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1

Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice  

PubMed Central

Previously we have shown that, unlike wild-type mice (WT), heme oxygenase-1 knockout (HO-1?/?) mice developed nitrate tolerance and were not protected from inflammation caused by ischemia-reperfusion (I/R) when preconditioned with a H2S donor. We hypothesized that stimulation (with BAY 41-2272) or activation (with BAY 60-2770) of soluble guanylate cyclase (sGC) would precondition HO-1?/? mice against an inflammatory effect of I/R and increase arterial nitrate responses. Intravital fluorescence microscopy was used to visualize leukocyte rolling and adhesion to postcapillary venules of the small intestine in anesthetized mice. Relaxation to ACh and BAY compounds was measured on superior mesenteric arteries isolated after I/R protocols. Preconditioning with either BAY compound 10 min (early phase) or 24 h (late phase) before I/R reduced postischemic leukocyte rolling and adhesion to sham control levels and increased superior mesenteric artery responses to ACh, sodium nitroprusside, and BAY 41-2272 in WT and HO-1?/? mice. Late-phase preconditioning with BAY 60-2770 was maintained in HO-1?/? and endothelial nitric oxide synthase knockout mice pretreated with an inhibitor (dl-propargylglycine) of enzymatically produced H2S. Pretreatment with BAY compounds also prevented the I/R increase in small intestinal TNF-?. We speculate that increasing sGC activity and related PKG acts downstream to H2S and disrupts signaling processes triggered by I/R in part by maintaining low cellular Ca2+. In addition, BAY preconditioning did not increase sGC levels, yet increased the response to agents that act on reduced heme-containing sGC. Collectively these actions would contribute to increased nitrate sensitivity and vascular function. PMID:23771693

Wang, Walter Z.; Wang, Meifang; Durante, William; Korthuis, Ronald J.

2013-01-01

2

Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO- and p38 MAPK-dependent mechanism.  

PubMed

Hydrogen sulfide (H(2)S) is one of three endogenous gases, along with carbon monoxide (CO) and nitric oxide (NO), that exert a variety of important vascular actions in vivo. Although it has been demonstrated that CO or NO can trigger the development of a preconditioned phenotype in postischemic tissues, it is unclear whether H(2)S may also induce protection in organs subsequently exposed to ischemia-reperfusion (I/R). In light of these observations, we postulated that preconditioning with the exogenous H(2)S donor sodium hydrosulfide (NaHS-PC) would inhibit leukocyte rolling (LR) and adhesion (LA) induced by I/R. We used intravital microscopic techniques to demonstrate that NaHS-PC 24 h, but not 1 h, before I/R causes postcapillary venules to shift to an anti-inflammatory phenotype in wild-type (WT) mice such that these vessels fail to support LR and LA during reperfusion. The protective effect of NaHS-PC on LR was largely abolished by coincident pharmacological inhibition of NO synthase (NOS) in WT animals and was absent in endothelial NOS-deficient (eNOS(-/-)) mice. A similar pattern of response was noted in WT mice treated concomitantly with NaHS plus p38 mitogen-activated protein kinase (MAPK) inhibitors (SB 203580 or SK-86002). Whereas the reduction in LA induced by antecedent NaHS was attenuated by pharmacological inhibition of NOS or p38 MAPK in WT mice, the antiadhesive effect of NaHS was still evident in eNOS(-/-) mice. Thus NaHS-PC prevents LR and LA by triggering the activation of an eNOS- and p38 MAPK-dependent mechanism. However, the role of eNOS in the antiadhesive effect of NaHS-PC was less prominent than its effect to reduce LR. PMID:19168723

Yusof, Mozow; Kamada, Kazuhiro; Kalogeris, Theodore; Gaskin, F Spencer; Korthuis, Ronald J

2009-03-01

3

Prevention of post-ischemic brain lipid conjugated diene production and neurological injury by hydroxyethyl starch-conjugated deferoxamine.  

PubMed

Hydroxyethyl starch conjugated deferoxamine (DFO) was administered to rats following resuscitation from 6.5 min cardiac arrest (CA) in an attempt to prevent the iron-catalyzed production of oxygen free radicals which may lead to neurologic injury and ultimately death following restoration of spontaneous circulation (ROSC). Brain conjugated dienes were analyzed spectrophotometrically 4 and 24 hr following ROSC, and were found to be significantly elevated when compared to non-ischemic controls. Hydroxyethyl starch-DFO treated rats demonstrated no increased conjugated diene production at either period. Neurologic injury was significantly less in drug treated rats surviving 24 or 72 hours when compared to controls. While mortality was similar in drug treated or control rats for the first 24 hours following ROSC, delayed mortality (days 1-10) was significantly less in drug treated animals, presumably as a result of neurologic protection afforded by post-ischemic drug administration. Administration of DFO conjugated to hydroxyethyl starch appears to modulate the neurologic injury which occurs during brain ischemia and reperfusion. PMID:1371490

Rosenthal, R E; Chanderbhan, R; Marshall, G; Fiskum, G

1992-01-01

4

Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts  

Microsoft Academic Search

INTRODUCTION: Postischemic injury to the coronary vascular endothelium, in particular to the endothelial glycocalyx, may provoke fluid extravasation. Shedding of the glycocalyx is triggered by redox stress encountered during reperfusion and should be alleviated by the radical scavenger nitric oxide (NO). The objective of this study was to investigate the effect of exogenous administration of NO during reperfusion on both

Dirk Bruegger; Markus Rehm; Matthias Jacob; Daniel Chappell; Mechthild Stoeckelhuber; Ulrich Welsch; Peter Conzen; Bernhard F Becker

2008-01-01

5

Preconditioning as a potential strategy for the prevention of Parkinson's disease.  

PubMed

Parkinson's disease (PD) is a chronic neurodegenerative movement disorder characterized by the progressive and massive loss of dopaminergic neurons by neuronal apoptosis in the substantia nigra pars compacta and depletion of dopamine in the striatum, which lead to pathological and clinical abnormalities. A numerous of cellular processes including oxidative stress, mitochondrial dysfunction, and accumulation of ?-synuclein aggregates are considered to contribute to the pathogenesis of Parkinson's disease. A further understanding of the cellular and molecular mechanisms involved in the pathophysiology of PD is crucial for developing effective diagnostic, preventative, and therapeutic strategies to cure this devastating disorder. Preconditioning (PC) is assumed as a natural adaptive process whereby a subthreshold stimulus can promote protection against a subsequent lethal stimulus in the brain as well as in other tissues that affords robust brain tolerance facing neurodegenerative insults. Multiple lines of evidence have demonstrated that preconditioning as a possible neuroprotective technique may reduce the neural deficits associated with neurodegenerative diseases such as PD. Throughout the last few decades, a lot of efforts have been made to discover the molecular determinants involved in preconditioning-induced protective responses; although, the accurate mechanisms underlying this "tolerance" phenomenon are not fully understood in PD. In this review, we will summarize pathophysiology and current therapeutic approaches in PD and discuss about preconditioning in PD as a potential neuroprotective strategy. Also the role of gene reprogramming and mitochondrial biogenesis involved in the preconditioning-mediated neuroprotective events will be highlighted. Preconditioning may represent a promising therapeutic weapon to combat neurodegeneration. PMID:24696268

Golpich, Mojtaba; Rahmani, Behrouz; Mohamed Ibrahim, Norlinah; Dargahi, Leila; Mohamed, Zahurin; Raymond, Azman Ali; Ahmadiani, Abolhassan

2015-02-01

6

Can endurance exercise preconditioning prevention disuse muscle atrophy?  

PubMed Central

Emerging evidence suggests that exercise training can provide a level of protection against disuse muscle atrophy. Endurance exercise training imposes oxidative, metabolic, and heat stress on skeletal muscle which activates a variety of cellular signaling pathways that ultimately leads to the increased expression of proteins that have been demonstrated to protect muscle from inactivity –induced atrophy. This review will highlight the effect of exercise-induced oxidative stress on endogenous enzymatic antioxidant capacity (i.e., superoxide dismutase, glutathione peroxidase, and catalase), the role of oxidative and metabolic stress on PGC1-?, and finally highlight the effect heat stress and HSP70 induction. Finally, this review will discuss the supporting scientific evidence that these proteins can attenuate muscle atrophy through exercise preconditioning. PMID:25814955

Wiggs, Michael P.

2015-01-01

7

Prevention of experimental stroke by hypercapnic-hypoxic preconditioning.  

PubMed

The effectiveness of hypercapnic hypoxic training in the prevention of acute disturbances in cerebral circulation was studied under experimental conditions. Hypercapnic hypoxic training was followed by a significant decrease in the severity of neurological deficit and locomotor and coordination disorders after cerebral ischemic injury. PMID:19240841

Yakushev, N N; Bespalov, A G; Kulikov, V P

2008-09-01

8

Prevention of experimental stroke by hypercapnic-hypoxic preconditioning  

Microsoft Academic Search

The effectiveness of hypercapnic hypoxic training in the prevention of acute disturbances in cerebral circulation was studied\\u000a under experimental conditions. Hypercapnic hypoxic training was followed by a significant decrease in the severity of neurological\\u000a deficit and locomotor and coordination disorders after cerebral ischemic injury.

N. N. Yakushev; A. G. Bespalov; V. P. Kulikov

2008-01-01

9

Trends in the use of preconditioning to hypoxia for early prevention of future life diseases.  

PubMed

Environmental factors during fetal life program the health outcomes regarding many diseases in future life. This idea has been supported by worldwide epidemiological studies, but the underlying mechanisms are still poorly understood. Three questions should be answered. (i) Does a common underlying cause of ordinary pathological fetal development exist? (ii) If such a cause exists, which mechanism might develop disease in later life? (iii) Is it possible to prevent this underlying cause and therefore the associated obstetric complications to primarily prevent future life diseases? The objective of this review is to attempt to answer these three questions by using PubMed (extending to October 2012) and other sources. Three data-based answers corresponding to these questions were found: (i) hypoxia, (ii) excessive stimulation of neurogenesis, and (iii) preconditioning/adaptation to hypoxia. The method for such preconditioning/adaptation is intermittent hypoxic training (IHT), in which air with low oxygen concentration is breathed through a mask to protect against subsequent strong adverse influences. Data are cited for IHT applications for the prevention/treatment of diseases in different fields, particularly in obstetrics. Data suggested that all common fetal origins of adult diseases are likely predetermined by changes in the fetal brain; therefore, early detection of these changes must be very important. The use of IHT may be a real means to primarily prevent obstetric complications and therefore, prevent future life diseases. PMID:23524890

Basovich, Simon N

2013-02-01

10

Coronary endothelial dysfunction after ischemia and reperfusion and its prevention by ischemic preconditioning.  

PubMed

In the coronary circulation, when reperfusion follows ischemia, endothelial dysfunction occurs. This is characterized by a reduced endothelial release of nitric oxide and by an increased release of reactive oxygen species and endothelin. The reduced availability of nitric oxide leads to the adhesion of neutrophils to the vascular endothelium, platelet aggregation and, with the contribution of endothelin, vasoconstriction, which are responsible for the "no-reflow" phenomenon. Neutrophil adhesion is followed by the release of the superoxide anion from neutrophils and endothelial cells. Preconditioning limits the endothelial damage by ischemia-reperfusion. A relevant role is attributed to the increased endothelial release of nitric oxide, while that of adenosine is controversial. Another effect of preconditioning on the coronary vasculature is the acceleration of vasodilation in reactive hyperemia after a brief coronary occlusion. The acceleration is prevented if myocardial protection is achieved by means of the activation of the mitochondrial adenosine triphosphate sensitive potassium channels by diazoxide and persists when ischemic preconditioning is induced after blockade of the same channels by 5-hydroxydecanoate. PMID:12898803

Pagliaro, Pasquale; Chiribiri, Amedeo; Mancardi, Daniele; Rastaldo, Raffaella; Gattullo, Donatella; Losano, Gianni

2003-06-01

11

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

PubMed Central

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

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

2014-01-01

12

The novel radical scavenger IAC is effective in preventing and protecting against post-ischemic brain damage in Mongolian gerbils.  

PubMed

The removal of pathologically generated free radicals produced during ischemia, reperfusion and intracranical hemorrhage seems to be a viable approach to neuroprotection. However, at present, no neuroprotective agent has proven effective in focal ischemic stroke phase III trials, despite the encouraging data in animal models. This study aimed to explore the effect of the brain penetrant low molecular weight radical scavenger bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)-decandioate (IAC) in neurological damage subsequent to ischemia-reperfusion injury in Mongolian gerbils. We examined the intraperitoneal effects of IAC on temporary bilateral common carotid artery occlusion (BCCO) by means of morphological and histological analysis of the hippocampus. Significant dose-dependent protective effects of IAC (1 to 10mg/kg b.w.) against neuropathological and morphological brain changes were seen when administered i.p. 1h before temporary BCCO in Mongolian gerbils. When administered up to 6h after BCCO, IAC actually reverses the neurodegenerative processes (e.g. hippocampal cell viability) induced by ischemia in a dose-dependent fashion. Data show that IAC is highly effective in protecting and preventing oxidative brain damage associated with cerebral flow disturbances. It is also effective even in late treatment of the insult, emphasizing its potential role for the management of ischemic stroke patients. PMID:19945716

Canistro, Donatella; Affatato, Alessandra A; Soleti, Antonio; Mollace, Vincenzo; Muscoli, Carolina; Sculco, Francesca; Sacco, Iolanda; Visalli, Valeria; Bonamassa, Barbara; Martano, Manuela; Iannone, Michelangelo; Sapone, Andrea; Paolini, Moreno

2010-03-15

13

Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats  

PubMed Central

Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage. PMID:23969972

Bakkal, B.H.; Gultekin, F.A.; Guven, B.; Turkcu, U.O.; Bektas, S.; Can, M.

2013-01-01

14

Glaucoma-Induced Degeneration of Retinal Ganglion Cells Prevented by Hypoxic Preconditioning: A Model of Glaucoma Tolerance  

PubMed Central

Like all cells, neurons adapt to stress by transient alterations in phenotype, an epigenetic response that forms the basis for preconditioning against acute ischemic injury in the central nervous system. We recently showed that a modified repetitive hypoxic preconditioning (RHP) regimen significantly extends the window of ischemic tolerance to acute retinal ischemic injury from days to months. The present study was undertaken to determine if this uniquely protracted neuroprotective phenotype would also confer resistance to glaucomatous neurodegeneration. Retinal ganglion cell death at somatic and axonal levels was assessed after both 3 and 10 wks of sustained intraocular hypertension in an adult mouse model of inducible, open-angle glaucoma, with or without RHP before intraocular pressure elevation. Loss of brn3-positive ganglion cell soma after 3 wks of experimental glaucoma, along with increases in several apoptotic endpoints, were all significantly and robustly attenuated in mice subjected to RHP. Soma protection by RHP was also confirmed after 10 wks of intraocular hypertension by brn3 and SMI32 immunostaining. In addition, quantification of axon density in the postlaminar optic nerve documented robust preservation in RHP-treated mice, and neurofilament immunostaining also revealed preconditioning-induced improvements in axon integrity/survival in both retina and optic nerve after 10 wks of experimental glaucoma. This uniquely protracted period of phenotypic change, established in retinal ganglion cells by the activation of latent antiapoptotic, prosurvival mechanisms at both somatic and axonal levels, reflects a novel form of inducible neuronal plasticity that may provide innovative therapeutic targets for preventing and treating glaucoma and other neurodegenerative diseases. PMID:22396016

Zhu, Yanli; Zhang, Lihong; Schmidt, Jimena F; Gidday, Jeffrey M

2012-01-01

15

Postischemic Treatment With Ethyl Pyruvate Prevents Adenosine Triphosphate Depletion, Ameliorates Inflammation, and Decreases Thrombosis in a Murine Model of Hind-Limb Ischemia and Reperfusion  

PubMed Central

Introduction Experiments were designed to investigate the effects of ethyl pyruvate (EP) in a murine model of hind-limb ischemia-reperfusion (IR) injury. Methods C57BL6 mice underwent 90 minutes of unilateral ischemia followed by 24 hours of reperfusion using two treatment protocols. For the preischemic treatment (pre-I) protocol, mice (n = 6) were given 300 mg/kg EP before ischemia, followed by 150 mg/kg of EP just before reperfusion and at 6 hours and 12 hours after reperfusion. In a postischemic treatment (post-I) protocol, mice (n = 7) were treated with 300 mg/kg EP at the end of the ischemic period, then 15 minutes later, and 2 hours after reperfusion and 150 mg/kg of EP at 4 hours, 6 hours, 10 hours, 16 hours, and 22 hours after reperfusion. Controls mice for both protocols were treated with lactated Ringers alone at time intervals identical to EP. Skeletal muscle levels of adenosine triphosphate (ATP), interleukin-1?, keratinocyte chemoattractant protein, and thrombin antithrombin-3 complex were measured. Skeletal muscle architectural integrity was assessed microscopically. Results ATP levels were higher in mice treated with EP compared with controls under the both treatment protocols (p = 0.02). Interleukin-1?, keratinocyte chemoattractant protein, thrombin antithrombin-3 complex (p < 0.05), and the percentage of injured fibers (p < 0.0001) were significantly decreased in treated versus control mice under the both protocols. Conclusion Muscle fiber injury and markers of tissue thrombosis and inflammation were reduced, and ATP was preserved with EP in pre-I and post-I protocols. Further investigation of the efficacy of EP to modulate IR injury in a larger animal model of IR injury is warranted. PMID:21217488

Crawford, Robert S.; Albadawi, Hassan; Atkins, Marvin D.; Jones, John J.; Conrad, Mark F.; Austen, William G.; Fink, Mitchell P.; Watkins, Michael T.

2011-01-01

16

The mitochondrial origin of postischemic arrhythmias  

PubMed Central

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

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

2005-01-01

17

Induction of GRP78 by Ischemic Preconditioning Reduces Endoplasmic Reticulum Stress and Prevents Delayed Neuronal Cell Death  

Microsoft Academic Search

Although the endoplasmic reticulum (ER) is implicated in neuronal degeneration in some situations, its role in delayed neuronal cell death (DND) after ischemia remains uncertain. The authors speculated that ER stress is involved in DND, that it is reduced by ischemic preconditioning, and that ER stress reduction by preconditioning is due to ER molecular chaperone induction. The phosphorylation status of

Takeshi Hayashi; Atsushi Saito; Shuzo Okuno; Michel Ferrand-Drake; Pak H. Chan

2003-01-01

18

Quercetin improves postischemic recovery of heart function in Doxorubicin-treated rats and prevents Doxorubicin-induced matrix metalloproteinase-2 activation and apoptosis induction.  

PubMed

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

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

2015-01-01

19

Preconditioning Balloons  

NSDL National Science Digital Library

Students use balloons (a polymer) to explore preconditioning—a viscoelastic material behavior that is important to understand when designing biomedical devices. They improve their understanding of preconditioning by measuring the force needed to stretch a balloon to the same displacement multiple times. Students gain experience in data collection and graph interpretation.

Integrated Teaching and Learning Program,

20

[Effect of a new derivative of glutamic and apovincaminic acids on brain metabolism in post-ischemic period].  

PubMed

Neuroprotective properties of the new derivative of glutamic and apovincaminic acids, ethyl -(3-alpha,16-alpha)-eburnamenin-14-carbopxylate of 2-aminopentadionic acid (LHT 1-02) were studied on a model of acute brain ischemia in cats. LHT 1-02 has proved to be more effective than the reference drugs vinpocetin and glycine in preventing the reperfusive damage, which was manifested by decreased postischemic hyperglycemia, activated utilization of oxygen in the brain, and suppressed postischemic metabolic lactate acidosis. Thus, the results of this comparative study show expediency of further investigations of LHT 1 - 02 as a potential neuroprotective drug. PMID:24791334

Makarova, L M; Prikhod'ko, M A; Pogorely?, V E; Skachilova, S Ia; Mirzoian, R S

2014-01-01

21

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

PubMed Central

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.

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

2015-01-01

22

Immunizing Beef Calves: A Preconditioning Immunization Concept  

E-print Network

Properly vaccinating an entire herd, including pregnant cows, calves, replacement heifers and bulls, can prevent disease outbreaks caused by both dormant and incubating infections. This preconditioning immunization helps unborn, nursing and weanling...

Faries Jr., Floron C.

2000-12-20

23

Systemic vascular response to brachial arteries crossclamping may prognosticate the outcome of remote ischemic preconditioning.  

