of Jacobian linearization of these schemes for use in Newton's method is greatly simplified owing to exploitation of exact symmetries which exist in the system. These variants have been implemented in the "ELF" library for which example calculations will be shown. The FV, FS and DG schemes also permit discrete maximum principle analysis and enforcement which greatly adds to the robustness of the methods. Some prevalent limiting strategies will be reviewed. Next, we consider embedding these nonlinear space discretizations into exact and inexact Newton solvers which are <span class="hlt">preconditioned</span> using a nonoverlapping (Schur complement) domain decomposition technique. Elements of nonoverlapping domain decomposition for elliptic problems will be reviewed followed by the present extension to hyperbolic and elliptic-hyperbolic problems. Other issues of practical relevance such the meshing of geometries, code implementation, turbulence modeling, global convergence, etc. will be addressed as needed.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22415473','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22415473"><span id="translatedtitle">Electrophilic surface sites as <span class="hlt">precondition</span> for the chemisorption of pyrrole on GaAs(001) surfaces</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Bruhn, Thomas; Fimland, Bjørn-Ove; Vogt, Patrick</p> <p>2015-03-14</p> <p>We report how the presence of electrophilic surface sites influences the adsorption mechanism of pyrrole on GaAs(001) surfaces. For this purpose, we have investigated the adsorption behavior of pyrrole on different GaAs(001) reconstructions with different stoichiometries and thus different surface chemistries. The interfaces were characterized by x-ray photoelectron spectroscopy, scanning tunneling microscopy, and by reflectance anisotropy spectroscopy in a spectral range between 1.5 and 5?eV. On the As-rich c(4 × 4) reconstruction that exhibits only nucleophilic surface sites, pyrrole was found to physisorb on the surface without any significant modification of the structural and electronic properties of the surface. On the Ga-rich GaAs(001)-(4 × 2)/(6 × 6) reconstructions which exhibit nucleophilic as well as electrophilic surface sites, pyrrole was found to form stable covalent bonds mainly to the electrophilic (charge deficient) Ga atoms of the surface. These results clearly demonstrate that the existence of electrophilic surface sites is a crucial <span class="hlt">precondition</span> for the chemisorption of pyrrole on GaAs(001) surfaces.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25562658','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25562658"><span id="translatedtitle">Indomethacin <span class="hlt">preconditioning</span> induces ischemic tolerance by modifying zinc availability in the brain.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Lee, Joo-Yong; Oh, Shin Bi; Hwang, Jung-Jin; Suh, Nayoung; Jo, Dong-Gyu; Kim, Jong S; Koh, Jae-Young</p> <p>2015-09-01</p> <p>Intracellular zinc overload causes neuronal injury during the course of neurological disorders, whereas mild levels of zinc are beneficial to neurons. Previous reports indicated that non-steroidal anti-inflammatory drugs, including indomethacin and aspirin, can reduce the risk of ischemic stroke. This study found that chronic pretreatment of rats with indomethacin, a non-selective cyclooxygenase inhibitor, provided tolerance to ischemic injuries in an animal model of stroke by eliciting moderate zinc elevation in neurons. Consecutive intraperitoneal injection of indomethacin (3mg/kg/day for 28days) led to modest increases in intraneuronal zinc as well as synaptic zinc content, with no significant stimulation of neuronal death. Furthermore, indomethacin induced the expressions of intracellular zinc homeostatic and neuroprotective proteins, rendering the brain resistant against ischemic damages and improving neurological outcomes. However, administration of a zinc-chelator, N,N,N',N'-tetra(2-picolyl)ethylenediamine (TPEN; 15mg/kg/day), immediately after indomethacin administration eliminated the beneficial actions of the drug. Therefore, indomethacin <span class="hlt">preconditioning</span> can modulate intracellular zinc availability, contributing to ischemic tolerance in the brain after stroke. PMID:25562658</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/1051208','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/1051208"><span id="translatedtitle">A <span class="hlt">preconditioning</span> technique for Schur complement systems arising in stochastic optimization</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Petra, C. G.; Anitescu, M.</p> <p>2012-01-01</p> <p>Deterministic sample average approximations of stochastic programming problems with recourse are suitable for a scenario-based parallelization. In this paper the parallelization is obtained by using an interior-point method and a Schur complement mechanism for the interior-point linear systems. However, the direct linear solves involving the dense Schur complement matrix are expensive, and adversely affect the scalability of this approach. We address this issue by proposing a stochastic preconditioner for the Schur complement matrix and by using Krylov iterative methods for the solution of the dense linear systems. The stochastic preconditioner is built based on a subset of existing scenarios and can be assembled and factorized on a separate process before the computation of the Schur complement matrix finishes on the remaining processes. The expensive factorization of the Schur complement is removed from the parallel execution flow and the scaling of the optimization solver is considerably improved with this approach. The spectral analysis indicates an exponentially fast convergence in probability to 1 of the eigenvalues of the <span class="hlt">preconditioned</span> matrix with the number of scenarios incorporated in the preconditioner. Numerical experiments performed on the relaxation of a unit commitment problem show good performance, in terms of both the accuracy of the solution and the execution time.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/types/cervical/patient/cervical-prevention-pdq#section/all','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.gov/types/cervical/patient/cervical-prevention-pdq#section/all"><span id="translatedtitle">Cervical Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Treatment Cervical Cancer <span class="hlt">Prevention</span> Cervical Cancer Screening Research Cervical Cancer <span class="hlt">Prevention</span> (PDQ®) What is <span class="hlt">prevention</span>? Cancer <span class="hlt">prevention</span> is ... to keep cancer from starting. General Information About Cervical Cancer Cervical cancer is a disease in which malignant ( ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4668996','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4668996"><span id="translatedtitle">Penehyclidine Hydrochloride <span class="hlt">Preconditioning</span> Provides Cardioprotection in a Rat Model of Myocardial Ischemia/Reperfusion Injury</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Lin, Duomao; Ma, Jun; Xue, Yanyan; Wang, Zhaoqi</p> <p>2015-01-01</p> <p>To investigate the impacts and related mechanisms of penehyclidine hydrochloride (PHC) on ischemia/reperfusion (I/R)-induced myocardial injury. A rat model of myocardial I/R injury was established by the ligation of left anterior descending coronary artery for 30 min followed by 3 h perfusion. Before I/R, the rats were pretreated with or without PHC. Cardiac function was measured by echocardiography. The activities/levels of myocardial enzymes, oxidants and antioxidant enzymes were detected. Evans blue/TTC double staining was performed to assess infarct size. Cardiomyocyte apoptosis was evaluated by TUNEL assay. The release of inflammatory cytokines and inflammatory mediators was detected by ELISA. Western blot was performed to analyze the expression of COX-2, I?B, p-I?B and NF-?B. Meanwhile, the rats were given a single injection of H-PHC before I/R. The effects of PHC on myocardial infarct and cardiac function were investigated after 7 days post-reperfusion. We found that PHC remarkably improved cardiac function, alleviated myocardial injury by decreasing myocardial enzyme levels and attenuated oxidative stress in a dose-dependent manner. Additionally, PHC <span class="hlt">preconditioning</span> significantly reduced infarct size and the apoptotic rate of cardiomyocytes. Administration of PHC significantly decreased serum TNF-?, IL-1?, IL-6 and PGE2 levels and myocardium COX-2 level. Meanwhile, the expression levels of p-I?B and NF-?B were downregulated, while I?B expression was upregulated. H-PHC also exerted long-term cardioprotection in a rat model of I/R injury by decreasing infarct size and improving cardiac function. These results suggest that PHC can efficiently protect the rats against I/R-induced myocardial injury. PMID:26632817</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4393211','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4393211"><span id="translatedtitle">Impact of ischemic <span class="hlt">preconditioning</span> on functional sympatholysis during handgrip exercise in humans</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Horiuchi, Masahiro; Endo, Junko; Thijssen, Dick H J</p> <p>2015-01-01</p> <p>Repeated bouts of ischemia followed by reperfusion, known as ischemic <span class="hlt">preconditioning</span> (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance, we examined the hypothesis that IPC improves functional sympatholysis in healthy, young humans. In a randomized study, 15 healthy young men performed a 10-min resting period, dynamic handgrip exercise at 10% maximal voluntary contraction (MVC), and 25% MVC. This protocol was preceded by IPC (IPC; 4 × 5-min 220-mmHg unilateral occlusion) or a sham intervention (CON; 4 × 5-min 20-mmHg unilateral occlusion). Near-infrared spectroscopy was used to assess changes in oxygenated hemoglobin and myoglobin in skeletal muscle (HbO2 + MbO2) in response to sympathetic activation (via cold pressor test (CPT)) at baseline and during handgrip exercise (at 10% and 25%). In resting conditions, HbO2 + MbO2 significantly decreased during CPT (?11.0 ± 1.0%), which was significantly larger during the IPC-trial (?13.8 ± 1.2%, P = 0.006). During handgrip exercise at 10% MVC, changes in HbO2 + MbO2 in response to the CPT were blunted after IPC (?8.8 ± 1.5%) and CON (?8.3 ± 0.4%, P = 0.593). During handgrip exercise at 25% MVC, HbO2 + MbO2 in response to the CPT increased (2.0 ± 0.4%), whereas this response was significantly larger when preceded by IPC (4.2 ± 0.6%, P = 0.027). Collectively, these results indicate that IPC-induced different vascular changes at rest and during moderate exercise in response to sympathetic activation. This suggests that, in healthy volunteers, exposure to IPC may alter tissue oxygenation during sympathetic stimulation at rest and during exercise. PMID:25713329</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_16");'>16</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li class="active"><span>18</span></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_18 --> <div id="page_19" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li class="active"><span>19</span></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="361"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26536910','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26536910"><span id="translatedtitle">Beneficial Effects of Hypoxic <span class="hlt">Preconditioning</span> on Human Umbilical Cord Mesenchymal Stem Cells.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhang, Li; Yang, Jing; Tian, Yan-Ming; Guo, Hui; Zhang, Yi</p> <p>2015-10-31</p> <p>As human umbilical cord mesenchymal stem cells (hUC-MSCs) transplanation may be promising in heart failure treatment, it is important to know whether hypoxic <span class="hlt">preconditioning</span> (HP) promote hUC-MSCs proliferation and differentiation and protect them against chemical hypoxic damages. This study aimed to investigate the effects of HP on proliferation and differentiation of human umbilical cord mesenchymal stem cells (hUC-MSCs). The study also aimed to confirm our hypothesis that HP could promote hUC-MSCs proliferation and differentiation to cardiomyocyte-like cells as well as effectively protecting hUC-MSCs and cardiomyocyte-like cells against chemical hypoxic damages. Isolated hUC-MSCs were cultured in hypoxia at 1%, 3% and 5% O? for 72 hours. 5-azacytidine (5-AZA) induced differentiation of hUC-MSCs to cardiomyocyte-like cells was determined by streptavidin-perosidase (SP) immunohistochemical staining and the content of troponin (TnI). Flow cytometry was used to measure cell cycle in hUC-MSCs and cardiomyocyte-like cells. The mitochondrial membrane potential (??m) and mitochondrial Ca²? concentration ([Ca²?]m), were measured in hUC-MSCs and cardiomyocyte-like cells during chemical hypoxia induced by cobalt chloride (100 ?mol/L). HP optimally promoted the proliferation of hUC-MSCs at 3% O? and enhanced the differentiation of hUC-MSCs to cardiomyocyte-like cells by 5-AZA in a concentration-dependent manner. The cell cycle distribution of cardiomyocyte-like cells, but not hUC-MSCs, was clearly changed by HP. Chemical hypoxic damage, decreased ??m and increased [Ca²?]m, were alleviated significantly in HP-treated cells compared with the normaxia-treated cells. The results demonstrate that HP promoted hUC-MSCs proliferation and differentiation to cardiomyocyte-like cells, and protected both cell types against chemical hypoxic damage. PMID:26536910</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26301824','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26301824"><span id="translatedtitle">Hyperbaric oxygen <span class="hlt">preconditioning</span> attenuates neuroinflammation after intracerebral hemorrhage in rats by regulating microglia characteristics.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yang, Liming; Tang, Jun; Chen, Qianwei; Jiang, Bing; Zhang, Bo; Tao, Yihao; Li, Lin; Chen, Zhi; Zhu, Gang</p> <p>2015-11-19</p> <p>Intracerebral Hemorrhage (ICH) results in a detrimental neurologic disorder with complicated secondary brain injury. Hyperbaric oxygen <span class="hlt">preconditioning</span> (HBOP) may be a safe and effective therapeutic method for ICH victims. Our previous studies have demonstrated that HBOP induces neuroprotection in cerebral ischemia and traumatic brain injury. This study aimed to investigate whether HBOP could alleviate neuroinflammation by regulating changes in microglia characteristics in a rat model of ICH. ICH was induced by autologous arterial blood injection, and animals were sacrificed at 12, 24, and 72h post injury. We measured motor function and brain water content to evaluate the extent of inflammation. Fluoro-Jade C and TNF-? staining was used to characterize neuronal degeneration and neuroinflammatory cytokines, and immunofluorescence staining was performed for CD11b to show activated microglia and Iba-1 to show microglia. Our results indicate that motor dysfunction and brain water content are alleviated by HBOP, and Fluoro-Jade C staining demonstrates that neuron degeneration decreased in the HBOP group. The growth of Iba-1-positive microglia decreased in the HBOP group. Moreover, TNF-? was dynamically reduced in the HBOP group compared with the ICH group. CD11b-Iba-1 double staining demonstrated that the ratio of CD11b and Iba-1 was significantly decreased in the HBOP group. Overall, the data demonstrated that HBOP could significantly alleviate the ICH-induced neuroinflammation by regulating microglia characteristics changing. The phenomenon may propel the progress of the relation between microglia and HBOP and represent a novel target for ICH treatment. PMID:26301824</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/19910017785','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/19910017785"><span id="translatedtitle">A nonrecursive order N <span class="hlt">preconditioned</span> conjugate gradient: Range space formulation of MDOF dynamics</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Kurdila, Andrew J.</p> <p>1990-01-01</p> <p>While excellent progress has been made in deriving algorithms that are efficient for certain combinations of system topologies and concurrent multiprocessing hardware, several issues must be resolved to incorporate transient simulation in the control design process for large space structures. Specifically, strategies must be developed that are applicable to systems with numerous degrees of freedom. In addition, the algorithms must have a growth potential in that they must also be amenable to implementation on forthcoming parallel system architectures. For mechanical system simulation, this fact implies that algorithms are required that induce parallelism on a fine scale, suitable for the emerging class of highly parallel processors; and transient simulation methods must be automatically load balancing for a wider collection of system topologies and hardware configurations. These problems are addressed by employing a combination range space/<span class="hlt">preconditioned</span> conjugate gradient formulation of multi-degree-of-freedom dynamics. The method described has several advantages. In a sequential computing environment, the method has the features that: by employing regular ordering of the system connectivity graph, an extremely efficient preconditioner can be derived from the 'range space metric', as opposed to the system coefficient matrix; because of the effectiveness of the preconditioner, preliminary studies indicate that the method can achieve performance rates that depend linearly upon the number of substructures, hence the title 'Order N'; and the method is non-assembling. Furthermore, the approach is promising as a potential parallel processing algorithm in that the method exhibits a fine parallel granularity suitable for a wide collection of combinations of physical system topologies/computer architectures; and the method is easily load balanced among processors, and does not rely upon system topology to induce parallelism.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3796499','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3796499"><span id="translatedtitle">Apolipoprotein A-I Is a Potential Mediator of Remote Ischemic <span class="hlt">Preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hibert, Pierre; Prunier-Mirebeau, Delphine; Beseme, Olivia; Chwastyniak, Maggy; Tamareille, Sophie; Lamon, Delphine; Furber, Alain; Pinet, Florence; Prunier, Fabrice</p> <p>2013-01-01</p> <p>Background Remote ischemic <span class="hlt">preconditioning</span> (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach. Methods and Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5?) or 10-min (RIPC 10?) reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10?. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI). Conclusions RIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism. PMID:24155931</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26052960','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26052960"><span id="translatedtitle">EFFECTS OF HELIUM <span class="hlt">PRECONDITIONING</span> ON INTESTINAL ISCHEMIA AND REPERFUSION INJURY IN RATS.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Du, Lei; Zhang, Rongjia; Luo, Tianhang; Nie, Mingming; Bi, Jianwei</p> <p>2015-10-01</p> <p>Intestinal ischemia-reperfusion (I/R) injury can occur in clinical settings such as organ transplantation, cardiopulmonary bypass and trauma. The noble gas helium attenuates I/R injury in a number of animal organs and thus may offer a strategy for reducing I/R-induced intestinal injury in clinical settings. In the present study, we used four different helium <span class="hlt">preconditioning</span> (HPC) profiles to investigate the potential beneficial effect of HPC on I/R-induced intestinal injury. Male Sprague-Dawley rats were pretreated with three cycles of air breathing for 5?min combined with three cycles of breathing a 70% helium:30% oxygen mixture for either 2, 5, 10, or 15?min, after which they were subjected to 60-min intestinal ischemia and 60-min reperfusion. Sixty minutes after reperfusion, the intestinal tissues of the variously treated rats were analyzed using histology, immunohistochemistry, terminal dUTP nick-end labeling staining, myeloperoxidase activity assay, Western blotting, and enzyme-linked immunosorbent assay for tumor necrosis factor ? and macrophage inflammatory protein 1?. Intestinal permeability was assayed by measuring fluorescein isothiocyanate-dextran release in blood samples. The results showed that the HPC profile consisting of three cycles of 10 or 15?min of helium breathing and three cycles of 5?min of air breathing reduced I/R-induced intestinal injury, cell apoptosis, and the inflammatory response. However, the 2- or 5-min helium breathing did not confer any protective effects. It seems that longer helium episodes should be used in HPC profiles designed to attenuate intestinal I/R injury. PMID:26052960</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26359484','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26359484"><span id="translatedtitle">Effects of ischemic <span class="hlt">preconditioning</span> on maximal constant-load cycling performance.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cruz, Rogério Santos de Oliveira; de Aguiar, Rafael Alves; Turnes, Tiago; Pereira, Kayo Leonardo; Caputo, Fabrizio</p> <p>2015-11-01</p> <p>This study investigated the effects of ischemic <span class="hlt">preconditioning</span> (IPC) on the ratings of perceived exertion (RPE), surface electromyography, and pulmonary oxygen uptake (V?o2) onset kinetics during cycling until exhaustion at the peak power output attained during an incremental test. A group of 12 recreationally trained cyclists volunteered for this study. After determination of peak power output during an incremental test, they were randomly subjected on different days to a performance protocol preceded by intermittent bilateral cuff pressure inflation to 220 mmHg (IPC) or 20 mmHg (control). To increase data reliability, the performance visits were replicated, also in a random manner. There was an 8.0% improvement in performance after IPC (control: 303 s, IPC 327 s, factor SDs of ×/÷1.13, P = 0.01). This change was followed by a 2.9% increase in peak V?o2 (control: 3.95 l/min, IPC: 4.06 l/min, factor SDs of ×/÷1.15, P = 0.04), owing to a higher amplitude of the slow component of the V?o2 kinetics (control: 0.45 l/min, IPC: 0.63 l/min, factor SDs of ×/÷2.21, P = 0.05). There was also an attenuation in the rate of increase in RPE (P = 0.01) and a progressive increase in the myoelectrical activity of the vastus lateralis muscle (P = 0.04). Furthermore, the changes in peak V?o2 (r = 0.73, P = 0.007) and the amplitude of the slow component (r = 0.79, P = 0.002) largely correlated with performance improvement. These findings provide a link between improved aerobic metabolism and enhanced severe-intensity cycling performance after IPC. Furthermore, the delayed exhaustion after IPC under lower RPE and higher skeletal muscle activation suggest they have a role on the ergogenic effects of IPC on endurance performance. PMID:26359484</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26500182','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26500182"><span id="translatedtitle">Activation of inositol 1,4,5-trisphosphate receptors during <span class="hlt">preconditioning</span> low-frequency stimulation suppresses subsequent induction of long-term potentiation in hippocampal CA1 neurons.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Yamazaki, Y; Fujii, S; Goto, J-I; Fujiwara, H; Mikoshiba, K</p> <p>2015-12-17</p> <p>We investigated the role of inositol 1,4,5-trisphosphate receptors (IP3Rs) activated during <span class="hlt">preconditioning</span> low-frequency stimulation (LFS) in the subsequent high-frequency stimulation (HFS)-induced induction of long-term potentiation (LTP) in CA1 neurons in hippocampal slices from mature guinea pigs. Induction of LTP in the field excitatory postsynaptic potential (EPSP) or the population spike (PS) by delivery of HFS (a tetanus of 100 pulses at 100Hz) to the Schaffer collateral-commissural pathway to CA1 neuron synapses was suppressed when the CA1 synapses were <span class="hlt">preconditioned</span> by LFS of 1000 pulses at 1Hz. This effect was inhibited when the <span class="hlt">preconditioning</span> LFS was applied in the presence of an N-methyl-d-aspartate receptors (NMDARs) antagonist, a metabotropic glutamate receptor (mGluR) antagonist, IP3R antagonist, a calmodulin-dependent kinase II inhibitor or a calcineurin inhibitor. Furthermore, blockade of group I mGluRs immediately before the delivery of HFS blocked the inhibitory effect of the <span class="hlt">preconditioning</span> LFS on subsequent induction of LTP by HFS. These results suggest that, in hippocampal CA1 neuron synapses, co-activation of NMDARs and IP3Rs during a <span class="hlt">preconditioning</span> LFS results in both phosphorylation and dephosphorylation events that lead to prolonged activation of group I mGluRs that is responsible for the failure of LTP induction. PMID:26500182</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4665727','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4665727"><span id="translatedtitle">Pharmacological <span class="hlt">preconditioning</span> and postconditioning with nicorandil attenuates ischemia/reperfusion-induced myocardial necrosis and apoptosis in hypercholesterolemic rats</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>LI, WENNA; WU, NAN; SHU, WENQI; JIA, DALIN; JIA, PENGYU</p> <p>2015-01-01</p> <p>Pharmacological <span class="hlt">preconditioning</span> and postconditioning may reduce myocardial necrosis and apoptosis during ischemia/reperfusion (I/R), however, hypercholesterolemia interferes with the associated cardioprotective mechanisms. The present study investigated whether pharmacological <span class="hlt">preconditioning</span> and postconditioning with nicorandil could attenuate myocardial necrosis and apoptosis induced by I/R in hypercholesterolemic rats, and explored the possible mechanisms involved. Male Wistar rats (n=160) were fed normal (normocholesterolemic group, n=10) or high-cholesterol (hypercholesterolemic group, n=150) diets for 8 weeks. Hearts harvested from the normal and hypercholesterolemic rats were subsequently placed on modified Langendorff perfusion apparatus and 30-min global ischemia was performed, followed by 120-min reperfusion. Nicorandil (1, 3, 10, 30, 100 µmol/l), and mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channel blocker 5-hydroxydecanoic acid sodium salt (5-HD) (100 µmol/l) or soluble guanylyl cyclase (sGC) blocker 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (10 µmol/l) were perfused for 10 min, prior to ischemia or at the onset of reperfusion. The myocardial infarct size was determined by triphenyltetrazolium chloride staining, and cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. In order to investigate the potential mechanisms, the expression levels of caspase-3, B-cell lymphoma-2 (Bcl-2) proteins and Bcl-2-associated X protein (Bax) were measured using western blot analysis. The present study demonstrated that, in hypercholesterolemic rats, pharmacological <span class="hlt">preconditioning</span> and postconditioning with nicorandil decreased I/R-induced myocardial necrosis and apoptosis in a concentration-dependent manner. The optimal <span class="hlt">preconditioning</span> and postconditioning concentration of nicorandil determined to have anti-infarct and anti-apoptosis effects was 30 µmol/l, which significantly (P<0.05) reduced the infarct size to 14.88±3.25% and 15.96±3.29%, and attenuated the percentage of cardiomyocyte apoptosis to 25.20±3.93% and 26.18±4.82%, respectively, compared with the I/R group. However, the cardioprotective effects of nicorandil were partially suppressed by cotreatment with 5-HD or ODQ. Western blot analysis demonstrated that pharmacological <span class="hlt">preconditioning</span> and postconditioning with nicorandil significantly downregulated caspase-3 and Bax expression, and upregulated Bcl-2 expression compared with the I/R group (P<0.05). The results of the present study suggest that pharmacological <span class="hlt">preconditioning</span> and postconditioning with nicorandil may protect hypercholesterolemic hearts against I/R-induced necrosis and apoptosis; and the cardioprotective effects of nicorandil may be due to the dual pharmacological mechanisms of opening the mitoKATP channels and a nitric oxide/sGC-dependent mechanism, and regulation of the expression of caspase-3, Bax and Bcl-2. PMID:26668616</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25416193','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25416193"><span id="translatedtitle">Interval exercise, but not endurance exercise, <span class="hlt">prevents</span> endothelial ischemia-reperfusion injury in healthy subjects.