PubMed

Remote ischemic preconditioning (RIPC) is a recent trend in cardiovascular medicine. From the literature, it may be deduced that physiological changes resulted from repeated episodes of brachial-cuff inflation/deflation during RIPC provoke, in some way, systemic "training" of the whole organism. At the same time, the effectiveness of such a "training" is substantially different in different humans, and the latter remains unclear. We propose the hypothesis as follows: the magnitude of real-time response of cardiovascular system to transient upper limb ischemia serves as a predictive indicator of the organismal sensitivity to RIPC preventive procedure and RIPC clinical efficiency in a particular person. The hypothesized prognosis of the RIPC-induced different resistance to post-ischemic reperfusion injury in different patients is represented in a quantitative manner using dynamic infrared examination of all human limbs simultaneously. With this screening method, it is clearly shown that different cohorts of healthy individuals exhibit different organismal responsiveness to upper limb arterial transient crossclamping. If proven, our hypothesis could have important implications for emergency medicine. PMID:25655222

Vainer, Boris G; Markel, Arcady L

2015-04-01

24

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

PubMed Central

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

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

2010-01-01

25

Gender and post-ischemic recovery of hypertrophied rat hearts  

PubMed Central

Background Gender influences the cardiac response to prolonged increases in workload, with differences at structural, functional, and molecular levels. However, it is unknown if post-ischemic function or metabolism of female hypertrophied hearts differ from male hypertrophied hearts. Thus, we tested the hypothesis that gender influences post-ischemic function of pressure-overload hypertrophied hearts and determined if the effect of gender on post-ischemic outcome could be explained by differences in metabolism, especially the catabolic fate of glucose. Methods Function and metabolism of isolated working hearts from sham-operated and aortic-constricted male and female Sprague-Dawley rats before and after 20 min of no-flow ischemia (N = 17 to 27 per group) were compared. Parallel series of hearts were perfused with Krebs-Henseleit solution containing 5.5 mM [5-3H/U-14C]-glucose, 1.2 mM [1-14C]-palmitate, 0.5 mM [U-14C]-lactate, and 100 mU/L insulin to measure glycolysis and glucose oxidation in one series and oxidation of palmitate and lactate in the second. Statistical analysis was performed using two-way analysis of variance. The sequential rejective Bonferroni procedure was used to correct for multiple comparisons and tests. Results Female gender negatively influenced post-ischemic function of non-hypertrophied hearts, but did not significantly influence function of hypertrophied hearts after ischemia such that mass-corrected hypertrophied heart function did not differ between genders. Before ischemia, glycolysis was accelerated in hypertrophied hearts, but to a greater extent in males, and did not differ between male and female non-hypertrophied hearts. Glycolysis fell in all groups after ischemia, except in non-hypertrophied female hearts, with the reduction in glycolysis after ischemia being greatest in males. Post-ischemic glycolytic rates were, therefore, similarly accelerated in hypertrophied male and female hearts and higher in female than male non-hypertrophied hearts. Glucose oxidation was lower in female than male hearts and was unaffected by hypertrophy or ischemia. Consequently, non-oxidative catabolism of glucose after ischemia was lowest in male non-hypertrophied hearts and comparably elevated in hypertrophied hearts of both sexes. These differences in non-oxidative glucose catabolism were inversely related to post-ischemic functional recovery. Conclusion Gender does not significantly influence post-ischemic function of hypertrophied hearts, even though female sex is detrimental to post-ischemic function in non-hypertrophied hearts. Differences in glucose catabolism may contribute to hypertrophy-induced and gender-related differences in post-ischemic function. PMID:16509993

Saeedi, Ramesh; Wambolt, Richard B; Parsons, Hannah; Antler, Christine; Leong, Hon S; Keller, Angelica; Dunaway, George A; Popov, Kirill M; Allard, Michael F

2006-01-01

26

5'-Nucleotidase inhibition enhances postischemic myocardial performance.  

PubMed

Adenosine methylene diphosphate (AMPCP), a 5'-nucleotidase inhibitor, was evaluated as an adjunct to cold crystalloid cardioplegic myocardial protection. Cardiopulmonary bypass (CPB) was instituted at 28 degrees C in two groups of mongrel dogs (each, n = 6). Myocardial ischemia was induced for 150 min by aortic cross clamping. Crystalloid cardioplegia (4 degrees C) was infused into the aortic root at 15 ml/kg/20 min in the control group (CP). The experimental group (CP + AMPCP) received identical doses of cardioplegia supplemented with 250 microM AMPCP. While on CPB, the mean arterial pressure was 70 mm Hg and the myocardial temperature ranged from 16 to 22 degrees C. Hemodynamic parameters were recorded prior to institution of CPB and at 15 and 45 min following the termination of CPB. Starling curves were constructed for cardiac index (CI), mean arterial pressure (MAP), mean left ventricular pressure (LVP), +dP/dt and -dP/dt at each time point for left atrial pressures between 5 and 12.5 mm Hg. The area under each curve was calculated and expressed as a percentage of prebypass values. Statistical analysis was performed with Student's two-tailed t test. The data demonstrate that although recovery of CI, MAP, heart rate, and LVP was similar in both groups, statistically significant improvement in recovery of myocardial compliance (-dP/dt) and systolic function (+dP/dt) was seen with AMPCP. The addition of the 5'-nucleotidase inhibitor, AMPCP, to cold crystalloid cardioplegia enhances postischemic myocardial performance in vivo and may be useful during prolonged periods of global myocardial ischemia. PMID:8152230

Schwann, T A; Lobdell, K W; Braxton, J; Condos, S; Baldwin, J C; Kopf, G S

1994-04-01

27

Molecular mechanism of preconditioning.  

PubMed

During the last 20 years, since the appearance of the first publication on ischemic preconditioning (PC), our knowledge of this phenomenon has increased exponentially. PC is defined as an increased tolerance to ischemia and reperfusion induced by previous sublethal period ischemia. This is the most powerful mechanism known to date for limiting the infract size. This adaptation occurs in a biphasic pattern (i) early preconditioning (lasts for 2-3 h) and (ii) late preconditioning (starting at 24 h lasting until 72-96 h after initial ischemia). Early preconditioning is more potent than delayed preconditioning in reducing infract size. Late preconditioning attenuates myocardial stunning and requires genomic activation with de novo protein synthesis. Early preconditioning depends on adenosine, opioids and to a lesser degree, on bradykinin and prostaglandins, released during ischemia. These molecules activate G-protein-coupled receptor, initiate activation of K(ATP) channel and generate oxygen-free radicals, and stimulate a series of protein kinases, which include protein kinase C, tyrosine kinase, and members of MAP kinase family. Late preconditioning is triggered by a similar sequence of events, but in addition essentially depends on newly synthesized proteins, which comprise iNOS, COX-2, manganese superoxide dismutase, and possibly heat shock proteins. The final mechanism of PC is still not very clear. The present review focuses on the possible role signaling molecules that regulate cardiomyocyte life and death during ischemia and reperfusion. PMID:18344203

Das, Manika; Das, Dipak K

2008-04-01

28

Revisiting cerebral postischemic reperfusion injury: new insights in understanding reperfusion failure, hemorrhage, and edema.  

PubMed

Cerebral postischemic reperfusion injury is defined as deterioration of ischemic brain tissue that parallels and antagonizes the benefits of restoring cerebral circulation after therapeutic thrombolysis for acute ischemic stroke. To understand the paradox of injury caused by treatment, we first emphasize the phenomenon in which recanalization of an occluded artery does not lead to tissue reperfusion. Additionally, no-reflow after recanalization may be due to injury of the neurovascular unit, distal microthrombosis, or both, and certainly worsens outcome. We examine the mechanism of molecular and subcellular damage in the neurovascular unit, notably oxidative stress, mitochondrial dysfunction, and apoptosis. At the level of the neurovascular unit, which mediates crosstalk between the damaged brain and systemic responses in blood, we summarize emerging evidence demonstrating that individual cell components play unique and cumulative roles that lead to damage of the blood-brain barrier and neurons. Furthermore, we review the latest developments in establishing a link between the immune system and microvascular dysfunction during ischemic reperfusion. Progress in assessing reperfusion injury has also been made, and we review imaging studies using various magnetic resonance imaging modalities. Lastly, we explore potential treatment approaches, including ischemic preconditioning, postconditioning, pharmacologic agents, and hypothermia. PMID:25598025

Bai, Jilin; Lyden, Patrick D

2015-02-01

29

Transient Ureteral Obstruction Prevents against Kidney Ischemia/Reperfusion Injury via Hypoxia-Inducible Factor (HIF)-2? Activation  

PubMed Central

Although the protective effect of transient ureteral obstruction (UO) prior to ischemia on subsequent renal ischemia/reperfusion (I/R) injury has been documented, the underlying molecular mechanism remains to be understood. We showed in the current study that 24 h of UO led to renal tubular hypoxia in the ipsilateral kidney in mice, with the accumulation of hypoxia-inducible factor (HIF)-2?, which lasted for a week after the release of UO. To address the functions of HIF-2? in UO-mediated protection of renal IRI, we utilized the Mx-Cre/loxP recombination system to knock out target genes. Inactivation of HIF-2?, but not HIF-1? blunted the renal protective effects of UO, as demonstrated by much higher serum creatinine level and severer histological damage. UO failed to prevent postischemic neutrophil infiltration and apoptosis induction in HIF-2? knockout mice, which also diminished the postobstructive up-regulation of the protective molecule, heat shock protein (HSP)-27. The renal protective effects of UO were associated with the improvement of the postischemic recovery of intra-renal microvascular blood flow, which was also dependent on the activation of HIF-2?. Our results demonstrated that UO protected the kidney via activation of HIF-2?, which reduced tubular damages via preservation of adequate renal microvascular perfusion after ischemia. Thus, preconditional HIF-2? activation might serve as a novel therapeutic strategy for the treatment of ischemic acute renal failure. PMID:22295069

Chen, Xiao-Song; Zhang, Ming; Xu, Long-Mei; Zhang, Jian-Jun; Xia, Qiang

2012-01-01

30

EEG, CT and neurosonographic findings in patients with postischemic seizures  

Microsoft Academic Search

Seventy-two patients with postischemic seizures were evaluated with electroencephalography (EEG), computerized tomography (CT) and neurosonography. There were 24% early-onset and 76% late-onset initial seizures. Early-onset seizure was more likely to be simple partial (53%), whereas late-onset seizure was more likely to be primarily generalized (56%). 76% early-onset and 80% late-onset seizures were single. Status epilepticus was more frequent in early-onset

Susanna Horner; Xiu-Shi Ni; Margret Duft; Kurt Niederkorn; Helmut Lechner

1995-01-01

31

Hyperbaric oxygen preconditioning attenuates postoperative cognitive impairment in aged rats.  

PubMed

Cognitive decline after surgery in the elderly population is a major clinical problem with high morbidity. Hyperbaric oxygen (HBO) preconditioning can induce significant neuroprotection against acute neurological injury. We hypothesized that HBO preconditioning would prevent the development of postoperative cognitive impairment. Elderly male rats (20 months old) underwent stabilized tibial fracture operation under general anesthesia after HBO preconditioning (once a day for 5 days). Separate cohorts of animals were tested for cognitive function with fear conditioning and Y-maze tests, or euthanized at different times to assess the blood-brain barrier integrity, systemic and hippocampal proinflammatory cytokines, and caspase-3 activity. Animals exhibited significant cognitive impairment evidenced by a decreased percentage of freezing time and an increased number of learning trials on days 1, 3, and 7 after surgery, which were significantly prevented by HBO preconditioning. Furthermore, HBO preconditioning significantly ameliorated the increase in serum and hippocampal proinflammatory cytokines tumor necrosis factor-?, interleukin-1 ? (IL-1?), IL-6, and high-mobility group protein 1 in surgery-challenged animals. Moreover, HBO preconditioning markedly improved blood-brain barrier integrity and caspase-3 activity in the hippocampus of surgery-challenged animals. These findings suggest that HBO preconditioning could significantly mitigate surgery-induced cognitive impairment, which is strongly associated with the reduction of systemic and hippocampal proinflammatory cytokines and caspase-3 activity. PMID:24870985

Sun, Li; Xie, Keliang; Zhang, Changsheng; Song, Rui; Zhang, Hong

2014-06-18

32

Permanent Reduction of Seizure Threshold in Post-Ischemic CA3 Pyramidal Neurons  

E-print Network

Permanent Reduction of Seizure Threshold in Post-Ischemic CA3 Pyramidal Neurons PATRICE CONGAR thresh- old in post-ischemic CA3 pyramidal neurons. J. Neurophysiol. 83: 2040­2046, 2000. The effects of ischemia were examined on CA3 pyramidal neurons recorded in hippocampal slices 2­4 mo after a global

Cossart, Rosa

33

Delayed Postischemic Hypothermia: A Six Month Survival Study Using Behavioral and Histological A ssessments of Neuroprotection  

Microsoft Academic Search

In the gerbil, brief global forebrain ischemia induces pro- found habituation and working memory impairments that stem from delayed hippocampal CA1 death. Short duration postischemic hypothermia has been shown to reduce CA1 loss, but such reports are controversial, as it is thought that protection may be transient. The purpose of this study was to investigate whether prolonged postischemic hypo- thermia

Frederick Colbourne; Dale Corbett

34

Post-ischemic inflammation regulates neural damage and protection  

PubMed Central

Post-ischemic inflammation is important in ischemic stroke pathology. However, details of the inflammation process, its resolution after stroke and its effect on pathology and neural damage have not been clarified. Brain swelling, which is often fatal in ischemic stroke patients, occurs at an early stage of stroke due to endothelial cell injury and severe inflammation by infiltrated mononuclear cells including macrophages, neutrophils, and lymphocytes. At early stage of inflammation, macrophages are activated by molecules released from necrotic cells [danger-associated molecular patterns (DAMPs)], and inflammatory cytokines and mediators that increase ischemic brain damage by disruption of the blood–brain barrier are released. After post-ischemic inflammation, macrophages function as scavengers of necrotic cell and brain tissue debris. Such macrophages are also involved in tissue repair and neural cell regeneration by producing tropic factors. The mechanisms of inflammation resolution and conversion of inflammation to neuroprotection are largely unknown. In this review, we summarize information accumulated recently about DAMP-induced inflammation and the neuroprotective effects of inflammatory cells, and discuss next generation strategies to treat ischemic stroke. PMID:25352781

Shichita, Takashi; Ito, Minako; Yoshimura, Akihiko

2014-01-01

35

Neutrophil recruitment in the reperfused-injured rat liver was effectively attenuated by repertaxin, a novel allosteric noncompetitive inhibitor of CXCL8 receptors: a therapeutic approach for the treatment of post-ischemic hepatic syndromes.  

PubMed

Hepatic reperfusion injury represents a crucial problem in several clinical situations including liver transplantation, extensive hepatectomy and hypovolemic shock with resuscitation. Repertaxin is a new non-competitive allosteric blocker of interleukin-8 (CXCL8) receptors, which by locking CXCR1/R2 in an inactive conformation, prevents receptor signaling and polymorphonuclear leukocyte (PMN) chemotaxis. The present study shows that repertaxin dramatically prevents rat post-ischemic hepatocellular necrosis (80% of inhibition) and PMN infiltration (96% of inhibition) at a clinically-relevant time (24 h) of reperfusion. Treatment with repertaxin by continuous infusion is demonstrated to be the optimal route of administration of the compound especially in view of its clinical therapeutic use. Because repertaxin has proven to be safe and well tolerated in different animal studies and in phase I studies in human volunteers, it is in fact a candidate novel therapeutic agent for the prevention and treatment of hepatic post-ischemic injury. PMID:16164828

Cavalieri, B; Mosca, M; Ramadori, P; Perrelli, M-G; De Simone, L; Colotta, F; Bertini, R; Poli, G; Cutrìn, J C

2005-01-01

36

Intestinal injury can be reduced by intra-arterial postischemic perfusion with hypertonic saline  

PubMed Central

AIM: To investigate the effect of local intestinal perfusion with hypertonic saline (HTS) on intestinal ischemia-reperfusion injury (IRI) in both ex vivo and in vivo rat models. METHODS: All experiments were performed on male Wistar rats anesthetized with pentobarbital sodium given intraperitoneally at a dose of 60 mg/kg. Ex vivo vascularly perfused rat intestine was subjected to 60-min ischemia and either 30-min reperfusion with isotonic buffer (controls), or 5 min with HTS of 365 or 415 mOsm/L osmolarity (HTS365mOsm or HTS415mOsm, respectively) followed by 25-min reperfusion with isotonic buffer. The vascular intestinal perfusate flow (IPF) rate was determined by collection of the effluent from the portal vein in a calibrated tube. Spontaneous intestinal contraction rate was monitored throughout. Irreversible intestinal injury or area of necrosis (AN) was evaluated histochemically using 2.3.5-triphenyltetrazolium chloride staining. In vivo, 30-min ischemia was followed by either 30-min blood perfusion or 5-min reperfusion with HTS365mOsm through the superior mesenteric artery (SMA) followed by 25-min blood perfusion. Arterial blood pressure (BP) was measured in the common carotid artery using a miniature pressure transducer. Histological injury was evaluated in both preparations using the Chui score. RESULTS: Ex vivo, intestinal IRI resulted in a reduction in the IPF rate during reperfusion (P < 0.05 vs sham). The postischemic recovery of the IPF rate did not differ between the controls and the HTS365mOsm group. In the HTS415mOsm group, postischemic IPF rates were lower than in the controls and the HTS365mOsm group (P < 0.05). The intestinal contraction rate was similar at baseline in all groups. An increase in this parameter was observed during the first 10 min of reperfusion in the control group as compared to the sham-treated group, but no such increase was seen in the HTS365mOsm group. In controls, AN averaged 14.8% ± 5.07% of the total tissue volume. Administration of HTS365mOsm for 5 min after 60-min ischemia resulted in decrease in AN (5.1% ± 1.20% vs controls, P < 0.01). However, perfusion of the intestine with the HTS of greater osmolarity (HTS415mOsm) failed to protect the intestine from irreversible injury. The Chiu score was lower in the HTS365mOsm group in comparison with controls (2.4 ± 0.54 vs 3.2 ± 0.44, P = 0.042), while intestinal perfusion with HTS415mOsm failed to improve the Chiu score. Intestinal reperfusion with HTS365mOsm in the in vivo series secured rapid recovery of BP after its transient fall, whereas in the controls no recovery was seen. The Chiu score was lower in the HTS365mOsm group vs controls (3.1 ± 0.26 and 3.8 ± 0.22, P = 0.0079 respectively,), although the magnitude of the effect was lower than in the ex vivo series. CONCLUSION: Brief intestinal postischemic perfusion with HTS365mOsm through the SMA followed by blood flow restoration is a protective procedure that could be used for the prevention of intestinal IRI. PMID:23345943

Kornyushin, Oleg; Galagudza, Michael; Kotslova, Anna; Nutfullina, Gelfia; Shved, Nina; Nevorotin, Alexey; Sedov, Valeriy; Vlasov, Timur

2013-01-01

37

TOWARD THE OPTIMAL PRECONDITIONED EIGENSOLVER: LOCALLY OPTIMAL BLOCK PRECONDITIONED  

E-print Network

advocate the standard preconditioned conjugate gradient method for finding an eigenvector as an element of Colorado at Boulder, 1999, and at the Sixth Copper Mountain Conference on Iterative Methods, Copper

Knyazev, Andrew

38

Preconditioning provides neuroprotection in models of CNS disease: paradigms and clinical significance.  

PubMed

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, surgical brain injury, 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. PMID:24389580

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

2014-03-01

39

An improved algorithm of fiber tractography demonstrates postischemic cerebral reorganization  

NASA Astrophysics Data System (ADS)

In vivo white matter tractography by diffusion tensor imaging (DTI) accurately represents the organizational architecture of white matter in the vicinity of brain lesions and especially ischemic brain. In this study, we suggested an improved fiber tracking algorithm based on TEND, called TENDAS, for tensor deflection with adaptive stepping, which had been introduced a stepping framework for interpreting the algorithm behavior as a function of the tensor shape (linear-shaped or not) and tract history. The propagation direction at each step was given by the deflection vector. TENDAS tractography was used to examine a 17-year-old recovery patient with congenital right hemisphere artery stenosis combining with fMRI. Meaningless picture location was used as spatial working memory task in this study. We detected the shifted functional localization to the contralateral homotypic cortex and more prominent and extensive left-sided parietal and medial frontal cortical activations which were used directly as seed mask for tractography for the reconstruction of individual spatial parietal pathways. Comparing with the TEND algorithms, TENDAS shows smoother and less sharp bending characterization of white matter architecture of the parietal cortex. The results of this preliminary study were twofold. First, TENDAS may provide more adaptability and accuracy in reconstructing certain anatomical features, whereas it is very difficult to verify tractography maps of white matter connectivity in the living human brain. Second, our study indicates that combination of TENDAS and fMRI provide a unique image of functional cortical reorganization and structural modifications of postischemic spatial working memory.

Liu, Xiao-dong; Lu, Jie; Yao, Li; Li, Kun-cheng; Zhao, Xiao-jie

2008-03-01

40

Protein kinase C beta in postischemic brain mitochondria.  

PubMed

PKC is implicated in the regulation of mitochondrial metabolism. We examined the association of PKC? with mitochondria and followed postischemic changes in its amount in mitochondria isolated from ischemia-vulnerable (CA1) and ischemia-resistant (CA2-4,DG) hippocampus in gerbil model of transient brain ischemia. Our observations suggest that transient ischemic episode induces a significant, rapid and long lasting increase of PKC? in mitochondria in CA2-4,DG, which may bespeak neuroprotection. In organotypic hippocampal culture (OHC) model of neurodegeneration, PKC? inhibition imposed over NMDA toxicity extended the death area beyond the CA1. These results suggest that PKC? might have a protective effect against excitotoxic damage in rat OHC. The pull-down method and LC-MS/MS analysis revealed mitochondrial proteins that can bind directly with PKC??. The proteins were parts of i) mitochondrial redox carriers forming the electron transport chain including ATP synthase and ii) MPTP: ANT and creatine kinase. PKC? acting through mitochondrial proteins could play a role in protecting the cells from death by e.g. influencing ROS and ATP production after ischemia in CA2-4,DG region of the hippocampus. PMID:21704734

Kowalczyk, Joanna E; Kawalec, Maria; Ber?sewicz, Ma?gorzata; D?bski, Janusz; Dadlez, Micha?; Zab?ocka, Barbara

2012-01-01

41

The iron chelator desferrioxamine attenuates postischemic ventricular dysfunction  

SciTech Connect

Recent evidence suggests that postischemic myocardial dysfunction (stunning) may be mediated by oxygen free radicals, but the mechanism by which they produce myocellular damage remains unknown. Since iron catalyzes formation of hydroxyl radicals (HO{center dot}) as well as HO{center dot}-initiated lipid peroxidation, the authors explored the potential role of this metal in the pathogenesis of myocardial stunning. Open-chest dogs undergoing a 15-min occlusion of the left anterior descending coronary artery (LAD) followed by 4 h of reperfusion (REP) received the iron chelator desferrioxamine intravenously or normal saline. Regional myocardial function was assessed by measuring systolic wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under base-line conditions and similar degrees of dyskinesis during ischemia. After REP, however, recovery of contractile function as considerably greater in desferrioxamine-treated compared with control dogs. These differences could not be ascribed to hemodynamic factors. The results suggest that iron-catalyzed reactions (possibly HO{center dot} generation) play a significant role in myocardial stunning after a brief episode of reversible regional ischemia.

Bolli, R.; Patel, B.S.; Zhu, Weixi; O'Neill, P.G.; Hartley, C.J.; Charlat, M.L.; Roberts, R. (Baylor College of Medicine, Houston, TX (US))

1987-12-01

42

Postischemic generation of superoxide anion by newborn pig brain.  

PubMed

Cerebral superoxide anion generation during reperfusion after total cerebral ischemia was measured in newborn pigs. Superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction was determined using two closed cranial windows inserted over the parietal cortices. Twenty minutes of total cerebral ischemia was produced by increasing intracranial pressure, and SOD-inhibitable NBT reduction was determined during 20 min of reperfusion. SOD-inhibitable NBT reduction (8.7 +/- 1.5 pmol.mm-2.20 min-1) was greater in piglets subjected to cerebral ischemia followed by reperfusion than in control piglets not exposed to ischemia (1.6 +/- 1.3 pmol.mm-2.20 min-1). Pretreatment with indomethacin (5 mg/kg iv) markedly reduced postischemia SOD-inhibitable NBT reduction (2.8 +/- 1.1 pmol.mm-2.20 min-1). We conclude that superoxide anion radical is produced by newborn pig brain during postischemic reperfusion. Furthermore, cyclooxygenase metabolism of arachidonic acid appears to be a major source of this activated oxygen during reperfusion of ischemic piglet brain. PMID:2841877

Armstead, W M; Mirro, R; Busija, D W; Leffler, C W

1988-08-01

43

Long-term effects of pre and post-ischemic exercise following global cerebral ischemia on astrocyte and microglia functions in hippocampus from Wistar rats.  

PubMed

Persistent effects of pre- and postischemic exercise on glial cells activation after global cerebral ischemia remains poorly understood. Here, we investigated the effect of both pre and postischemic treadmill exercise protocols (20min/day during 2 weeks) on glial cells immunostaining in the hippocampus of Wistar rats submitted to global ischemia. A synergistic effect between ischemia and postischemic exercise on the astrocytic area was demonstrated. Postischemic exercise partially reversed the ischemia-induced increase on the area occupied by microglia, without any effect of pre-ischemic protocol. In conclusion, postischemic exercise distinctly modulates astrocyte and microglia immunostaining in the hippocampal dentate gyrus following global cerebral ischemia in Wistar rats. PMID:25192647

Lovatel, Gisele Agustini; Bertoldi, Karine; Elsnerb, Viviane Rostirola; Piazza, Francele Valente; Basso, Carla Giovana; Moysés, Felipe Dos Santos; Worm, Paulo Valdeci; Netto, Carlos Alexandre; Marcuzzo, Simone; Siqueira, Ionara Rodrigues

2014-10-31

44

PRECONDITIONING HIGHLY INDEFINITE AND NONSYMMETRIC MATRICES \\Lambda  

E-print Network

) preconditioners and iterative solvers were tested on a set of standard problems from chemical engineering, nonsymmetric problems which cause difficulties for preconditioned iterative solvers. Our numerical experiments indicate that the reliability and performance of preconditioned iterative solvers are greatly enhanced

Tùma, Miroslav

45

Preconditioning stimuli induce autophagy via sphingosine kinase 2 in mouse cortical neurons.  

PubMed

Sphingosine kinase 2 (SPK2) and autophagy are both involved in brain preconditioning, but whether preconditioning-induced SPK2 up-regulation and autophagy activation are linked mechanistically remains to be elucidated. In this study, we used in vitro and in vivo models to explore the role of SPK2-mediated autophagy in isoflurane and hypoxic preconditioning. In primary mouse cortical neurons, both isoflurane and hypoxic preconditioning induced autophagy. Isoflurane and hypoxic preconditioning protected against subsequent oxygen glucose deprivation or glutamate injury, whereas pretreatment with autophagy inhibitors (3-methyladenine or KU55933) abolished preconditioning-induced tolerance. Pretreatment with SPK2 inhibitors (ABC294640 and SKI-II) or SPK2 knockdown prevented preconditioning-induced autophagy. Isoflurane also induced autophagy in mouse in vivo as shown by Western blots for LC3 and p62, LC3 immunostaining, and electron microscopy. Isoflurane-induced autophagy in mice lacking the SPK1 isoform (SPK1(-/-)), but not in SPK2(-/-)mice. Sphingosine 1-phosphate and the sphingosine 1-phosphate receptor agonist FTY720 did not protect against oxygen glucose deprivation in cultured neurons and did not alter the expression of LC3 and p62, suggesting that SPK2-mediated autophagy and protections are not S1P-dependent. Beclin 1 knockdown abolished preconditioning-induced autophagy, and SPK2 inhibitors abolished isoflurane-induced disruption of the Beclin 1/Bcl-2 association. These results strongly indicate that autophagy is involved in isoflurane preconditioning both in vivo and in vitro and that SPK2 contributes to preconditioning-induced autophagy, possibly by disrupting the Beclin 1/Bcl-2 interaction. PMID:24928515

Sheng, Rui; Zhang, Tong-Tong; Felice, Valeria D; Qin, Tao; Qin, Zheng-Hong; Smith, Charles D; Sapp, Ellen; Difiglia, Marian; Waeber, Christian

2014-07-25

46

Liver ischemia preconditions the heart against ischemia-reperfusion arrhythmias  

PubMed Central

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

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

2015-01-01

47

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

E-print Network

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

Witzgall, Ralph - Naturwissenschaftliche Fakultät III

48

Induction of neuro-protective\\/regenerative genes in stem cells infiltrating post-ischemic brain tissue  

Microsoft Academic Search

BACKGROUND-: Although the therapeutic potential of bone marrow-derived stromal stem cells (BMSC) has been demonstrated in different experimental models of ischemic stroke, it remains unclear how stem cells (SC) induce neuroprotection following stroke. In this study, we describe a novel method for isolating BMSC that infiltrate postischemic brain tissue and use this method to identify the genes that are persistently

Gokhan Yilmaz; J Steven Alexander; Cigdem Erkuran Yilmaz; D Neil Granger

2010-01-01

49

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

E-print Network

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

Duong, Timothy Q.

50

Exercise and Cardiac Preconditioning Against Ischemia Reperfusion Injury  

PubMed Central

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

Quindry, John C; Hamilton, Karyn L

2013-01-01

51

Preconditioning Operators on Unstructured Grids  

NASA Technical Reports Server (NTRS)

We consider systems of mesh equations that approximate elliptic boundary value problems on arbitrary (unstructured) quasi-uniform triangulations and propose a method for constructing optimal preconditioning operators. The method is based upon two approaches: (1) the fictitious space method, i.e., the reduction of the original problem to a problem in an auxiliary (fictitious) space, and (2) the multilevel decomposition method, i.e., the construction of preconditioners by decomposing functions on hierarchical meshes. The convergence rate of the corresponding iterative process with the preconditioner obtained is independent of the mesh step. The preconditioner has an optimal computational cost: the number of arithmetic operations required for its implementation is proportional to the number of unknowns in the problem. The construction of the preconditioning operators for three dimensional problems can be done in the same way.

Nepomnyaschikh, S. V.

1996-01-01

52

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

PubMed Central

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

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

2014-01-01

53

Neuroprotective Effect of Graded Postischemic Reoxygenation in Spinal Cord Ischemia in the Rabbit  

Microsoft Academic Search

Early ischemia\\/reperfusion-induced changes of four phospholipid compounds bound to the inner cell membrane leaflet, i.e., phosphatidic acid, inositol phospholipids, serine phospholipids, and ethanolamine plasmalogens, were studied in a model of spinal cord ischemia in the rabbit during normoxic and graded postischemic reoxygenation. Light and electron microscopic analysis after normoxic reoxygenation disclosed neuronal membrane argyrophilia of the interneuronal pool located in

Nadežda Luká?ová; Martin Maršala; Gabriel Halát; Jozef Maršala

1997-01-01

54

Preclinical Evaluation of Postischemic Dehydroascorbic Acid Administration in a Large-Animal Stroke Model  

Microsoft Academic Search

Dehydroascorbic acid (DHA), a blood–brain barrier transportable form of ascorbic acid, confers robust neuroprotection following\\u000a murine stroke. In an effort to translate this promising neuroprotective strategy into human clinical trial, we evaluated postischemic\\u000a DHA administration in a large-animal stroke model. Thirty-six adult male baboons were initially randomized to undergo transorbital\\u000a craniectomy to induce transient cerebral artery occlusion and to receive

Andrew F. Ducruet; William J. Mack; J. Mocco; Daniel J. Hoh; Alexander L. Coon; Anthony L. D’Ambrosio; Christopher J. Winfree; David J. Pinsky; E. Sander Connolly

55

Effects of antioxidants on the blood-brain barrier and postischemic hyperemia.  

PubMed

The role of free oxygen radicals in blood-brain barrier (BBB) disruption and postischemic hyperemia was evaluated in the rabbit model of focal cerebral ischemia-reperfusion. Six groups of rabbits underwent clipping of the anterior cerebral, middle cerebral, and intracranial internal carotid arteries. Cerebral blood flow (CBF) was measured by using radiolabeled microspheres, before, during, and 15 minutes after 1-hour occlusion of these arteries. After 50 minutes of ischemia, Group 1 animals (control) received a placebo. Animals in Groups 2-4 received one of three drugs: catalase at 10 mg/kg, methimazole at 5 mg/kg, or indomethacin at 10 mg/kg. A fifth group received a tungsten-supplemented diet for 14 days before ischemia was induced, and a sixth group was sham operated. Microvascular integrity within the brain was determined by the presence or absence of Evan's Blue (EB)-albumin dye leakage across the BBB and was measured by microspectrofluorometry. In the control group during ischemia, CBF dropped to 14%, 7%, and 11% of preischemic levels in rostral, middle, and caudal sections of the brain, respectively, as characterized by extensive EB-albumin dye leakage through the BBB into the ischemic hemisphere. During early reperfusion, postischemic hyperemia was associated with an increase in CBF of 128%, 123%, and 129% of control in the rostral, middle, and caudal sections of the brain, respectively. In all treated groups and in the group receiving a tungsten-supplemented diet, BBB integrity was protected during reperfusion without inhibition of postischemic hyperemia. This study suggests that early disruption of the BBB to large molecules is mediated by free oxygen radicals, which inhibit rather than cause postischemic hyperemia. PMID:7754839

Tasdemiroglu, E; Christenberry, P D; Ardell, J L; Chronister, R B; Taylor, A E

1994-01-01

56

Insulin-like Growth Factor1 Reduces Postischemic White Matter Injury in Fetal Sheep  

Microsoft Academic Search

Insulin-like growth factor-1 (IGF-1) is known to be important for oligodendrocyte survival and myelination. In the current study, the authors examined the hypothesis that exogenous IGF-1 could reduce postischemic white matter injury. Bilateral brain injury was induced in near-term fetal sheep by 30 minutes of reversible carotid artery occlusion. Ninety minutes after ischemia, either vehicle (n = 8) or a

Jian Guan; Laura Bennet; Shirley George; David Wu; Harry J. Waldvogel; Peter D. Gluckman; Richard L. M. Faull; Philip S. Crosier; Alistair J. Gunn

2001-01-01

57

Cortical spreading depression-induced preconditioning in mouse neocortex is lamina specific.  

PubMed

Cortical spreading depression (CSD) is able to confer neuroprotection when delivered at least 1 day in advance of an ischemic event. However, its ability to confer neuroprotection in a more immediate time frame has not previously been investigated. Here we have used mouse neocortical brain slices to study the effects of repeated episodes of CSD in layer V and layer II/III pyramidal neurons. In layer V, CSD evoked at 15-min intervals caused successively smaller membrane depolarizations and increases in intracellular calcium compared with the response to the first CSD. With an inter-CSD interval of 30 min this preconditioning effect was much less marked, indicating that preconditioning lasts between 15 and 30 min. A single episode of CSD also provided a degree of protection in oxygen-glucose deprivation (OGD) by significantly lengthening the time a cell could withstand OGD before anoxic depolarization occurred. In layer II/III pyramidal neurons no preconditioning by CSD on subsequent episodes of CSD was observed, demonstrating that the response of pyramidal neurons to repeated CSD is lamina specific. The A1 receptor antagonist 8-cyclopentyl theophylline (8-CPT) reduced the layer V preconditioning in a concentration-related manner. Inhibition of extracellular formation of adenosine by blocking ecto-5'-nucleotidase with ?,?-methyleneadenosine 5'-diphosphate prevented preconditioning in most but not all cells. Block of equilibrative nucleoside transporters 1 and 2 with dipyramidole alone or in combination with 6-[(4-nitrobenzyl)thio]-9-?-d-ribofuranosylpurine also prevented preconditioning in some but not all cells. These data provide evidence that rapid preconditioning of one CSD by another is primarily mediated by adenosine. PMID:23515796

Gniel, Helen M; Martin, Rosemary L

2013-06-01

58

Chemogenetic Silencing of Neurons in Retrosplenial Cortex Disrupts Sensory Preconditioning  

PubMed Central

An essential aspect of episodic memory is the formation of associations between neutral sensory cues in the environment. In light of recent evidence that this critical aspect of learning does not require the hippocampus, we tested the involvement of the retrosplenial cortex (RSC) in this process using a chemogenetic approach that allowed us to temporarily silence neurons along the entire rostrocaudal extent of the RSC. A viral vector containing the gene for a synthetic inhibitory G-protein-coupled receptor (hM4Di) was infused into RSC. When the receptor was later activated by systemic injection of clozapine-N-oxide, neural activity in RSC was transiently silenced (confirmed using a patch-clamp procedure). Rats expressing hM4Di and control rats were trained in a sensory preconditioning procedure in which a tone and light were paired on some trials and a white noise stimulus was presented alone on the other trials during the Preconditioning phase. Thus, rats were given the opportunity to form an association between a tone and a light in the absence of reinforcement. Later, the light was paired with food. During the test phase when the auditory cues were presented alone, controls exhibited more conditioned responding during presentation of the tone compared with the white noise reflecting the prior formation of a tone-light association. Silencing RSC neurons during the Preconditioning phase prevented the formation of an association between the tone and light and eliminated the sensory preconditioning effect. These findings indicate that RSC may contribute to episodic memory formation by linking essential sensory stimuli during learning. PMID:25122898

Robinson, Siobhan; Todd, Travis P.; Pasternak, Anna R.; Luikart, Bryan W.; Skelton, Patrick D.; Urban, Daniel J.

2014-01-01

59

Preconditioning the diabetic human myocardium  

PubMed Central

Abstract Our objective was to determine whether human diabetic myocardium is amenable to the cardioprotective actions of ischaemic preconditioning. Human right atrial appendages were harvested from diabetic and non-diabetic patients undergoing elective coronary artery bypass graft surgery. The atrial trabeculae were isolated and subjected to 90 min. of hypoxia followed by 120 min. of reoxygenation, following which the percentage recovery of baseline contractile function was determined. The atrial trabeculae were randomized to: (i) controls (groups 1 and 3); (ii) standard hypoxic preconditioning (HPC) protocol consisting of 4 min. of hypoxia/16 min. of reoxygenation before the 90 min. index hypoxic period (groups 2 and 4); (iii) Prolonged HPC protocol consisting of: 7 min. of hypoxia /16 min. of reoxygenation before the index hypoxic period (group 5). In addition, basal levels of Akt phosphorylation were determined in right atrial appendages harvested from non-diabetic patients and diabetic patients to determine whether PI3K-Akt signalling is down-regulated in the diabetic heart. Standard HPC improved baseline contractile function in human atrial trabeculae harvested from non-diabetic patients (52.4 ± 3.8% with HPC versus 30.0 ± 3.2% in control: P= 0.001; N= 6/group), but not in atrial trabeculae isolated from diabetic patients (22.6 ± 3.3% with HPC versus 28.5 ± 1.9% in control: P > 0.05; N= 6/group). However, the prolonged HPC protocol did improve baseline contractile function in atrial trabeculae harvested from diabetic patients (42.0 ± 2.4% with HPC versus 28.5 ± 1.9% in control: P= 0.001; N? 6/group). Western blot analysis demonstrated lower levels of phosphorylated Akt in diabetic myocardium compared to non-diabetic myocardium (0.13 ± 0.03 arbitrary units versus 0.39 ± 0.11 arbitrary units: P= 0.047; N? 4/group). From the data obtained it appears that the threshold for preconditioning the diabetic myocardium is elevated which may be related to the down-regulation of the PI3K-Akt pathway. PMID:19508386

Sivaraman, Vivek; Hausenloy, Derek J; Wynne, Abigail M; Yellon, Derek M

2010-01-01

60

Preconditioning Strategy in Stem Cell Transplantation Therapy  

PubMed Central

Stem cell transplantation therapy has emerged as a promising regenerative medicine for ischemic stroke and other neurodegenerative disorders. However, many issues and problems remain to be resolved before successful clinical applications of the cell-based therapy. To this end, some recent investigations have sought to benefit from well-known mechanisms of ischemic/hypoxic preconditioning. Ischemic/hypoxic preconditioning activates endogenous defense mechanisms that show marked protective effects against multiple insults found in ischemic stroke and other acute attacks. As in many other cell types, a sub-lethal hypoxic exposure significantly increases the tolerance and regenerative properties of stem cells and progenitor cells. So far, a variety of preconditioning triggers have been tested on different stem cells and progenitor cells. Preconditioned stem cells and progenitors generally show much better cell survival, increased neuronal differentiation, enhanced paracrine effects leading to increased trophic support, and improved homing to the lesion site. Transplantation of preconditioned cells helps to suppress inflammatory factors and immune responses, and promote functional recovery. Although the preconditioning strategy in stem cell therapy is still an emerging research area, accumulating information from reports over the last few years already indicates it as an attractive, if not essential, prerequisite for transplanted cells. It is expected that stem cell preconditioning and its clinical applications will attract more attention in both the basic research field of preconditioning as well as in the field of stem cell translational research. This review summarizes the most important findings in this active research area, covering the preconditioning triggers, potential mechanisms, mediators, and functional benefits for stem cell transplant therapy. PMID:23914259

Yu, Shan Ping; Wei, Zheng; Wei, Ling

2013-01-01

61

Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning.  