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Seeger, Joost P H; Lenting, Charlotte J; Schreuder, Tim H A; Landman, Thijs R J; Cable, N Timothy; Hopman, Maria T E; Thijssen, Dick H J</p> <p>2015-02-15</p> <p>Endothelial ischemia-reperfusion (I/R) injury importantly contributes to the poor prognosis during ischemic (myocardial) events. <span class="hlt">Preconditioning</span>, i.e., repeated exposure to short periods of ischemia, effectively reduces endothelial I/R injury. In the present study, we examined the hypothesis that exercise has <span class="hlt">preconditioning</span> effects on endothelial I/R injury. Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. In 17 healthy young subjects, we examined changes in brachial artery endothelial function using flow-mediated dilation (FMD) before and after a bout of high-intensity interval exercise, moderate-intensity endurance exercise, or a control intervention. Subsequently, I/R injury was induced by inflation of a blood pressure cuff around the upper arm to 220 mmHg for 20 min and 20 min of reperfusion followed by another FMD measurement. Near-infrared spectrometry was used to examine local tissue oxygenation during exercise. No differences in brachial artery FMD were found at baseline for the three conditions. I/R induced a significant decline in FMD (7.1±2.3 to 4.3±2.3, P<0.001). When preceded by the interval exercise bout, no change in FMD was present after I/R (7.7±3.1 to 7.2±3.1, P=0.56), whereas the decrease in FMD after I/R could not be <span class="hlt">prevented</span> by the endurance exercise bout (7.8±3.1 to 3.8±1.7, P<0.001). In conclusion, a single bout of lower limb interval exercise, but not moderate-intensity endurance exercise, effectively <span class="hlt">prevents</span> brachial artery endothelial I/R injury. This indicates the presence of a remote <span class="hlt">preconditioning</span> effect of exercise, which is selectively present after short-term interval but not continuous exercise in healthy young subjects. PMID:25416193</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/types/liver/patient/liver-prevention-pdq#section/_28','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.gov/types/liver/patient/liver-prevention-pdq#section/_28"><span id="translatedtitle">Liver (Hepatocellular) Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Treatment Liver Cancer <span class="hlt">Prevention</span> Liver Cancer Screening Research Liver (Hepatocellular) Cancer <span class="hlt">Prevention</span> (PDQ®) What is <span class="hlt">prevention</span>? Cancer ... to keep cancer from starting. General Information About Liver (Hepatocellular) Cancer Key Points Liver cancer is a ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.polioeradication.org/Polioandprevention.aspx','NIH-MEDLINEPLUS'); return false;" href="http://www.polioeradication.org/Polioandprevention.aspx"><span id="translatedtitle">Polio and <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Library Members Site Web Polio and <span class="hlt">prevention</span> Key countries Data and monitoring Post-eradication Research Financing Media room You are here: Polio and <span class="hlt">prevention</span> The virus The vaccines History of polio Polio and <span class="hlt">prevention</span> Polio is a ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/20120010416','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/20120010416"><span id="translatedtitle">Method for <span class="hlt">Pre-Conditioning</span> a Measured Surface Height Map for Model Validation</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Sidick, Erkin</p> <p>2012-01-01</p> <p>This software allows one to up-sample or down-sample a measured surface map for model validation, not only without introducing any re-sampling errors, but also eliminating the existing measurement noise and measurement errors. Because the re-sampling of a surface map is accomplished based on the analytical expressions of Zernike-polynomials and a power spectral density model, such re-sampling does not introduce any aliasing and interpolation errors as is done by the conventional interpolation and FFT-based (fast-Fourier-transform-based) spatial-filtering method. Also, this new method automatically eliminates the measurement noise and other measurement errors such as artificial discontinuity. The developmental cycle of an optical system, such as a space telescope, includes, but is not limited to, the following two steps: (1) deriving requirements or specs on the optical quality of individual optics before they are fabricated through optical modeling and simulations, and (2) validating the optical model using the measured surface height maps after all optics are fabricated. There are a number of computational issues related to model validation, one of which is the "<span class="hlt">pre-conditioning</span>" or pre-processing of the measured surface maps before using them in a model validation software tool. This software addresses the following issues: (1) up- or down-sampling a measured surface map to match it with the gridded data format of a model validation tool, and (2) eliminating the surface measurement noise or measurement errors such that the resulted surface height map is continuous or smoothly-varying. So far, the preferred method used for re-sampling a surface map is two-dimensional interpolation. The main problem of this method is that the same pixel can take different values when the method of interpolation is changed among the different methods such as the "nearest," "linear," "cubic," and "spline" fitting in Matlab. The conventional, FFT-based spatial filtering method used to eliminate the surface measurement noise or measurement errors can also suffer from aliasing effects. During re-sampling of a surface map, this software preserves the low spatial-frequency characteristic of a given surface map through the use of Zernike-polynomial fit coefficients, and maintains mid- and high-spatial-frequency characteristics of the given surface map by the use of a PSD model derived from the two-dimensional PSD data of the mid- and high-spatial-frequency components of the original surface map. Because this new method creates the new surface map in the desired sampling format from analytical expressions only, it does not encounter any aliasing effects and does not cause any discontinuity in the resultant surface map.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4509368','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4509368"><span id="translatedtitle">Effect of hyperbaric oxygen <span class="hlt">preconditioning</span> on peri-hemorrhagic focal edema and aquaporin-4 expression</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>FANG, JINYONG; LI, HONGLING; LI, GUANGLEI; WANG, LICHUN</p> <p>2015-01-01</p> <p>The aim of the present study was to investigate the effect of hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) on peri-hemorrhagic focal edema and aquaporin-4 (AQP-4) expression in an experimental intracerebral hemorrhage (ICH) rat model. Sixty-six Sprague Dawley® rats were divided into three groups: The sham-surgery group (SHG; n=6); the control group (A-ICH; n=30), in which the rats were injected with autologous blood; and the experimental HBO-PC group (P-HBO; n=30). The rats underwent brain edema and AQP-4 detection at 5 postoperative time-points (24, 48 and 72 h and 5 and 7 days). The water content in the brain tissues of the A-ICH animals was higher than that in the brain tissues of the SHG rats at each time-point (P<0.05), and the edema in the P-HBO was significantly more severe 24 and 48 h postoperatively than that at 7 days postoperatively (P<0.05). The difference between the P-HBO and A-ICH was significant at 48 and 72 h postoperatively (P<0.05). AQP-4 was expressed in the post-hemorrhagic rat brains of all groups; the SHG animals exhibited low expression, while the A-ICH animals exhibited an increased expression 24 h postoperatively. In the A-ICH, expression peaked at 48 h postoperatively and began to decrease gradually after 72 h. At the 7-day time-point, the expression level in the A-ICH was closer to but still higher than that of the SHG animals (P<0.05). The differences between the P-HBO and A-ICH animals at the postoperative 24-h, 48-h and 7-day time-points were statistically significant (P<0.05). In conclusion, HBO-PC may downregulate AQP-4 expression to reduce the intracerebral edema, thus strengthening tolerance to ICH and protecting the nerves. PMID:26622378</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22215256','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22215256"><span id="translatedtitle">Involvement of SIRT1 in hypoxic down-regulation of c-Myc and ?-catenin and hypoxic <span class="hlt">preconditioning</span> effect of polyphenols</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Hong, Kyung-Soo; Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan ; Park, Jun-Ik; Kim, Mi-Ju; Kim, Hak-Bong; Lee, Jae-Won; Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan ; Dao, Trong Tuan; Oh, Won Keun; Kang, Chi-Dug; Kim, Sun-Hee; Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan </p> <p>2012-03-01</p> <p>SIRT1 has been found to function as a Class III deacetylase that affects the acetylation status of histones and other important cellular nonhistone proteins involved in various cellular pathways including stress responses and apoptosis. In this study, we investigated the role of SIRT1 signaling in the hypoxic down-regulations of c-Myc and ?-catenin and hypoxic <span class="hlt">preconditioning</span> effect of the red wine polyphenols such as piceatannol, myricetin, quercetin and resveratrol. We found that the expression of SIRT1 was significantly increased in hypoxia-exposed or hypoxic <span class="hlt">preconditioned</span> HepG2 cells, which was closely associated with the up-regulation of HIF-1? and down-regulation of c-Myc and ?-catenin expression via deacetylation of these proteins. In addition, blockade of SIRT1 activation using siRNA or amurensin G, a new potent SIRT1 inhibitor, abolished hypoxia-induced HIF-1? expression but increased c-Myc and ?-catenin expression. SIRT1 was also found to stabilize HIF-1? protein and destabilize c-Myc, ?-catenin and PHD2 under hypoxia. We also found that myricetin, quercetin, piceatannol and resveratrol up-regulated HIF-1? and down-regulated c-Myc, PHD2 and ?-catenin expressions via SIRT1 activation, in a manner that mimics hypoxic <span class="hlt">preconditioning</span>. This study provides new insights of the molecular mechanisms of hypoxic <span class="hlt">preconditioning</span> and suggests that polyphenolic SIRT1 activators could be used to mimic hypoxic/ischemic <span class="hlt">preconditioning</span>. -- Graphical abstract: Polyphenols mimicked hypoxic <span class="hlt">preconditioning</span> by up-regulating HIF-1? and SIRT1 and down-regulating c-Myc, PHD2, and ?-catenin. HepG2 cells were pretreated with the indicated doses of myricetin (MYR; A), quercetin (QUR; B), or piceatannol (PIC; C) for 4 h and then exposed to hypoxia for 4 h. Levels of HIF-1?, SIRT1, c-Myc, ?-catenin, and PHD2 were determined by western blot analysis. The data are representative of three individual experiments. Highlights: ? SIRT1 expression is increased in hypoxia-exposed or hypoxic <span class="hlt">preconditioned</span> cells. ? SIRT1 deacetylates c-Myc and ?-catenin ? HIF-1? is up-regulated by down-regulation of c-Myc and ?-catenin expression. ? Polyphenolic SIRT1 activators mimics hypoxic <span class="hlt">preconditioning</span>.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/servlets/purl/1047191','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/servlets/purl/1047191"><span id="translatedtitle">REACTIVE TRANSPORT MODELING USING A PARALLEL FULLY-COUPLED SIMULATOR BASED ON <span class="hlt">PRECONDITIONED</span> JACOBIAN-FREE NEWTON-KRYLOV</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Luanjing Guo; Chuan Lu; Hai Huang; Derek R. Gaston</p> <p>2012-06-01</p> <p>Systems of multicomponent reactive transport in porous media that are large, highly nonlinear, and tightly coupled due to complex nonlinear reactions and strong solution-media interactions are often described by a system of coupled nonlinear partial differential algebraic equations (PDAEs). A <span class="hlt">preconditioned</span> Jacobian-Free Newton-Krylov (JFNK) solution approach is applied to solve the PDAEs in a fully coupled, fully implicit manner. The advantage of the JFNK method is that it avoids explicitly computing and storing the Jacobian matrix during Newton nonlinear iterations for computational efficiency considerations. This solution approach is also enhanced by physics-based blocking <span class="hlt">preconditioning</span> and multigrid algorithm for efficient inversion of preconditioners. Based on the solution approach, we have developed a reactive transport simulator named RAT. Numerical results are presented to demonstrate the efficiency and massive scalability of the simulator for reactive transport problems involving strong solution-mineral interactions and fast kinetics. It has been applied to study the highly nonlinearly coupled reactive transport system of a promising in situ environmental remediation that involves urea hydrolysis and calcium carbonate precipitation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4605744','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4605744"><span id="translatedtitle">Red Blood Cells <span class="hlt">Preconditioned</span> with Hemin Are Less Permissive to Plasmodium Invasion In Vivo and In Vitro</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Gaudreault, Véronique; Wirbel, Jakob; Jardim, Armando; Rohrbach, Petra; Scorza, Tatiana</p> <p>2015-01-01</p> <p>Malaria is a parasitic disease that causes severe hemolytic anemia in Plasmodium-infected hosts, which results in the release and accumulation of oxidized heme (hemin). Although hemin impairs the establishment of Plasmodium immunity in vitro and in vivo, mice <span class="hlt">preconditioned</span> with hemin develop lower parasitemia when challenged with Plasmodium chabaudi adami blood stage parasites. In order to understand the mechanism accounting for this resistance as well as the impact of hemin on eryptosis and plasma levels of scavenging hemopexin, red blood cells were labeled with biotin prior to hemin treatment and P. c. adami infection. This strategy allowed discriminating hemin-treated from de novo generated red blood cells and to follow the infection within these two populations of cells. Fluorescence microscopy analysis of biotinylated-red blood cells revealed increased P. c. adami red blood cells selectivity and a decreased permissibility of hemin-conditioned red blood cells for parasite invasion. These effects were also apparent in in vitro P. falciparum cultures using hemin-<span class="hlt">preconditioned</span> human red blood cells. Interestingly, hemin did not alter the turnover of red blood cells nor their replenishment during in vivo infection. Our results assign a function for hemin as a protective agent against high parasitemia, and suggest that the hemolytic nature of blood stage human malaria may be beneficial for the infected host. PMID:26465787</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/19331821','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/19331821"><span id="translatedtitle">Transcriptional signature of human adipose tissue-derived stem cells (hASCs) <span class="hlt">preconditioned</span> for chondrogenesis in hypoxic conditions.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Pilgaard, L; Lund, P; Duroux, M; Lockstone, H; Taylor, J; Emmersen, J; Fink, T; Ragoussis, J; Zachar, V</p> <p>2009-07-01</p> <p>Hypoxia is an important factor involved in the control of stem cells. To obtain a better insight into the phenotypical changes brought about by hypoxic <span class="hlt">preconditioning</span> prior to chondrogenic differentiation; we have investigated growth, colony-forming and chondrogenic capacity, and global transcriptional responses of six adipose tissue-derived stem cell lines expanded at oxygen concentrations ranging from ambient to 1%. The assessment of cell proliferation and colony-forming potential revealed that the hypoxic conditions corresponding to 1% oxygen played a major role. The chondrogenic inducibility, examined by high-density pellet model, however, did not improve on hypoxic <span class="hlt">preconditioning</span>. While the microarray analysis revealed a distinctive inter-donor variability, the exposure to 1% hypoxia superseded the biological variability and produced a specific expression profile with 2581 significantly regulated genes and substantial functional enrichment in the pathways of cell proliferation and apoptosis. Additionally, exposure to 1% oxygen resulted in upregulation of factors related to angiogenesis and cell growth. In particular, leptin (LEP), the key regulator of body weight and food intake was found to be highly upregulated. In conclusion, the results of this investigation demonstrate the significance of donor demographics and the importance of further studies into the use of regulated oxygen tension as a tool for preparation of ASCs in order to exploit their full potential. PMID:19331821</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22209779','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22209779"><span id="translatedtitle">Transcriptional signature of human adipose tissue-derived stem cells (hASCs) <span class="hlt">preconditioned</span> for chondrogenesis in hypoxic conditions</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Pilgaard, L.; Lund, P.; Duroux, M.; Lockstone, H.; Taylor, J.; Emmersen, J.; Fink, T.; Ragoussis, J.; Zachar, V.</p> <p>2009-07-01</p> <p>Hypoxia is an important factor involved in the control of stem cells. To obtain a better insight into the phenotypical changes brought about by hypoxic <span class="hlt">preconditioning</span> prior to chondrogenic differentiation; we have investigated growth, colony-forming and chondrogenic capacity, and global transcriptional responses of six adipose tissue-derived stem cell lines expanded at oxygen concentrations ranging from ambient to 1%. The assessment of cell proliferation and colony-forming potential revealed that the hypoxic conditions corresponding to 1% oxygen played a major role. The chondrogenic inducibility, examined by high-density pellet model, however, did not improve on hypoxic <span class="hlt">preconditioning</span>. While the microarray analysis revealed a distinctive inter-donor variability, the exposure to 1% hypoxia superseded the biological variability and produced a specific expression profile with 2581 significantly regulated genes and substantial functional enrichment in the pathways of cell proliferation and apoptosis. Additionally, exposure to 1% oxygen resulted in upregulation of factors related to angiogenesis and cell growth. In particular, leptin (LEP), the key regulator of body weight and food intake was found to be highly upregulated. In conclusion, the results of this investigation demonstrate the significance of donor demographics and the importance of further studies into the use of regulated oxygen tension as a tool for preparation of ASCs in order to exploit their full potential.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25818106','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25818106"><span id="translatedtitle"><span class="hlt">Preconditioning</span> With Tauroursodeoxycholic Acid Protects Against Contrast-Induced HK-2 Cell Apoptosis by Inhibiting Endoplasmic Reticulum Stress.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Peng, Pingan; Ma, Qian; Wang, Le; Zhang, Ou; Han, Hongya; Liu, Xiaoli; Zhou, Yujie; Zhao, Yingxin</p> <p>2015-11-01</p> <p>To investigate whether tauroursodeoxycholic acid (TUDCA) could attenuate contrast media (CM)-induced renal tubular cell apoptosis by inhibiting endoplasmic reticulum stress (ERS), we exposed HK-2 cells to increasing doses of meglumine diatrizoate (20, 40, and 80 mg I/mL) for 2 to 16 hours, with/without TUDCA <span class="hlt">preconditioning</span> for 24 hours. Cell viability test, Hoechst 33258 staining, and flow cytometry were used to detect meglumine diatrizoate-induced cell apoptosis, while real-time polymerase chain reaction and Western blot analysis were used to measure the expressions of ERS markers of glucose-regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), and the apoptosis-related marker of caspase 12. Cell apoptosis and messenger RNA (mRNA) expression of GRP78 (P = .005), ATF4 (P = .01), and caspase 12 (P = .001) were significantly higher in the CM 4 hours group than the control as well as the protein expressions. The TUDCA <span class="hlt">preconditioning</span> reduced the mRNA expression of GRP78, ATF4, and caspase 12 in the CM 4 hours groups (P = .009, .019, and .003, respectively) as well as the protein expression. In conclusion, TUDCA could protect renal tubular cells from meglumine diatrizoate-induced apoptosis by inhibiting ERS. PMID:25818106</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3890329','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3890329"><span id="translatedtitle">Modifications in Rat Plasma Proteome after Remote Ischemic <span class="hlt">Preconditioning</span> (RIPC) Stimulus: Identification by a SELDI-TOF-MS Approach</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hibert, Pierre; Prunier-Mirebeau, Delphine; Beseme, Olivia; Chwastyniak, Maggy; Tamareille, Sophie</p> <p>2014-01-01</p> <p>Remote ischemic <span class="hlt">preconditioning’s</span> (RIPC) ability to render the myocardium resistant to subsequent prolonged ischemia is now clearly established in different species, including humans. Strong evidence suggests that circulating humoral mediators play a key role in signal transduction, but their identities still need to be established. Our study sought to identify potential circulating RIPC mediators using a proteomic approach. Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5?) or 10-min (RIPC 10?) reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were isolated for proteomic analysis using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). A total of seven proteins, including haptoglobin and transthyretin, were detected as up- or down-regulated in response to RIPC. These proteins had previously been identified as associated with organ protection, anti-inflammation, and various cellular and molecular responses to ischemia. In conclusion, this study indicates that RIPC results in significant modulations of plasma proteome. PMID:24454915</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_17");'>17</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li class="active"><span>19</span></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_19 --> <div id="page_20" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li class="active"><span>20</span></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="381"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED014097.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED014097.pdf"><span id="translatedtitle">"AN OUNCE OF <span class="hlt">PREVENTION</span>..."</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>HASELKORN, FLORENCE</p> <p></p> <p><span class="hlt">PREVENTION</span> AS FUNCTION, VALUE ISSUE, CONCEPTUAL SHORTCOMING, AND PRACTICE IS DISCUSSED AND RELATED TO EDUCATIONAL TASK. <span class="hlt">PREVENTION</span> AS FUNCTION IS GENERATED BY OUR VALUE PREMISES. IN SEEKING TO <span class="hlt">PREVENT</span> SOME FORMS OF SOCIAL DYSFUNCTION, WE MAY BE PERPETUATING OTHERS. THE CONCEPT OF <span class="hlt">PREVENTION</span> IS AMBIGUOUS. CRUCIAL CONCEPTUAL ISSUES INCLUDE THE…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4216952','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4216952"><span id="translatedtitle">High-fat diet-induced impairment of skeletal muscle insulin sensitivity is not <span class="hlt">prevented</span> by SIRT1 overexpression</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>White, Amanda T.; Philp, Andrew; Fridolfsson, Heidi N.; Schilling, Jan M.; Murphy, Anne N.; Hamilton, D. Lee; McCurdy, Carrie E.; Patel, Hemal H.</p> <p>2014-01-01</p> <p>Skeletal muscle sirtuin 1 (SIRT1) expression is reduced under insulin-resistant conditions, such as those resulting from high-fat diet (HFD) feeding and obesity. Herein, we investigated whether constitutive activation of SIRT1 in skeletal muscle <span class="hlt">prevents</span> HFD-induced muscle insulin resistance. To address this, mice with muscle-specific overexpression of SIRT1 (mOX) and wild-type (WT) littermates were fed a control diet (10% calories from fat) or HFD (60% of calories from fat) for 12 wk. Magnetic resonance imaging and indirect calorimetry were used to measure body composition and energy expenditure, respectively. Whole body glucose metabolism was assessed by oral glucose tolerance test, and insulin-stimulated glucose uptake was measured at a physiological insulin concentration in isolated soleus and extensor digitorum longus muscles. Although SIRT1 was significantly overexpressed in muscle of mOX vs. WT mice, body weight and percent body fat were similarly increased by HFD for both genotypes, and energy expenditure was unaffected by diet or genotype. Importantly, impairments in glucose tolerance and insulin-mediated activation of glucose uptake in skeletal muscle that occurred with HFD feeding were not <span class="hlt">prevented</span> in mOX mice. In contrast, mOX mice showed enhanced <span class="hlt">postischemic</span> cardiac functional recovery compared with WT mice, confirming the physiological functionality of the SIRT1 transgene in this mouse model. Together, these results demonstrate that activation of SIRT1 in skeletal muscle alone does not <span class="hlt">prevent</span> HFD-induced glucose intolerance, weight gain, or insulin resistance. PMID:25159328</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/20850491','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/20850491"><span id="translatedtitle"><span class="hlt">Preconditioning</span> with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Kwak, Hyun-Jeong; Park, Kyoung-Mi; Lee, Seahyoung; Lim, Hyun-Joung; Go, Sang-Hee; Eom, Sang-Mi; Park, Hyun-Young . E-mail: hypark65@nih.go.kr</p> <p>2006-12-01</p> <p>Nitric oxide (NO) signaling pathways are important in both the maintenance of vascular homeostasis and disease progression. Overproduction of NO has been associated with ischemia/reperfusion (I/R) injury. Growing evidences suggest that NO <span class="hlt">preconditioning</span> has cytoprotective effects against I/R injury. However, the mechanism with which NO mediates these effects remains to be elucidated. The purpose of this study was to examine the mechanism of how NO <span class="hlt">preconditioning</span> inhibits subsequent NO-induced apoptosis in vascular smooth muscle cells (VSMC), specifically focusing on heme oxygenase-1 (HO-1). According to our data, sodium nitroprusside (SNP) increased HO-1 expression in a concentration dependent manner. <span class="hlt">Preconditioning</span> with low concentration SNP (0.3 mM) inhibited subsequent high concentration SNP (1.5 mM)-induced apoptosis, and this effect was reversed by the HO-1 inhibitor SnPP. Low concentration SNP-mediated protection involved p38 kinase inactivation and increased Bcl-2 expression. Furthermore, mitochondrial membrane potential was concomitantly increased with decreased expressions of Bax, Apaf-1, and activity of caspase-3, which was reversed by SnPP treatment. Our results show that low concentration SNP <span class="hlt">preconditioning</span> suppresses subsequent high concentration SNP-induced apoptosis by inhibiting p38 kinase and mitochondrial death pathway via HO-1-dependent mechanisms in VSMC.