PubMed

Reductions in the blood supply produce considerable injury if the duration of ischemia is prolonged. Paradoxically, restoration of perfusion to ischemic organs can exacerbate tissue damage and extend the size of an evolving infarct. Being highly metabolic organs, the heart and brain are particularly vulnerable to the deleterious effects of ischemia/reperfusion (I/R). While the pathogenetic mechanisms contributing to I/R-induced tissue injury and infarction are multifactorial, the relative importance of each contributing factor remains unclear. However, an emerging body of evidence indicates that the generation of reactive oxygen species (ROS) by mitochondria plays a critical role in damaging cellular components and initiating cell death. In this review, we summarize our current understanding of the mechanisms whereby mitochondrial ROS generation occurs in I/R and contributes to myocardial infarction and stroke. In addition, mitochondrial ROS have been shown to participate in preconditioning by several pharmacologic agents that target potassium channels (e.g., ATP-sensitive potassium (mKATP) channels or large conductance, calcium-activated potassium (mBKCa) channels) to activate cell survival programs that render tissues and organs more resistant to the deleterious effects of I/R. Finally, we review novel therapeutic approaches that selectively target mROS production to reduce postischemic tissue injury, which may prove efficacious in limiting myocardial dysfunction and infarction and abrogating neurocognitive deficits and neuronal cell death in stroke. PMID:24944913

Kalogeris, Theodore; Bao, Yimin; Korthuis, Ronald J

2014-01-01

62

Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs preconditioning  

PubMed Central

Reductions in the blood supply produce considerable injury if the duration of ischemia is prolonged. Paradoxically, restoration of perfusion to ischemic organs can exacerbate tissue damage and extend the size of an evolving infarct. Being highly metabolic organs, the heart and brain are particularly vulnerable to the deleterious effects of ischemia/reperfusion (I/R). While the pathogenetic mechanisms contributing to I/R-induced tissue injury and infarction are multifactorial, the relative importance of each contributing factor remains unclear. However, an emerging body of evidence indicates that the generation of reactive oxygen species (ROS) by mitochondria plays a critical role in damaging cellular components and initiating cell death. In this review, we summarize our current understanding of the mechanisms whereby mitochondrial ROS generation occurs in I/R and contributes to myocardial infarction and stroke. In addition, mitochondrial ROS have been shown to participate in preconditioning by several pharmacologic agents that target potassium channels (e.g., ATP-sensitive potassium (mKATP) channels or large conductance, calcium-activated potassium (mBKCa) channels) to activate cell survival programs that render tissues and organs more resistant to the deleterious effects of I/R. Finally, we review novel therapeutic approaches that selectively target mROS production to reduce postischemic tissue injury, which may prove efficacious in limiting myocardial dysfunction and infarction and abrogating neurocognitive deficits and neuronal cell death in stroke. PMID:24944913

Kalogeris, Theodore; Bao, Yimin; Korthuis, Ronald J.

2014-01-01

63

A mouse model of peripheral postischemic dysesthesia: involvement of reperfusion-induced oxidative stress and TRPA1 channel.  

PubMed

Peripheral postischemic dysesthesia was examined behaviorally in mice and we investigated the underlying molecular mechanism with a focus on oxidative stress. Hind-paw ischemia was induced by tight compression of the ankle with a rubber band, and reperfusion was achieved by cutting the rubber tourniquet. We found that reperfusion after ischemia markedly provoked licking of the reperfused hind paw, which was significantly inhibited by systemic administration of the antioxidant N-acetyl-l-cysteine and the transient receptor potential (TRP) A1 channel blocker HC-030031 [2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide]. Postischemic licking was also significantly inhibited by an intraplantar injection of another antioxidant, phenyl-N-tert-butylnitrone. The TRPV1 channel blocker BCTC [N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)tetrahydropyrazine-1(2H)-carboxamide] did not inhibit postischemic licking. An intraplantar injection of hydrogen peroxide elicited hind-paw licking, which was inhibited by N-acetyl-l-cysteine, phenyl-N-tert-butylnitrone, and HC-030031. Postischemic licking was not affected by chemical depletion of sensory C-fibers, but it was inhibited by morphine, which has been shown to inhibit the C- and A?-fiber-evoked responses of dorsal horn neurons. Interestingly, postischemic licking was not inhibited by gabapentin and pregabalin, which have been shown to inhibit the C-fiber- but not A?-fiber-evoked response. The present results suggest that ischemia-reperfusion induces oxidative stress, which activates TRPA1 channels to provoke postischemic licking. It has been suggested that this behavior is mediated by myelinated (probably A?-type) afferent fibers. Oxidative stress and TRPA1 channels may be potential targets to treat peripheral ischemia-associated dysesthesia. PMID:25228635

Sasaki, Atsushi; Mizoguchi, Shizuka; Kagaya, Kenta; Shiro, Mai; Sakai, Akiho; Andoh, Tsugunobu; Kino, Yurika; Taniguchi, Hiroyuki; Saito, Yukako; Takahata, Hiroki; Kuraishi, Yasushi

2014-12-01

64

Progranulin Deficiency Promotes Post-Ischemic Blood–Brain Barrier Disruption  

PubMed Central

Loss-of-function mutations of progranulin (PGRN) have been linked to frontotemporal dementia, but little is known about the effects of PGRN deficiency on the brain in health and disease. PGRN has been implicated in neurovascular development, inflammation, and Wnt signaling, a pathway involved in the formation of the blood–brain barrier (BBB). Because BBB alterations and inflammation contribute to ischemic brain injury, we examined the role of PGRN in the brain damage produced by ischemia-reperfusion. PGRN+/? and PGRN?/? mice underwent middle cerebral artery occlusion (MCAO) with monitoring of cerebral blood flow. Infarct volume and motor deficits were assessed 72 h later. Post-ischemic inflammation was examined by expression of inflammatory genes and flow cytometry. BBB structure and permeability were examined by electron microscopy (EM) and Evans blue (EB) extravasation, respectively. MCAO resulted in ?60% larger infarcts in PGRN+/? and PGRN?/? mice, an effect independent of hemodynamic factors or post-ischemic inflammation. Rather, massive hemorrhages and post-ischemic BBB disruption were observed, unrelated to degradation of tight junction (TJ) proteins or matrix metalloproteinases (MMPs). By EM, TJ were 30–52% shorter, fewer, and less interlocking, suggesting a weaker seal between endothelial cells. Intracerebral injection of platelet-derived growth factor-CC (PDGF-CC), which increases BBB permeability, resulted in a more severe BBB breakdown in PGRN+/? and PGRN?/? than wild-type mice. We describe a previously unrecognized involvement of PGRN in the expression of key ultrastructural features of the BBB. Such a novel vasoprotective role of PGRN may contribute to brain dysfunction and damage in conditions associated with reduced PGRN function. PMID:24336722

Jackman, Katherine; Kahles, Timo; Lane, Diane; Garcia-Bonilla, Lidia; Abe, Takato; Capone, Carmen; Hochrainer, Karin; Voss, Henning; Zhou, Ping; Ding, Aihao; Anrather, Josef

2013-01-01

65

Preconditioning techniques for stochastic partial differential equations  

E-print Network

This thesis is about preconditioning techniques for time dependent stochastic Partial Differential Equations arising in the broader context of Uncertainty Quantification. State-of-the-art methods for an efficient integration ...

Spantini, Alessio

2013-01-01

66

40 CFR 1065.518 - Engine preconditioning.  

Code of Federal Regulations, 2014 CFR

...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...

2014-07-01

67

Hypoxic preconditioning with cobalt ameliorates hypobaric hypoxia induced pulmonary edema in rat.  

PubMed

Exposure to high altitude results in hypobaric hypoxia which is considered as an acute physiological stress and often leads to high altitude maladies such as high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The best way to prevent high altitude injuries is hypoxic preconditioning which has potential clinical usefulness and can be mimicked by cobalt chloride. Preconditioning with cobalt has been reported to provide protection in various tissues against ischemic injury. However, the effect of preconditioning with cobalt against high altitude induced pulmonary edema has not been investigated in vivo. Therefore, in the present study, rats pretreated with saline or cobalt (12.5mg/kg body weight) for 7days were exposed to hypobaric hypoxia of 9142m for 5h at 24°C. Formation of pulmonary edema was assessed by measuring transvascular leakage of sodium fluorescein dye and lung water content. Total protein content, albumin content, vascular endothelial growth factor (VEGF) and cytokine levels were measured in bronchoalveolar lavage fluid. Expression of HO-1, MT, NF-?B DNA binding activity and lung tissue pathology were evaluated to determine the effect of preconditioning on HAPE. Hypobaric hypoxia induced increase in transvascular leakage of sodium fluorescein dye, lung water content, lavage total protein, albumin, VEGF levels, pro-inflammatory cytokine levels, tissue expression of cell adhesion molecules and NF-?B DNA binding activity were reduced significantly after hypoxic preconditioning with cobalt. Expression of anti-inflammatory protein HO-1, MT, TGF-? and IL-6 were increased after hypoxic preconditioning. These data suggest that hypoxic preconditioning with cobalt has protective effect against HAPE. PMID:21296072

Shukla, Dhananjay; Saxena, Saurabh; Purushothaman, Jayamurthy; Shrivastava, Kalpana; Singh, Mrinalini; Shukla, Shirish; Malhotra, Vineet Kumar; Mustoori, Sairam; Bansal, Anju

2011-04-10

68

Laser thermal preconditioning enhances dermal wound repair  

NASA Astrophysics Data System (ADS)

Preconditioning tissues with an initial mild thermal stress, thereby eliciting a stress response, can serve to protect tissue from subsequent stresses. Patients at risk for impaired healing, such as diabetics, can benefit from therapeutic methods which enhance wound repair. We present a laser thermal preconditioning protocol that accelerates cutaneous wound repair in a murine model. A pulsed diode laser (? = 1.86 ?m, ? p = 2 ms, 50 Hz, H = 7.64 mJ/cm2) was used to precondition mouse skin before incisional wounds were made. The preconditioning protocol was optimized in vitro and in vivo using hsp70 expression, cell viability, and temperature measurements as benchmarks. Hsp70 expression was non-invasively monitored using a transgenic mouse strain with the hsp70 promoter driving luciferase expression. Tissue temperature recordings were acquired in real time using an infrared camera. Wound repair was assessed by measuring hsp70 expression, biomechanical properties, and wound histology for up to 24 d. Bioluminescence (BLI) was monitored with the IVIS 200 System (Xenogen) and tensile properties with a tensiometer (BTC-2000). The in vivo BLI studies indicated that the optimized laser preconditioning protocol increased hsp70 expression by 15-fold. The tensiometer data revealed that laser preconditioned wounds are ~40% stronger than control wounds at 10 days post surgery. Similar experiments in a diabetic mouse model also enhanced wound repair strength. These results indicate that 1) noninvasive imaging methods can aid in the optimization of novel laser preconditioning methods; 2) that optimized preconditioning with a 1.86 ?m diode laser enhances early wound repair.

Wilmink, Gerald J.; Carter, Terry; Davidson, Jeffrey M.; Jansen, E. Duco

2008-02-01

69

Sivelestat Attenuates Myocardial Reperfusion Injury during Brief Low Flow Postischemic Infusion  

PubMed Central

The neutrophil elastase inhibitor sivelestat (ONO-5046) possesses unknown mechanisms of cardioprotection when infused following global ischemia, even in the absence of neutrophils. Since myocardial ischemia-reperfusion injury is strongly associated with endothelial dysfunction and reactive oxygen species (ROS) generation during reperfusion, we have tested the hypothesis that infusion of sivelestat during postischemic low flow would preserve endothelial and contractile function and reduce infarct size through an ROS-mediated mechanism. Isolated male rat hearts, subjected to global ischemia of 25 minutes, were reperfused with low flow with or without sivelestat followed by a full flow reperfusion. Hearts treated with sivelestat showed a significant improvement of LV contractile function and a reduction in infarct size. Infusion of L-NAME (nonspecific blocker of endothelial nitric oxide synthase (eNOS)) along with sivelestat during reperfusion reversed the preservation of contractile function and infarct size. In vitro EPR spin trapping experiments showed that sivelestat treatment decreased superoxide adduct formation in bovine aortic endothelial cells (BAECs) subjected to hypoxia-reoxygenation. Similarly, dihydroethidine (DHE) staining showed decreased superoxide production in LV sections from sivelestat-treated hearts. Taken together, these results indicate that sivelestat infusion during postischemic low flow reduces infarct size and preserves vasoreactivity in association with decreased ROS formation and the preservation of nitric oxide. PMID:23766850

Aune, Sverre E.; Yeh, Steve T.; Kuppusamy, Periannan; Kuppusamy, M. Lakshmi; Khan, Mahmood; Angelos, Mark G.

2013-01-01

70

Optimal preconditioning of lattice Boltzmann methods  

NASA Astrophysics Data System (ADS)

A preconditioning technique to accelerate the simulation of steady-state problems using the single-relaxation-time (SRT) lattice Boltzmann (LB) method was first proposed by Guo et al. [Z. Guo, T. Zhao, Y. Shi, Preconditioned lattice-Boltzmann method for steady flows, Phys. Rev. E 70 (2004) 066706-1]. The key idea in this preconditioner is to modify the equilibrium distribution function in such a way that, by means of a Chapman-Enskog expansion, a time-derivative preconditioner of the Navier-Stokes (NS) equations is obtained. In the present contribution, the optimal values for the free parameter ? of this preconditioner are searched both numerically and theoretically; the later with the aid of linear-stability analysis and with the condition number of the system of NS equations. The influence of the collision operator, single- versus multiple-relaxation-times (MRT), is also studied. Three steady-state laminar test cases are used for validation, namely: the two-dimensional lid-driven cavity, a two-dimensional microchannel and the three-dimensional backward-facing step. Finally, guidelines are suggested for an a priori definition of optimal preconditioning parameters as a function of the Reynolds and Mach numbers. The new optimally preconditioned MRT method derived is shown to improve, simultaneously, the rate of convergence, the stability and the accuracy of the lattice Boltzmann simulations, when compared to the non-preconditioned methods and to the optimally preconditioned SRT one. Additionally, direct time-derivative preconditioning of the LB equation is also studied.

Izquierdo, Salvador; Fueyo, Norberto

2009-09-01

71

Support graph preconditioning for elliptic finite element problems  

E-print Network

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 symmetric diagonally...

Wang, Meiqiu

2009-05-15

72

Xenon preconditioning: molecular mechanisms and biological effects  

PubMed Central

Xenon is one of noble gases and has been recognized as an anesthetic for more than 50?years. Xenon possesses many of the characteristics of an ideal anesthetic, but it is not widely applied in clinical practice mainly because of its high cost. In recent years, numerous studies have demonstrated that xenon as an anesthetic can exert neuroprotective and cardioprotective effects in different models. Moreover, xenon has been applied in the preconditioning, and the neuroprotective and cardioprotective effects of xenon preconditioning have been investigated in a lot of studies in which some mechanisms related to these protections are proposed. In this review, we summarized these mechanisms and the biological effects of xenon preconditioning. PMID:23305274

2013-01-01

73

Ischemic preconditioning enhances integrity of coronary endothelial tight junctions  

SciTech Connect

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.

Li, Zhao [Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007 (United States)] [Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007 (United States); Jin, Zhu-Qiu, E-mail: zhu-qiu.jin@sdstate.edu [Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007 (United States)] [Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007 (United States)

2012-08-31

74

Sound preconditioning therapy inhibits ototoxic hearing loss in mice  

PubMed Central

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

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

2013-01-01

75

Improving Reconstituted HDL Composition for Efficient Post-Ischemic Reduction of Ischemia Reperfusion Injury  

PubMed Central

Background New evidence shows that high density lipoproteins (HDL) have protective effects beyond their role in reverse cholesterol transport. Reconstituted HDL (rHDL) offer an attractive means of clinically exploiting these novel effects including cardioprotection against ischemia reperfusion injury (IRI). However, basic rHDL composition is limited to apolipoprotein AI (apoAI) and phospholipids; addition of bioactive compound may enhance its beneficial effects. Objective The aim of this study was to investigate the role of rHDL in post-ischemic model, and to analyze the potential impact of sphingosine-1-phosphate (S1P) in rHDL formulations. Methods and Results The impact of HDL on IRI was investigated using complementary in vivo, ex vivo and in vitro IRI models. Acute post-ischemic treatment with native HDL significantly reduced infarct size and cell death in the ex vivo, isolated heart (Langendorff) model and the in vivo model (-48%, p<0.01). Treatment with rHDL of basic formulation (apoAI + phospholipids) had a non-significant impact on cell death in vitro and on the infarct size ex vivo and in vivo. In contrast, rHDL containing S1P had a highly significant, protective influence ex vivo, and in vivo (-50%, p<0.01). This impact was comparable with the effects observed with native HDL. Pro-survival signaling proteins, Akt, STAT3 and ERK1/2 were similarly activated by HDL and rHDL containing S1P both in vitro (isolated cardiomyocytes) and in vivo. Conclusion HDL afford protection against IRI in a clinically relevant model (post-ischemia). rHDL is significantly protective if supplemented with S1P. The protective impact of HDL appears to target directly the cardiomyocyte. PMID:25781943

Brulhart-Meynet, Marie-Claude; Braunersreuther, Vincent; Brinck, Jonas; Montecucco, Fabrizio; Prost, Jean-Christophe; Thomas, Aurelien; Galan, Katia; Pelli, Graziano; Pedretti, Sarah; Vuilleumier, Nicolas; Mach, François; Lecour, Sandrine; James, Richard W.; Frias, Miguel A.

2015-01-01

76

Preconditioning 9.1 The General Approach  

E-print Network

is computed by solving Mz = s. 1David Hilbert (1862 ­ 1943) 46 #12;The matrix form of the preconditioned be a Hilbert1 space with the inner product (·, ·)H and L : H H be a linear map. This map is called self

John, Volker

77

Improvement of postischemic myocardial function and metabolism induced by administration of deferoxamine at the time of reflow: the role of iron in the pathogenesis of reperfusion injury.  

PubMed

Reperfusion of ischemic myocardium has been postulated to result in a specific oxygen radical-mediated component of tissue injury. In a previous study we demonstrated improved recovery of ventricular function and metabolism when the superoxide radical scavenger superoxide dismutase was administered at the time of postischemic reflow. Studies in vitro, have suggested that superoxide toxicity might be mediated via the generation of more reactive hydroxyl radicals in an iron-catalyzed reaction. The present study was designed to test the hypothesis that myocardial reperfusion injury might be reduced by administration of the iron chelator deferoxamine at the time of reflow, most likely by preventing hydroxyl radical formation. Sixteen isolated Langendorff rabbit hearts, perfused within the bore of a superconducting magnet, were subjected to 30 min of normothermic (37 degrees C) total global ischemia followed by 45 min of reperfusion. At reflow eight treated hearts received a 10 ml bolus containing 50 mumol of deferoxamine followed by an infusion of 11 mumol/min for the first 15 min of reflow. The hearts were then perfused with standard perfusate for an additional 30 min. Eight untreated control hearts received a similar bolus of perfusate followed by 45 min of standard reperfusion. Serial 5 min 31P nuclear magnetic resonance spectra were recorded. Myocardial phosphocreatine (PCr) content fell to 5% to 7% of control during ischemia in both groups of hearts. Deferoxamine-treated hearts recovered 99 +/- 10% of control PCr content, while untreated hearts recovered 60 +/- 16% (p less than .05). Intracellular pH fell to 5.9 during ischemia in both groups, before showing more rapid and complete recovery in treated hearts (p less than .01). Recovery of developed pressure reached 70 +/- 6% of control in treated hearts compared with 35 +/- 10% in untreated hearts (p less than .05). Iron content of the perfusate was 7 microM, and by electron paramagnetic resonance spectroscopy was in the form of Fe3+-EDTA complexes. In the effluent of treated hearts iron was in the form of Fe3+-deferoxamine chelates. In summary, administration of the iron chelator deferoxamine at the time of postischemic reflow results in greater recovery of myocardial function and energy metabolism, which supports the hypothesis that iron plays an important role in the pathogenesis of reperfusion injury. PMID:2820615

Ambrosio, G; Zweier, J L; Jacobus, W E; Weisfeldt, M L; Flaherty, J T

1987-10-01

78

Condition number estimation of preconditioned matrices.  

PubMed

The present paper introduces a condition number estimation method for preconditioned matrices. The newly developed method provides reasonable results, while the conventional method which is based on the Lanczos connection gives meaningless results. The Lanczos connection based method provides the condition numbers of coefficient matrices of systems of linear equations with information obtained through the preconditioned conjugate gradient method. Estimating the condition number of preconditioned matrices is sometimes important when describing the effectiveness of new preconditionerers or selecting adequate preconditioners. Operating a preconditioner on a coefficient matrix is the simplest method of estimation. However, this is not possible for large-scale computing, especially if computation is performed on distributed memory parallel computers. This is because, the preconditioned matrices become dense, even if the original matrices are sparse. Although the Lanczos connection method can be used to calculate the condition number of preconditioned matrices, it is not considered to be applicable to large-scale problems because of its weakness with respect to numerical errors. Therefore, we have developed a robust and parallelizable method based on Hager's method. The feasibility studies are curried out for the diagonal scaling preconditioner and the SSOR preconditioner with a diagonal matrix, a tri-daigonal matrix and Pei's matrix. As a result, the Lanczos connection method contains around 10% error in the results even with a simple problem. On the other hand, the new method contains negligible errors. In addition, the newly developed method returns reasonable solutions when the Lanczos connection method fails with Pei's matrix, and matrices generated with the finite element method. PMID:25816331

Kushida, Noriyuki

2015-01-01

79

Condition Number Estimation of Preconditioned Matrices  

PubMed Central

The present paper introduces a condition number estimation method for preconditioned matrices. The newly developed method provides reasonable results, while the conventional method which is based on the Lanczos connection gives meaningless results. The Lanczos connection based method provides the condition numbers of coefficient matrices of systems of linear equations with information obtained through the preconditioned conjugate gradient method. Estimating the condition number of preconditioned matrices is sometimes important when describing the effectiveness of new preconditionerers or selecting adequate preconditioners. Operating a preconditioner on a coefficient matrix is the simplest method of estimation. However, this is not possible for large-scale computing, especially if computation is performed on distributed memory parallel computers. This is because, the preconditioned matrices become dense, even if the original matrices are sparse. Although the Lanczos connection method can be used to calculate the condition number of preconditioned matrices, it is not considered to be applicable to large-scale problems because of its weakness with respect to numerical errors. Therefore, we have developed a robust and parallelizable method based on Hager’s method. The feasibility studies are curried out for the diagonal scaling preconditioner and the SSOR preconditioner with a diagonal matrix, a tri-daigonal matrix and Pei’s matrix. As a result, the Lanczos connection method contains around 10% error in the results even with a simple problem. On the other hand, the new method contains negligible errors. In addition, the newly developed method returns reasonable solutions when the Lanczos connection method fails with Pei’s matrix, and matrices generated with the finite element method. PMID:25816331

Kushida, Noriyuki

2015-01-01

80

Expression of Id1 mRNA and Protein in the Post-Ischemic Regenerating Rat Kidney  

Microsoft Academic Search

The basic helix-loop-helix (bHLH) class of proteins are of major importance in controlling tissue-specific gene expression. The actions of the bHLH proteins are inhibited by a related class of proteins, inhibitors of differentiation (Id). We have studied the expression of one of these latter proteins, Id-1, in the normal and post-ischemic regenerating rat kidney by immunocytochemistry, Western blot and RNase

Göran L. Matejka; Maria Thornemo; Annika Kernholt; Anders Lindahl

1998-01-01

81

Noopept Reduces the Postischemic Functional and Metabolic Disorders in the Brain of Rats with Different Sensitivity to Hypoxia  

Microsoft Academic Search

Chronic cerebral ischemia was induced by ligation of both common carotid arteries in Wistar rats, divided by sensitivity to\\u000a hypoxia into highly sensitive and low-sensitive. Noopept (peptide preparation), injected (0.5 mg\\/kg) during 7 days after occlusion\\u000a of the carotid arteries, reduced the neurological disorders in rats with high and low sensitivity to hypoxia and improved\\u000a their survival during the postischemic

I. V. Zarubina; P. D. Shabanov

2009-01-01

82

Effect of post-ischemic hypothermia on spinal cord damage induced by transient ischemic insult in rabbits  

Microsoft Academic Search

Objective: The effect of post-ischemic mild hypothermia applied immediately after induced transient ischemia on the extent of neuronal\\u000a damage to the spinal cord was investigated in rabbit.Subjects and Method: A 15-minute period of transient abdominal aortic occlusion for spinal cord ischemia at a rectal temperature of 37.3±0.3°C\\u000a was performed just below the left renal vein via median laparotomy. Three groups

Koji Tsutsumi; Toshihiko Ueda; Hideyuki Shimizu; Kenichi Hashizume; Yoshimi Tino; Shiaki Kawada

2002-01-01

83

Effect of ischemia and postischemic dysfunction on myocardial uptake of technetium-99m-labeled methoxyisobutyl isonitrile and thallium-201  

Microsoft Academic Search

The myocardial uptake of a new technetium-99m-labeled myocardial perfusion agent, methoxyisobutyl isonitrile (Tc-99m MIBI), and thallium-201 was correlated with microsphere flow in an open chest canine model of low coronary flow and postischemic dysfunction. Eighteen dogs were given an injection of thallium-201 (0.5 mCi) and Tc-99m MIBI (5 mCi) either after 40 min of partial left anterior descending artery occlusion

Albert J. Sinusas; Denny D. Watson; James M. Cannon Jr; George A. Beller

1989-01-01

84

Biodegradable gelatin microspheres enhance the neuroprotective potency of osteopontin via quick and sustained release in the post-ischemic brain.  

PubMed

Gelatin microspheres (GMSs) are widely used as drug carriers owing to their excellent biocompatibilities and toxicologically safe degradation products. The drug release profile is easily tailored by controlling the cross-linking density and surface-to-volume ratio, i.e. size, of the GMS. In this study, we employed GMSs which are 25 ?m in diameter and cross-linked with 0.03125% glutaraldehyde, to enable rapid initial and a subsequent sustained release. Therapeutic potency of human recombinant osteopontin (rhOPN) with or without encapsulation into GMSs was investigated after administrating them to rat stroke model (Sprague-Dawley; middle cerebral artery occlusion, MCAO). The administration of rhOPN/GMS (100 ng/100 ?g) at 1h post-MCAO reduced the mean infarct volume by 81.8% of that of the untreated MCAO control and extended the therapeutic window at least to 12h post-MCAO, demonstrating a markedly enhanced therapeutic potency for the use of OPN in the post-ischemic brain. Scanning electron microscopy micrographs revealed that GMSs maintained the three-dimensional shape for more than 5 days in normal brain but were degraded rapidly in the post-ischemic brain, presumably due to high levels of gelatinase induction. After encapsulation with GMS, the duration of OPN release was markedly extended; from the period of 2 days to 5 days in normal brain, and from 2 days to 4 days in the post-ischemic brain; these encompass the critical period for recovery processes, such as vascularization, and controlling inflammation. Together, these results indicate that GMS-mediated drug delivery has huge potential when it was used in the hyperacute period in the post-ischemic brain. PMID:24607857

Jin, Yinchuan; Kim, In-Yong; Kim, Il-Doo; Lee, Hye-Kyung; Park, Jin-Young; Han, Pyung-Lim; Kim, Kyekyoon Kevin; Choi, Hyungsoo; Lee, Ja-Kyeong

2014-07-01

85

Direct Evidence that Oxygen-Derived Free Radicals Contribute to Postischemic Myocardial Dysfunction in the Intact Dog  

Microsoft Academic Search

Electron paramagnetic resonance (EPR) spectroscopy was used to investigate whether (i) the free radicals produced in the ``stunned'' myocardium (myocardium with postischemic contractile dysfunction) are derived from O2, (ii) inhibition of radical reactions improves function, and (iii) i.v. spin traps are effective. Open-chest dogs undergoing a 15-min coronary occlusion received an i.v. infusion of the spin trap, alpha -phenyl N-tert-butylnitrone

Roberto Bolli; Mohamed O. Jeroudi; Bharat S. Patel; Coit M. Dubose; Edward K. Lai; Robert Roberts; Paul B. McCay

1989-01-01

86

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

PubMed Central

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

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

87

Preserving Symmetry in Preconditioned Krylov Subspace Methods  

NASA Technical Reports Server (NTRS)

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.

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

1996-01-01

88

M-step preconditioned conjugate gradient methods  

NASA Technical Reports Server (NTRS)

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.

Adams, L.

1983-01-01

89

Preconditioned Multigrid Methods for Unsteady Incompressible Flows  

Microsoft Academic Search

A highly efficient numerical approach based on multigrid and preconditioning methods is developed for modeling 3D steady and time-dependent incompressible flows. Thek-? turbulence model is used to estimate the effects of turbulence. The model equations are solved together with the N-S equations in a strongly coupled way, and acceleration techniques like the multigrid method are also used for the turbulence

C. Liu; X. Zheng; C. H. Sung

1998-01-01

90

On polynomial preconditioning for indefinite Hermitian matrices  

NASA Technical Reports Server (NTRS)

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.

Freund, Roland W.

1989-01-01

91

Is longer sevoflurane preconditioning neuroprotective in permanent focal cerebral ischemia?  

PubMed Central

Sevoflurane preconditioning has neuroprotective effects in the cerebral ischemia/reperfusion model. However, its influence on permanent cerebral ischemia remains unclear. In the present study, the rats were exposed to sevoflurane for 15, 30, 60, and 120 minutes, followed by induction of permanent cerebral ischemia. Results demonstrated that 30- and 60-minute sevoflurane preconditioning significantly reduced the infarct volume at 24 hours after cerebral ischemia, and 60-minute lurane preconditioning additionally reduced the number of TUNEL- and caspase-3-positive cells in the ischemic penumbra. However, 120-minute sevoflurane preconditioning did not show evident neuroprotective effects. Moreover, 60-minute sevoflurane preconditioning significantly attenuated neurological deficits and infarct volume in rats at 4 days after cerebral ischemia. These findings indicated that 60-minute sevoflurane preconditioning can induce the best neuroprotective effects in rats with permanent cerebral ischemia through the inhibition of apoptosis. PMID:25206521

Qiu, Caiwei; Sheng, Bo; Wang, Shurong; Liu, Jin

2013-01-01

92

MFGE8 inhibits inflammasome-induced IL-1? production and limits postischemic cerebral injury  

PubMed Central

Milk fat globule-EGF 8 (MFGE8) plays important, nonredundant roles in several biological processes, including apoptotic cell clearance, angiogenesis, and adaptive immunity. Several recent studies have reported a potential role for MFGE8 in regulation of the innate immune response; however, the precise mechanisms underlying this role are poorly understood. Here, we show that MFGE8 is an endogenous inhibitor of inflammasome-induced IL-1? production. MFGE8 inhibited necrotic cell–induced and ATP-dependent IL-1? production by macrophages through mediation of integrin ?3 and P2X7 receptor interactions in primed cells. Itgb3 deficiency in macrophages abrogated the inhibitory effect of MFGE8 on ATP-induced IL-1? production. In a setting of postischemic cerebral injury in mice, MFGE8 deficiency was associated with enhanced IL-1? production and larger infarct size; the latter was abolished after treatment with IL-1 receptor antagonist. MFGE8 supplementation significantly dampened caspase-1 activation and IL-1? production and reduced infarct size in wild-type mice, but did not limit cerebral necrosis in Il1b-, Itgb3-, or P2rx7-deficient animals. In conclusion, we demonstrated that MFGE8 regulates innate immunity through inhibition of inflammasome-induced IL-1? production. PMID:23454767

Deroide, Nicolas; Li, Xuan; Lerouet, Dominique; Van Vré, Emily; Baker, Lauren; Harrison, James; Poittevin, Marine; Masters, Leanne; Nih, Lina; Margaill, Isabelle; Iwakura, Yoichiro; Ryffel, Bernhard; Pocard, Marc; Tedgui, Alain; Kubis, Nathalie; Mallat, Ziad

2013-01-01

93

Ischemic preconditioning reduces intestinal epithelial apoptosis in rats.  

PubMed

Recent experimental studies have described protective effect of ischemic preconditioning (IPC) on ischemia-reperfusion (I/R) injury of the intestine. We hypothesize that to reach a new point of view on the effect of IPC in intestinal barrier function, the relationship between I/R-induced mucosal injury and apoptosis must first be clarified. The present study was undertaken to investigate the role of IPC on intestinal apoptosis and probable contributions of bcl-2 expression to this process. We also investigated the effect of intestinal IPC on ileal malondyaldihyde levels. Forty-four male Wistar rats were randomized into four groups each consisting of 11 rats: sham-operated control, I/R group (30 min of superior mesenteric artery occlusion), IPC-I/R group (10 min of temporary artery occlusion prior before an ischemic insult of 30 min), and IPC alone group (10 min of preconditioning). Twenty-four hours later, ileum samples were obtained. Ileal malondyaldihyde levels were increased in the I/R group (31.9 +/- 18.8 vs. 106.8 +/- 39.8) but not in the IPC alone and IPC-I/R groups (38.1 +/- 13.6 and 44.7 +/- 12.7; P < 0.01). The number of apoptotic cells was significantly lower in IPC-I/R group than that of I/R group, and these findings were further supported by DNA laddering and M30 findings. Diminished bcl-2 expression observed in the ileal specimens of I/R group was prevented by IPC. Our results indicate that IPC may provide a protective effect on ileal epithelium and that this effect is probably the result of a significant increase in the expression of bcl-2 after the insult. The reversal of apoptosis by IPC might help preserving the vitality of intestinal structures that have a critical function, cessation of which often leads to multiorgan dysfunction syndrome. PMID:12785017

Cinel, Ismail; Avlan, Dincer; Cinel, Leyla; Polat, Gurbuz; Atici, Sebnem; Mavioglu, Ilhan; Serinol, Hasan; Aksoyek, Selim; Oral, Ugur

2003-06-01

94

Approximate polynomial preconditioning applied to biharmonic equations on vector supercomputers  

NASA Technical Reports Server (NTRS)

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.

Wong, Yau Shu; Jiang, Hong

1987-01-01

95

The acetylation of RelA in Lys310 dictates the NF-?B-dependent response in post-ischemic injury  

PubMed Central

The activation of nuclear factor kappa B (NF-?B) p50/RelA is a key event in ischemic neuronal injury, as well as in brain ischemic tolerance. We tested whether epigenetic mechanisms affecting the acetylation state of RelA might discriminate between neuroprotective and neurotoxic activation of NF-?B during ischemia. NF-?B activation and RelA acetylation were investigated in cortices of mice subjected to preconditioning brain ischemia or lethal middle cerebral artery occlusion (MCAO) and primary cortical neurons exposed to preconditioning or lethal oxygen-glucose deprivation (OGD). In mice subjected to MCAO and in cortical neurons exposed to lethal OGD, activated RelA displayed a high level of Lys310 acetylation in spite of reduced total acetylation. Also, acetylated RelA on Lys310 interacted strongly with the CREB-binding protein (CBP). Conversely, RelA activated during preconditioning ischemia appeared deacetylated on Lys310. Overexpressing RelA increased Bim promoter activity and neuronal cell death both induced by lethal OGD, whereas overexpressing the acetylation-resistant RelA-K310R, carrying a mutation from Lys310 to arginine, prevented both responses. Pharmacological manipulation of Lys310 acetylation by the sirtuin 1 activator resveratrol repressed the activity of the Bim promoter and reduced the neuronal cell loss. We conclude that the acetylation of RelA in Lys310 dictates NF-?B-dependent pro-apoptotic responses and represents a suitable target to dissect pathological from neuroprotective NF-?B activation in brain ischemia. PMID:21368872

Lanzillotta, A; Sarnico, I; Ingrassia, R; Boroni, F; Branca, C; Benarese, M; Faraco, G; Blasi, F; Chiarugi, A; Spano, P; Pizzi, M

2010-01-01

96

The acetylation of RelA in Lys310 dictates the NF-?B-dependent response in post-ischemic injury.  

PubMed

The activation of nuclear factor kappa B (NF-?B) p50/RelA is a key event in ischemic neuronal injury, as well as in brain ischemic tolerance. We tested whether epigenetic mechanisms affecting the acetylation state of RelA might discriminate between neuroprotective and neurotoxic activation of NF-?B during ischemia. NF-?B activation and RelA acetylation were investigated in cortices of mice subjected to preconditioning brain ischemia or lethal middle cerebral artery occlusion (MCAO) and primary cortical neurons exposed to preconditioning or lethal oxygen-glucose deprivation (OGD). In mice subjected to MCAO and in cortical neurons exposed to lethal OGD, activated RelA displayed a high level of Lys310 acetylation in spite of reduced total acetylation. Also, acetylated RelA on Lys310 interacted strongly with the CREB-binding protein (CBP). Conversely, RelA activated during preconditioning ischemia appeared deacetylated on Lys310. Overexpressing RelA increased Bim promoter activity and neuronal cell death both induced by lethal OGD, whereas overexpressing the acetylation-resistant RelA-K310R, carrying a mutation from Lys310 to arginine, prevented both responses. Pharmacological manipulation of Lys310 acetylation by the sirtuin 1 activator resveratrol repressed the activity of the Bim promoter and reduced the neuronal cell loss. We conclude that the acetylation of RelA in Lys310 dictates NF-?B-dependent pro-apoptotic responses and represents a suitable target to dissect pathological from neuroprotective NF-?B activation in brain ischemia. PMID:21368872

Lanzillotta, A; Sarnico, I; Ingrassia, R; Boroni, F; Branca, C; Benarese, M; Faraco, G; Blasi, F; Chiarugi, A; Spano, P; Pizzi, M

2010-01-01

97

ISOFLURANE PRECONDITIONING AND POSTCONDITIONING IN RAT HIPPOCAMPAL NEURONS  

PubMed Central

The volatile anesthetic isoflurane is capable of inducing preconditioning and postconditioning effects in the brain. However, the mechanisms for these neuroprotective effects are not fully understood. Here, we showed that rat hippocampal neuronal cultures exposed to 2% isoflurane for 30 min at 24 h before a 1-h oxygen-glucose deprivation (OGD) and a 24-h simulated reperfusion had a reduced lactate dehydrogenase release. Similarly, this OGD and simulated reperfusion-induced lactate dehydrogenase release was attenuated by exposing the neuronal cultures to 2% isoflurane for 1 h at various times after the onset of the simulated reperfusion (isoflurane postconditioning). The combination of isoflurane preconditioning and postconditioning induced a better neuroprotection than either alone. Inhibition of the calcium/calmodulin-dependent protein kinase II (CaMKII), inhibition of N-methyl D-aspartate (NMDA) receptors, or activation of adenosine A2A receptors resulted in reduction of the OGD and simulated reperfusion-induced cell injury. The combination of CaMKII inhibition and isoflurane preconditioning or postconditioning did not provide better protection than CaMKII inhibition, isoflurane preconditioning, or isoflurane postconditioning alone. The combination of NMDA receptor inhibition and isoflurane postconditioning was not better than NMDA receptor inhibition or isoflurane postconditioning alone for neuroprotection. However, the combination of adenosine A2A receptor activation with either isoflurane preconditioning or isoflurane postconditioning induced a better neuroprotective effect than adenosine A2A receptor activation, isoflurane preconditioning, or isoflurane postconditioning alone. The combination of NMDA receptor inhibition and isoflurane preconditioning caused a better neuroprotective effect than NMDA receptor inhibition or isoflurane preconditioning alone. These results suggest that isoflurane preconditioning- and postconditioning-induced neuroprotection can be additive. Isoflurane preconditioning and isoflurane postconditioning may involve CaMKII inhibition, but may not involve adenosine A2A receptor activation. Inhibition of NMDA receptors may mediate the effects of isoflurane postconditioning, but not isoflurane preconditioning. PMID:20709037

McMurtrey, Richard J.; Zuo, Zhiyi

2010-01-01

98

Reproductive Senescence Blunts Response of Estrogen Receptor-? Expression to Estrogen Treatment in Rat Post-Ischemic Cerebral Microvessels  

PubMed Central

Background Several studies demonstrate that estrogen treatment improves cerebral blood flow in ischemic brain regions of young ovariectomized (OVX) rats. Estrogen receptor-? (ER-?) may mediate estrogen’s beneficial actions via its effects on the cerebral microvasculature. However, estrogen-derived benefit may be attenuated in aged, reproductively senescent (RS) rats. Our goal was to determine the effects of aging, estrogen deprivation and estrogen repletion with oral conjugated estrogens (CE) on postischemic cerebral microvascular protein expression of ER-? and ER-?. Methods Fisher-344 (n?=?37) female rats were randomly divided into the following groups: OVX, OVX CE-treated, RS untreated, and RS CE-treated. After 30 days pretreatment with CE (0.01 mg/kg) rats were subjected to15 min. transient global cerebral ischemia. Non-ischemic naïve, OVX and RS rats were used as controls. Expression of ER-? and ER-? in isolated cortical cerebral microvessels (20 to 100 µm in diameter) was assessed using Western blot and immunohistochemistry techniques. Results Age and reproductive status blunted nonischemic ER-? expression in microvessels of OVX rats (0.31±0.05) and RS rats (0.33±0.06) compared to naïve rats (0.45±0.02). Postischemic microvascular expression of ER-? in OVX rats (0.01±0.0) was increased by CE treatment (0.04±0.01). Expression of ER-? in microvessels of RS rats (0.03±0.02) was unaffected by CE treatment (0.01±0.02). Western blot data are presented as a ratio of ER-? or ER-? proteins to ?-actin and. Oral CE treatment had no effect on ER-? expression in postischemic microvessels of OVX and RS rats. Statistical analysis was performed by One-Way ANOVA and a Newman-Keuls or Student’s post-hoc test. Conclusion Chronic treatment with CE increases ER-? but not ER-? expression in cerebral microvessels of OVX rats. Aging appears to reduce the normal ability of estrogen to increase ER-? expression in postischemic cerebral microvessels. PMID:25010766

Zeynalov, Emil; Rezvani, Niloofar; Miyazaki, Chikao; Liu, Xiaoguang; Littleton-Kearney, Marguerite T.