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=80762&keyword=%28Myocardial+AND+infarction%29&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=42959666&CFTOKEN=79134144','EPA-EIMS'); return false;" href="http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=80762&keyword=%28Myocardial+AND+infarction%29&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=42959666&CFTOKEN=79134144"><span id="translatedtitle">HSP70.1 AND -70.3 ARE REQUIRED FOR LATE-PHASE PROTECTION INDUCED BY ISCHEMIC <span class="hlt">PRECONDITIONING</span> OF MOUSE HEARTS</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>Heat-Shock Proteins 70.1 and 70.3 Are Required for Late-phase Protection<br>Induced by Ischemic <span class="hlt">Preconditioning</span> of the Mouse Heart<br>Craig R. Hampton 1 , Akira Shimamoto 1 , Christine L. Rothnie 1 , Jeaneatte Griscavage-Ennis 1 ,<br>Albert Chong 1 , David J. Dix 2 , Edward D. Ve...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/19133028','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/19133028"><span id="translatedtitle">Endothelial cell retention on a viscoelastic nanocomposite vascular conduit is improved by exposure to shear stress <span class="hlt">preconditioning</span> prior to physiological flow.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Vara, Dina S; Punshon, Geoffrey; Sales, Kevin M; Sarkar, Sandip; Hamilton, George; Seifalian, Alexander M</p> <p>2008-12-01</p> <p>In this study, endothelial cell (EC)-seeded nanocomposite grafts were <span class="hlt">preconditioned</span> with 1-2 dynes/cm(2) in vitro to establish whether low shear stress resulted in improved cell adherence prior to physiological shear stress (15 dynes/cm(2)). Alamar blue cell viability was assessed. Polymerase chain reaction was conducted for glyceraldehyde-3-phosphate dehydrogenase, transforming growth factor beta-1 (TGFbeta-1), vascular endothelial growth factor receptor-1 (VEGFR-1), platelet EC adhesion molecule-1, and vascular endothelial growth factor receptor-2 (VEGFR-2). The Alamar blue results demonstrated improved cellular retention following <span class="hlt">preconditioning</span> (P < 0.001). VEGFR-2 and TGFbeta-1 expression was up-regulated, and VEGFR-1 down-regulated following <span class="hlt">preconditioning</span>. This investigation confirms previous findings regarding the potential benefits of <span class="hlt">preconditioning</span>, and demonstrates that these benefits can be applied to ECs seeded on the nanocomposite employed. It also demonstrates further the suitability and potential of nanocomposite for future use in tissue-engineered cardiovascular devices. PMID:19133028</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED354638.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED354638.pdf"><span id="translatedtitle">Graduate Follow-Up: An Examination of NCATE's <span class="hlt">Precondition</span> Criteria, CEC's Criteria, and the State of the Knowledge Base. Information Bulletin #41.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Berkeley, Terry R.</p> <p></p> <p>Graduates of professional preparation programs in special education are followed up in order to know about the status of professionals who completed their training in programs receiving federal support from the Office of Special Education Programs Division of Personnel Preparation. This bulletin discusses graduate follow-up <span class="hlt">precondition</span> criteria…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25757750','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25757750"><span id="translatedtitle"><span class="hlt">Preconditioning</span> cortical lesions reduce the incidence of peri-infarct depolarizations during focal ischemia in the Spontaneously Hypertensive Rat: interaction with prior anesthesia and the impact of hyperglycemia.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhao, Liang; Nowak, Thaddeus S</p> <p>2015-07-01</p> <p>The relationship between peri-infarct depolarizations (PIDs) and infarction was investigated in a model of <span class="hlt">preconditioning</span> by cortical freeze lesions (cryogenic lesions, CL) in the Spontaneously Hypertensive Rat. Small (< 5 mm(3)) lesions produced 24 hours before permanent focal ischemia were protective, without impacting baseline cerebral blood flow (CBF) and metabolism. Prior CL reduced infarct volume, associated with improved penumbral CBF as previously showed for ischemic <span class="hlt">preconditioning</span>. The brief initial procedure avoided sham effects on infarct volume after subsequent occlusion under brief anesthesia. However, under prolonged isoflurane anesthesia for perfusion monitoring both sham and CL rats showed reduced PID incidence relative to naive animals. This anesthesia effect could be eliminated by using ?-chloralose during perfusion imaging. As an additional methodological concern, blood glucose was frequently elevated at the time of the second surgery, reflecting buprenorphine-induced pica and other undefined mechanisms. Even modest hyperglycemia (>10 mmol/L) reduced PID incidence. In normoglycemic animals CL <span class="hlt">preconditioning</span> reduced PID number by 50%, demonstrating associated effects on PID incidence, penumbral perfusion, and infarct progression. Hyperglycemia suppressed PIDs without affecting the relationship between CBF and infarction. This suggests that the primary effect of <span class="hlt">preconditioning</span> is to improve penumbral perfusion, which in turn impacts PID incidence and infarct size. PMID:25757750</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2015EGUGA..17.7687C','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2015EGUGA..17.7687C"><span id="translatedtitle">Using pan-Arctic, springtime, surface radiation observations to quantify atmospheric <span class="hlt">preconditioning</span> processes that impact the sea ice melt season</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Cox, Christopher; Uttal, Taneil; Starkweather, Sandy; Intrieri, Janet; Maturilli, Marion; Kustov, Vasily; Konopleva, Elena; Crepinsek, Sara; Long, Chuck</p> <p>2015-04-01</p> <p>Accurate, seasonal-scale forecasts of sea ice extent and distribution are critical for weather forecasting, transportation, the energy industry and local Arctic communities. Current forecasting methods capture an overall trend of decreasing sea ice on decadal scales, but do not reliably predict inter-annual variability. Recent work using satellite observations identified a relationship between spring-time, cloud modulated, shortwave radiation, and late season sea-ice extent; this relationship suggested an atmospheric <span class="hlt">preconditioning</span> process that modulates the ice-albedo feedback and sets the stage for the melt season. Due to a general lack of emphasis on the role of the atmosphere on the evolution of the summer sea-ice, compounded by biases in cloud properties within models, this <span class="hlt">preconditioning</span> process is poorly represented in current forecasting methods. Longwave and shortwave radiation data collected at the surface from stations surrounding the Arctic Basin as part of the Baseline Surface Radiation Network (BSRN) provide high-quality, continuous observations of the surface radiation budget. This includes downwelling fluxes and surface-cloud radiative interactions which cannot be directly acquired by satellites. These BSRN data are used to investigate the role of the atmosphere and clouds in seasonal scale variability of sea ice conditions, and the potential for improving predictability by incorporating these atmospheric observations into prediction strategies. We find that the downwelling fluxes measured at the land stations in spring are well correlated with sea ice conditions in September, especially in regions of the Arctic Ocean where late summer sea ice concentration has large inter-annual variability. Using observations of the total radiative flux (longwave + shortwave) at the surface, it is possible to make a seasonal sea-ice extent forecast that is within the range of uncertainty of forecasts currently incorporated into the Sea Ice Prediction Network (SIPN). Cloud variability and associated shortwave modulation of the ice-albedo feedback are found to be important, but the shortwave anomaly alone is insufficient unless combined with the longwave anomaly, which dominates and is opposite in sign in the presence of clouds. The amount of open water in the Western Arctic in September and October then controls cloud cover during the autumn freeze-up, potentially revealing a <span class="hlt">preconditioning</span> mechanism that persists into the following melt season.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/23546740','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/23546740"><span id="translatedtitle">Involvement of volume-activated chloride channels in H2O 2 <span class="hlt">preconditioning</span> against oxidant-induced injury through modulating cell volume regulation mechanisms and membrane permeability in PC12 cells.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Zhu, Linyan; Zuo, Wanhong; Yang, Haifeng; Zhang, Haifeng; Luo, Hai; Ye, Dong; Lin, Xi; Mao, Jianwen; Feng, Jianqiang; Chen, Lixin; Wang, Liwei</p> <p>2013-08-01</p> <p>The functions of chloride channels in <span class="hlt">preconditioning</span>-induced cell protection remain unclear. In this report, we show that the volume-activated chloride channels play a key role in hydrogen peroxide (H2O2) <span class="hlt">preconditioning</span>-induced cell protection in pheochromocytoma PC12 cells. The <span class="hlt">preconditioning</span> with 100 ?M H2O2 for 90 min protected the cells from injury induced by long period exposure to 300 ?M H2O2. The protective effect was attenuated by pretreatment with the chloride channel blockers, 5-nitro-2-3-phenylpropylamino benzoic acid (NPPB) and tamoxifen. H2O2 <span class="hlt">preconditioning</span> directly activated a chloride current, which was moderately outward-rectified and sensitive to the chloride channel blockers and hypertonicity-induced cell shrinkage. H2O2 <span class="hlt">preconditioning</span> functionally up-regulated the activities of volume-activated chloride channels and enhanced the regulatory volume decrease when exposure to extracellular hypotonic challenges. In addition, acute application of H2O2 showed distinctive actions on cell volume and membrane permeability in H2O2 <span class="hlt">preconditioned</span> cells. In H2O2 <span class="hlt">preconditioned</span> cells, acute application of 300 ?M H2O2 first promptly induced a decrease of cell volume and enhancement of cell membrane permeability, and then, cell volume was maintained at a relatively stable level and the facilitation of membrane permeability was reduced. Conversely, in control cells, 300 ?M H2O2 induced a slow but persistent apoptotic volume decrease (AVD) and facilitation of membrane permeability. H2O2 <span class="hlt">preconditioning</span> also significantly up-regulated the expression of ClC-3 protein, the molecular candidate of the volume-activated chloride channel. These results suggest that H2O2 <span class="hlt">preconditioning</span> can enhance the expression and functional activities of volume-activated chloride channels, thereby modulate cell volume and cell membrane permeability, which may contribute to neuroprotection against oxidant-induced injury. PMID:23546740</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/20976979','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/20976979"><span id="translatedtitle">Biological stress response terminology: Integrating the concepts of adaptive response and <span class="hlt">preconditioning</span> stress within a hormetic dose-response framework</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Calabrese, Edward J. . E-mail: edwardc@schoolph.umass.edu; Bachmann, Kenneth A.; Bailer, A. John; Bolger, P. Michael; Borak, Jonathan; Cai, Lu; Cedergreen, Nina; Cherian, M. George; Chiueh, Chuang C.; Clarkson, Thomas W.; Cook, Ralph R.; Diamond, David M.; Doolittle, David J.; Dorato, Michael A.; Duke, Stephen O.; Feinendegen, Ludwig; Gardner, Donald E.; Hart, Ronald W.; Hastings, Kenneth L.; Hayes, A. Wallace; Hoffmann, George R.; Ives, John A.; Jaworowski, Zbigniew; Johnson, Thomas E.; Jonas, Wayne B.; Kaminski, Norbert E.</p> <p>2007-07-01</p> <p>Many biological subdisciplines that regularly assess dose-response relationships have identified an evolutionarily conserved process in which a low dose of a stressful stimulus activates an adaptive response that increases the resistance of the cell or organism to a moderate to severe level of stress. Due to a lack of frequent interaction among scientists in these many areas, there has emerged a broad range of terms that describe such dose-response relationships. This situation has become problematic because the different terms describe a family of similar biological responses (e.g., adaptive response, <span class="hlt">preconditioning</span>, hormesis), adversely affecting interdisciplinary communication, and possibly even obscuring generalizable features and central biological concepts. With support from scientists in a broad range of disciplines, this article offers a set of recommendations we believe can achieve greater conceptual harmony in dose-response terminology, as well as better understanding and communication across the broad spectrum of biological disciplines.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4541236','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4541236"><span id="translatedtitle">Electroacupuncture <span class="hlt">preconditioning</span> attenuates ischemic brain injury by activation of the adenosine monophosphate-activated protein kinase signaling pathway</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ran, Qiang-qiang; Chen, Huai-long; Liu, Yan-li; Yu, Hai-xia; Shi, Fei; Wang, Ming-shan</p> <p>2015-01-01</p> <p>Electroacupuncture has therapeutic effects on ischemic brain injury, but its mechanism is still poorly understood. In this study, mice were stimulated by electroacupuncture at the Baihui (GV20) acupoint for 30 minutes at 1 mA and 2/15 Hz for 5 consecutive days. A cerebral ischemia model was established by ligating the bilateral common carotid artery for 15 minutes. At 72 hours after injury, neuronal injury in the mouse hippocampus had lessened, and the number of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling-positive cells reduced after electroacupuncture treatment. Moreover, expression of adenosine monophosphate-activated protein kinase ? (AMPK?) and phosphorylated AMPK? was up-regulated. Intraperitoneal injection of the AMPK antagonist, compound C, suppressed this phenomenon. Our findings suggest that electroacupuncture <span class="hlt">preconditioning</span> alleviates ischemic brain injury via AMPK activation. PMID:26330828</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/381776','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/381776"><span id="translatedtitle">Parallel block <span class="hlt">preconditioning</span> techniques for the numerical simulation of the shallow water flow using finite element methods</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Cai, Y.; Navon, I.M.</p> <p>1995-11-01</p> <p>In this paper, the authors report their work on applying Krylov iterative methods, accelerated by parallelizable domain-decomposed (DD) preconditioners, to the solution of nonsymmetric linear algebraic equations arising from implicit time discretization of a finite element model of the shallow water equations on a limited-area domain. Two types of previously proposed DD preconditioners are employed and a novel one is advocated to accelerate, with post-<span class="hlt">preconditioning</span>, the convergence of three popular and competitive Krylov iterative linear solvers. Performance sensitivities of these preconditioners to inexact subdomain solvers are also reported. Autotasking, the parallel processing capability representing the third phase of multitasking libraries on CRAY Y-MP, has been exploited and successfully applied to both loop and subroutine level parallelization. Satisfactory speedup results were obtained. On the other hand, automatic loop-level parallelization, made possible by the autotasking preprocessor, attained only a speedup smaller than a factor of two. 39 refs., 2 figs., 6 tabs.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2009JSAST..52..135L','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2009JSAST..52..135L"><span id="translatedtitle">Combined Analysis of Thruster Plume Behavior in Rarefied Region by <span class="hlt">Preconditioned</span> Navier-Stokes and DSMC Methods</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Lee, Kyun Ho; Lee, Sung Nam; Yu, Myoung Jong; Kim, Su Kyum; Baek, Seung Wook</p> <p></p> <p>Satellite attitude is usually controlled by plume exhaust from thrusters into the vacuum of space. To study the plume effects in the highly rarefied region, the Direct Simulation Monte Carlo (DSMC) method is usually used, because the plume flow field contains the entire range of flow regime from the near-continuum near the nozzle exit through the transitional state to free molecular state at the far field region from the nozzle. The purpose of this study is to investigate the behavior of a small monopropellant thruster plume in the vacuum region numerically by using the DSMC method. To obtain more accurate results, the <span class="hlt">preconditioned</span> Navier-Stokes algorithm is introduced to calculate continuum flow fields inside the thruster to predict nozzle exit properties, which are used for inlet conditions of DSMC method. As a result, the plume characteristics in the highly rarefied flow, such as strong nonequilibrium near nozzle exit, large back flow region, etc., are investigated.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://agcenter.ucdavis.edu/documents/IIPP_Ag_Guide.pdf','EPRINT'); return false;" href="http://agcenter.ucdavis.edu/documents/IIPP_Ag_Guide.pdf"><span id="translatedtitle">LEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span>, LEADERSHIP,</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Leistikow, Bruce N.</p> <p></p> <p>Group, Graphic Design Portions of this Guide were adapted from WOSHTEP's Taking Action for SafetyLEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span>, LEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span>, LEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span>, LEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span>, LEADERSHIP, ACTION, SKILLS, <span class="hlt">PREVENTION</span></p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3410886','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3410886"><span id="translatedtitle">Aromatase Inhibition Attenuates Desflurane-Induced <span class="hlt">Preconditioning</span> against Acute Myocardial Infarction in Male Mouse Heart In Vivo</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Jazbutyte, Virginija; Stumpner, Jan; Redel, Andreas; Lorenzen, Johan M.; Roewer, Norbert</p> <p>2012-01-01</p> <p>The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. We hypothesized that endogenous estrogens play a role as mediators of desflurane-induced <span class="hlt">preconditioning</span> against myocardial infarction. In this study, we tested the hypothesis that desflurane effects local estrogen synthesis by modulating enzyme aromatase expression and activity in the mouse heart. Aromatase metabolizes testosterone to 17?- estradiol (E2) and thereby significantly contributes to local estrogen synthesis. We tested aromatase effects in acute myocardial infarction model in male mice. The animals were randomized and subjected to four groups which were pre-treated with the selective aromatase inhibitor anastrozole (A group) and DES alone (DES group) or in combination (A+DES group) for 15 minutes prior to surgical intervention whereas the control group received 0.9% NaCl (CON group). All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. Anastrozole blocked DES induced <span class="hlt">preconditioning</span> and increased infarct size compared to DES alone (37.94±15.5% vs. 17.1±3.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model. PMID:22876297</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/21535300','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/21535300"><span id="translatedtitle"><span class="hlt">Preconditioning</span> induced by gentamicin protects against acute kidney injury: The role of prostaglandins but not nitric oxide</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Pessoa, Edson A.; Convento, Marcia B.; Ribas, Otoniel S.; Tristao, Vivian R.; Reis, Luciana Aparecida; Borges, Fernanda T.; Schor, Nestor</p> <p>2011-05-15</p> <p>Nephrotoxicity is the main side effect of gentamicin (GENTA). <span class="hlt">Preconditioning</span> (PC) refers to a situation in which an organ subjected to an injury responds less intensely when exposed to another injury. The aim of this study was to evaluate the effect of PC with GENTA on nephrotoxic acute kidney injury (AKI). GENTA group rats were injected daily with GENTA (40 mg/kg/BW) for 10 days. PC animals were injected with GENTA for 3 days (40 mg/kg/BW/daily) and, after one rest week, were injected daily with GENTA for 10 days. Animals of the L-NAME and DICLO groups were <span class="hlt">preconditioned</span> for 3 days and then received daily injections of GENTA for 10 days; they were concomitantly treated with L-NAME (10 mg/kg/BW) and diclofenac (DICLO, 5 mg/kg/BW) for 13 days. Blood and urine were collected for measurement of serum creatinine, urea, urine sodium, protein, hydroperoxides, lipid peroxidation and nitric oxide (NO). The animals were killed; kidneys were removed for histology and immunohistochemistry for apoptosis and cell proliferation. GENTA group rats showed an increase in plasma creatinine, urea, urine sodium, hydroperoxides, lipid peroxidation, proteinuria, necrosis and apoptosis, characterizing nephrotoxic AKI. PC animals showed a decrease in these parameters and increased proliferation. The blockade of NO synthesis by L-NAME potentiated the protective effect, suggesting that NO contributed to the injury caused by GENTA. The blockade of prostaglandin synthesis with DICLO increased serum and urinary parameters, blunting the protective effect of PC. Our data suggest that PC could be a useful tool to protect against nephrotoxic AKI.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25733102','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25733102"><span id="translatedtitle">Role of adaptor protein MyD88 in TLR-mediated <span class="hlt">preconditioning</span> and neuroprotection after acute excitotoxicity.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Larochelle, Antoine; Bellavance, Marc-André; Rivest, Serge</p> <p>2015-05-01</p> <p>Excitotoxic cell death is a crucial mechanism through which neurodegeneration occurs in numerous pathologies of the central nervous system (CNS), such as Alzheimer's disease, stroke and spinal cord injury. Toll-like receptors (TLRs) are strongly expressed on microglial cells and are key regulators of the innate immune response to neuronal damage. However, it is still unclear whether their stimulation is protective or harmful in excitotoxic contexts. In this study, we demonstrate that systemic administration of lipopolysaccharide (LPS) or Pam3CSK4 24h prior to an intrastriatal injection of kainic acid (KA) significantly protected cortical neurons in the acute phase of injury. Protection could not be detected with the TLR3 ligand poly-IC. Histological analyses revealed that microglia of LPS and Pam3CSK4 <span class="hlt">pre-conditioned</span> group were primed to react to injury and exhibited a stronger expression of Tnf and Tlr2 mRNA. We also found that mice deficient for MyD88, a critical adaptor protein for most TLR, were more vulnerable than WT mice to KA-induced excitotoxicity at early (12h and 24h) and late (10days) time points. Finally, bone-marrow chimeric mice revealed that MyD88 signaling in CNS resident cells, but not in cells of hematopoietic origin, mediates the protective effect. This study unravels the potential of TLR2 and TLR4 agonists to induce a protective state of <span class="hlt">preconditioning</span> against KA-mediated excitotoxicity and further highlights the beneficial role of cerebral MyD88 signaling in this context. PMID:25733102</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4624762','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4624762"><span id="translatedtitle">Sevoflurane <span class="hlt">Preconditioning</span> Reduces Intestinal Ischemia-Reperfusion Injury: Role of Protein Kinase C and Mitochondrial ATP-Sensitive Potassium Channel</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Shen, Zhiwen; Miao, Liping; Zhang, Kun; Wang, Fei; Li, Yujuan</p> <p>2015-01-01</p> <p>Ischemic <span class="hlt">preconditioning</span> (IPC) has been considered to be a potential therapy to reduce ischemia-reperfusion injury (IRI) since the 1980s. Our previous study indicated that sevoflurane <span class="hlt">preconditioning</span> (SPC) also reduced intestinal IRI in rats. However, whether the protective effect of SPC is similar to IPC and the mechanisms of SPC are unclear. Thus, we compared the efficacy of SPC and IPC against intestinal IRI and the role of protein kinase C (PKC) and mitochondrial ATP-sensitive potassium channel (mKATP) in SPC. A rat model of intestinal IRI was used in this study. The superior mesenteric artery (SMA) was clamped for 60 min followed by 120 min of reperfusion. Rats with IPC underwent three cycles of SMA occlusion for 5 min and reperfusion for 5 min before intestinal ischemia. Rats with SPC inhaled sevoflurane at 0.5 minimum alveolar concentration (MAC) for 30 min before the intestinal ischemic insult. Additionally, the PKC inhibitor Chelerythrine (CHE) or mKATP inhibitor 5-Hydroxydecanoic (5-HD) was injected intraperitoneally before sevoflurane inhalation. Both SPC and IPC ameliorated intestinal IRI-induced histopathological changes, decreased Chiu’s scores, reduced terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL) positive cells in the epithelium, and inhibited the expression of malondialdehyde (MDA) and tumor necrosis factor-? (TNF-?). These protective effects of SPC were similar to those of IPC. Pretreatment with PKC or mKATP inhibitor abolished SPC—induced protective effects by increasing Chiu’s scores, down-regulated the expression of Bcl-2 and activated caspase-3. Our results suggest that pretreatment with 0.5 MAC sevoflurane is as effective as IPC against intestinal IRI. The activation of PKC and mKATP may be involved in the protective mechanisms of SPC. PMID:26505750</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4002880','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4002880"><span id="translatedtitle">The endoplasmic reticulum stress inhibitor salubrinal inhibits the activation of autophagy and neuroprotection induced by brain ischemic <span class="hlt">preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Gao, Bo; Zhang, Xiang-yang; Han, Rong; Zhang, Tong-tong; Chen, Cheng; Qin, Zheng-hong; Sheng, Rui</p> <p>2013-01-01</p> <p>Aim: To investigate whether endoplasmic reticulum (ER) stress participates in the neuroprotective effects of ischemic <span class="hlt">preconditioning</span> (IPC)-induced neuroprotection and autophagy activation in rat brains. Methods: The right middle cerebral artery in SD rats was occluded for 10 min to induce focal cerebral IPC, and was occluded permanently 24 h later to induce permanent focal ischemia (PFI). ER stress inhibitor salubrinal (SAL) was injected via intracerebral ventricle infusion 10 min before the onset of IPC. Infarct volume and motor behavior deficits were examined after the ischemic insult. The protein levels of LC3, p62, HSP70, glucose-regulated protein 78 (GRP 78), p-eIF2? and caspase-12 in the ipsilateral cortex were analyzed using immunoblotting. LC3 expression pattern in the sections of ipsilateral cortex was observed with immunofluorescence. Results: Pretreatment with SAL (150 pmol) abolished the neuroprotective effects of IPC, as evidenced by the significant increases in mortality, infarct volume and motor deficits after PFI. At the molecular levels, pretreatment with SAL (150 pmol) significantly increased p-eIF2? level, and decreased GRP78 level after PFI, suggesting that SAL effectively inhibited ER stress in the cortex. Furthermore, the pretreatment with SAL blocked the IPC-induced upregulation of LC3-II and downregulation of p62 in the cortex, thus inhibiting the activation of autophagy. Moreover,SAL blocked the upregulation of HSP70, but significantly increased the cleaved caspase-12 level, thus promoting ER stress-dependent apoptotic signaling in the cortex. Conclusion: ER stress-induced autophagy might contribute to the neuroprotective effect of brain ischemic <span class="hlt">preconditioning</span>. PMID:23603983</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4102512','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4102512"><span id="translatedtitle">Hypoxic <span class="hlt">Preconditioning</span> Differentially Affects GABAergic and Glutamatergic Neuronal Cells in the Injured Cerebellum of the Neonatal Rat</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Patterson, Sean I.; Muñoz, Estela M.; Seltzer, Alicia M.