2014-01-01

99

Time-derivative preconditioning for viscous flows  

NASA Technical Reports Server (NTRS)

A time-derivative preconditioning algorithm that is effective over a wide range of flow conditions from inviscid to very diffusive flows and from low speed to supersonic flows was developed. This algorithm uses a viscous set of primary dependent variables to introduce well-conditioned eigenvalues and to avoid having a nonphysical time reversal for viscous flow. The resulting algorithm also provides a mechanism for controlling the inviscid and viscous time step parameters to be of order one for very diffusive flows, thereby ensuring rapid convergence at very viscous flows as well as for inviscid flows. Convergence capabilities are demonstrated through computation of a wide variety of problems.

Choi, Yunho; Merkle, Charles L.

1991-01-01

100

A limited role for regulatory T cells in post-ischemic neovascularization  

PubMed Central

Abstract Recently, it was demonstrated that arteriogenesis is enhanced in mice deficient in regulatory T cells (CD4+CD25+FoxP3+ T cell), which can suppress effector T cell responses. The present study investigates the effects of these regulatory T cells on arteriogenesis in more detail by either specific expanding or depleting regulatory T cells. Hind limb ischemia was induced by electro-coagulation of the femoral artery in mice. Regulatory T cells were either expanded by injecting mice with a complex of interleukin (IL)-2 with the IL-2 monoclonal antibody JES6–1, or depleted by anti-CD25 antibody or diphtheria toxin injections in DEREG mice (depletion of regulatory T cells). Blood flow restoration was monitored using laser Doppler perfusion imaging. Collateral arteries were visualized by immunohistochemistry. Regulatory T cell expansion led to a moderate though significant suppression of blood flow restoration after ischemia induction. Surprisingly, depletion of regulatory T cells resulted in minor increase on blood flow recovery. However, collateral and capillary densities in the post-ischemic skeletal muscle were significantly increased in DEREG mice depleted for regulatory T cells. The presence of regulatory T cells after ischemia induction when analysed in non-depleted DEREG mice could be demonstrated by green fluorescent protein staining only in lymph nodes in the ischemic area, and not in the ischemic muscle tissue. The current study demonstrates that, even under conditions of major changes in regulatory T cell content, the contribution of regulatory T cells to the regulation of the arteriogenic response is only moderate. PMID:21426486

Hellingman, AA; van der Vlugt, LEPM; Lijkwan, MA; Bastiaansen, AJNM; Sparwasser, T; Smits, HH; Hamming, JF; Quax, PHA

2012-01-01

101

Kinin receptor agonism restores hindlimb postischemic neovascularization capacity in diabetic mice.  

PubMed

Limb ischemia is a major complication of thromboembolic diseases. Diabetes worsens prognosis by impairing neovascularization. Genetic or pharmacological inactivation of the kallikrein-kinin system aggravates limb ischemia in nondiabetic animals, whereas angiotensin I-converting enzyme/kininase II inhibition improves outcome. The role of kinins in limb ischemia in the setting of diabetes is not documented. We assessed whether selective activation of kinin receptors by pharmacological agonists can influence neovascularization in diabetic mice with limb ischemia and have a therapeutic effect. Selective pseudopeptide kinin B1 or B2 receptor agonists resistant to peptidase action were administered by osmotic minipumps at a nonhypotensive dosage for 14 days after unilateral femoral artery ligation in mice previously rendered diabetic by streptozotocin. Comparison was made with ligatured, nonagonist-treated nondiabetic and diabetic mice. Diabetes reduced neovascularization, assessed by microangiography and histologic capillary density analysis, by roughly 40%. B1 receptor agonist or B2 receptor agonist similarly restored neovascularization in diabetic mice. Neovascularization in agonist-treated diabetic mice was indistinguishable from nondiabetic mice. Both treatments restored blood flow in the ischemic hindfoot, measured by laser-Doppler perfusion imaging. Macrophage infiltration increased 3-fold in the ischemic gastrocnemius muscle during B1 receptor agonist or B2 receptor agonist treatment, and vascular endothelial growth factor (VEGF) level increased 2-fold. Both treatments increased, by 50-100%, circulating CD45/CD11b-positive monocytes and CD34(+)/VEGFR2(+) progenitor cells. Thus, selective pharmacological activation of B1 or B2 kinin receptor overcomes the effect of diabetes on postischemic neovascularization and restores tissue perfusion through monocyte/macrophage mobilization. Kinin receptors are potential therapeutic targets in limb ischemia in diabetes. PMID:25398240

Desposito, Dorinne; Potier, Louis; Chollet, Catherine; Gobeil, Fernand; Roussel, Ronan; Alhenc-Gelas, Francois; Bouby, Nadine; Waeckel, Ludovic

2015-02-01

102

A limited role for regulatory T cells in post-ischemic neovascularization.  

PubMed

Recently, it was demonstrated that arteriogenesis is enhanced in mice deficient in regulatory T cells (CD4(+) CD25(+) FoxP3(+) T cell), which can suppress effector T cell responses. The present study investigates the effects of these regulatory T cells on arteriogenesis in more detail by either specific expanding or depleting regulatory T cells. Hind limb ischemia was induced by electro-coagulation of the femoral artery in mice. Regulatory T cells were either expanded by injecting mice with a complex of interleukin (IL)-2 with the IL-2 monoclonal antibody JES6-1, or depleted by anti-CD25 antibody or diphtheria toxin injections in DEREG mice (depletion of regulatory T cells). Blood flow restoration was monitored using laser Doppler perfusion imaging. Collateral arteries were visualized by immunohistochemistry. Regulatory T cell expansion led to a moderate though significant suppression of blood flow restoration after ischemia induction. Surprisingly, depletion of regulatory T cells resulted in minor increase on blood flow recovery. However, collateral and capillary densities in the post-ischemic skeletal muscle were significantly increased in DEREG mice depleted for regulatory T cells. The presence of regulatory T cells after ischemia induction when analysed in non-depleted DEREG mice could be demonstrated by green fluorescent protein staining only in lymph nodes in the ischemic area, and not in the ischemic muscle tissue. The current study demonstrates that, even under conditions of major changes in regulatory T cell content, the contribution of regulatory T cells to the regulation of the arteriogenic response is only moderate. PMID:21426486

Hellingman, A A; van der Vlugt, L E P M; Lijkwan, M A; Bastiaansen, A J N M; Sparwasser, T; Smits, H H; Hamming, J F; Quax, P H A

2012-02-01

103

Equivalent operator preconditioning for elliptic problems  

NASA Astrophysics Data System (ADS)

The numerical solution of linear elliptic partial differential equations most often involves a finite element or finite difference discretization. To preserve sparsity, the arising system is normally solved using an iterative solution method, commonly a preconditioned conjugate gradient method. Preconditioning is a crucial part of such a solution process. In order to enable the solution of very large-scale systems, it is desirable that the total computational cost will be of optimal order, i.e. proportional to the degrees of freedom of the approximation used, which also induces mesh independent convergence of the iteration. This paper surveys the equivalent operator approach, which has proven to provide an efficient general framework to construct such preconditioners. Hereby one first approximates the given differential operator by some simpler differential operator, and then chooses as preconditioner the discretization of this operator for the same mesh. In this survey we give a uniform presentation of this approach, including theoretical foundation and several practically important applications for both symmetric and nonsymmetric equations and systems, and some nonlinear examples in the context of Newton linearization.

Axelsson, O.; Karátson, J.

2009-03-01

104

Pre-conditioning with low-level laser (light) therapy: light before the storm.  

PubMed

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

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

2014-12-01

105

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

PubMed Central

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

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

2014-01-01

106

A Molecular Approach to Epilepsy Management: from Current Therapeutic Methods to Preconditioning Efforts.  

PubMed

Epilepsy is the most common and chronic neurological disorder characterized by recurrent unprovoked seizures. The key aim in treating patients with epilepsy is the suppression of seizures. An understanding of focal changes that are involved in epileptogenesis may therefore provide novel approaches for optimal treatment of the seizure. Although the actual pathogenesis of epilepsy is still uncertain, recently growing lines of evidence declare that microglia and astrocyte activation, oxidative stress and reactive oxygen species (ROS) production, mitochondria dysfunction, and damage of blood-brain barrier (BBB) are involved in its pathogenesis. Impaired GABAergic function in the brain is probably the most accepted hypothesis regarding the pathogenesis of epilepsy. Clinical neuroimaging of patients and experimental modeling have demonstrated that seizures may induce neuronal apoptosis. Apoptosis signaling pathways are involved in the pathogenesis of several types of epilepsy such as temporal lobe epilepsy (TLE). The quality of life of patients is seriously affected by treatment-related problems and also by unpredictability of epileptic seizures. Moreover, the available antiepileptic drugs (AED) are not significantly effective to prevent epileptogenesis. Thus, novel therapies that are proficient to control seizure in people who are suffering from epilepsy are needed. The preconditioning method promises to serve as an alternative therapeutic approach because this strategy has demonstrated the capability to curtail epileptogenesis. For this reason, understanding of molecular mechanisms underlying brain tolerance induced by preconditioning is crucial to delineate new neuroprotective ways against seizure damage and epileptogenesis. In this review, we summarize the work to date on the pathogenesis of epilepsy and discuss recent therapeutic strategies in the treatment of epilepsy. We will highlight that novel therapy targeting such as preconditioning process holds great promise. In addition, we will also highlight the role of gene reprogramming and mitochondrial biogenesis in the preconditioning-mediated neuroprotective events. PMID:25195699

Amini, Elham; Rezaei, Mohsen; Mohamed Ibrahim, Norlinah; Golpich, Mojtaba; Ghasemi, Rasoul; Mohamed, Zahurin; Raymond, Azman Ali; Dargahi, Leila; Ahmadiani, Abolhassan

2014-09-01

107

Preconditioning Triggered by Carbon Monoxide (CO) Provides Neuronal Protection Following Perinatal Hypoxia-Ischemia  

PubMed Central

Perinatal hypoxia-ischemia is a major cause of acute mortality in newborns and cognitive and motor impairments in children. Cerebral hypoxia-ischemia leads to excitotoxicity and necrotic and apoptotic cell death, in which mitochondria play a major role. Increased resistance against major damage can be achieved by preconditioning triggered by subtle insults. CO, a toxic molecule that is also generated endogenously, may have a role in preconditioning as low doses can protect against inflammation and apoptosis. In this study, the role of CO-induced preconditioning on neurons was addressed in vitro and in vivo. The effect of 1 h of CO treatment on neuronal death (plasmatic membrane permeabilization and chromatin condensation) and bcl-2 expression was studied in cerebellar granule cells undergoing to glutamate-induced apoptosis. CO's role was studied in vivo in the Rice-Vannucci model of neonatal hypoxia-ischemia (common carotid artery ligature +75 min at 8% oxygen). Apoptotic cells, assessed by Nissl staining were counted with a stereological approach and cleaved caspase 3-positive profiles in the hippocampus were assessed. Apoptotic hallmarks were analyzed in hippocampal extracts by Western Blot. CO inhibited excitotoxicity-induced cell death and increased Bcl-2 mRNA in primary cultures of neurons. In vivo, CO prevented hypoxia-ischemia induced apoptosis in the hippocampus, limited cytochrome c released from mitochondria and reduced activation of caspase-3. Still, Bcl-2 protein levels were higher in hippocampus of CO pre-treated rat pups. Our results show that CO preconditioning elicits a molecular cascade that limits neuronal apoptosis. This could represent an innovative therapeutic strategy for high-risk cerebral hypoxia-ischemia patients, in particular neonates. PMID:22952602

Widerøe, Marius; Alves, Paula M.; Vercelli, Alessandro; Vieira, Helena L. A.

2012-01-01

108

Hyperbaric oxygen preconditioning protects skin from UV-A damage.  

PubMed

Hyperbaric oxygen therapy (HBOT) is used for a number of applications, including the treatment of diabetic foot ulcers and CO poisoning. However, we and others have shown that HBOT can mobilize cellular antioxidant defenses, suggesting that it may also be useful under circumstances in which tissue protection from oxidative damage is desired. To test the protective properties of hyperbaric oxygen (HBO) on a tissue level, we evaluated the ability of a preconditioning treatment regimen to protect cutaneous tissue from UV-A-induced oxidative damage. Three groups of hairless SKH1-E mice were exposed to UV-A 3 days per week for 22 weeks, with two of these groups receiving an HBO pretreatment either two or four times per week. UV-A exposure increased apoptosis and proliferation of the skin tissue, indicating elevated levels of epithelial damage and repair. Pretreatment with HBO significantly reduced UV-A-induced apoptosis and proliferation. A morphometric analysis of microscopic tissue folds also showed a significant increase in skin creasing following UV-A exposure, which was prevented by HBO pretreatment. Likewise, skin elasticity was found to be greatest in the group treated with HBO four times per week. The effects of HBO were also apparent systemically as reductions in caspase-3 activity and expression were observed in the liver. Our findings support a protective function of HBO pretreatment from a direct oxidative challenge of UV-A to skin tissue. Similar protection of other tissues may likewise be achievable. PMID:22855227

Fuller, Ashley M; Giardina, Charles; Hightower, Lawrence E; Perdrizet, George A; Tierney, Cassandra A

2013-01-01

109

Mitochondria: The Missing Link Between Preconditioning and Neuroprotection  

PubMed Central

The quote “what does not kill you makes you stronger” perfectly describes the preconditioning phenomenon – a paradigm that affords robust brain tolerance in the face of neurodegenerative insults. Over the last few decades, many attempts have been made to identify the molecular mechanisms involved in preconditioning-induced protective responses, and recent data suggests that many of these mechanisms converge on the mitochondria, positing mitochondria as master regulators of preconditioning-triggered endogenous neuroprotection. In this review, we critically discuss evidence for the involvement of mitochondria within the preconditioning paradigm. We will highlight the crucial targets and mediators by which mitochondria are integrated into neuroprotective signaling pathways that underlie preconditioning, putting focus on mitochondrial respiratory chain and mitochondrial reactive oxygen species, mitochondrial ATP-sensitive potassium channels, mitochondrial permeability transition pore, uncoupling proteins, and mitochondrial antioxidant enzyme manganese superoxide dismutase. We also discuss the role of mitochondria in the induction of hypoxia-inducible factor-1, a transcription factor engaged in preconditioning-mediated neuroprotective effects. The identification of intrinsic mitochondrial mechanisms involved in preconditioning will provide new insights which can be translated into potential pharmacological interventions aimed at counteracting neurodegeneration. PMID:20463394

Correia, Sónia C.; Santos, Renato X.; Perry, George; Zhu, Xiongwei; Moreira, Paula I.; Smith, Mark A.

2010-01-01

110

Development of Resistance of an Organism under Various Conditions of Hypoxic Preconditioning: Role of the Hypoxic Period and Reoxygenation  

Microsoft Academic Search

Single exposure to moderate (10% O2) hypobaric, normobaric, and intermittent hypoxia is followed by a preconditioning response of the organism. The mechanisms\\u000a for immediate adaptation are activated during the hypoxic period. Intermittent reoxygenation not only delays, but even suppresses\\u000a this process. However, periods of oxygenation during the course of hypoxic training reduce the effect of hypoxia and prevent\\u000a the possibility

L. D. Lukyanova; E. L. Germanova; R. A. Kopaladze

2009-01-01

111

Preconditioning by Cilostazol Protects against Cold Hepatic Ischemia-Reperfusion Injury.  

PubMed

Background In liver transplantation, prolonged cold storage and post-transplant reperfusion are associated with endothelial inflammation, organ dysfunction, and graft failure. We herein studied whether cilostazol, a phosphodiesterase-3-inhibitor, attenuates post-ischemic liver injury after prolonged cold storage. Material and Methods Sprague-Dawley rats were assigned to 5 groups (n=6 each): sham animals (cold storage time (CST): 1 h), vehicle-treated (NaCl 0.9%) controls (CST: 24 h), and animals receiving 0.1, 1.0, or 10.0 mg/kg body weight (BW) cilostazol pre-treatment (CST: 24 h). After organ explantation, all livers were stored at 4°C in HTK solution, followed by 60 min of reperfusion with 37°C Krebs Henseleit buffer in a non-recirculating ex situ system. Bile flow was measured to evaluate liver function. To analyze inflammation and morphology, liver tissue samples were taken and histology, immunohistochemistry, and Western blotting were conducted. Results In vehicle-treated controls, prolonged cold storage and warm reperfusion induced inflammation, organ dysfunction, and cell death. This was indicated by an increase of hepatocellular vacuolization, endothelial ICAM-1 expression, and apoptotic cell death compared to sham animals. Cilostazol pre-treatment protected against cold hepatic ischemia-reperfusion injury by preventing hepatocellular disintegration, ICAM-1-associated endothelial inflammation, and apoptotic death. Conclusions Inhibition of PDE3 reduces endothelial cell activation and hepatocellular injury in cold ischemia/reperfusion of the liver. PMID:25811412

von Heesen, Maximilian; Müller, Simon; Keppler, Ulrich; Strowitzki, Moritz J; Scheuer, Claudia; Schilling, Martin K; Menger, Michael D; Moussavian, Mohammed R

2015-01-01

112

A fast, preconditioned conjugate gradient Toeplitz solver  

NASA Technical Reports Server (NTRS)

A simple factorization is given of an arbitrary hermitian, positive definite matrix in which the factors are well-conditioned, hermitian, and positive definite. In fact, given knowledge of the extreme eigenvalues of the original matrix A, an optimal improvement can be achieved, making the condition numbers of each of the two factors equal to the square root of the condition number of A. This technique is to applied to the solution of hermitian, positive definite Toeplitz systems. Large linear systems with hermitian, positive definite Toeplitz matrices arise in some signal processing applications. A stable fast algorithm is given for solving these systems that is based on the preconditioned conjugate gradient method. The algorithm exploits Toeplitz structure to reduce the cost of an iteration to O(n log n) by applying the fast Fourier Transform to compute matrix-vector products. Matrix factorization is used as a preconditioner.

Pan, Victor; Schrieber, Robert

1989-01-01

113

Simple characterizations for commutativity of quantum weakest preconditions  

E-print Network

In a recent letter [Information Processing Letters~104 (2007) 152-158], it has shown some sufficient conditions for commutativity of quantum weakest preconditions. This paper provides some alternative and simple characterizations for the commutativity of quantum weakest preconditions, i.e., Theorem \\ref{thm3}, Theorem \\ref{thm4} and Proposition \\ref{pro5} in what follows. We also show that to characterize the commutativity of quantum weakest preconditions in terms of $[M,N]$ ($=MN-NM$) is hard in the sense of Proposition \\ref{pro7} and Proposition \\ref{pro8}.

T. Lin

2013-12-02

114

Progress in Parallel Schur Complement Preconditioning for Computational Fluid Dynamics  

NASA Technical Reports Server (NTRS)

We consider preconditioning methods for nonself-adjoint advective-diffusive systems based on a non-overlapping Schur complement procedure for arbitrary triangulated domains. The ultimate goal of this research is to develop scalable preconditioning algorithms for fluid flow discretizations on parallel computing architectures. In our implementation of the Schur complement preconditioning technique, the triangulation is first partitioned into a number of subdomains using the METIS multi-level k-way partitioning code. This partitioning induces a natural 2X2 partitioning of the p.d.e. discretization matrix. By considering various inverse approximations of the 2X2 system, we have developed a family of robust preconditioning techniques. A computer code based on these ideas has been developed and tested on the IBM SP2 and the SGI Power Challenge array using MPI message passing protocol. A number of example CFD calculations will be presented to illustrate and assess various Schur complement approximations.