</p> <p>2014-01-01</p> <p>In this study we examined cerebellar alterations in a neonatal rat model of hypoxic-ischemic brain injury with or without hypoxic <span class="hlt">preconditioning</span> (Pc). Between postnatal days 7 and 15, the cerebellum is still undergoing intense cellular proliferation, differentiation and migration, dendritogenesis and synaptogenesis. The expression of glutamate decarboxylase 1 (GAD67) and the differentiation factor NeuroD1 were examined as markers of Purkinje and granule cells, respectively. We applied quantitative immunohistochemistry to sagittal cerebellar slices, and Western blot analysis of whole cerebella obtained from control (C) rats and rats submitted to Pc, hypoxia-ischemia (L) and a combination of both treatments (PcL). We found that either hypoxia-ischemia or Pc perturbed the granule cells in the posterior lobes, affecting their migration and final placement in the internal granular layer. These effects were partially attenuated when the Pc was delivered prior to the hypoxia-ischemia. Interestingly, whole nuclear NeuroD1 levels in Pc animals were comparable to those in the C rats. However, a subset of Purkinje cells that were severely affected by the hypoxic-ischemic insult—showing signs of neuronal distress at the levels of the nucleus, cytoplasm and dendritic arborization—were not protected by Pc. A monoclonal antibody specific for GAD67 revealed a three-band pattern in cytoplasmic extracts from whole P15 cerebella. A ?110 kDa band, interpreted as a potential homodimer of a truncated form of GAD67, was reduced in Pc and L groups while its levels were close to the control animals in PcL rats. Additionally we demonstrated differential glial responses depending on the treatment, including astrogliosis in hypoxiated cerebella and a selective effect of hypoxia-ischemia on the vimentin-immunolabeled intermediate filaments of the Bergmann glia. Thus, while both glutamatergic and GABAergic cerebellar neurons are compromised by the hypoxic-ischemic insult, the former are protected by a <span class="hlt">preconditioning</span> hypoxia while the latter are not. PMID:25032984</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_18");'>18</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li class="active"><span>20</span></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_20 --> <div id="page_21" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li class="active"><span>21</span></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="401"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26505750','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26505750"><span id="translatedtitle">Sevoflurane <span class="hlt">Preconditioning</span> Reduces Intestinal Ischemia-Reperfusion Injury: Role of Protein Kinase C and Mitochondrial ATP-Sensitive Potassium Channel.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Liu, Chuiliang; Liu, Yanhui; Shen, Zhiwen; Miao, Liping; Zhang, Kun; Wang, Fei; Li, Yujuan</p> <p>2015-01-01</p> <p>Ischemic <span class="hlt">preconditioning</span> (IPC) has been considered to be a potential therapy to reduce ischemia-reperfusion injury (IRI) since the 1980s. Our previous study indicated that sevoflurane <span class="hlt">preconditioning</span> (SPC) also reduced intestinal IRI in rats. However, whether the protective effect of SPC is similar to IPC and the mechanisms of SPC are unclear. Thus, we compared the efficacy of SPC and IPC against intestinal IRI and the role of protein kinase C (PKC) and mitochondrial ATP-sensitive potassium channel (mKATP) in SPC. A rat model of intestinal IRI was used in this study. The superior mesenteric artery (SMA) was clamped for 60 min followed by 120 min of reperfusion. Rats with IPC underwent three cycles of SMA occlusion for 5 min and reperfusion for 5 min before intestinal ischemia. Rats with SPC inhaled sevoflurane at 0.5 minimum alveolar concentration (MAC) for 30 min before the intestinal ischemic insult. Additionally, the PKC inhibitor Chelerythrine (CHE) or mKATP inhibitor 5-Hydroxydecanoic (5-HD) was injected intraperitoneally before sevoflurane inhalation. Both SPC and IPC ameliorated intestinal IRI-induced histopathological changes, decreased Chiu's scores, reduced terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL) positive cells in the epithelium, and inhibited the expression of malondialdehyde (MDA) and tumor necrosis factor-? (TNF-?). These protective effects of SPC were similar to those of IPC. Pretreatment with PKC or mKATP inhibitor abolished SPC-induced protective effects by increasing Chiu's scores, down-regulated the expression of Bcl-2 and activated caspase-3. Our results suggest that pretreatment with 0.5 MAC sevoflurane is as effective as IPC against intestinal IRI. The activation of PKC and mKATP may be involved in the protective mechanisms of SPC. PMID:26505750</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4619554','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4619554"><span id="translatedtitle">Renoprotective Mechanism of Remote Ischemic <span class="hlt">Preconditioning</span> Based on Transcriptomic Analysis in a Porcine Renal Ischemia Reperfusion Injury Model</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kim, Sook Young; Cho, Young In; Lee, Kwang Suk; Kim, Kwang Hyun; Yang, Seung Choul; Han, Woong Kyu</p> <p>2015-01-01</p> <p>Ischemic <span class="hlt">preconditioning</span> (IPC) is a well-known phenomenon in which tissues are exposed to a brief period of ischemia prior to a longer ischemic event. This technique produces tissue tolerance to ischemia reperfusion injury (IRI). Currently, IPC’s mechanism of action is poorly understood. Using a porcine single kidney model, we performed remote IPC with renal IRI and evaluated the IPC mechanism of action. Following left nephrectomy, 15 female Yorkshire pigs were divided into three groups: no IPC and 90 minutes of warm ischemia (control), remote IPC immediately followed by 90 minutes of warm ischemia (rIPCe), and remote IPC with 90 minutes of warm ischemia performed 24 hours later (rIPCl). Differential gene expression analysis was performed using a porcine-specific microarray. The microarray analysis of porcine renal tissues identified 1,053 differentially expressed probes in <span class="hlt">preconditioned</span> pigs. Among these, 179 genes had altered expression in both the rIPCe and rIPCl groups. The genes were largely related to oxidation reduction, apoptosis, and inflammatory response. In the rIPCl group, an additional 848 genes had altered expression levels. These genes were primarily related to immune response and inflammation, including those coding for cytokines and cytokine receptors and those that play roles in the complement system and coagulation cascade. In the complement system, the membrane attack complex was determined to be sublytic, because it colocalized with phosphorylated extracellular signal-regulated kinase. Furthermore, alpha 2 macroglobulin, tissue plasminogen activator, uterine plasmin trypsin inhibitor, and arginase-1 mRNA levels were elevated in the rIPCl group. These findings indicate that remote IPC produces renoprotective effects through multiple mechanisms, and these effects develop over a long timeframe rather than immediately following IPC. PMID:26489007</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26322727','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26322727"><span id="translatedtitle">Combining climatic and geo-hydrological <span class="hlt">preconditions</span> as a method to determine world potential for aquifer thermal energy storage.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Bloemendal, Martin; Olsthoorn, Theo; van de Ven, Frans</p> <p>2015-12-15</p> <p>A heat pump combined with Aquifer Thermal Energy Storage (ATES) is proven technology to economically and sustainably provide space heating and cooling. The two most important <span class="hlt">preconditions</span> for the applicability of ATES are favorable climatic conditions and the availability of a suitable aquifer. This paper shows how these two <span class="hlt">preconditions</span> can be combined to identify where in the world ATES potential is present, or will become present as a consequence of climate change. Countries and regions are identified where regulation and stimulation measures may increase application of ATES technologies and thus help reduce CO2-emissions. Two types of data determine ATES suitability, and their combination with a 3rd identifies potential hot-spots in the world: 1) geo-hydrological conditions, 2) current and projected climate classification and 3) urbanization. Our method combines the data into an ATES-suitability score as explained in this paper. On the one hand the results confirm the suitability for ATES where it is already applied and on the other they identify places where the technology is or will become suitable. About 15% of urban population lived in areas with high potential for ATES at the start of the 21st century, but this figure will decrease to about 5% during the 21st century as a consequence of expected climate change. Around 50% of urban population currently lives in areas of medium ATES suitability, a percentage that will remain constant. Demand for ATES is likely to exceed available subsurface space in a significant part of the urban areas. PMID:26322727</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/cholesterol/prevention.htm','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/cholesterol/prevention.htm"><span id="translatedtitle">High Blood Cholesterol <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/bloodpressure/healthy_living.htm','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/bloodpressure/healthy_living.htm"><span id="translatedtitle"><span class="hlt">Preventing</span> High Blood Pressure</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/types/head-and-neck/patient/oral-prevention-pdq#section/all','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.gov/types/head-and-neck/patient/oral-prevention-pdq#section/all"><span id="translatedtitle">Oral Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Oral Cavity and Oropharyngeal Cancer Screening Research Oral Cavity and Oropharyngeal Cancer <span class="hlt">Prevention</span> (PDQ®) What is <span class="hlt">prevention</span>? ... and How to Quit General Information About Oral Cavity and Oropharyngeal Cancer Key Points Oral cavity cancer ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.aad.org/dermatology-a-to-z/diseases-and-treatments/a---d/bedbugs/tips','NIH-MEDLINEPLUS'); return false;" href="https://www.aad.org/dermatology-a-to-z/diseases-and-treatments/a---d/bedbugs/tips"><span id="translatedtitle">Bedbugs: Tips for <span class="hlt">Preventing</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Z Diseases and treatments A - D Bedbugs Tips Bedbugs: Tips for <span class="hlt">preventing</span> Travel tip : To <span class="hlt">prevent</span> bedbugs ... about a year without eating. Traveling: Check for bedbugs when you check in Many people get bedbugs ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://kidshealth.org/teen/your_body/skin_stuff/prevent_acne.html','NIH-MEDLINEPLUS'); return false;" href="http://kidshealth.org/teen/your_body/skin_stuff/prevent_acne.html"><span id="translatedtitle">Can I <span class="hlt">Prevent</span> Acne?</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Smart Snacking Losing Weight Safely Can I <span class="hlt">Prevent</span> Acne? KidsHealth > Teens > Body > Skin Stuff > Can I <span class="hlt">Prevent</span> ... this article? What Causes Acne? Treatments What Causes Acne? Contrary to what you may have heard, acne ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.preventblindness.org/','NIH-MEDLINEPLUS'); return false;" href="http://www.preventblindness.org/"><span id="translatedtitle"><span class="hlt">Prevent</span> Blindness America</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... How You Can Help About Us News <span class="hlt">Prevent</span> Blindness in your State Online Store Discussion Forum Planned ... Season Support the sight-saving work of <span class="hlt">Prevent</span> Blindness. Please Donate Vision Problems in the U.S. Prevalence ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/antioxidants-fact-sheet','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/antioxidants-fact-sheet"><span id="translatedtitle">Antioxidants and Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Partners & Collaborators Spotlight on Scientists Research Areas Cancer Biology Cancer Genomics Causes of Cancer Diagnosis <span class="hlt">Prevention</span> Screening & ... Collaborators Spotlight on Scientists NCI Research Areas Cancer Biology Cancer Genomics Causes of Cancer Diagnosis <span class="hlt">Prevention</span> Screening & ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.hrsonline.org/Patient-Resources/Risk-Factors-Prevention','NIH-MEDLINEPLUS'); return false;" href="http://www.hrsonline.org/Patient-Resources/Risk-Factors-Prevention"><span id="translatedtitle">Risk Factors and <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... atherosclerosis (“clogged” arteries) and High Blood Pressure . <span class="hlt">Preventing</span> Arrhythmias and Heart Disease <span class="hlt">Prevent</span> heart disease by lowering ... cholesterol, diabetes, and thyroid disease. Risk Factors For Arrhythmias and Heart Disease The following conditions can increase ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://kidshealth.org/teen/your_body/beautiful/prevent_acne.html','NIH-MEDLINEPLUS'); return false;" href="http://kidshealth.org/teen/your_body/beautiful/prevent_acne.html"><span id="translatedtitle">Can I <span class="hlt">Prevent</span> Acne?</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Myths About Acne Peer Pressure Can I <span class="hlt">Prevent</span> Acne? KidsHealth > Teens > Body > Skin Stuff > Can I <span class="hlt">Prevent</span> ... this article? What Causes Acne? Treatments What Causes Acne? Contrary to what you may have heard, acne ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://womenshealth.gov/hiv-aids/preventing-hiv-infection/preventing-hiv-with-medicine.html','NIH-MEDLINEPLUS'); return false;" href="http://womenshealth.gov/hiv-aids/preventing-hiv-infection/preventing-hiv-with-medicine.html"><span id="translatedtitle"><span class="hlt">Preventing</span> HIV with Medicine</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... information in Spanish ( en español ) <span class="hlt">Preventing</span> HIV with medicine Get medicine right after you are exposed to ... to top More information on <span class="hlt">Preventing</span> HIV with medicine Explore other publications and websites National HIV and ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.bioeng.ucla.edu/wp-content/uploads/bioeng/HSSEAS-Bioengineering-IIPP-Rev-Apr-2015-MBS1.pdf','EPRINT'); return false;" href="http://www.bioeng.ucla.edu/wp-content/uploads/bioeng/HSSEAS-Bioengineering-IIPP-Rev-Apr-2015-MBS1.pdf"><span id="translatedtitle">Injury & Illness <span class="hlt">Prevention</span> Program</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Levine, Alex J.</p> <p></p> <p>Injury & Illness <span class="hlt">Prevention</span> Program (IIPP) Manual Henry Samueli School of Engineering & Applied Bioengineering IIPP i April 2015 Injury & Illness <span class="hlt">Prevention</span> Program Henry Samueli School of Engineering ............................................................5-1 Section 6: Incident, Injury & Illness Reporting and Investigations</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/cancer/cervical/basic_info/infographic.htm','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/cancer/cervical/basic_info/infographic.htm"><span id="translatedtitle"><span class="hlt">Prevent</span> Cervical Cancer</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... professional printing [PDF-1.5MB] Cancer Home “<span class="hlt">Prevent</span> Cervical Cancer” Infographic Language: English Español (Spanish) Recommend on Facebook Tweet Share Compartir <span class="hlt">Prevent</span> Cervical Cancer with the Right Test at the Right Time ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.healthychildren.org/English/health-issues/conditions/skin/Pages/Sunburn-Treatment-and-Prevention.aspx','NIH-MEDLINEPLUS'); return false;" href="https://www.healthychildren.org/English/health-issues/conditions/skin/Pages/Sunburn-Treatment-and-Prevention.aspx"><span id="translatedtitle">Sunburn: Treatment and <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Text Size Email Print Share Sunburn: Treatment and <span class="hlt">Prevention</span> Article Body While those with darker skin coloring ... by your pediatrician or the nearest emergency facility. <span class="hlt">Prevention</span> Many parents incorrectly assume that the sun is ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26359087','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26359087"><span id="translatedtitle">Diazoxide <span class="hlt">preconditioning</span> of endothelial progenitor cells from streptozotocin-induced type 1 diabetic rats improves their ability to repair diabetic cardiomyopathy.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ali, Muhammad; Mehmood, Azra; Anjum, Muhammad Sohail; Tarrar, Moazzam Nazir; Khan, Shaheen N; Riazuddin, Sheikh</p> <p>2015-12-01</p> <p>Type 1 diabetes mellitus (DM) is a strong risk factor for the development of diabetic cardiomyopathy (DCM) which is the leading cause of morbidity and mortality in the type 1 diabetic patients. Stem cells may act as a therapeutic agent for the repair of DCM. However, deteriorated functional abilities and survival of stem cells derived from type 1 diabetic subjects need to be overcome for obtaining potential outcome of the stem cell therapy. Diazoxide (DZ) a highly selective mitochondrial ATP-sensitive K(+) channel opener has been previously shown to improve the ability of mesenchymal stem cells for the repair of heart failure. In the present study, we evaluated the effects of DZ <span class="hlt">preconditioning</span> in improving the ability of streptozotocin-induced type 1 diabetes affected bone marrow-derived endothelial progenitor cells (DM-EPCs) for the repair of DCM in the type 1 diabetic rats. DM-EPCs were characterized by immunocytochemistry, flow cytometry, and reverse transcriptase PCR for endothelial cell-specific markers like vWF, VE cadherin, VEGFR2, PECAM, CD34, and eNOS. In vitro studies included <span class="hlt">preconditioning</span> of DM-EPCs with 200 ?M DZ for 30 min followed by exposure to either 200 ?M H2O2 for 2 h (for oxidative stress induction) or 30 mM glucose media (for induction of hyperglycemic stress) for 48 h. Non-<span class="hlt">preconditioned</span> EPCs with and without exposure to H2O2 and 30 mM high glucose served as controls. These cells were then evaluated for survival (by MTT and XTT cell viability assays), senescence, paracrine potential (by ELISA for VEGF), and alteration in gene expression [VEGF, stromal derived factor-1? (SDF-1?), HGF, bFGF, Bcl2, and Caspase-3]. DZ <span class="hlt">preconditioned</span> DM-EPCs demonstrated significantly increased survival and VEGF release while reduced cell injury and senescence. Furthermore, DZ <span class="hlt">preconditioned</span> DM-EPCs exhibited up-regulated expression of prosurvival genes (VEGF, SDF-1?, HGF, bFGF, and Bcl2) on exposure to H2O2, and VEGF and Bcl2 on exposure to hyperglycemia while down regulation of Caspase-3 gene. Eight weeks after type 1 diabetes induction, DZ <span class="hlt">preconditioned</span>, and non-<span class="hlt">preconditioned</span> DM-EPCs were transplanted into left ventricle of diabetic rats (at a dose of 2 × 10(6) DM-EPCs/70 ?l serum free medium). After 4 weeks, DZ <span class="hlt">preconditioned</span> DM-EPCs transplantation improved cardiac function as assessed by Millar's apparatus. There was decrease in collagen content estimated by Masson's trichrome and sirius red staining. Furthermore, reduced cell injury was observed as evidenced by decreased expression of Caspase-3 and increased expression of prosurvival genes Bcl2, VEGF, and bFGF by semi-quantitative real-time PCR. In conclusion, the present study demonstrated that DZ <span class="hlt">preconditioning</span> enhanced EPCs survival under oxidative and hyperglycemic stress and their ability to treat DCM. PMID:26359087</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2936581','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2936581"><span id="translatedtitle">The Suicide <span class="hlt">Prevention</span> Continuum</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Caldwell, Dawn</p> <p>2010-01-01</p> <p>The suicide <span class="hlt">prevention</span> continuum illustrates a practical approach to the complex issue of suicide <span class="hlt">prevention</span>. The continuum evolved from discussions with two Aboriginal communities in Atlantic Canada about suicide and the different types of interventions available. The continuum offers a framework and reference tool to differentiate between the different stages of suicide risk. It illustrates where the Aboriginal Community Youth Resilience Network (ACYRN) fits into suicide <span class="hlt">prevention</span> and how it contributes to <span class="hlt">prevention</span> knowledge, capacity building, and policy development. PMID:20835376</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=Wildfires&pg=3&id=ED472789','ERIC'); return false;" href="http://eric.ed.gov/?q=Wildfires&pg=3&id=ED472789"><span id="translatedtitle">Wildfire <span class="hlt">Prevention</span> Strategies.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>National Wildlife Coordinating Group, Boise, ID.</p> <p></p> <p>This document provides information and guidance on wildfire <span class="hlt">prevention</span> strategies. Chapters include: (1) "Introduction"; (2) "How to Use this Guide"; (3) "Fire Cause Classification"; (4) "Relative Effectiveness"; (5) "Degree of Difficulty"; (6) "Intervention Techniques"; (7) "<span class="hlt">Prevention</span> Activities"; (8) "Sample <span class="hlt">Prevention</span> Strategies"; and (9)…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=42462&keyword=energy+AND+conservation+AND+methods&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=53504583&CFTOKEN=12733101','EPA-EIMS'); return false;" href="http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=42462&keyword=energy+AND+conservation+AND+methods&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=53504583&CFTOKEN=12733101"><span id="translatedtitle">FACILITY POLLUTION <span class="hlt">PREVENTION</span> GUIDE</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>The U.S. Environmental Protection Agency (U.S. EPA) has developed the Facility Pollution <span class="hlt">Prevention</span> Guide for those who are interested in and responsible for pollution <span class="hlt">prevention</span> in industrial or service facilities. t summarizes the benefits of a company-wide pollution <span class="hlt">prevention</span>...</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_19");'>19</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li class="active"><span>21</span></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_21 --> <div id="page_22" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li class="active"><span>22</span></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="421"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.socialwork.lsu.edu/downloads/researchinitiatives/lpi/CPPC%20Implementation%20Plan%202009.pdf','EPRINT'); return false;" href="http://www.socialwork.lsu.edu/downloads/researchinitiatives/lpi/CPPC%20Implementation%20Plan%202009.pdf"><span id="translatedtitle">Child Povertyy <span class="hlt">Prevention</span> Council</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Harms, Kyle E.</p> <p></p> <p>Child Povertyy <span class="hlt">Prevention</span> Council for Louisianafor Louisiana Implementation Plan February 2009eb ua In response to ACT 559 of the 2008 Regular Session of the Louisiana Legislature #12;Child Poverty <span class="hlt">Prevention</span> Council for Louisiana Implementation Plan ­ 2009 #12;Child Poverty <span class="hlt">Prevention</span> Council for Louisiana 3</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=release+AND+stress&pg=5&id=ED251747','ERIC'); return false;" href="http://eric.ed.gov/?q=release+AND+stress&pg=5&id=ED251747"><span id="translatedtitle">Suicide <span class="hlt">Prevention</span> Triangle.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Cutter, Fred</p> <p></p> <p>This manual provides resource tools and strategies to enhance the suicide <span class="hlt">prevention</span> capabilities of health professionals and the health care setting in which care is provided. In the first section, terms are defined and the suicide <span class="hlt">prevention</span> triangle model is described. Applications of the model and good practices for suicide <span class="hlt">prevention</span> in any…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=Dysentery&id=ED121956','ERIC'); return false;" href="http://eric.ed.gov/?q=Dysentery&id=ED121956"><span id="translatedtitle"><span class="hlt">Prevention</span> of Food Poisoning.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Army Quartermaster School, Ft. Lee, VA.</p> <p></p> <p>The programed text provides a single lesson, four-hour, correspondence subcourse on the <span class="hlt">prevention</span> of food poisoning. It covers the following areas: a definition of food poisoning; chemical food poisoning; biological food poisoning; causes and <span class="hlt">prevention</span> of trichinosis; six factors controlling bacteria growth; bacterial infection; <span class="hlt">prevention</span> of…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED102384.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED102384.pdf"><span id="translatedtitle">Fire <span class="hlt">Prevention</span> Education.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Ehmann, Jeanne; Claus, William C.</p> <p></p> <p>The fire <span class="hlt">prevention</span> education bulletin helps schools continue their work to make the home, school, and community safe places in which to live and to help children and young people live in safe ways without developing undue fears. Briefly discussed are the goals of a fire <span class="hlt">prevention</span> program, who should be concerned with fire <span class="hlt">prevention</span> education,…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.chem.ucr.edu/documents/safetyinformation/injuryandillnesspreventionplan.pdf','EPRINT'); return false;" href="http://www.chem.ucr.edu/documents/safetyinformation/injuryandillnesspreventionplan.pdf"><span id="translatedtitle">INJURY & ILLNESS <span class="hlt">PREVENTION</span> PLAN</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Reed, Christopher A.</p> <p></p> <p>INJURY & ILLNESS <span class="hlt">PREVENTION</span> PLAN (IIPP) University of California Riverside (UCR) Injury & Illness) Title 8, Section 3203. University of California Riverside #12;Injury & Illness <span class="hlt">Prevention</span> Plan and Illness <span class="hlt">Prevention</span> Plan (IIPP) this document... Template online at http://ehs.ucr.edu under the Programs</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4590236','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4590236"><span id="translatedtitle">Exercise <span class="hlt">preconditioning</span> exhibits neuroprotective effects on hippocampal CA1 neuronal damage after cerebral ischemia</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Shamsaei, Nabi; Khaksari, Mehdi; Erfani, Sohaila; Rajabi, Hamid; Aboutaleb, Nahid</p> <p>2015-01-01</p> <p>Recent evidence has suggested the neuroprotective effects of physical exercise on cerebral ischemic injury. However, the role of physical exercise in cerebral ischemia-induced hippocampal damage remains controversial. The aim of the present study was to evaluate the effects of pre-ischemia treadmill training on hippocampal CA1 neuronal damage after cerebral ischemia. Male adult rats were randomly divided into control, ischemia and exercise + ischemia groups. In the exercise + ischemia group, rats were subjected to running on a treadmill in a designated time schedule (5 days per week for 4 weeks). Then rats underwent cerebral ischemia induction through occlusion of common carotids followed by reperfusion. At 4 days after cerebral ischemia, rat learning and memory abilities were evaluated using passive avoidance memory test and rat hippocampal neuronal damage was detected using Nissl and TUNEL staining. Pre-ischemic exercise significantly reduced the number of TUNEL-positive cells and necrotic cell death in the hippocampal CA1 region as compared to the ischemia group. Moreover, pre-ischemic exercise significantly <span class="hlt">prevented</span> ischemia-induced memory dysfunction. Pre-ischemic exercise mighct <span class="hlt">prevent</span> memory deficits after cerebral ischemia through rescuing hippocampal CA1 neurons from ischemia-induced degeneration. PMID:26487851</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24618542','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24618542"><span id="translatedtitle">Hypoxia <span class="hlt">preconditioning</span> increases survival and decreases expression of Toll-like receptor 4 in pulmonary artery endothelial cells exposed to lipopolysaccharide.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ali, Irshad; Nanchal, Rahul; Husnain, Fouad; Audi, Said; Konduri, G Ganesh; Densmore, John C; Medhora, Meetha; Jacobs, Elizabeth R</p> <p>2013-09-01</p> <p>Abstract Pulmonary or systemic infections and hypoxemic respiratory failure are among the leading causes of admission to intensive care units, and these conditions frequently exist in sequence or in tandem. Inflammatory responses to infections are reproduced by lipopolysaccharide (LPS) engaging Toll-like receptor 4 (TLR4). Apoptosis is a hallmark of lung injury in sepsis. This study was conducted to determine whether preexposure to LPS or hypoxia modulated the survival of pulmonary artery endothelial cells (PAECs). We also investigated the role TLR4 receptor expression plays in apoptosis due to these conditions. Bovine PAECs were cultured in hypoxic or normoxic environments and treated with LPS. TLR4 antagonist TAK-242 was used to probe the role played by TLR4 receptors in cell survival. Cell apoptosis and survival were measured by caspase 3 activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) incorporation. TLR4 expression and tumor necrosis factor ? (TNF-?) production were also determined. LPS increased caspase 3 activity in a TAK-242-sensitive manner and decreased MTT incorporation. Apoptosis was decreased in PAECs <span class="hlt">preconditioned</span> with hypoxia prior to LPS exposure. LPS increased TNF-? production, and hypoxic <span class="hlt">preconditioning</span> blunted it. Hypoxic <span class="hlt">preconditioning</span> reduced LPS-induced TLR4 messenger RNA and TLR4 protein. TAK-242 decreased to baseline the LPS-stimulated expression of TLR4 messenger RNA regardless of environmental conditions. In contrast, LPS followed by hypoxia substantially increased apoptosis and cell death. In conclusion, protection from LPS-stimulated PAEC apoptosis by hypoxic <span class="hlt">preconditioning</span> is attributable in part to reduction in TLR4 expression. If these signaling pathways apply to septic patients, they may account for differing sensitivities of individuals to acute lung injury depending on oxygen tensions in PAECs in vivo. PMID:24618542</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4070795','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4070795"><span id="translatedtitle">Hypoxia <span class="hlt">preconditioning</span> increases survival and decreases expression of Toll-like receptor 4 in pulmonary artery endothelial cells exposed to lipopolysaccharide</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Nanchal, Rahul; Audi, Said; Konduri, G. Ganesh; Medhora, Meetha</p> <p>2013-01-01</p> <p>Abstract Pulmonary or systemic infections and hypoxemic respiratory failure are among the leading causes of admission to intensive care units, and these conditions frequently exist in sequence or in tandem. Inflammatory responses to infections are reproduced by lipopolysaccharide (LPS) engaging Toll-like receptor 4 (TLR4). Apoptosis is a hallmark of lung injury in sepsis. This study was conducted to determine whether preexposure to LPS or hypoxia modulated the survival of pulmonary artery endothelial cells (PAECs). We also investigated the role TLR4 receptor expression plays in apoptosis due to these conditions. Bovine PAECs were cultured in hypoxic or normoxic environments and treated with LPS. TLR4 antagonist TAK-242 was used to probe the role played by TLR4 receptors in cell survival. Cell apoptosis and survival were measured by caspase 3 activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) incorporation. TLR4 expression and tumor necrosis factor ? (TNF-?) production were also determined. LPS increased caspase 3 activity in a TAK-242-sensitive manner and decreased MTT incorporation. Apoptosis was decreased in PAECs <span class="hlt">preconditioned</span> with hypoxia prior to LPS exposure. LPS increased TNF-? production, and hypoxic <span class="hlt">preconditioning</span> blunted it. Hypoxic <span class="hlt">preconditioning</span> reduced LPS-induced TLR4 messenger RNA and TLR4 protein. TAK-242 decreased to baseline the LPS-stimulated expression of TLR4 messenger RNA regardless of environmental conditions. In contrast, LPS followed by hypoxia substantially increased apoptosis and cell death. In conclusion, protection from LPS-stimulated PAEC apoptosis by hypoxic <span class="hlt">preconditioning</span> is attributable in part to reduction in TLR4 expression. If these signaling pathways apply to septic patients, they may account for differing sensitivities of individuals to acute lung injury depending on oxygen tensions in PAECs in vivo. PMID:24618542</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://adsabs.harvard.edu/abs/2013GeoJI.194.1250K','NASAADS'); return false;" href="http://adsabs.harvard.edu/abs/2013GeoJI.194.1250K"><span id="translatedtitle">On acoustic waveform tomography of wide-angle OBS data—strategies for <span class="hlt">pre-conditioning</span> and inversion</span></a></p> <p><a target="_blank" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p>Kamei, R.; Pratt, R. G.; Tsuji, T.</p> <p>2013-08-01</p> <p>We successfully apply the acoustic Laplace-Fourier waveform tomography method to delineate P-wave velocity structures of the mega-splay fault system in the central part of the seismogenic Nankai subduction zone offshore Japan, using densely sampled wide-angle ocean bottom seismograph (OBS) data originally acquired in 2004. Our success is due to new and carefully designed data <span class="hlt">preconditioning</span> and inversion strategies to mitigate (i) the well-known non-linearity of waveform inversion, (ii) the challenges arising from crustal-scale survey designs (e.g. undersampling of the OBSs), and (iii) modelling errors due to the use of the acoustic assumption. We identify a sixfold set of key components that together lead to the success of the high-resolution waveform tomography image: (i) Availability of low-frequency components (starting at 2.25 Hz) reducing the non-linearity, and access to large offset data (up to 55 km) increasing the depth of illumination and the recovery of low wavenumber components. (ii) A highly accurate traveltime tomography result (with an rms error of approximately 60 ms) that further mitigates the non-linearity. (iii) A hierarchical inversion approach in which phase spectra are inverted first to reduce artefacts from the acoustic assumption, and amplitude information is only incorporated in the final stages. (iv) A Laplace-Fourier domain approach that facilitates a multiscale approach to mitigate non-linearity by restricting the inversion to the low frequency components and early arrivals first, and sequentially including higher frequencies and later arrivals. (v) A <span class="hlt">pre-conditioning</span> strategy for eliminating undesirable high wavenumber components from the the gradient. (vi) A strategy for source estimation that reduce the influence of the instrumental design. In the OBS case study used for illustration purposes, Laplace-Fourier waveform tomography retrieves velocity anomalies as small as 700 m (horizontally) and 350 m (vertically) above the top of the Philippine Sea Plate. The resulting velocity structures include low-velocity zones and thrust structures which have not been previously identified clearly. The velocity models are validated by scrutiny of synthetic and observed waveforms, by evaluating the coherency of source estimates, and by comparison with 3-D pre-stack migrated (PreSDM) images. Chequerboard tests and point-scatter tests demonstrate both the reliability and the limitations of the acoustic implementation.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.nhlbi.nih.gov/health/health-topics/topics/hbp/prevention','NIH-MEDLINEPLUS'); return false;" href="http://www.nhlbi.nih.gov/health/health-topics/topics/hbp/prevention"><span id="translatedtitle"><span class="hlt">Prevention</span> of High Blood Pressure</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... page from the NHLBI on Twitter. <span class="hlt">Prevention</span> of High Blood Pressure Healthy lifestyle habits, proper use of medicines, and ... <span class="hlt">prevent</span> high blood pressure or its complications. <span class="hlt">Preventing</span> High Blood Pressure Onset Healthy lifestyle habits can help <span class="hlt">prevent</span> high ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://familydoctor.org/familydoctor/en/prevention-wellness/staying-healthy/healthy-living/preventive-services-for-healthy-living.printerview.all.html','NIH-MEDLINEPLUS'); return false;" href="http://familydoctor.org/familydoctor/en/prevention-wellness/staying-healthy/healthy-living/preventive-services-for-healthy-living.printerview.all.html"><span id="translatedtitle"><span class="hlt">Preventive</span> Services for Healthy Living</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>MENU Return to Web version <span class="hlt">Preventive</span> Services for Healthy Living <span class="hlt">Preventive</span> Services for Healthy Living How can my doctor help me stay healthy? ... <span class="hlt">preventive</span> service"? A <span class="hlt">preventive</span> service might be a test, or it might be advice from your doctor. ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/1062744','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/1062744"><span id="translatedtitle">A Parallel, Fully Coupled, Fully Implicit Solution to Reactive Transport in Porous Media Using the <span class="hlt">Preconditioned</span> Jacobian-Free Newton-Krylov Method</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Luanjing Guo; Hai Huang; Derek Gaston; Cody Permann; David Andrs; George Redden; Chuan Lu; Don Fox; Yoshiko Fujita</p> <p>2013-03-01</p> <p>Modeling large multicomponent reactive transport systems in porous media is particularly challenging when the governing partial differential algebraic equations (PDAEs) are highly nonlinear and tightly coupled due to complex nonlinear reactions and strong solution-media interactions. Here we present a <span class="hlt">preconditioned</span> Jacobian-Free Newton-Krylov (JFNK) solution approach to solve the governing PDAEs in a fully coupled and fully implicit manner. A well-known advantage of the JFNK method is that it does not require explicitly computing and storing the Jacobian matrix during Newton nonlinear iterations. Our approach further enhances the JFNK method by utilizing physics-based, block <span class="hlt">preconditioning</span> and a multigrid algorithm for efficient inversion of the preconditioner. This <span class="hlt">preconditioning</span> strategy accounts for self- and optionally, cross-coupling between primary variables using diagonal and off-diagonal blocks of an approximate Jacobian, respectively. Numerical results are presented demonstrating the efficiency and massive scalability of the solution strategy for reactive transport problems involving strong solution-mineral interactions and fast kinetics. We found that the physics-based, block preconditioner significantly decreases the number of linear iterations, directly reducing computational cost; and the strongly scalable algebraic multigrid algorithm for approximate inversion of the preconditioner leads to excellent parallel scaling performance.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2145456','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2145456"><span id="translatedtitle">Values in <span class="hlt">Preventive</span> Medicine</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hoffmaster, Barry</p> <p>1992-01-01</p> <p>We know how lifestyle affects health, yet concern for <span class="hlt">preventing</span> illness by promoting healthy lifestyles remains marginal in medical practice. Effective <span class="hlt">preventive</span> strategies can raise daunting moral and political problems about the extent to which individual freedoms may be infringed, particularly on paternalistic grounds. Evaluative questions also arise about more specific matters, such as identifying risk and causal factors, determining what level of risk is acceptable, and deciding how compelling the evidence must be to take <span class="hlt">preventive</span> action. PMID:11651426</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://researchtoreality.cancer.gov/sites/default/files/Laing_PCD_HealthLinks%20pilot_2012.pdf','NCI'); return false;" href="https://researchtoreality.cancer.gov/sites/default/files/Laing_PCD_HealthLinks%20pilot_2012.pdf"><span id="translatedtitle"><span class="hlt">Preventing</span> Chronic Disease</span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p><span class="hlt">Preventing</span> Chronic Disease (PCD) is a peer-reviewed electronic journal established by the National Center for Chronic Disease <span class="hlt">Prevention</span> and Health Promotion to address the interface between applied public health research, practice, and policy. Articles focus on <span class="hlt">preventing</span> and controlling chronic diseases and conditions, promoting health, and examining the biological, behavioral, physical, and social determinants of health and their impact on quality of life, morbidity, and mortality across the life span.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www-ehs.ucsd.edu/ih/hazaware_contractors.pdf','EPRINT'); return false;" href="http://www-ehs.ucsd.edu/ih/hazaware_contractors.pdf"><span id="translatedtitle">awareness and pollution <span class="hlt">prevention</span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Aluwihare, Lihini</p> <p></p> <p>..............................................5 Storm Water Pollution <span class="hlt">Prevention</span>.....................5 Sanitary Sewer System Management.................................................................. 12 Lead-Based Paint Awareness............................ 13 Reproductive Hazards in the Workplace</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4492986','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4492986"><span id="translatedtitle"><span class="hlt">Preconditioning</span> L6 Muscle Cells with Naringin Ameliorates Oxidative Stress and Increases Glucose Uptake</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Dhanya, R.; Arun, K. B.; Nisha, V. M.; Syama, H. P.; Nisha, P.; Santhosh Kumar, T. R.; Jayamurthy, P.</p> <p>2015-01-01</p> <p>Enhanced oxidative stress contributes to pathological changes in diabetes and its complications. Thus, strategies to reduce oxidative stress may alleviate these pathogenic processes. Herein, we have investigated Naringin mediated regulation of glutathione (GSH) & intracellular free radical levels and modulation of glucose uptake under oxidative stress in L6 cell lines. The results from the study demonstrated a marked decrease in glutathione with a subsequent increase in free radical levels, which was reversed by the pretreatment of Naringin. We also observed that the increased malondialdehyde level, the marker of lipid peroxidation on induction of oxidative stress was retrieved on Naringin pretreatment. Addition of Naringin (100 ?M) showed approximately 40% reduction in protein glycation in vitro. Furthermore, we observed a twofold increase in uptake of fluorescent labeled glucose namely 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose (2 - NBDG) on Naringin treatment in differentiated L6 myoblast. The increased uptake of 2-NBDG by L6 myotubes may be attributed due to the enhanced translocation of GLUT4. Our results demonstrate that Naringin activate GSH synthesis through a novel antioxidant defense mechanism against excessive Reactive Oxygen Species (ROS) production, contributing to the <span class="hlt">prevention</span> of oxidative damage in addition to its effect on glycemic control. PMID:26147673</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/355499','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/355499"><span id="translatedtitle">Risk reduction during chemical flooding: <span class="hlt">Preconditioning</span> DNAPL density in situ prior to recovery by miscible displacement</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Lunn, S.R.D.; Kueper, B.H.</p> <p>1999-05-15</p> <p>Dense, nonaqueous phase liquids (DNAPLs) are separate phase compounds that commonly contaminate groundwater supplies. Miscible displacement methods using surfactants and alcohols to recover the DNAPLs have been proposed, but concerns have been raised about mobilizing the DNAPLs deeper into previously uncontaminated media. In this paper, the concerns are addressed by reducing DNAPL density prior to elimination of interfacial tension. Laboratory-measured equilibrium phase behavior demonstrates the ability of 2-butanol to reverse the density contrast between tetrachloroethene (PCE) and water prior to miscibility, resulting in a DNAPL phase less dense than the aqueous phase. Laboratory experiments using an upward gradient flow cell demonstrate that 2-butanol, introduced as an aqueous solution to a PCE pool suspended within a water-saturated sandpack, partitions strongly into the PCE. Pools of PCE exposed to 1 pore volume of water saturated with 2-butanol and subsequently recovered by miscible displacements with 1-propanol showed that between 56.6% and 97.6% of the DNAPL mass was recovered for total alcohol /complements of between 0.24 and 1.0 pore volume. In all two-phase samples produced, the NAPL phase was less dense than the aqueous phase. Analysis of a static DNAPL pool shows that the use of a 2-butanol preflood may <span class="hlt">prevent</span> the downward mobilization predicted to occur for more conventional alcohol floods.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/22202407','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/22202407"><span id="translatedtitle">Brief exposure to carbon monoxide <span class="hlt">preconditions</span> cardiomyogenic cells against apoptosis in ischemia-reperfusion</span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>Kondo-Nakamura, Mihoko; Shintani-Ishida, Kaori; Uemura, Koichi; Yoshida, Ken-ichi</p> <p>2010-03-12</p> <p>We examined whether and how pretreatment with carbon monoxide (CO) <span class="hlt">prevents</span> apoptosis of cardioblastic H9c2 cells in ischemia-reperfusion. Reperfusion (6 h) following brief ischemia (10 min) induced cytochrome c release, activation of caspase-9 and caspase-3, and apoptotic nuclear condensation. Brief CO pretreatment (10 min) or a caspase-9 inhibitor (Z-LEHD-FMK) attenuated these apoptotic changes. Ischemia-reperfusion increased phosphorylation of Akt at Ser472/473/474, and this was enhanced by CO pretreatment. A specific Akt inhibitor (API-2) blunted the anti-apoptotic effects of CO in reperfusion. In normoxic cells, CO enhanced O{sub 2}{sup -} generation, which was inhibited by a mitochondrial complex III inhibitor (antimycin A) but not by a NADH oxidase inhibitor (apocynin). The CO-enhanced Akt phosphorylation was suppressed by an O{sub 2}{sup -} scavenger (Tiron), catalase or a superoxide dismutase (SOD) inhibitor (DETC). These results suggest that CO pretreatment induces mitochondrial generation of O{sub 2}{sup -}, which is then converted by SOD to H{sub 2}O{sub 2}, and subsequent Akt activation by H{sub 2}O{sub 2} attenuates apoptosis in ischemia-reperfusion.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24426021','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24426021"><span id="translatedtitle">Chemical composition and physical quality characteristics of Ghanaian cocoa beans as affected by pulp <span class="hlt">pre-conditioning</span> and fermentation.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Afoakwa, Emmanuel Ohene; Quao, Jennifer; Takrama, Jemmy; Budu, Agnes Simpson; Saalia, Firibu Kwesi</p> <p>2013-12-01</p> <p>Investigations were conducted to evaluate the effects of pod storage (as a means of pulp <span class="hlt">preconditioning</span>) and fermentation on the chemical composition and physical characteristics of Ghanaian cocoa beans. A 4?×?2 full factorial design with factors as pod storage (0, 7, 14, 21 days) and cocoa treatment (fermented and unfermented) were conducted. Samples were analyzed for their chemical composition (moisture, crude fat, crude protein, ash and carbohydrate content) and mineral content using standard analytical methods. The physical qualities of the beans were analyzed for their proportions of cocoa nibs, shells and germ. Fermentation and increasing pod storage resulted in significant (P?<?0.05) decreases in ash (3.48-2.92%), protein (21.63-17.62%) and fat (55.21-50.40%) content of the beans while carbohydrate content increased from 15.47% to 24.93% with both treatments. As well, increasing pod storage and fermentation significantly (P?<?0.05) increased the copper content of the beans from while reductions in Mg and K occurred. Amongst the minerals studied, potassium was the most abundant mineral followed by magnesium, phosphorus and calcium in the fermented cocoa beans. Proportion of cocoa nibs also increased from with increasing pod storage and fermentation whiles reductions in shell content and no appreciable changes in germ proportions were noted. PMID:24426021</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/23537951','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/23537951"><span id="translatedtitle">Hyperbaric oxygen <span class="hlt">preconditioning</span> attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Soejima, Yoshiteru; Hu, Qin; Krafft, Paul R; Fujii, Mutsumi; Tang, Jiping; Zhang, John H</p> <p>2013-09-01</p> <p>Hyperglycemia dramatically aggravates brain infarct and hemorrhagic transformation (HT) after ischemic stroke. Oxidative stress and matrix metalloproteinases (MMPs) play an important role in the pathophysiology of HT. Hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) has been proved to decrease oxidative stress and has been demonstrated to be neuroprotective in experimental stroke models. The present study determined whether HBO-PC would ameliorate HT by a pre-ischemic increase of reactive oxygen species (ROS) generation, and a suppression of MMP-2 and MMP-9 in hyperglycemic middle cerebral artery occlusion (MCAO) rats. Rats were pretreated with HBO (100% O?, 2.5 atmosphere absolutes) 1 h daily for 5 days before MCAO. Acute hyperglycemia was induced by an injection of 50% dextrose. Neurological deficits, infarction volume and hemorrhagic volume were assessed 24 h and 7 days after ischemia. ROS scavenger n-acetyl cysteine (NAC), hypoxia-inducible factor-1? (HIF-1?), inhibitor 2-methoxyestradiol (2ME2) and activator cobalt chloride (CoCl?), and MMP inhibitor SB-3CT were administrated for mechanism study. The activity of MMP-2 and MMP-9, and the expression HIF-1? were measured. HBO-PC improved neurological deficits, and reduced hemorrhagic volume; the expression of HIF-1? was significantly decreased, and the activity of MMP-2 and MMP-9 was reduced by HBO-PC compared with vehicle group. Our results suggested that HBO-PC attenuated HT via decreasing HIF-1? and its downstream MMP-2 and MMP-9 in hyperglycemic MCAO rats. PMID:23537951</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_20");'>20</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li class="active"><span>22</span></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_22 --> <div id="page_23" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li class="active"><span>23</span></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="441"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/25261534','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/25261534"><span id="translatedtitle">Interaction of risk factors, comorbidities, and comedications with ischemia/reperfusion injury and cardioprotection by <span class="hlt">preconditioning</span>, postconditioning, and remote conditioning.