Barth, Timothy J.; Chan, Tony F.; Tang, Wei-Pai; Chancellor, Marisa K. (Technical Monitor)

1997-01-01

115

Pharmacological preconditioning to improve outcome in free tissue transfer   

E-print Network

in models of visceral IRI. Aim: to investigate whether HA could be used to improve outcome in myocutaneous flaps. Objectives: (1) to establish a reliable model of myocutaneous IRI (2) to assess the effects of pharmacological preconditioning with HA...

Edmunds, Marie-Claire

2013-11-29

116

Behavioral/Systems/Cognitive Octopamine Mediates Thermal Preconditioning of the  

E-print Network

., 2003). At the moment of heat- induced rhythm failure, there is an abrupt rise in extracellular) in the metathoracic ganglion decreased during heat stress. We measured l OA) mimicked heat shock preconditioning and improved the thermotolerance of the motor pattern

Robertson, Meldrum

117

40 CFR 1065.516 - Sample system decontamination and preconditioning.  

Code of Federal Regulations, 2014 CFR

...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...

2014-07-01

118

Ischemic Preconditioning and the b-Adrenergic Signal Transduction Pathway  

Microsoft Academic Search

Background—Previous studies from our laboratory showed cyclic increases in tissue cAMP during a multiple-cycle preconditioning (PC) protocol, followed by attenuated cAMP accumulation during sustained ischemia. The aim of this study was to determine whether ischemia-induced activation of the b-adrenergic signaling pathway could act as a trigger in eliciting protection. Methods and Results—Isolated perfused rat hearts were preconditioned by 3 35

Amanda Lochner; Sonia Genade; Erna Tromp; Thomas Podzuweit; Johan A. Moolman

119

Green tea polyphenols precondition against cell death induced by oxygen-glucose deprivation via stimulation of laminin receptor, generation of reactive oxygen species, and activation of protein kinase C?.  

PubMed

As the development of synthetic drugs for the prevention of stroke has proven challenging, utilization of natural products capable of preconditioning neuronal cells against ischemia-induced cell death would be a highly useful complementary approach. In this study using an oxygen-glucose deprivation and reoxygenation (OGD/R) model in PC12 cells, we show that 2-day pretreatment with green tea polyphenols (GTPP) and their active ingredient, epigallocatechin-3-gallate (EGCG), protects cells from subsequent OGD/R-induced cell death. A synergistic interaction was observed between GTPP constituents, with unfractionated GTPP more potently preconditioning cells than EGCG. GTPP-induced preconditioning required the 67-kDa laminin receptor (67LR), to which EGCG binds with high affinity. 67LR also mediated the generation of reactive oxygen species (ROS) via activation of NADPH oxidase. An exogenous ROS-generating system bypassed 67LR to induce preconditioning, suggesting that sublethal levels of ROS are indeed an important mediator in GTPP-induced preconditioning. This role for ROS was further supported by the fact that antioxidants blocked GTPP-induced preconditioning. Additionally, ROS induced an activation and translocation of protein kinase C (PKC), particularly PKC? from the cytosol to the membrane/mitochondria, which was also blocked by antioxidants. The crucial role of PKC in GTPP-induced preconditioning was supported by use of its specific inhibitors. Preconditioning was increased by conditional overexpression of PKC? and decreased by its knock-out with siRNA. Collectively, these results suggest that GTPP stimulates 67LR and thereby induces NADPH oxidase-dependent generation of ROS, which in turn induces activation of PKC, particularly prosurvival isoenzyme PKC?, resulting in preconditioning against cell death induced by OGD/R. PMID:22879598

Gundimeda, Usha; McNeill, Thomas H; Elhiani, Albert A; Schiffman, Jason E; Hinton, David R; Gopalakrishna, Rayudu

2012-10-01

120

[Brain tissue leukotrienes in cerebral ischemia and the effect of inhibitor of SRS-A release on postischemic cerebral edema].  

PubMed

Arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to test the development of lipoxygenase metabolites of arachidonic acid in cerebral ischemia, we measured free arachidonic acid and slow reacting substance of anaphylaxis (SRS-A) and leukotriene C4 in the brain tissue. Moreover, we studied the influence of inhibitor of SRS-A release on postischemic cerebral edema. Severe forebrain ischemia in rats was induced by the modification of the method described by Pulsinelli and Brierley. Both vertebral arteries were electrocauterized through the alar foramen and then bilateral common carotid arteries were clamped by aneurysmal clips and mean arterial pressure was reduced to 80-90 mmHg. EEG activity was isoelectric throughout the period of carotid clamping. After forebrain ischemia had been maintained for 30 minutes, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Following the desired ischemic or postischemic periods, the brains were frozen in situ with liquid nitrogen. The brains were then chiselled out during irrigation with liquid nitrogen and stored at -80 degrees C until analysis. The brain extracts were analysed by high performance liquid chromatography for free arachidonic acid, by bioassay using the ileum of guinea pig for SRS-A and by radioimmunoassay for leukotriene C4. Brain water content was calculated with dry weight method. Inhibitor of SRS-A release, tranilast, was given intraperitoneally, 100 mg/kg 30 minutes before induction of ischemia and 50 mg/kg immediately before recirculation.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2465014

Mabe, H; Suzuka, T; Nagai, H; Nagai, H; Koda, A

1988-07-01

121

Attenuation of Focal Cerebral Ischemic Injury Following Post-Ischemic Inhibition of Angiotensin Converting Enzyme (ACE) Activity in Normotensive Rat  

PubMed Central

Background Central renin angiotensin system has an important role on the cerebral microcirculation and metabolism. Our previous work showed that inhibition of angiotensin converting enzyme () activity prior to induction of ischemia protected the brain from severe ischemia/reperfusion (I/R) injuries. This study evaluated the impacts of post-ischemic inhibition of , enalapril, on brain infarction in normotensive rats. Methods Rats were anesthetized with chloral hydrate (400 mg/kg). Focal cerebral ischemia was induced by 60-min intraluminal occlusion of right middle cerebral artery (MCA). Intraperitoneal injection of enalapril (0.03 or 0.1 mg/kg) was done after MCA reopening (reperfusion). Neurological deficit score (NDS) was evaluated after 24 h and the animals randomly assigned for the assessments of infarction, absolute brain water content (ABWC) and index of brain edema Results Severe impaired motor functions (NDS = 2.78 ± 0.28), massive infarction (cortex = 214 ± 19 mm3, striatum = 86 ± 5 mm3) and edema (ABWC = 83.1 ± 0.46%) were observed in non-treated ischemic rats. Non-hypotensive dose of enalapril (0.03 mg/kg) significantly reduced NDS (1.5 ± 0.22), infarction (cortex = 102 ± 16 mm3, striatum = 38 ± 5 mm3) and edema (ABWC = 80.9 ± 0.81%). Enalapril at dose of 0.1 mg/kg significantly lowered arterial pressure could not improve NDS (2.0 ± 0.45) and reduce infarction (cortex = 166 ± 26 mm3, striatum = 71 ± 11 mm3). Conclusion Post-ischemic ACE inhibition in the normotensive rats without affecting arterial pressure protects the brain from reperfusion injuries; however, this beneficial action is masked by hypotension. PMID:23183619

Panahpour, Hamdollah; Dehghani, Gholam Abbas

2012-01-01

122

BWR Fuel Thermomechanical Evaluation for Preconditioning Procedures With FEMAXI-V  

SciTech Connect

Burnup limitations are normally set to limit stresses in the fuel assembly components. The defined limits provide guidance to the fuel designer to minimize fuel failure during steady sate operation, and also prevent against some thermal and mechanical phenomena that could occur during overpower transients. In particular, a LHGR limit value is set to take into account physical phenomena that could lead to pellet-cladding interaction. This limit value directly relates to a PCI limit, which may be set based on experimental ramp tests. Thus, to avoid violating the PCI limit, fuel conditioning procedures are still required for both barrier and non-barrier fuel. Simulation of the power ramp procedures to be performed by the reactor operator during startup or power increase maneuvers is advisable as a preventive measure of possible overpower consequences on the fuel thermomechanical behavior. In this paper, the thermomechanical behavior of two different kinds of BWR fuel rods is analyzed for fuel preconditioning procedures. Five different preconditioning computations were performed, each with three different ascending linear power rate ramps. The starting point of the ramps was taken from data of the Cycle 8 of the Unit 1 of the Laguna Verde Nuclear Power Plant, located in Mexico. The top limit of the ramps was the threshold linear power at which failure by PCI could occur, as a function of burnup. The analysis was performed with the FEMAXI-V code. (authors)

Hernandez-Lopez, Hector; Lucatero, Marco A.; Ortiz-Villafuerte, Javier [Instituto Nacional de Investigaciones Nucleares, 52045 Ocoyoacac, Edo. de Mexico (Mexico)

2006-07-01

123

A Weakest Precondition Approach to Robustness  

NASA Astrophysics Data System (ADS)

With the increasing complexity of information management computer systems, security becomes a real concern. E-government, web-based financial transactions or military and health care information systems are only a few examples where large amount of information can reside on different hosts distributed worldwide. It is clear that any disclosure or corruption of confidential information in these contexts can result fatal. Information flow controls constitute an appealing and promising technology to protect both data confidentiality and data integrity. The certification of the security degree of a program that runs in untrusted environments still remains an open problem in the area of language-based security. Robustness asserts that an active attacker, who can modify program code in some fixed points (holes), is unable to disclose more private information than a passive attacker, who merely observes unclassified data. In this paper, we extend a method recently proposed for checking declassified non-interference in presence of passive attackers only, in order to check robustness by means of weakest precondition semantics. In particular, this semantics simulates the kind of analysis that can be performed by an attacker, i.e., from public output towards private input. The choice of semantics allows us to distinguish between different attacks models and to characterize the security of applications in different scenarios.

Balliu, Musard; Mastroeni, Isabella

124

Reduction in postsystolic wall thickening during late preconditioning.  

PubMed

Brief coronary artery occlusion (CAO) and reperfusion induce myocardial stunning and late preconditioning. Postsystolic wall thickening (PSWT) also develops with CAO and reperfusion. However, the time course of PSWT during stunning and the regional function pattern of the preconditioned myocardium remain unknown. The goal of this study was to investigate the evolution of PSWT during myocardial stunning and its modifications during late preconditioning. Dogs were chronically instrumented to measure (sonomicrometry) systolic wall thickening (SWT), PSWT, total wall thickening (TWT = SWT + PSWT), and maximal rate of thickening (dWT/dt(max)). Two 10-min CAO (circumflex artery) were performed 24 h apart (day 0 and day 1, n = 7). At day 0, CAO decreased SWT and increased PSWT. During the first hours of the subsequent stunning, evolution of PSWT was symmetrical to that of SWT. At day 1, baseline SWT was similar to day 0, but PSWT was reduced (-66%), while dWT/dt(max) and SWT/TWT ratio increased (+48 and +14%, respectively). After CAO at day 1, stunning was reduced, indicating late preconditioning. Simultaneously vs. day 0, PSWT was significantly reduced, and dWT/dt(max) as well as SWT/TWT ratio were increased, i.e., a greater part of TWT was devoted to ejection. Similar decrease in PSWT was observed with a nonischemic preconditioning stimulus (rapid ventricular pacing, n = 4). In conclusion, a major contractile adaptation occurs during late preconditioning, i.e., the rate of wall thickening is enhanced and PWST is almost abolished. These phenotype adaptations represent potential approaches for characterizing stunning and late preconditioning with repetitive ischemia in humans. PMID:16920813

Monnet, Xavier; Lucats, Laurence; Colin, Patrice; Derumeaux, Geneviève; Dubois-Rande, Jean-Luc; Hittinger, Luc; Ghaleh, Bijan; Berdeaux, Alain

2007-01-01

125

Fetal asphyctic preconditioning alters the transcriptional response to perinatal asphyxia  

PubMed Central

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

2014-01-01

126

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

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

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

2014-01-01

127

Nanoparticle Pre-Conditioning for Enhanced Thermal Therapies in Cancer  

PubMed Central

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

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

2011-01-01

128

Fast curve estimation using preconditioned generalized Radon transform.  

PubMed

A new algorithm for fast curve parameter estimation based on the generalized Radon transform is proposed. The algorithm works on binary images, obtained, e.g., by edge filtering or deconvolution. The fundamental idea of the suggested algorithm is the use of a precondition map to reduce the computational cost of the generalized Radon transform. The precondition map is composed of irregular regions in the parameter domain, which contain peaks that represent curves in the image. To generate the precondition map, a fast mapping procedure named image point mapping is developed. As the image point mapping scheme maps image points into the corresponding parameter values in the parameter domain, it is possible to improve computational efficiency by recognizing image points with value zero. Initially, the suggested algorithm estimates the precondition map and subsequently applies the generalized Radon transform within the regions specified by the precondition map. The required parameter domain sampling and the resulting blurring are also investigated. The suggested algorithm is successfully applied to the identification of hyperbolas in seismic images, and two numerical examples are given. PMID:18290082

Hansen, K V; Toft, P A

1996-01-01

129

Implementation of Preconditioned Dual-Time Procedures in OVERFLOW  

NASA Technical Reports Server (NTRS)

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.

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

2003-01-01

130

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

Code of Federal Regulations, 2010 CFR

...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...

2010-07-01

131

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

Code of Federal Regulations, 2011 CFR

... 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)...

2011-07-01

132

40 CFR 85.2218 - Preconditioned idle test-EPA 91.  

Code of Federal Regulations, 2011 CFR

... 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...

2011-07-01

133

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

Code of Federal Regulations, 2011 CFR

...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...

2011-07-01

134

Impact of hypoglycemic agents on myocardial ischemic preconditioning  

PubMed Central

Murry et al in 1986 discovered the intrinsic mechanism of profound protection called ischemic preconditioning. The complex cellular signaling cascades underlying this phenomenon remain controversial and are only partially understood. However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C (PKC). This leads to the translocation of PKC from the cytoplasm to the sarcolemma, where it stimulates the opening of the ATP-sensitive K+ channel, which confers resistance to ischemia. It is known that a range of different hypoglycemic agents that activate the same signaling cascades at various cellular levels can interfere with protection from ischemic preconditioning. This review examines the effects of several hypoglycemic agents on myocardial ischemic preconditioning in animal studies and clinical trials. PMID:24936247

Rahmi Garcia, Rosa Maria; Rezende, Paulo Cury; Hueb, Whady

2014-01-01

135

On adaptive weighted polynomial preconditioning for Hermitian positive definite matrices  

NASA Technical Reports Server (NTRS)

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.

Fischer, Bernd; Freund, Roland W.

1992-01-01

136

Operator-Based Preconditioning of Stiff Hyperbolic Systems  

SciTech Connect

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.

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

2009-02-09

137

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

NASA Technical Reports Server (NTRS)

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.

Wong, G. S.

1973-01-01

138

Resistance to Reperfusion Injury Following Short Term Postischemic Administration of Natural Honey in Globally Ischemic Isolated Rat Heart  

PubMed Central

Purpose: Results of our previous study revealed that preischemic perfusion of honey before zero flow global ischemia had cardioprotective effects in rat. The present study investigated potential resistance to reperfusion injury following short term postischemic administration of natural honey in globally ischemic isolated rat heart. Methods: Male Wistar rats were divided into five groups (n=10-13). The rat hearts were isolated, mounted on a Langendorff apparatus, allowed to equilibrate for 30 min then subjected to 30 min global ischemia. In the control group, the hearts were reperfused with drug free normal Krebs-Henseleit (K/H) solution before ischemia and during 120 min reperfusion. In the treatment groups, reperfusion was initiated with K/H solution containing different concentration of honey (0.25, 0.5, 1 and 2%) for 15 min and was resumed until the end of 120 min with normal K/H solution. Results: In the control group, VEBs number was 784±199, while in honey concentration of 0.25, 0.5, 1 and 2%, it decreased to 83±23 (P<0.001), 138±48 (P<0.01), 142±37 (P<0.001) and 157±40 (P<0.01), respectively. Number and duration of VT and time spent in reversible VF were also reduced by honey. In the control group, the infarct size was 54.1±7.8%, however; honey (0.25, 0.5, 1 and 2%) markedly lowered the value to 12.4±2.4, 12.7±3.3, 11.3±2.6 and 7.9±1.7 (P<0.001), respectively. Conclusion: Postischemic administration of natural honey in global ischemia showed protective effects against ischemia/reperfusion (I/R) injuries in isolated rat heart. Antioxidant and radical scavenging activity, lipoperoxidation inhibition, reduction of necrotized tissue, presence of rich energy sources, various type of vitamins, minerals and enzymes and formation of NO-contain metabolites may probably involve in those cardioprotective effects. PMID:24312792

Vaez, Haleh; Samadzadeh, Mehrban; Zahednezhad, Fahimeh; Najafi, Moslem

2012-01-01

139

In vivo inhibition of the mitochondrial H+-ATP synthase in neurons promotes metabolic preconditioning  

PubMed Central

A key transducer in energy conservation and signaling cell death is the mitochondrial H+-ATP synthase. The expression of the ATPase inhibitory factor 1 (IF1) is a strategy used by cancer cells to inhibit the activity of the H+-ATP synthase to generate a ROS signal that switches on cellular programs of survival. We have generated a mouse model expressing a mutant of human IF1 in brain neurons to assess the role of the H+-ATP synthase in cell death in vivo. The expression of hIF1 inhibits the activity of oxidative phosphorylation and mediates the shift of neurons to an enhanced aerobic glycolysis. Metabolic reprogramming induces brain preconditioning affording protection against quinolinic acid-induced excitotoxicity. Mechanistically, preconditioning involves the activation of the Akt/p70S6K and PARP repair pathways and Bcl-xL protection from cell death. Overall, our findings provide the first in vivo evidence highlighting the H+-ATP synthase as a target to prevent neuronal cell death. PMID:24521670

Formentini, Laura; Pereira, Marta P; Sánchez-Cenizo, Laura; Santacatterina, Fulvio; Lucas, José J; Navarro, Carmen; Martínez-Serrano, Alberto; Cuezva, José M

2014-01-01

140

Ischemic preconditioning for cell-based therapy and tissue engineering.  

PubMed

Cell- and tissue-based therapies are innovative strategies to repair and regenerate injured hearts. Despite major advances achieved in optimizing these strategies in terms of cell source and delivery method, the clinical outcome of cell-based therapy remains unsatisfactory. The non-genetic approach of ischemic/hypoxic preconditioning to enhance cell- and tissue-based therapies has received much attention in recent years due to its non-invasive drug-free application. Here we discuss the current development of hypoxic/ischemic preconditioning to enhance stem cell-based cardiac repair and regeneration. PMID:24321597

Hsiao, Sarah T; Dilley, Rodney J; Dusting, Gregory J; Lim, Shiang Y

2014-05-01

141

Choice of Variables and Preconditioning for Time Dependent Problems  

NASA Technical Reports Server (NTRS)

We consider the use of low speed preconditioning for time dependent problems. These are solved using a dual time step approach. We consider the effect of this dual time step on the parameter of the low speed preconditioning. In addition, we compare the use of two sets of variables, conservation and primitive variables, to solve the system. We show the effect of these choices on both the convergence to a steady state and the accuracy of the numerical solutions for low Mach number steady state and time dependent flows.

Turkel, Eli; Vatsa, Verr N.

2003-01-01

142

Differential Effect of Ischemic and Pharmacological Preconditioning on PKC Isoform Translocation in Adult Rat Cardiac Myocytes  

Microsoft Academic Search

The role of PKC isoforms in the protection of ischemic preconditioning remains controversial. The aim of the present study was to compare PKC translocation in ischemic and pharmacological preconditioning and to test the hypothesis that induction of the preconditioned state results in a sustained translocation of PKC during the following ischemic period. Isolated rat cardiac myocytes were subjected to established

Vasiliki Tsouka; Thomais Markou; Antigone Lazou

2002-01-01

143

Syndecan 1 plays a novel role in enteral glutamine's gut-protective effects of the postischemic gut.  