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Ferdinandy, Péter; Hausenloy, Derek J; Heusch, Gerd; Baxter, Gary F; Schulz, Rainer</p> <p>2014-10-01</p> <p>Pre-, post-, and remote conditioning of the myocardium are well described adaptive responses that markedly enhance the ability of the heart to withstand a prolonged ischemia/reperfusion insult and provide therapeutic paradigms for cardioprotection. Nevertheless, more than 25 years after the discovery of ischemic <span class="hlt">preconditioning</span>, we still do not have established cardioprotective drugs on the market. Most experimental studies on cardioprotection are still undertaken in animal models, in which ischemia/reperfusion is imposed in the absence of cardiovascular risk factors. However, ischemic heart disease in humans is a complex disorder caused by, or associated with, cardiovascular risk factors and comorbidities, including hypertension, hyperlipidemia, diabetes, insulin resistance, heart failure, altered coronary circulation, and aging. These risk factors induce fundamental alterations in cellular signaling cascades that affect the development of ischemia/reperfusion injury per se and responses to cardioprotective interventions. Moreover, some of the medications used to treat these risk factors, including statins, nitrates, and antidiabetic drugs, may impact cardioprotection by modifying cellular signaling. The aim of this article is to review the recent evidence that cardiovascular risk factors and their medication may modify the response to cardioprotective interventions. We emphasize the critical need to take into account the presence of cardiovascular risk factors and concomitant medications when designing preclinical studies for the identification and validation of cardioprotective drug targets and clinical studies. This will hopefully maximize the success rate of developing rational approaches to effective cardioprotective therapies for the majority of patients with multiple risk factors. PMID:25261534</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/23103716','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/23103716"><span id="translatedtitle">Dietary polyphenols <span class="hlt">preconditioning</span> protects 3T3-L1 preadipocytes from mitochondrial alterations induced by oxidative stress.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Baret, Pascal; Septembre-Malaterre, Axelle; Rigoulet, Michel; Lefebvre d'Hellencourt, Christian; Priault, Muriel; Gonthier, Marie-Paule; Devin, Anne</p> <p>2013-01-01</p> <p>Numerous studies indicate that an increase in reactive oxygen species (ROS) significantly affects white adipose tissue biology and leads to an inflammatory profile and insulin resistance, which could contribute to obesity-associated diabetes and cardiovascular diseases. Mitochondria play a key role in adipose tissue energy metabolism and constitute the main source of cellular ROS such as H(2)O(2). Polyphenols constitute the most abundant antioxidants provided by the human diet. Indeed, they are widely distributed in fruits, vegetables and some plant-derived beverages such as coffee and tea. Thus, the biological effects of dietary polyphenols that may increase the antioxidant capacity of the body against obesity-induced oxidative stress are of high interest. Here, we studied the capacity of polyphenols to modulate the impact of oxidative stress on the mitochondria of preadipocytes, which are important cells governing the adipose tissue development for energy homeostasis. Whereas H(2)O(2) treatment induces a proliferation arrest associated with an increase in mitochondrial content in 3T3-L1 preadipocytes, <span class="hlt">preconditioning</span> with some major dietary polyphenols totally or partially protects the cells against oxidative stress consequences. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy. PMID:23103716</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED538758.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED538758.pdf"><span id="translatedtitle"><span class="hlt">Prevention</span> at Community Colleges. <span class="hlt">Prevention</span> Update</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Higher Education Center for Alcohol, Drug Abuse, and Violence Prevention, 2012</p> <p>2012-01-01</p> <p>According to "Community College Student Alcohol Use: Developing Context-Specific Evidence and <span class="hlt">Prevention</span> Approaches," community colleges have traditionally had a threefold mission that includes preparing students for transfer to four-year colleges, developmental education, and workforce preparation. The researchers point out that the demographic…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=Helen+AND+keller&pg=7&id=EJ613181','ERIC'); return false;" href="http://eric.ed.gov/?q=Helen+AND+keller&pg=7&id=EJ613181"><span id="translatedtitle">Teaching <span class="hlt">Prevention</span> in Pediatrics.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Cheng, Tina L.; Greenberg, Larrie; Loeser, Helen; Keller, David</p> <p>2000-01-01</p> <p>Reviews methods of teaching <span class="hlt">preventive</span> medicine in pediatrics and highlights innovative programs. Methods of teaching <span class="hlt">prevention</span> in pediatrics include patient interactions, self-directed learning, case-based learning, small-group learning, standardized patients, computer-assisted instruction, the Internet, student-centered learning, and lectures.…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=Crime+AND+prevention&id=EJ678227','ERIC'); return false;" href="http://eric.ed.gov/?q=Crime+AND+prevention&id=EJ678227"><span id="translatedtitle">IMPACT Youth Crime <span class="hlt">Prevention</span>.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Warrington, Georgina; Wright, Paul</p> <p>2003-01-01</p> <p>Four models of crime <span class="hlt">prevention</span> are discussed that arise from differing views of the causes of crime: criminal justice, situational, developmental, and social development models. Two activity-based youth crime <span class="hlt">prevention</span> projects in Queensland (Australia) use developmental and social development models and expand local youth service…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3534321','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3534321"><span id="translatedtitle"><span class="hlt">Prevention</span> of Preeclampsia</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Bezerra Maia e Holanda Moura, Sammya; Marques Lopes, Laudelino</p> <p>2012-01-01</p> <p>Preeclampsia (PE) affects around 2–5% of pregnant women. It is a major cause of maternal and perinatal morbidity and mortality. In an attempt to <span class="hlt">prevent</span> preeclampsia, many strategies based on antenatal care, change in lifestyle, nutritional supplementation, and drugs have been studied. The aim of this paper is to review recent evidence about primary and secondary <span class="hlt">prevention</span> of preeclampsia. PMID:23316362</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED123479.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED123479.pdf"><span id="translatedtitle">Police Burglary <span class="hlt">Prevention</span> Programs.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>White, Thomas W.; And Others</p> <p></p> <p>The study is designed to assist police and other law enforcement agencies, as well as local government officials, in planning new burglary <span class="hlt">prevention</span> activities and modifying existing ones. Information was compiled from (1) a survey of 50 United States police departments, (2) site visits to 12 departments with operating burglary <span class="hlt">prevention</span>…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=fire+AND+prevention&pg=2&id=ED221738','ERIC'); return false;" href="http://eric.ed.gov/?q=fire+AND+prevention&pg=2&id=ED221738"><span id="translatedtitle">Fire <span class="hlt">Prevention</span> Inspection Procedures.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Pribyl, Paul F.</p> <p></p> <p>Lesson plans are provided for a fire <span class="hlt">prevention</span> inspection course of the Wisconsin Fire Service Training program. Objectives for the course are to enable students to describe and conduct fire <span class="hlt">prevention</span> inspections, to identify and correct hazards common to most occupancies, to understand the types of building construction and occupancy, and to…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=39075&keyword=financial+AND+risk+AND+management&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=46109018&CFTOKEN=27064954','EPA-EIMS'); return false;" href="http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=39075&keyword=financial+AND+risk+AND+management&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=46109018&CFTOKEN=27064954"><span id="translatedtitle">MEASURING POLLUTION <span class="hlt">PREVENTION</span> PROGRESS</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>The workshop, "Measuring Pollution <span class="hlt">Prevention</span> Progress," was held in Salem, MA, March 31 - April 2, 1993. he purpose of this workshop was to present the latest significant research and practical findings related to pollution <span class="hlt">prevention</span> measurement from ongoing and recently comple...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=DuPont&pg=6&id=EJ659225','ERIC'); return false;" href="http://eric.ed.gov/?q=DuPont&pg=6&id=EJ659225"><span id="translatedtitle"><span class="hlt">Prevention</span>, Not Punishment.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>DuPont Robert L.</p> <p>2003-01-01</p> <p>Describes eight suggestions for implementing a drug-testing program based on study of nine successful programs: Stress student health and safety, make it part of comprehensive education and <span class="hlt">prevention</span> program, get it in writing, protect student privacy, focus on <span class="hlt">prevention</span>, not punishment, involve parents and community from the start, evaluate and…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=132612&keyword=Guatemala&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=41835632&CFTOKEN=28041653','EPA-EIMS'); return false;" href="http://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=132612&keyword=Guatemala&actType=&TIMSType=+&TIMSSubTypeID=&DEID=&epaNumber=&ntisID=&archiveStatus=Both&ombCat=Any&dateBeginCreated=&dateEndCreated=&dateBeginPublishedPresented=&dateEndPublishedPresented=&dateBeginUpdated=&dateEndUpdated=&dateBeginCompleted=&dateEndCompleted=&personID=&role=Any&journalID=&publisherID=&sortBy=revisionDate&count=50&CFID=41835632&CFTOKEN=28041653"><span id="translatedtitle">DIABETES <span class="hlt">PREVENTION</span> PROGRAM</span></a></p> <p><a target="_blank" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p></p> <p></p> <p>The Diabetes <span class="hlt">Prevention</span> Program (DPP) was a major clinical trial, or research study, aimed at discovering whether either diet and exercise or the oral diabetes drug metformin (Glucophage) could <span class="hlt">prevent</span> or delay the onset of type 2 diabetes in people with impaired glucose toleranc...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26045616','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26045616"><span id="translatedtitle">Metformin <span class="hlt">prevents</span> ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cahova, Monika; Palenickova, Eliska; Dankova, Helena; Sticova, Eva; Burian, Martin; Drahota, Zdenek; Cervinkova, Zuzana; Kucera, Otto; Gladkova, Christina; Stopka, Pavel; Krizova, Jana; Papackova, Zuzana; Oliyarnyk, Olena; Kazdova, Ludmila</p> <p>2015-07-15</p> <p>Nonalcoholic fatty liver disease is associated with chronic oxidative stress. In our study, we explored the antioxidant effect of antidiabetic metformin on chronic [high-fat diet (HFD)-induced] and acute oxidative stress induced by short-term warm partial ischemia-reperfusion (I/R) or on a combination of both in the liver. Wistar rats were fed a standard diet (SD) or HFD for 10 wk, half of them being administered metformin (150 mg·kg body wt(-1)·day(-1)). Metformin treatment <span class="hlt">prevented</span> acute stress-induced necroinflammatory reaction, reduced alanine aminotransferase and aspartate aminotransferase serum activity, and diminished lipoperoxidation. The effect was more pronounced in the HFD than in the SD group. The metformin-treated groups exhibited less severe mitochondrial damage (markers: cytochrome c release, citrate synthase activity, mtDNA copy number, mitochondrial respiration) and apoptosis (caspase 9 and caspase 3 activation). Metformin-treated HFD-fed rats subjected to I/R exhibited increased antioxidant enzyme activity as well as attenuated mitochondrial respiratory capacity and ATP resynthesis. The exposure to I/R significantly increased NADH- and succinate-related reactive oxygen species (ROS) mitochondrial production in vitro. The effect of I/R was significantly alleviated by previous metformin treatment. Metformin downregulated the I/R-induced expression of proinflammatory (TNF-?, TLR4, IL-1?, Ccr2) and infiltrating monocyte (Ly6c) and macrophage (CD11b) markers. Our data indicate that metformin reduces mitochondrial performance but concomitantly protects the liver from I/R-induced injury. We propose that the beneficial effect of metformin action is based on a combination of three contributory mechanisms: increased antioxidant enzyme activity, lower mitochondrial ROS production, and reduction of <span class="hlt">postischemic</span> inflammation. PMID:26045616</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/26197102','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/26197102"><span id="translatedtitle">[<span class="hlt">Prevention</span> of alcohol dependence].</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Trova, A C; Paparrigopoulos, Th; Liappas, I; Ginieri-Coccossis, M</p> <p>2015-01-01</p> <p>With the exception of cardiovascular diseases, no other medical condition causes more serious dysfunction or premature deaths than alcohol-related problems. Research results indicate that alcohol dependent individuals present an exceptionally poor level of quality of life. This is an outcome that highlights the necessity of planning and implementing <span class="hlt">preventive</span> interventions on biological, psychological or social level, to be provided to individuals who make alcohol abuse, as well as to their families. <span class="hlt">Preventive</span> interventions can be considered on three levels of <span class="hlt">prevention</span>: (a) primary <span class="hlt">prevention</span>, which is focused on the protection of healthy individuals from alcohol abuse and dependence, and may be provided on a universal, selective or indicated level, (b) secondary <span class="hlt">prevention</span>, which aims at the <span class="hlt">prevention</span> of deterioration regarding alcoholic dependence and relapse, in the cases of individuals already diagnosed with the condition and (c) tertiary <span class="hlt">prevention</span>, which is focused at minimizing deterioration of functioning in chronically sufferers from alcoholic dependence. The term "quaternary <span class="hlt">prevention</span>" can be used for the <span class="hlt">prevention</span> of relapse. As for primary <span class="hlt">prevention</span>, interventions focus on assessing the risk of falling into problematic use, enhancing protective factors and providing information and health education in general. These interventions can be delivered in schools or in places of work and recreation for young people. In this context, various programs have been applied in different countries, including Greece with positive results (Preventure, Alcolocks, LST, SFP, Alcohol Ignition Interlock Device). Secondary <span class="hlt">prevention</span> includes counseling and structured help with the delivery of programs in schools and in high risk groups for alcohol dependence (SAP, LST). These programs aim at the development of alcohol refusal skills and behaviors, the adoption of models of behaviors resisting alcohol use, as well as reinforcement of general social skills. In the context of relevant interventions, various techniques are used, such as role playing. At the level of social policy, different measures may contribute to increase the effectiveness of <span class="hlt">preventive</span> programs (e.g. prohibition of sale of alcohol in young people). Interventions of tertiary <span class="hlt">prevention</span> aim at the development of motivation for abstinence in alcohol dependent individuals and the <span class="hlt">prevention</span> of relapse, as well as the acquisition of new behaviors, which support modification of the problem of alcohol dependence. These interventions can take place in the context of psychotherapeutic follow-up provided to alcohol dependent individuals, and may include various short-term interventions, such as motivational interviewing, but also alternative forms of treatment (e.g. acupuncture, meditation). Elements of <span class="hlt">prevention</span> in combination with elements of promotion of mental health may be incorporated in the same programme for alcohol dependence, endorsing similar or different activities, which may be complementary and may reinforce the effectiveness of the <span class="hlt">prevention</span> program. Finally, it is necessary to raise the awareness of mental health professionals regarding <span class="hlt">prevention</span> and provide specialized education to those who work in drug addiction programmes. Mental health professionals may act as therapists and as intervention coordinators, and performing these roles, they may contribute to the effectiveness of <span class="hlt">preventive</span> programs and more generally to the treatment of disorders connected with alcohol use. PMID:26197102</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1424764','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1424764"><span id="translatedtitle">The limits of <span class="hlt">prevention</span>.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>McGinnis, J M</p> <p>1985-01-01</p> <p>Recent years have been marked by unprecedented accomplishments in <span class="hlt">preventing</span> disease and reducing mortality. More gains can be expected, but there are limits. The forces shaping the nature and potential of <span class="hlt">prevention</span> programs can be characterized as points falling along a spectrum ranging from the purely scientific to the purely social. This paper focuses on four elements of that spectrum, discussing some of the limitations to <span class="hlt">prevention</span> that are presented by biological, technical, ethical, and economic factors. The author concludes with an essentially optimistic perspective on the prospects, special opportunities, and imperatives inherent in each of the categories of limitations discussed. PMID:3923530</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/11758049','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/11758049"><span id="translatedtitle">Screening and <span class="hlt">preventable</span> illness.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Byrne, M M; Thompson, P</p> <p>2001-11-01</p> <p>If an agent does not discount the future at a constant rate, as in some forms of myopia, her optimal strategy is unattainable without some commitment device. We apply this familiar idea to a model of screening and disease <span class="hlt">prevention</span>, and explore how financial incentives can correct suboptimal health choices. In general, myopia need not imply under-screening. While the optimal intervention for <span class="hlt">prevention</span> effort is a state-invariant subsidy, the optimal intervention for screening may involve a tax or a subsidy. When screening and <span class="hlt">prevention</span> are coincident, a simple and practical subsidy equal to one minus the discount factor to both screening and intervention is indicated. PMID:11758049</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4345883','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4345883"><span id="translatedtitle">Extending Injury- and Disease-Resistant CNS Phenotypes by Repetitive Epigenetic Conditioning</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Gidday, Jeffrey M.</p> <p>2015-01-01</p> <p>Significant reductions in the extent of acute injury in the CNS can be achieved by exposure to different <span class="hlt">preconditioning</span> stimuli, but the duration of the induced protective phenotype is typically short-lasting, and thus is deemed as limiting its clinical applicability. Extending the period over which such adaptive epigenetic changes persist – in effect, expanding conditioning’s “therapeutic window” – would significantly broaden the potential applications of such a treatment approach in patients. The frequency of the conditioning stimulus may hold the key. While transient (1–3?days) protection against CNS ischemic injury is well established preclinically following a single <span class="hlt">preconditioning</span> stimulus, repetitively presenting <span class="hlt">preconditioning</span> stimuli extends the duration of ischemic tolerance by many weeks. Moreover, repetitive intermittent postconditioning enhances <span class="hlt">post-ischemic</span> recovery metrics and improves long-term survival. Intermittent conditioning is also efficacious for <span class="hlt">preventing</span> or delaying injury in preclinical models of chronic neurodegenerative disease, and for promoting long-lasting functional improvements in a number of other pathologies as well. Although the detailed mechanisms underlying these protracted kinds of neuroplasticity remain largely unstudied, accumulating empirical evidence supports the contention that all of these adaptive phenotypes are epigenetically mediated. Going forward, additional preclinical demonstrations of the ability to induce sustained beneficial phenotypes that reduce the burden of acute and chronic neurodegeneration, and experimental interrogations of the regulatory constructs responsible for these epigenetic responses, will accelerate the identification of not only efficacious but also practical, adaptive epigenetics-based treatments for individuals with neurological disease. PMID:25784897</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3387090','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3387090"><span id="translatedtitle">Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic <span class="hlt">preconditioning</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Sarkar, Kakali; Cai, Zheqing; Gupta, Rigu; Parajuli, Nirmal; Fox-Talbot, Karen; Darshan, Medha S.; Gonzalez, Frank J.; Semenza, Gregg L.</p> <p>2012-01-01</p> <p>Infarction occurs when myocardial perfusion is interrupted for prolonged periods of time. Short episodes of ischemia and reperfusion protect against tissue injury when the heart is subjected to a subsequent prolonged ischemic episode, a phenomenon known as ischemic <span class="hlt">preconditioning</span> (IPC). Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates adaptive responses to hypoxia/ischemia and is required for IPC. In this study, we performed a cellular and molecular characterization of the role of HIF-1 in IPC. We analyzed mice with knockout of HIF-1? or HIF-1? in Tie2+ lineage cells, which include bone marrow (BM) and vascular endothelial cells, compared with control littermates. Hearts were subjected to 30 min of ischemia and 120 min of reperfusion, either as ex vivo Langendorff preparations or by in situ occlusion of the left anterior descending artery. The IPC stimulus consisted of two cycles of 5-min ischemia and 5-min reperfusion. Mice lacking HIF-1? or HIF-1? in Tie2+ lineage cells showed complete absence of protection induced by IPC, whereas significant protection was induced by adenosine infusion. Treatment of mice with a HIF-1 inhibitor (digoxin or acriflavine) 4 h before Langendorff perfusion resulted in loss of IPC, as did administration of acriflavine directly into the perfusate immediately before IPC. We conclude that HIF-1 activity in endothelial cells is required for acute IPC. Expression and dimerization of the HIF-1? and HIF-1? subunits is required, suggesting that the heterodimer is functioning as a transcriptional activator, despite the acute nature of the response. PMID:22699503</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/22699503','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/22699503"><span id="translatedtitle">Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic <span class="hlt">preconditioning</span>.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Sarkar, Kakali; Cai, Zheqing; Gupta, Rigu; Parajuli, Nirmal; Fox-Talbot, Karen; Darshan, Medha S; Gonzalez, Frank J; Semenza, Gregg L</p> <p>2012-06-26</p> <p>Infarction occurs when myocardial perfusion is interrupted for prolonged periods of time. Short episodes of ischemia and reperfusion protect against tissue injury when the heart is subjected to a subsequent prolonged ischemic episode, a phenomenon known as ischemic <span class="hlt">preconditioning</span> (IPC). Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates adaptive responses to hypoxia/ischemia and is required for IPC. In this study, we performed a cellular and molecular characterization of the role of HIF-1 in IPC. We analyzed mice with knockout of HIF-1? or HIF-1? in Tie2(+) lineage cells, which include bone marrow (BM) and vascular endothelial cells, compared with control littermates. Hearts were subjected to 30 min of ischemia and 120 min of reperfusion, either as ex vivo Langendorff preparations or by in situ occlusion of the left anterior descending artery. The IPC stimulus consisted of two cycles of 5-min ischemia and 5-min reperfusion. Mice lacking HIF-1? or HIF-1? in Tie2(+) lineage cells showed complete absence of protection induced by IPC, whereas significant protection was induced by adenosine infusion. Treatment of mice with a HIF-1 inhibitor (digoxin or acriflavine) 4 h before Langendorff perfusion resulted in loss of IPC, as did administration of acriflavine directly into the perfusate immediately before IPC. We conclude that HIF-1 activity in endothelial cells is required for acute IPC. Expression and dimerization of the HIF-1? and HIF-1? subunits is required, suggesting that the heterodimer is functioning as a transcriptional activator, despite the acute nature of the response. PMID:22699503</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4660753','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4660753"><span id="translatedtitle">Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic <span class="hlt">preconditioning</span> in transient cerebral ischemia</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Hong, Seongkweon; Ahn, Ji Yun; Cho, Geum-Sil; Kim, In Hye; Cho, Jeong Hwi; Ahn, Ji Hyeon; Park, Joon Ha; Won, Moo-Ho; Chen, Bai Hui; Shin, Bich-Na; Tae, Hyun-Jin; Park, Seung Min; Cho, Jun Hwi; Choi, Soo Young; Lee, Jae-Chul</p> <p>2015-01-01</p> <p>Monocarboxylate transporters (MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic <span class="hlt">preconditioning</span> (IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups (sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region (CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC + ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/11834251','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/11834251"><span id="translatedtitle">Involvement of alpha-calcitonin gene-related peptide in monophosphoryl lipid A-induced delayed <span class="hlt">preconditioning</span> in rat hearts.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Peng, Jun; Lu, Rong; Deng, Han Wu; Li, Yuan Jian</p> <p>2002-02-01</p> <p>Recent study has shown that monophosphoryl lipid A-induced delayed <span class="hlt">preconditioning</span> enhanced preservation with cardioplegia and that the protective effects of monophosphoryl lipid A were related to stimulation of calcitonin gene-related peptide (CGRP) release. The purpose of the present study was to explore whether the elevated release of CGRP induced by monophosphoryl lipid A is secondary to stimulation of CGRP synthesis via the nitric oxide (NO) pathway and to characterize the isoform of CGRP. Sprague-Dawley rats were pretreated with monophosphoryl lipid A 24 h before the experiment, and then the left main coronary artery of rat hearts was subjected to 1 h occlusion followed by 3 h reperfusion. Infarct size, plasma creatine kinase activity, the plasma level of CGRP, and the expression of CGRP isoforms (alpha- and beta-CGRP) mRNA in lumbar dorsal root ganglia were measured. Pretreatment with monophosphoryl lipid A (500 microg/kg, i.p.) significantly reduced infarct size and creatine kinase release. Monophosphoryl lipid A caused a significant increase in the expression of alpha-CGRP mRNA, but not of beta-CGRP mRNA, concomitantly with an increase in plasma concentrations of CGRP, and the increased level of CGRP expression happened before stimulation of CGRP release. The effect of monophosphoryl lipid A was completely abolished by pretreatment with L-nitroarginine methyl ester (L-NAME, 10 mg/kg, i.p.), an inhibitor of NO synthase or capsaicin (50 mg/kg, s.c.), which selectively depletes transmitters in capsaicin-sensitive sensory nerves. The results suggest that the delayed cardioprotection afforded by monophosphoryl lipid A involves the synthesis and release of CGRP via the NO pathway, and that the protection is mainly mediated by the alpha-CGRP isoform. PMID:11834251</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li class="active"><span>23</span></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_23 --> <div id="page_24" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li class="active"><span>24</span></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="461"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4046194','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4046194"><span id="translatedtitle">The Molecular Mechanism Underlying the Proliferating and <span class="hlt">Preconditioning</span> Effect of Vitamin C on Adipose-Derived Stem Cells</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kim, Ji Hye; Kim, Wang-Kyun; Sung, Young Kwan; Kwack, Mi Hee; Song, Seung Yong; Choi, Joon-Seok; Park, Sang Gyu; Yi, TacGhee; Lee, Hyun-Joo; Kim, Dae-Duk; Seo, Hyun Min</p> <p>2014-01-01</p> <p>Although adipose-derived stem cells (ASCs) show promise for cell therapy, there is a tremendous need for developing ASC activators. In the present study, we investigated whether or not vitamin C increases the survival, proliferation, and hair-regenerative potential of ASCs. In addition, we tried to find the molecular mechanisms underlying the vitamin C-mediated stimulation of ASCs. Sodium-dependent vitamin C transporter 2 (SVCT2) is expressed in ASCs, and mediates uptake of vitamin C into ASCs. Vitamin C increased the survival and proliferation of ASCs in a dose-dependent manner. Vitamin C increased ERK1/2 phosphorylation, and inhibition of the mitogen-activated protein kinase (MAPK) pathway attenuated the proliferation of ASCs. Microarray and quantitative polymerase chain reaction showed that vitamin C primarily upregulated expression of proliferation-related genes, including Fos, E2F2, Ier2, Mybl1, Cdc45, JunB, FosB, and Cdca5, whereas Fos knock-down using siRNA significantly decreased vitamin C-mediated ASC proliferation. In addition, vitamin C-treated ASCs accelerated the telogen-to-anagen transition in C3H/HeN mice, and conditioned medium from vitamin C-treated ASCs increased the hair length and the Ki67-positive matrix keratinocytes in hair organ culture. Vitamin C increased the mRNA expression of HGF, IGFBP6, VEGF, bFGF, and KGF, which may mediate hair growth promotion. In summary, vitamin C is transported via SVCT2, and increased ASC proliferation is mediated by the MAPK pathway. In addition, vitamin C <span class="hlt">preconditioning</span> enhanced the hair growth promoting effect of ASCs. Because vitamin C is safe and effective, it could be used to increase the yield and regenerative potential of ASCs. PMID:24524758</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://hdl.handle.net/2060/19990032494','NASA-TRS'); return false;" href="http://hdl.handle.net/2060/19990032494"><span id="translatedtitle">WARP3D-Release 10.8: Dynamic Nonlinear Analysis of Solids using a <span class="hlt">Preconditioned</span> Conjugate Gradient Software Architecture</span></a></p> <p><a target="_blank" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p>Koppenhoefer, Kyle C.; Gullerud, Arne S.; Ruggieri, Claudio; Dodds, Robert H., Jr.; Healy, Brian E.</p> <p>1998-01-01</p> <p>This report describes theoretical background material and commands necessary to use the WARP3D finite element code. WARP3D is under continuing development as a research code for the solution of very large-scale, 3-D solid models subjected to static and dynamic loads. Specific features in the code oriented toward the investigation of ductile fracture in metals include a robust finite strain formulation, a general J-integral computation facility (with inertia, face loading), an element extinction facility to model crack growth, nonlinear material models including viscoplastic effects, and the Gurson-Tver-gaard dilatant plasticity model for void growth. The nonlinear, dynamic equilibrium equations are solved using an incremental-iterative, implicit formulation with full Newton iterations to eliminate residual nodal forces. The history integration of the nonlinear equations of motion is accomplished with Newmarks Beta method. A central feature of WARP3D involves the use of a linear-<span class="hlt">preconditioned</span> conjugate gradient (LPCG) solver implemented in an element-by-element format to replace a conventional direct linear equation solver. This software architecture dramatically reduces both the memory requirements and CPU time for very large, nonlinear solid models since formation of the assembled (dynamic) stiffness matrix is avoided. Analyses thus exhibit the numerical stability for large time (load) steps provided by the implicit formulation coupled with the low memory requirements characteristic of an explicit code. In addition to the much lower memory requirements of the LPCG solver, the CPU time required for solution of the linear equations during each Newton iteration is generally one-half or less of the CPU time required for a traditional direct solver. All other computational aspects of the code (element stiffnesses, element strains, stress updating, element internal forces) are implemented in the element-by- element, blocked architecture. This greatly improves vectorization of the code on uni-processor hardware and enables straightforward parallel-vector processing of element blocks on multi-processor hardware.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/24980267','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/24980267"><span id="translatedtitle">In vivo detection of the effects of <span class="hlt">preconditioning</span> on LNCaP tumors by a TNF-? nanoparticle construct using MRI.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Iltis, Isabelle; Choi, Jeunghwan; Vollmers, Manda; Shenoi, Mithun; Bischof, John; Metzger, Gregory J</p> <p>2014-09-01</p> <p>The outcome of systemic and local therapies (e.g. chemotherapy, radiotherapy, surgery, focal ablation) for prostate cancer can be significantly improved by using tumor-specific adjuvants prior to treatment ("<span class="hlt">preconditioning</span>"). We propose to use dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) to monitor the in vivo response of a mouse model of prostate cancer treated with a vascular disruptive agent, TNF-?, delivered on a gold nanoparticle (NP-TNF). Six male nude mice bearing 4-5 week old LNCaP tumors were scanned at 9.4 T. DCE-MRI was performed two days before and 4-5 h after treatment with NP-TNF. An intraperitoneal (i.p.) bolus of gadolinium-DTPA (Gd) was administered and contrast enhancement was measured for 90 min. Concentration-time curves of Gd were calculated and the area under the Gd curve (AUGC) was determined pre- and post-treatment. NP-TNF treatment caused an increase in contrast uptake in tumors. Interestingly, the early concentration (10 min post Gd bolus i.p.) was similar in both untreated and treated conditions; however, 90 min after injection, [Gd] was 3.4 times higher than before treatment. AUGC doubled from (11 ± 6) [Gd] × min before treatment to (22 ± 9) [Gd] × min after treatment. An increase in signal enhancement was also observed in the muscle but to a lesser degree. We also evaluated the kinetics of intravenous Gd administration in mice bearing a jugular vein catheter to mimic the delivery method used in clinical trials. The overall treatment effects were independent of the delivery pathway of the contrast agent. In conclusion, we show that DCE-MRI is suitable to detect changes associated with a vascular disruptive agent in a mouse model of prostate cancer. The ability to characterize the effects of nanoparticle therapy in vivo with non-destructive methods is important, as such compounds, in combination with treatment strategies, are progressing towards clinical trials. PMID:24980267</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3698768','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3698768"><span id="translatedtitle">Effect of Remote Ischemic <span class="hlt">Preconditioning</span> on Phosphorylated Protein Signaling in Children Undergoing Tetralogy of Fallot Repair: A Randomized Controlled Trial</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Pepe, Salvatore; Liaw, Norman Y.; Hepponstall, Michele; Sheeran, Freya L.; Yong, Matthew S.; d'Udekem, Yves; Cheung, Michael M.; Konstantinov, Igor E.</p> <p>2013-01-01</p> <p>Background Our previous randomized controlled trial demonstrated cardiorespiratory protection by remote ischemic <span class="hlt">preconditioning</span> (RIPC) in children before cardiac surgery. However, the impact of RIPC on myocardial prosurvival intracellular signaling remains unknown in cyanosis. RIPC may augment phosphorylated protein signaling in myocardium and circulating leukocytes during tetralogy of Fallot (ToF) repair. Methods and Results Children (n=40) undergoing ToF repair were double?blind randomized to RIPC (n=11 boys, 9 girls) or control (sham RIPC: n=9 boys, 11 girls). Blood samples were taken before, immediately after, and 24 hours after cardiopulmonary bypass. Resected right ventricular outflow tract muscle and leukocytes were processed for protein expression and mitochondrial respiration. There was no difference in age (7.1±3.4 versus 7.1±3.4 months), weight (7.7±1.8 versus 7.5±1.9 kg), or bypass or aortic cross?clamp times between the groups (control versus RIPC, mean±SD). No differences were seen between the groups for an increase in the ratio of phosphorylated to total protein for protein kinase B, p38 mitogen activated protein kinase, signal transducer and activator of transcription 3, glycogen synthase kinase 3?, heat shock protein 27, Connexin43, or markers associated with promotion of necrosis (serum cardiac troponin I), apoptosis (Bax, Bcl?2), and autophagy (Parkin, Beclin?1, LC3B). A high proportion of total proteins were in phosphorylated form in control and RIPC myocardium. In leukocytes, mitochondrial respiration and assessed protein levels did not differ between groups. Conclusions In patients with cyanotic heart disease, a high proportion of proteins are in phosphorylated form. RIPC does not further enhance phosphorylated protein signaling in myocardium or circulating leukocytes in children undergoing ToF repair. Clinical Trial Registration URL: (http://www.anzctr.org.au/trial_view.aspx?id=335613. Unique identifier: Australian New Zealand Clinical Trials Registry number ACTRN12610000496011. PMID:23666460</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/16289119','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/16289119"><span id="translatedtitle">Effect of acute hypoxic <span class="hlt">preconditioning</span> on qEEG and functional recovery after cardiac arrest in rats.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Geocadin, Romergryko G; Malhotra, Amit D; Tong, Shanbao; Seth, Akhil; Moriwaki, Goroku; Hanley, Daniel F; Thakor, Nitish V</p> <p>2005-12-01</p> <p>Acute hypoxic <span class="hlt">preconditioning</span> (AHPC) can confer neuroprotection from global cerebral ischemia such as cardiac arrest. We hypothesize that acute neuroprotection by AHPC will be detected early by quantitative EEG (qEEG) entropy analysis after asphyxial cardiac arrest (aCA). Cerebral ischemia lowers EEG signal randomness leading to low entropy. A qEEG entropy index defined as the duration when the entropy measure is 15% below uninjured baseline entropy is used as a measure of injury. We compared 3 groups of adult Wistar rats: (1) untreated controls that were subjected to 5 min of aCA and were resuscitated (n = 5); (2) AHPC-treated group with 10% FI O2 for 30 min, then 25 min of room air, 5 min of aCA followed by resuscitation (n = 5); and (3) a surgical sham group (no aCA) (n = 3). Functional outcome was assessed by neurodeficit score (NDS) which consisted of level of consciousness, cranial nerve, motor-sensory function, and simple behavioral tests (best = 100 and brain dead = 0). We found that increasing entropy index of injury at 0-5 h from return of spontaneous circulation (ROSC) is associated with worsening NDS at 24 h (linear regression: r = 0.81, P < 0.001). The NDS of the group sham (84.7 +/- 2.8) (mean +/- SEM) and AHPC group (84.6 +/- 2.9, P > 0.05) was better than control injury group (52.2 +/- 8.4, P < 0.05) (ANOVA with Tukey test). We therefore conclude that AHPC confers acute neuroprotection at 24 h, which was detected by qEEG entropy during the first 5 h after injury. PMID:16289119</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4651366','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4651366"><span id="translatedtitle">Determinants of the Efficacy of Cardiac Ischemic <span class="hlt">Preconditioning</span>: A Systematic Review and Meta-Analysis of Animal Studies</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Wever, Kimberley E.; Hooijmans, Carlijn R.; Riksen, Niels P.; Sterenborg, Thomas B.; Sena, Emily S.; Ritskes-Hoitinga, Merel; Warlé, Michiel C.</p> <p>2015-01-01</p> <p>Background Ischemic <span class="hlt">preconditioning</span> (IPC) of the heart is a protective strategy in which a brief ischemic stimulus immediately before a lethal ischemic episode potently limits infarct size. Although very promising in animal models of myocardial infarction, IPC has not yet been successfully translated to benefit for patients. Objective To appraise all preclinical evidence on IPC for myocardial infarction and identify factors hampering translation. Methods and results Using systematic review and meta-analysis, we identified 503 animal studies reporting infarct size data from 785 comparisons between IPC-treated and control animals. Overall, IPC reduced myocardial infarction by 24.6% [95%CI 23.5, 25.6]. Subgroup analysis showed that IPC efficacy was reduced in comorbid animals and non-rodents. Efficacy was highest in studies using 2–3 IPC cycles applied <45 minutes before myocardial infarction. Local and remote IPC were equally effective. Reporting of study quality indicators was low: randomization, blinding and a sample size calculation were reported in 49%, 11% and 2% of publications, respectively. Conclusions Translation of IPC to the clinical setting may be hampered by the observed differences between the animals used in preclinical IPC studies and the patient population, regarding comorbidity, sex and age. Furthermore, the IPC protocols currently used in clinical trials could be optimized in terms of timing and the number of ischemic cycles applied. In order to inform future clinical trials successfully, future preclinical studies on IPC should aim to maximize both internal and external validity, since poor methodological quality may limit the value of the preclinical evidence. PMID:26580958</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4139144','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4139144"><span id="translatedtitle">In vivo detection of the effects of <span class="hlt">preconditioning</span> on LNCaP tumors by a TNF-? nanoparticle construct using MRI</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Iltis, Isabelle; Choi, Jeunghwan; Vollmers, Manda; Shenoi, Mithun; Bischof, John; Metzger, Gregory J.</p> <p>2014-01-01</p> <p>The outcome of systemic and local therapies (e.g., chemotherapy, radiotherapy, surgery, focal ablation) for prostate cancer can be significantly improved by using tumor-specific adjuvants prior to treatment (“<span class="hlt">preconditioning</span>”). We propose to use dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) to monitor the in vivo response of a mouse model of prostate cancer treated with a vascular disruptive agent, TNF-?, delivered on a gold nanoparticle (NP-TNF). Six male nude mice bearing 4–5 weeks old LNCaP tumors were scanned at 9.4T. DCE-MRI was performed two days before and 4–5 hours after treatment with NP-TNF. An intraperitoneal bolus of Gadolinium-DTPA (Gd) was administered and contrast enhancement was measured for 90 minutes. Concentration time curves of Gd were calculated and the area under the Gd curve (AUGC) was determined pre and post treatment. NP-TNF treatment caused an increase in contrast uptake in tumors. Interestingly, the early concentration (10 minutes post Gd bolus i.p.) was similar in both untreated and treated conditions; however, 90 minutes after injection, [Gd] was 3.4 times higher after treatment compared to before. AUGC doubled from 11 ± 6 [Gd] × min before treatment to 22 ± 9 [Gd] × min after treatment. An increase in signal enhancement was also observed in the muscle but to a lesser degree. We also evaluated the kinetics of intravenous gadolinium administration in mice bearing a jugular vein catheter to mimic the delivery method used in clinical trials. The overall treatment effects were independent of the delivery pathway of the contrast agent. In conclusion, we show that DCE-MRI is suitable to detect changes associated with a vascular disruptive agent in a mouse model of prostate cancer. The ability to characterize the effects of nanoparticle therapy in vivo with non-destructive methods is important as such compounds, in combination with treatment strategies, progress towards clinical trials. PMID:24980267</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2786351','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2786351"><span id="translatedtitle">In Vitro Sensitivity Testing of Leishmania Clinical Field Isolates: <span class="hlt">Preconditioning</span> of Promastigotes Enhances Infectivity for Macrophage Host Cells?</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Inocêncio da Luz, Raquel; Vermeersch, Marieke; Dujardin, Jean-Claude; Cos, Paul; Maes, Louis</p> <p>2009-01-01</p> <p>Diagnostic material from patients with leishmaniasis is generally available as promastigotes, and proper testing for susceptibility to first-line drugs by the intracellular amastigote assay is frequently hampered by the poor infectivity of the promastigotes for the macrophage host cell. Several conditions for optimization of the in vitro metacyclogenesis and cell infectivity of Leishmania donovani, L. guyanensis, and L. braziliensis field strains obtained from patients receiving standard antimony medication were investigated. Triggering log-phase promastigotes to become amastigote-like by increasing the temperature or acidifying the culture medium was not successful. Adequate metacyclogenesis and the highest levels of macrophage infection were obtained after 5-day-old late-log-phase promastigote cultures were <span class="hlt">preconditioned</span> at 25°C to pH 5.4 for 24 h in Schneider's medium prior to infection. The susceptibility assay with primary peritoneal mouse macrophages included pentavalent antimony (SbV; sodium stibogluconate), trivalent antimony (SbIII; potassium antimonyl tartrate), miltefosine, and the experimental drug PX-6518. All strains were sensitive to miltefosine (50% inhibitory concentration [IC50] < 10 ?M) and PX-6518 (IC50 < 2 ?g/ml) but showed distinct susceptibility to SbV and/or SbIII, depending on whether they were derived from cured, relapse, or nonresponder patients. Within the available set of Leishmania species and strains, simultaneous SbV-SbIII resistance was clearly associated with treatment failure; however, a larger set of isolates is still needed to judge the predictive value of SbV-SbIII susceptibility profiling on treatment outcome. In conclusion, the proposed conditioning protocol further contributes toward a more standardized laboratory model for evaluation of the drug sensitivities of field isolates. PMID:19752271</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.facingdisability.com/expert-topics/preventing-pressure-sores','SCIGOVIMAGE-MEDLINEPLUS'); return false;" href="http://www.facingdisability.com/expert-topics/preventing-pressure-sores"><span id="translatedtitle"><span class="hlt">Preventing</span> Pressure Sores</span></a></p> <p><a target="_blank" href="http://www.nlm.nih.gov/medlineplus/videosandcooltools.html">MedlinePLUS Videos and Cool Tools</a></p> <p></p> <p></p> <p>... sores? What's the best way to do daily skin inspections? What are the most important things for ... in bed to <span class="hlt">prevent</span> pressure sores? What is “skin tolerance” and how can it be increased? What ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/research/progress/discovery/skin-cancer','NCI'); return false;" href="http://www.cancer.gov/research/progress/discovery/skin-cancer"><span id="translatedtitle">Discovery – <span class="hlt">Preventing</span> Skin Cancer</span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p>Cancer research includes stopping cancer before it spreads. NCI funded the development of the Melanoma Risk Assessment Tool and the ABC method. Both help to diagnose high-risk patients and <span class="hlt">prevent</span> melanoma earlier in the fight against skin cancer.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/listeria/prevention.html','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/listeria/prevention.html"><span id="translatedtitle"><span class="hlt">Prevention</span> of Listeriosis</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... risk. General recommendations to <span class="hlt">prevent</span> an infection with Listeria : FDA recommendations for washing and handling food. Rinse ... handling and preparing uncooked foods. Be aware that Listeria monocytogenes can grow in foods in the refrigerator. ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://uncw.edu/care/documents/ViolencePreventionBrochureEmployees.pdf','EPRINT'); return false;" href="http://uncw.edu/care/documents/ViolencePreventionBrochureEmployees.pdf"><span id="translatedtitle"><span class="hlt">Preventing</span> Interpersonal Understanding Your</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>Olszewski Jr., Edward A.</p> <p></p> <p>-2222 Response to campus safety and security issues, including criminal investigations. RAD self-defense classes. Student Health Services..................962-3280 Confidential medical care, including free STI testing and free <span class="hlt">preventative</span> medication for STI's and pregnancy. Counseling Center........................962</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://kidshealth.org/parent/firstaid_safe/home/safety_choking.html','NIH-MEDLINEPLUS'); return false;" href="http://kidshealth.org/parent/firstaid_safe/home/safety_choking.html"><span id="translatedtitle">Household Safety: <span class="hlt">Preventing</span> Choking</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... room a child shouldn't enter to <span class="hlt">prevent</span> wandering into places that haven't been properly childproofed. ... the activities that develop your child's body and mind. Reviewed by: Mary L. Gavin, MD Date reviewed: ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.geteyesmart.org/eyesmart/living/eye-injuries/preventing.cfm','NIH-MEDLINEPLUS'); return false;" href="http://www.geteyesmart.org/eyesmart/living/eye-injuries/preventing.cfm"><span id="translatedtitle"><span class="hlt">Preventing</span> Eye Injuries</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... the Sun Eye Health News Consumer Alerts <span class="hlt">Preventing</span> Eye Injuries Tweet Protecting your eyes from injury is ... as possible, even if the injury seems minor. Eye Injury Facts and Myths Men are more likely ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://dceg.cancer.gov/research/what-we-study/lifestyle/polyp-prevention-trial','NCI'); return false;" href="http://dceg.cancer.gov/research/what-we-study/lifestyle/polyp-prevention-trial"><span id="translatedtitle">Polyp <span class="hlt">Prevention</span> Trial</span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p>The primary objective of the Polyp <span class="hlt">Prevention</span> Trial (PPT) is to determine whether a low fat, high fiber, high vegetable and fruit eating plan will decrease the recurrence of adenomatous polyps of the large bowel.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('https://www.nia.nih.gov/health/publication/can-we-prevent-aging','NIH-MEDLINEPLUS'); return false;" href="https://www.nia.nih.gov/health/publication/can-we-prevent-aging"><span id="translatedtitle">Can We <span class="hlt">Prevent</span> Aging?</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... help delay or <span class="hlt">prevent</span> age-related health problems. Hormones Hormones are chemical messengers that set in motion ... part of menopausal hormone therapy) Dehydroepiandrosterone (DHEA) How Hormones Work A hormone acts upon a cell much ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.osti.gov/scitech/biblio/77999','SCIGOV-STC'); return false;" href="http://www.osti.gov/scitech/biblio/77999"><span id="translatedtitle">Profiting from pollution <span class="hlt">prevention</span></span></a></p> <p><a target="_blank" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p>LoPilato, A.J.; Eng, D.B.</p> <p>1994-12-31</p> <p>In the case of pollution <span class="hlt">prevention</span>, national environmental goals coincide with industry`s economic interests. Most, if not all businesses have strong incentives to reduce the toxicity and quantities of wastes generated. These incentives include not only the ever increasing cost of compliance within a growing framework of regulations, but may include a firms desire to reduce the risk of criminal and civil liability, reduce overall operating costs, improve employee morale and participation, enhance corporate image in the community and insure protection of both public health and the environment. Although some businesses may invest in a pollution <span class="hlt">prevention</span> program because it is the green thin to do, most businesses will weight their initial and long-term pollution <span class="hlt">prevention</span> program investments on sound economic analyses. An effective pollution <span class="hlt">prevention</span> program can provide cost savings that will more than offset the initial development and implementation costs.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2379184','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2379184"><span id="translatedtitle">Pneumoconioses and Their <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Grzybowski, Stefan</p> <p>1978-01-01</p> <p>This article classifies the types of occupational lung disease, details the known hazards of several substances and looks at <span class="hlt">prevention</span>, both in terms of host factors and improvement of working environment. Current screening procedures are evaluated. PMID:21301505</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://eric.ed.gov/?q=suicide+AND+prevention&pg=3&id=EJ793216','ERIC'); return false;" href="http://eric.ed.gov/?q=suicide+AND+prevention&pg=3&id=EJ793216"><span id="translatedtitle">Youth Suicide <span class="hlt">Prevention</span> Programs</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Kalafat, John</p> <p>2006-01-01</p> <p>Youth suicide <span class="hlt">prevention</span> programs are described that promote the identification and referral of at-risk youth, address risk factors, and promote protective factors. Emphasis is on programs that are both effective and sustainable in applied settings.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.sprc.org/basics/roles-suicide-prevention','NIH-MEDLINEPLUS'); return false;" href="http://www.sprc.org/basics/roles-suicide-prevention"><span id="translatedtitle">Roles in Suicide <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... SAMHSA or DHHS for the information on this web site is intended or should be inferred. The Suicide <span class="hlt">Prevention</span> Resource Center (SPRC) is a project in EDC's Health and Human Development Division 43 Foundry Avenue, Waltham, MA 02453-8313. ...</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li class="active"><span>24</span></li> <li><a href="#" onclick='return showDiv("page_25");'>25</a></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_24 --> <div id="page_25" class="hiddenDiv"> <div class="row"> <div class="col-sm-12"> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li class="active"><span>25</span></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div> </div> <div class="row"> <div class="col-sm-12"> <ol class="result-class" start="481"> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.niddk.nih.gov/about-niddk/research-areas/diabetes/diabetes-prevention-program-dpp/Pages/default.aspx','NIH-MEDLINEPLUS'); return false;" href="http://www.niddk.nih.gov/about-niddk/research-areas/diabetes/diabetes-prevention-program-dpp/Pages/default.aspx"><span id="translatedtitle">Diabetes <span class="hlt">Prevention</span> Program (DPP)</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... Recruiting Patients & Families Consortia, Networks & Centers Reports & Planning Diabetes <span class="hlt">Prevention</span> Program (DPP) Page Content On this page: ... increased risk of developing diabetes. [ Top ] Type 2 Diabetes and Prediabetes Type 2 diabetes is a disorder ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/HomeandRecreationalSafety/Poisoning/preventiontips.htm','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/HomeandRecreationalSafety/Poisoning/preventiontips.htm"><span id="translatedtitle">Tips to <span class="hlt">Prevent</span> Poisonings</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... below were adapted from the American Association of Poison Control Centersâ?? poison <span class="hlt">prevention</span> tips for children and adults. Drugs and ... Children Safe from Poisoning Be Prepared Put the poison help number, 1-800-222-1222, on or ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/parasites/scabies/prevent.html','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/parasites/scabies/prevent.html"><span id="translatedtitle">Scabies: <span class="hlt">Prevention</span> and Control</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... message, please visit this page: About CDC.gov . Parasites - Scabies Parasites Home Share Compartir <span class="hlt">Prevention</span> & Control When a person ... Cases Publications Information For: Institutions Travelers Related Links Parasites A-Z Index Parasites Glossary Neglected Tropical Diseases ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/cholera/prevention.html','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/cholera/prevention.html"><span id="translatedtitle">Cholera <span class="hlt">Prevention</span> and Control</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... <span class="hlt">Prevention</span> of cholera is dependent on access to safe water, adequate sanitation, and basic hygiene needs. The following ... Water Global Water, Sanitation, and Hygiene (WASH) The Safe Water System Division of Foodborne, Waterborne, and Environmental Diseases ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/calcium-fact-sheet','NCI'); return false;" href="http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/calcium-fact-sheet"><span id="translatedtitle">Calcium and Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://www.cancer.gov">Cancer.gov</a></p> <p></p> <p></p> <p>A fact sheet that summarizes the results of studies on calcium and cancer <span class="hlt">prevention</span>. It includes information about dietary recommendations for calcium, and the amount of calcium in foods and calcium supplements.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.gov/about-cancer/causes-prevention/risk/statins-fact-sheet','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.gov/about-cancer/causes-prevention/risk/statins-fact-sheet"><span id="translatedtitle">Statins and Cancer <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... types of cancer? What evidence is there that lipid-lowering drugs can <span class="hlt">prevent</span> skin cancer? Where can ... opposed to the use of another type of lipid-lowering drug, fibrates). [Statins and the risk of ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/16299672','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/16299672"><span id="translatedtitle"><span class="hlt">Preventing</span> parasites in cats.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Dryden, Michael W; Payne, Patricia A</p> <p>2005-01-01</p> <p>The monthly administration of broad-spectrum heartworm medications can effectively <span class="hlt">prevent</span> a variety of internal and external parasitic diseases in cats. Although not every parasite can be stopped, many of the common feline parasites are susceptible to these agents. This article discusses the epidemiology and <span class="hlt">prevention</span> strategies for those parasites that can be controlled by the administration of ivermectin, milbemycin oxime, or selamectin, either alone or in conjunction with an external parasiticide. PMID:16299672</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cdc.gov/ncbddd/birthdefects/prevention.html','NIH-MEDLINEPLUS'); return false;" href="http://www.cdc.gov/ncbddd/birthdefects/prevention.html"><span id="translatedtitle">Guidance for <span class="hlt">Preventing</span> Birth Defects</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... <span class="hlt">Prevention</span>. Commit to Healthy Choices to Help <span class="hlt">Prevent</span> Birth Defects Language: English Español (Spanish) Recommend on Facebook Tweet Share Compartir We know that not all birth defects can be <span class="hlt">prevented</span>. But, we also know ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.ncbi.nlm.nih.gov/pubmed/10926043','PUBMED'); return false;" href="http://www.ncbi.nlm.nih.gov/pubmed/10926043"><span id="translatedtitle">Teaching <span class="hlt">prevention</span> in pediatrics.</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p>Cheng, T L; Greenberg, L; Loeser, H; Keller, D</p> <p>2000-07-01</p> <p>Pediatrics has attempted to inculcate the "culture of <span class="hlt">prevention</span>" into practice, both through anticipatory guidance in well-child care and through behavioral interventions in sick care. The effectivenesses of many components of well-child care have not been conclusively demonstrated, particularly in health education, counseling, and anticipatory guidance, nor has teaching <span class="hlt">prevention</span> in pediatrics been thoroughly evaluated. This article reviews methods of teaching <span class="hlt">prevention</span> in pediatrics and highlights innovative programs. Teaching programs use the wide range of approaches now common in medical education, in a variety of inpatient and outpatient sites. Programs across the country are trying new approaches to teaching traditional topics or are introducing new topics into their curricula. Examples of specific programs are given, organized by the themes of the programs. The field needs to develop in three major directions. First, there is a need to develop competencies and curricula in <span class="hlt">prevention</span> issues of contemporary importance, including the new morbidities, cross-cultural issues, cost-effectiveness, quality of care, and practice in managed care and other community settings. Second, further work is needed to evaluate programs and measure educational outcomes. This feedback must in turn be used to redefine competencies, curricula, and programs, Third, there needs to be an accessible clearinghouse, and educational tools need to be disseminated. To be effective, a curriculum for <span class="hlt">prevention</span> in pediatrics cannot stand alone, but must be part of a vertically and horizontally integrated curriculum. Further, creating horizontally and vertically integrated curricula in <span class="hlt">prevention</span> teaching across disciplines should be the standard. PMID:10926043</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3289174','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3289174"><span id="translatedtitle"><span class="hlt">Prevention</span> of Football Injuries</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Kirkendall, Donald T; Junge, Astrid; Dvorak, Jiri</p> <p>2010-01-01</p> <p>Purpose Every sport has a unique profile of injury and risk of injury. In recent years, there have been numerous attempts at conducting injury <span class="hlt">prevention</span> trials for specific injuries or for injuries within specific sports to provide evidence useful to the sports medicine and sport community. Football has been a focus of a number of randomized injury <span class="hlt">prevention</span> trials. Methods MEDLINE was searched with the first order keywords of “injury <span class="hlt">prevention</span>” and “sport”. This list was restricted to “clinical trial” or “randomized controlled trial” which had been conducted on children and adults whose goal was <span class="hlt">preventing</span> common football injuries. Our objective was to find studies with an exercise-based training program, thus projects that used mechanical interventions were excluded. Results A structured, generalized warm-up has been shown to be effective at <span class="hlt">preventing</span> common injuries in football, reducing injuries by about one-third. Conclusion The huge participation numbers in the worldwide family of football would suggest that any reduction in injury should have a public health impact. Professionals in sports medicine need to promote injury <span class="hlt">prevention</span> programs that have been shown to be effective. PMID:22375195</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4470312','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4470312"><span id="translatedtitle">Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-? in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-<span class="hlt">preconditioned</span> rats</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Wang, C.; Hu, S.M.; Xie, H.; Qiao, S.G.; Liu, H.; Liu, C.F.</p> <p>2015-01-01</p> <p>This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-? in the delayed protective effects of sevoflurane <span class="hlt">preconditioning</span> using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane <span class="hlt">preconditioning</span> (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-? (p-PKC-?) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-? expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-? expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in <span class="hlt">preconditioning</span> against I/R injury, by regulating PKC-? phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion. PMID:25831209</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://arxiv.org/pdf/0907.3261v1','EPRINT'); return false;" href="http://arxiv.org/pdf/0907.3261v1"><span id="translatedtitle">Application of <span class="hlt">preconditioned</span> block BiCGGR to the Wilson-Dirac equation with multiple right-hand sides in lattice QCD</span></a></p> <p><a target="_blank" href="http://www.osti.gov/eprints/">E-print Network</a></p> <p>H. Tadano; Y. Kuramashi; T. Sakurai</p> <p>2009-07-19</p> <p>There exist two major problems in application of the conventional block BiCGSTAB method to the O(a)-improved Wilson-Dirac equation with multiple right-hand-sides: One is the deviation between the true and the recursive residuals. The other is the convergence failure observed at smaller quark masses for enlarged number of the right-hand-sides. The block BiCGGR algorithm which was recently proposed by the authors succeeds in solving the former problem. In this article we show that a <span class="hlt">preconditioning</span> technique allows us to improve the convergence behavior for increasing number of the right-hand-sides.</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4348939','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4348939"><span id="translatedtitle">Delayed cardioprotection by sevoflurane <span class="hlt">preconditioning</span>: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Xie, Hong; Liu, Qin; Qiao, Shigang; Jiang, Xiuli; Wang, Chen</p> <p>2015-01-01</p> <p>Sevoflurane <span class="hlt">preconditioning</span> has shown to exert delayed caridioprotection against subsequent ischemia and reperfusion injury, but the mechanisms underlying is unclear. Inhibition of autophagy by 3-methyladenine (3-MA) or knockdown of Beclin 1 leads to enhanced cardiac myocyte survival. Our study aimed to test whether sevoflurane <span class="hlt">preconditioning</span> provides a second window of anesthetic <span class="hlt">preconditioning</span> (SWOP) via inhibit Beclin 1-mediated autophagic cell death. H9c2 rat cardiomyocytes were randomly divided into five groups: Control (CON) group; hypoxia/reoxygenation (H/R) group, rat cardiomyocytes was exposed in the airtight container for 2 h followed by 1 h of reoxgenation; SWOP group, rat cardiomyocytes was exposed to 1 h of 2.5% sevoflurane 24 h before H/R; Autophagic inhibitors, 3-methyladenine (3-MA, 10 mM) was added to culture medium 15 min before sevoflurane exposure (3-MA+SWOP group) or cells were treated by 3-MA alone (3-MA group). The cell proliferation was significantly increased in SWOP group (79.49 ± 1.37%, P < 0.05) when compared to H/R group (62.2 ± 6.49%, P < 0.05). 3-MA administered before SWOP significantly attenuated the H/R induced autophagy and cell death. H/R injury up-regulated the expression of LC3-II and Beclin 1 proteins (342 ± 66% and 163 ± 18%, respectively, P < 0.05) compared to the CON group (100%), which were increased in SWOP group (202 ± 77% and 128 ± 8%, respectively, P < 0.05). The expression of LC3-II and Beclin 1 proteins was decreased in 3-MA group (110 ± 28% and 97 ± 6%, respectively) and 3-MA+SWOP group (93 ± 7% and 98 ± 6%, respectively) compared with H/R group, but Bcl-2 was upregulated in 3-MA group (158 ± 4%) and 3-MA+SWOP group (156 ± 5%) compared to H/R group (103 ± 7%). In conclusion, sevoflurane <span class="hlt">preconditioning</span> confers delayed cardioprotection via inhibition Beclin 1-mediated autophagic cell death in cardiac myocytes 24 h before exposed to H/R injury. PMID:25755708</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.cancer.net/research-and-advocacy/asco-care-and-treatment-recommendations-patients/preventing-and-treating-blood-clots','NIH-MEDLINEPLUS'); return false;" href="http://www.cancer.net/research-and-advocacy/asco-care-and-treatment-recommendations-patients/preventing-and-treating-blood-clots"><span id="translatedtitle"><span class="hlt">Preventing</span> and Treating Blood Clots</span></a></p> <p><a target="_blank" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p></p> <p></p> <p>... here Home > Research and Advocacy > ASCO Care and Treatment Recommendations for Patients > <span class="hlt">Preventing</span> and Treating Blood Clots Request Permissions Download PDF <span class="hlt">Preventing</span> and Treating Blood Clots ...</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3760559','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3760559"><span id="translatedtitle">Conditioning the heart to <span class="hlt">prevent</span> myocardial reperfusion injury during PPCI</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p></p> <p>2012-01-01</p> <p>For patients presenting with a ST-segment elevation myocardial infarction (STEMI), early myocardial reperfusion by primary percutaneous coronary intervention (PPCI) remains the most effective treatment strategy for limiting myocardial infarct size, preserving left ventricular systolic function, and <span class="hlt">preventing</span> the onset of heart failure. Recent advances in PCI technology to improve myocardial reperfusion and the introduction of novel anti-platelet and anti-thrombotic agents to maintain the patency of the infarct-related coronary artery continue to optimize PPCI procedure. However, despite these improvements, STEMI patients still experience significant major adverse cardiovascular events. One major contributing factor has been the inability to protect the heart against the lethal myocardial reperfusion injury, which accompanies PPCI. Past attempts to translate cardioprotective strategies, discovered in experimental studies to <span class="hlt">prevent</span> lethal myocardial reperfusion injury, into the clinical setting of PPCI have been disappointing. However, a number of recent proof-of-concept clinical studies suggest that the heart can be ‘conditioned’ to protect itself against lethal myocardial reperfusion injury, as evidenced by a reduction in myocardial infarct size. This can be achieved using either mechanical (such as ischaemic postconditioning, remote ischaemic <span class="hlt">preconditioning</span>, therapeutic hypothermia, or hyperoxaemia) or pharmacological (such as cyclosporin-A, natriuretic peptide, exenatide) ‘conditioning’ strategies as adjuncts to PPCI. Furthermore, recent developments in cardiac magnetic resonance (CMR) imaging can provide a non-invasive imaging strategy for assessing the efficacy of these novel adjunctive therapies to PPCI in terms of key surrogate clinical endpoints such as myocardial infarct size, myocardial salvage, left ventricular ejection fraction, and the presence of microvascular obstruction or intramyocardial haemorrhage. In this article, we review the therapeutic potential of ‘conditioning’ to protect the heart against lethal myocardial reperfusion injury in STEMI patients undergoing PPCI. PMID:24062884</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED474119.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED474119.pdf"><span id="translatedtitle">Community How To Guide On Underage Drinking <span class="hlt">Prevention</span>: <span class="hlt">Prevention</span> & Education.</span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>National Association of Governors' Highway Safety Representatives.</p> <p></p> <p>Underage drinking <span class="hlt">prevention</span> has two goals: <span class="hlt">prevent</span> harm to the individual drinker and <span class="hlt">prevent</span> harm to society. Modern <span class="hlt">prevention</span> programs should be measured not by their intentions, but by their consequences: reducing the number of criminal events, reducing the amount of harm to individuals, and reducing the harm to society. This guide discusses…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://files.eric.ed.gov/fulltext/ED532219.pdf','ERIC'); return false;" href="http://files.eric.ed.gov/fulltext/ED532219.pdf"><span id="translatedtitle">Gender-Based Violence <span class="hlt">Prevention</span>. Issues in <span class="hlt">Prevention</span></span></a></p> <p><a target="_blank" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p>Higher Education Center for Alcohol, Drug Abuse, and Violence Prevention, 2012</p> <p>2012-01-01</p> <p>This issue of "Issues in <span class="hlt">Prevention</span>" focuses on gender-based violence <span class="hlt">prevention</span>. This issue contains the following articles: (1) <span class="hlt">Preventing</span> Gender-Based Violence: An Overview (Linda Langford); (2) Q&A With Amelia Cobb; (3) Denim Day at HBCUs; (4) Dear Colleague Letter; (5) ED Grants for Violence <span class="hlt">Prevention</span>; and (6) Higher Education Center…</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2305865','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2305865"><span id="translatedtitle"><span class="hlt">Prevention</span> of Eye Injuries</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Pashby, Tom</p> <p>1981-01-01</p> <p>In Canada 30,000 people are registered as blind; in one third of these, blindness might have been avoided. <span class="hlt">Prevention</span> is the key to reducing the number of eye injuries and blind eyes. The role of the family physician in early identification of treatable conditions and in the education of patients is discussed, but responsibility for <span class="hlt">prevention</span> belongs to all physicians. The success of <span class="hlt">prevention</span> is seen in the great reduction in eye injuries in industry and sports since eye protectors have been commonly used. However, many dangers to the eyes are either not recognized or are not taken seriously enough. This paper discusses some of the common causes of serious eye injuries in the home, in sports and in industry. Imagesp464-aFig. 1Fig. 2Fig. 3Fig. 4 PMID:21289691</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4171685','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4171685"><span id="translatedtitle"><span class="hlt">Prevention</span> of Child Maltreatment</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Lane, Wendy Gwirtzman</p> <p>2014-01-01</p> <p>Pediatricians and other health care providers can play a number of important roles in the <span class="hlt">prevention</span> of child maltreatment. As part of routine patient care, pediatricians can provide anticipatory guidance for effective discipline and parent-child communication, screen for maltreatment risk factors, and refer parents and families to effective community-based programs. This article will help pediatricians incorporate child abuse <span class="hlt">prevention</span> into their practice. Resources for systematizing anticipatory guidance and child maltreatment risk factor screening will be described. The modalities and strengths and weaknesses of community-based <span class="hlt">prevention</span> programs will be discussed, and providers will be given tools to identify the effectiveness of available community-based programs. At a broader level, the article will describe ways that pediatricians can advocate at the local, state, and national level for policies and programs that support families and children. PMID:25242703</p> </li> <li> <p><a target="_blank" onclick="trackOutboundLink('http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2306666','PMC'); return false;" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2306666"><span id="translatedtitle">Trauma: A <span class="hlt">Preventable</span> Disease</span></a></p> <p><a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p>Ransford, Peter M.</p> <p>1982-01-01</p> <p>While driver restraints have reduced fatalities in those provinces which have enacted seatbelt legislation, motor vehicle accidents still account for 80% of all deaths in those aged 15-24. <span class="hlt">Prevention</span> is paramount, but better prehospital care could <span class="hlt">prevent</span> much morbidity and mortality. This article describes seven years' experience in British Columbia with emergency health services, including the organization of an ambulance service, construction of emergency vehicles, training of emergency medical assistants, operation of air ambulance services, and education of the public. Imagesp2016-ap2017-a PMID:21286541</p> </li> </ol> <div class="pull-right"> <ul class="pagination"> <li><a href="#" onclick='return showDiv("page_1");'>«</a></li> <li><a href="#" onclick='return showDiv("page_21");'>21</a></li> <li><a href="#" onclick='return showDiv("page_22");'>22</a></li> <li><a href="#" onclick='return showDiv("page_23");'>23</a></li> <li><a href="#" onclick='return showDiv("page_24");'>24</a></li> <li class="active"><span>25</span></li> <li><a href="#" onclick='return showDiv("page_25");'>»</a></li> </ul> </div> </div><!-- col-sm-12 --> </div><!-- row --> </div><!-- page_25 --> <center> <div class="footer-extlink text-muted"><small>Some links on this page may take you to non-federal websites. Their policies may differ from this site.</small> </div> </center> <div id="footer-wrapper"> <div class="footer-content"> <div id="footerOSTI" class=""> <div class="row"> <div class="col-md-4 text-center col-md-push-4 footer-content-center"><small><a href="http://www.science.gov/disclaimer.html">Privacy and Security</a></small> <div class="visible-sm visible-xs push_footer"></div> </div> <div class="col-md-4 text-center col-md-pull-4 footer-content-left"> <img src="http://www.osti.gov/images/DOE_SC31.png" alt="U.S. Department of Energy" usemap="#doe" height="31" width="177"><map style="display:none;" name="doe" id="doe"><area shape="rect" coords="1,3,107,30" href="http://www.energy.gov" alt="U.S. Deparment of Energy"><area shape="rect" coords="114,3,165,30" href="http://www.science.energy.gov" alt="Office of Science"></map> <a ref="http://www.osti.gov" style="margin-left: 15px;"><img src="http://www.osti.gov/images/footerimages/ostigov53.png" alt="Office of Scientific and Technical Information" height="31" width="53"></a> <div class="visible-sm visible-xs push_footer"></div> </div> <div class="col-md-4 text-center footer-content-right"> <a href="http://www.osti.gov/nle"><img src="http://www.osti.gov/images/footerimages/NLElogo31.png" alt="National Library of Energy" height="31" width="79"></a> <a href="http://www.science.gov"><img src="http://www.osti.gov/images/footerimages/scigov77.png" alt="science.gov" height="31" width="98"></a> <a href="http://worldwidescience.org"><img src="http://www.osti.gov/images/footerimages/wws82.png" alt="WorldWideScience.org" height="31" width="90"></a> </div> </div> </div> </div> </div> <p><br></p> </div><!-- container --> </body> </html>