PubMed

Syndecan 1 is the predominant heparan sulfate proteoglycan found on the surface of epithelial cells and, like glutamine, is essential in maintaining the intestinal epithelial barrier. We therefore hypothesized that loss of epithelial syndecan 1 would abrogate the gut-protective effects of enteral glutamine. Both an in vitro and in vivo model of gut ischemia-reperfusion (IR) was utilized. In vitro, intestinal epithelial cells underwent hypoxia-reoxygenation to mimic gut IR with 2 mM (physiologic) or 10 mM glutamine supplementation. Permeability, caspase activity, cell growth, and cell surface and shed syndecan 1 were assessed. In vivo, wild-type and syndecan 1 knockout (KO) mice received ± enteral glutamine followed by gut IR. Intestinal injury was assessed by fluorescent dye clearance and histopathology, permeability as mucosal-to-serosal clearance ex vivo in everted sacs, and inflammation by myeloperoxidase (MPO) activity. In an in vitro model of gut IR, glutamine supplementation reduced epithelial cell permeability and apoptosis and enhanced cell growth. Shed syndecan 1 was reduced by glutamine without an increase in syndecan 1 mRNA. In vivo, intestinal permeability, inflammation, and injury were increased after gut IR in wild-type mice and further increased in syndecan 1 KO mice. Glutamine's attenuation of IR-induced intestinal hyperpermeability, inflammation, and injury was abolished in syndecan 1 KO mice. These results suggest that syndecan 1 plays a novel role in the protective effects of enteral glutamine in the postischemic gut. PMID:22706022

Peng, Zhanglong; Ban, Kechen; Sen, Aritra; Grill, Raymond; Park, Pyong; Costantini, Todd W; Kozar, Rosemary

2012-07-01

144

Ephrin-B2–Activated Peripheral Blood Mononuclear Cells From Diabetic Patients Restore Diabetes-Induced Impairment of Postischemic Neovascularization  

PubMed Central

We hypothesized that in vitro treatment of peripheral blood mononuclear cells (PB-MNCs) from diabetic patients with ephrin-B2/Fc (EFNB2) improves their proangiogenic therapeutic potential in diabetic ischemic experimental models. Diabetes was induced in nude athymic mice by streptozotocin injections. At 9 weeks after hyperglycemia, 105 PB-MNCs from diabetic patients, pretreated by EFNB2, were intravenously injected in diabetic mice with hindlimb ischemia. Two weeks later, the postischemic neovascularization was evaluated. The mechanisms involved were investigated by flow cytometry analysis and in vitro cell biological assays. Paw skin blood flow, angiographic score, and capillary density were significantly increased in ischemic leg of diabetic mice receiving EFNB2-activated diabetic PB-MNCs versus those receiving nontreated diabetic PB-MNCs. EFNB2 bound to PB-MNCs and increased the adhesion and transmigration of PB-MNCs. Finally, EFNB2-activated PB-MNCs raised the number of circulating vascular progenitor cells in diabetic nude mice and increased the ability of endogenous bone marrow MNCs to differentiate into cells with endothelial phenotype and enhanced their proangiogenic potential. Therefore, EFNB2 treatment of PB-MNCs abrogates the diabetes-induced stem/progenitor cell dysfunction and opens a new avenue for the clinical development of an innovative and accessible strategy in diabetic patients with critical ischemic diseases. PMID:22596048

Broquères-You, Dong; Leré-Déan, Carole; Merkulova-Rainon, Tatiana; Mantsounga, Chris S.; Allanic, David; Hainaud, Patricia; Contrères, Jean-Olivier; Wang, Yu; Vilar, José; Virally, Marie; Mourad, Jean-Jacques; Guillausseau, Pierre-Jean; Silvestre, Jean-Sébastien; Lévy, Bernard I.

2012-01-01

145

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

SciTech Connect

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.

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

146

Preconditioning Eigenvalues and Some Comparison of Ronald B. Morgan  

E-print Network

method. Preconditioning of eigenvalue problems is only partly developed. However, work has been done, including Davidson [4], developed correction methods 1 #12;2 for their large symmetric matrices. In 1986-Davidson method [31] was developed in 1996. The inexact rational Krylov method [10] and truncated RQ [36

Morgan, Ron

147

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

E-print Network

that their solution constitutes a challenging test for nonlinear elliptic solvers. The flame sheet model adds only onePreconditioned 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

Zhang, Jun

148

Preconditioning Indefinite Systems in Interior Point Methods for Optimization  

Microsoft Academic Search

Every Newton step in an interior-point method for optimization requires a solution of a symmetric indefinite system of linear equations. Most of today's codes apply direct solution methods to perform this task. The use of logarithmic barriers in interior point methods causes unavoidable ill-conditioning of linear systems and, hence, iterative methods fail to provide sufficient accuracy unless appropriately preconditioned. Two

Luca Bergamaschi; Jacek Gondzio; Giovanni Zilli

2004-01-01

149

Preconditioning with cobalt chloride modifies pain perception in mice  

PubMed Central

Cobalt chloride (CoCl2) modifies mitochondrial permeability and has a hypoxic-mimetic effect; thus, the compound induces tolerance to ischemia and increases resistance to a number of injury types. The aim of the present study was to investigate the effects of CoCl2 hypoxic preconditioning for three weeks on thermonociception, somatic and visceral inflammatory pain, locomotor activity and coordination in mice. A significant pronociceptive effect was observed in the hot plate and tail flick tests after one and two weeks of CoCl2 administration, respectively (P<0.001). Thermal hyperalgesia (Plantar test) was present in the first week, but recovered by the end of the experiment. Contrary to the hyperalgesic effect on thermonociception, CoCl2 hypoxic preconditioning decreased the time spent grooming the affected area in the second phase of the formalin test on the orofacial and paw models. The first phase of formalin-induced pain and the writhing test were not affected by CoCl2 preconditioning. Thus, the present study demonstrated that CoCl2 preconditioning has a dual effect on pain, and these effects should be taken into account along with the better-known neuro-, cardio- and renoprotective effects of CoCl2. PMID:25780453

ALEXA, TEODORA; LUCA, ANDREI; DONDAS, ANDREI; BOHOTIN, CATALINA ROXANA

2015-01-01

150

Dexmedetomidine Preconditioning Attenuates Cisplatin-Induced Ototoxicity in Zebrafish  

PubMed Central

Objectives Utilisation of high-frequency drills is known to increase noise induced hearing loss due to increasing the damages of inner ear cells. This study aimed to investigate whether preconditioning by using dexmedetomidine (DEX) decreased the occurrence of ischemia in inner cells of the ear. Methods We utilised a transgenic zebrafish line Brn3C, and the embryos were collected from breeding adult zebrafish. Five-day-old larvae were cultured at the density of 50 embryos, and the larvae were classified into 4 groups: control, cisplatin group, DEX group, and DEX+yohimbine; adrenoreceptor blocker group. The DEX group was categorised into 3 subgroups by dosage; 0.1, 1, and 10 µM. Preconditioning was performed for 150 minutes and then exposed to cisplatin for 6 hours. The experiment was performed in 7 replicates for each group and the number of hair cells in 3 parts of the neuromasts of each fish was determined. Results Hair cell apoptosis by cisplatin was attenuated more significantly in the DEX preconditioning group than in the control group. However, the preconditioning effects were not blocked by yohimbine. Conclusion The results of this study suggest that hearing loss caused by vibration-induced noise could be reduced by using DEX and may occur through other mechanisms rather than adreno-receptors. PMID:25436046

Min, Too Jae; Ha, Young Ran; Jeong, In young; Yoo, Ji young

2014-01-01

151

Modern Preconditioned Eigensolvers for Spectral Image Segmentation and Graph Bisection  

E-print Network

on Clustering Large Data Sets Third IEEE International Conference on Data Mining (ICDM 2003) Andrew V. KnyazevModern Preconditioned Eigensolvers for Spectral Image Segmentation and Graph Bisection Workshop://www-math.cudenver.edu/~aknyazev e-mail: andrew.knyazev@cudenver.edu Original image Spectral segmentation 153.1405 sec Figure 1

Knyazev, Andrew

152

Learning Controller Preconditions for Physics-Based Character Animation  

E-print Network

as DANCE plug-ins. Using this software, we have produced a variety of physics-based animation results. 2Learning Controller Preconditions for Physics-Based Character Animation Petros Faloutsos, Michiel's College Road Toronto, ON M5S 3G4, Canada An ambitious goal in the area of physics-based computer animation

Faloutsos, Petros

153

Ischemic preconditioning: a potential role for protein S-thiolation?  

PubMed

Oxidant stress plays a crucial role in the triggering of cardioprotection involving ischemic preconditioning (IPC). We have used biotin-tagged cysteine to probe for redox-modified proteins in IPC protocols. Cysteine was biotinylated and introduced into isolated rat hearts. S-Thiolated proteins were detected and quantified using nonreducing western blots probed with streptavidin-horseradish peroxidase. Controls (15 min of aerobic perfusion plus 5 min of 0.5 mM biotin-cysteine plus 5 min of aerobic perfusion) showed low-level protein S-thiolation. Hearts preconditioned with 5 min of ischemia and reperfused for 5 min with biotin-cysteine plus 5 min of aerobic perfusion showed increased thiolation (160%) that was fully blocked by the antioxidant mercaptopropionylglycine, which is also known to block IPC. "Preconditioning" agonists (phorbol 12-myristate 13-acetate or phenylephrine) or oxidants (hydrogen peroxide or diamide) administered during aerobic preparations to biotin-cysteine-loaded hearts induced efficient protein S-thiolation. Preconditioning agonist-induced S-thiolation was significantly attenuated by diphenyleneiodonium (a flavoprotein inhibitor) or by the protein kinase C inhibitor bisindolylmaleimide I. Additional studies testing the role of a Nox2-containing NAD(P)H oxidase as the source of the oxidant stress essential to the triggering IPC showed that protein S-thiolation was the same in wild-type and Nox2 knockout mice. PMID:15998243

Eaton, Philip; Bell, Robert M; Cave, Alison C; Shattock, Michael J

2005-01-01

154

ISOFLURANE PRECONDITIONING NEUROPROTECTION IN EXPERIMENTAL FOCAL STROKE IS ANDROGEN-DEPENDENT IN MALE MICE  

PubMed Central

Isoflurane preconditioning neuroprotection in experimental stroke is male-specific. The role of androgens in the ischemic sensitivity of isoflurane preconditioned male brain and whether androgen effects are androgen receptor dependent were assessed. Male C57BL/6 mice were implanted with flutamide (androgen receptor antagonist), or castrated and implanted with testosterone, dihydrotestosterone, flutamide, letrozole (aromatase inhibitor), or vehicle 7–13 days before preconditioning. P450 estrogen aromatase wild-type and knockout mice were also evaluated. All mice were preconditioned for 4 h with 0% (sham preconditioning) or 1% isoflurane (isoflurane preconditioning) and recovered for 24 h. Mice then underwent 2 h of middle cerebral artery occlusion and were evaluated 22 h later for infarct volume. For neurobehavioral outcomes, sham and isoflurane preconditioned castrated male±dihydrotestosterone groups underwent 1 h of middle cerebral artery occlusion followed by 9 days of reperfusion. Isoflurane preconditioning neuroprotection relative to infarct volume outcomes were testosterone and dihydrotestosterone dose-specific and androgen receptor-dependent. Relative to long-term neurobehavioral outcomes, front paw sensorimotor function improved in isoflurane preconditioned mice regardless of androgen status while androgen replacement independently improved sensorimotor function. In contrast, isoflurane preconditioning improved cognitive function in castrates lacking endogenous androgens, but this improvement was absent in androgen replaced mice. Our findings suggest that androgen availability during isoflurane preconditioning may influence infarct volume and neurobehavioral outcomes in male mice following experimental stroke. PMID:20580788

ZHU, W.; WANG, L.; ZHANG, L.; PALMATEER, J. M.; LIBAL, N. L.; HURN, P. D.; HERSON, P. S.; MURPHY, S. J.

2010-01-01

155

Clinical applications of remote ischaemic preconditioning in native and transplant acute kidney injury.  

PubMed

Ischaemia-reperfusion (IR) injury is a composite of the injury sustained during a period of reduced or absent blood flow to a tissue or organ and the additional insult sustained upon reperfusion that limits the amount of tissue that can be salvaged. IR injury plays a central role in both native and transplant acute kidney injury (AKI). Native AKI is associated with increased morbidity and mortality in hospital inpatients, and transplant AKI contributes to graft dysfunction, ultimately limiting graft longevity. In this review, we discuss the potential therapeutic benefits of a cost-effective and low-risk intervention, remote ischaemic preconditioning (RIPC), and its applicability in the prevention and reduction of AKI. PMID:25280959

Veighey, Kristin; MacAllister, Raymond

2014-10-01

156

Preconditioning protects the heart in a prolonged uremic condition.  

PubMed

Metabolic diseases such as hyperlipidemia and diabetes attenuate the cardioprotective effect of ischemic preconditioning. In the present study, we examined whether another metabolic disease, prolonged uremia, affects ischemia/reperfusion injury and cardioprotection by ischemic preconditioning. Uremia was induced by partial nephrectomy in male Wistar rats. The development of uremia was verified 29 wk after surgery. Transthoracic echocardiography was performed to monitor cardiac function. At week 30, hearts of nephrectomized and sham-operated rats were isolated and subjected to a 30-min coronary occlusion followed by 120 min reperfusion with or without preceding preconditioning induced by three intermittent cycles of brief ischemia and reperfusion. In nephrectomized rats, plasma uric acid, carbamide, and creatinine as well as urine protein levels were increased as compared with sham-operated controls. Systolic anterior and septal wall thicknesses were increased in nephrectomized rats, suggesting the development of a minimal cardiac hypertrophy. Ejection fraction was decreased and isovolumic relaxation time was shortened in nephrectomized rats demonstrating a mild systolic and diastolic dysfunction. Infarct size was not affected significantly by nephrectomy itself. Ischemic preconditioning significantly decreased infarct size from 24.8 ± 5.2% to 6.6 ± 1.3% in the sham-operated group and also in the uremic group from 35.4 ± 9.5% to 11.9 ± 3.1% of the area at risk. Plasma ANG II and nitrotyrosine were significantly increased in the uremic rats. We conclude that although prolonged experimental uremia leads to severe metabolic changes and the development of a mild myocardial dysfunction, the cardioprotective effect of ischemic preconditioning is still preserved. PMID:22982778

Kocsis, Gabriella F; Sárközy, Márta; Bencsik, Péter; Pipicz, Márton; Varga, Zoltán V; Pálóczi, János; Csonka, Csaba; Ferdinandy, Péter; Csont, Tamás

2012-11-15

157

Development of resistance of an organism under various conditions of hypoxic preconditioning: role of the hypoxic period and reoxygenation.  

PubMed

Single exposure to moderate (10% O(2)) hypobaric, normobaric, and intermittent hypoxia is followed by a preconditioning response of the organism. The mechanisms for immediate adaptation are activated during the hypoxic period. Intermittent reoxygenation not only delays, but even suppresses this process. However, periods of oxygenation during the course of hypoxic training reduce the effect of hypoxia and prevent the possibility for "overdosage" of the adverse stimulus. Hence, they have a regulatory or normalizing role under these conditions. Our results indicate that hypoxitherapy in intermittent hypoxia mode provides optimum conditions for long-term adaptation. PMID:19704933

Lukyanova, L D; Germanova, E L; Kopaladze, R A

2009-04-01

158

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

PubMed

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

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

159

Strategies for Study of Neuroprotection from Cold-preconditioning  

PubMed Central

Neurological injury is a frequent cause of morbidity and mortality from general anesthesia and related surgical procedures that could be alleviated by development of effective, easy to administer and safe preconditioning treatments. We seek to define the neural immune signaling responsible for cold-preconditioning as means to identify novel targets for therapeutics development to protect brain before injury onset. Low-level pro-inflammatory mediator signaling changes over time are essential for cold-preconditioning neuroprotection. This signaling is consistent with the basic tenets of physiological conditioning hormesis, which require that irritative stimuli reach a threshold magnitude with sufficient time for adaptation to the stimuli for protection to become evident. Accordingly, delineation of the immune signaling involved in cold-preconditioning neuroprotection requires that biological systems and experimental manipulations plus technical capacities are highly reproducible and sensitive. Our approach is to use hippocampal slice cultures as an in vitro model that closely reflects their in vivo counterparts with multi-synaptic neural networks influenced by mature and quiescent macroglia / microglia. This glial state is particularly important for microglia since they are the principal source of cytokines, which are operative in the femtomolar range. Also, slice cultures can be maintained in vitro for several weeks, which is sufficient time to evoke activating stimuli and assess adaptive responses. Finally, environmental conditions can be accurately controlled using slice cultures so that cytokine signaling of cold-preconditioning can be measured, mimicked, and modulated to dissect the critical node aspects. Cytokine signaling system analyses require the use of sensitive and reproducible multiplexed techniques. We use quantitative PCR for TNF-? to screen for microglial activation followed by quantitative real-time qPCR array screening to assess tissue-wide cytokine changes. The latter is a most sensitive and reproducible means to measure multiple cytokine system signaling changes simultaneously. Significant changes are confirmed with targeted qPCR and then protein detection. We probe for tissue-based cytokine protein changes using multiplexed microsphere flow cytometric assays using Luminex technology. Cell-specific cytokine production is determined with double-label immunohistochemistry. Taken together, this brain tissue preparation and style of use, coupled to the suggested investigative strategies, may be an optimal approach for identifying potential targets for the development of novel therapeutics that could mimic the advantages of cold-preconditioning. PMID:20834222

Mitchell, Heidi M.; White, David M.; Kraig, Richard P.

2010-01-01

160

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: A target of uric acid treatment.  

PubMed

Ischemia impairs blood supply to the brain, and reperfusion is important to restore cerebral blood flow (CBF) and rescue neurons from cell death. However, reperfusion can induce CBF values exceeding the basal values before ischemia. This hyperemic effect has been associated with a worse ischemic brain damage, albeit the mechanisms that contribute to infarct expansion are not clear. In this study, we investigated the influence of early postischemic hyperemia on brain damage and middle cerebral artery (MCA) properties and the effect of treatment with the endogenous antioxidant uric acid (UA). The MCA was occluded for 90 min followed by 24 h reperfusion in adult male Sprague-Dawley rats. Cortical CBF increases at reperfusion beyond 20% of basal values were taken as indicative of hyperemia. UA (16 mg/kg) or vehicle (Locke's buffer) was administered intravenously 135 min after MCA occlusion. Hyperemic compared with nonhyperemic rats showed MCA wall thickening (sham: 22.4 ± 0.8 ?m; nonhyperemic: 23.1 ± 1.2 ?m; hyperemic: 27.8 ± 0.9 at 60 mmHg; P < 0.001, hyperemic vs. sham) involving adventitial cell proliferation, increased oxidative stress, and interleukin-18, and more severe brain damage. Thus MCA remodeling after ischemia-reperfusion takes place under vascular oxidative and inflammatory stress conditions linked to hyperemia. UA administration attenuated MCA wall thickening, induced passive lumen expansion, and reduced brain damage in hyperemic rats, although it did not increase brain UA concentration. We conclude that hyperemia at reperfusion following brain ischemia induces vascular damage that can be attenuated by administration of the endogenous antioxidant UA. PMID:25637543

Onetti, Yara; Dantas, Ana P; Pérez, Belén; Cugota, Roger; Chamorro, Angel; Planas, Anna M; Vila, Elisabet; Jiménez-Altayó, Francesc

2015-04-15

161

Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats.  

PubMed

Mitochondria-generated reactive oxygen species (ROS) play a crucial role in the pathogenesis of aging and age-associated diseases. In this study, we evaluated the effects of XJB-5-131 (XJB), a mitochondria-targeted ROS and electron scavenger, on cardiac resistance to ischemia-reperfusion (IR)-induced oxidative stress in aged rats. Male adult (5-month old, n=17) and aged (29-month old, n=19) Fischer Brown Norway (F344/BN) rats were randomly assigned to the following groups: adult (A), adult+XJB (AX), aged (O), and aged+XJB (OX). XJB was administered 3 times per week (3mg/kg body weight, IP) for four weeks. At the end of the treatment period, cardiac function was continuously monitored in excised hearts using the Langendorff technique for 30 min, followed by 20 min of global ischemia, and 60-min reperfusion. XJB improved post-ischemic recovery of aged hearts, as evidenced by greater left ventricular developed-pressures and rate-pressure products than the untreated, aged-matched group. The state 3 respiration rates at complexes I, II and IV of mitochondria isolated from XJB-treated aged hearts were 57% (P<0.05), 25% (P<0.05) and 28% (P<0.05), respectively, higher than controls. Ca(2+)-induced swelling, an indicator of permeability transition pore opening, was reduced in the mitochondria of XJB-treated aged rats. In addition, XJB significantly attenuated the H2O2-induced depolarization of the mitochondrial inner membrane as well as the total and mitochondrial ROS levels in cultured cardiomyocytes. This study underlines the importance of mitochondrial ROS in aging-induced cardiac dysfunction and suggests that targeting mitochondrial ROS may be an effective therapeutic approach to protect the aged heart against IR injury. PMID:25451170

Escobales, Nelson; Nuñez, Rebeca E; Jang, Sehwan; Parodi-Rullan, Rebecca; Ayala-Peña, Sylvette; Sacher, Joshua R; Skoda, Erin M; Wipf, Peter; Frontera, Walter; Javadov, Sabzali

2014-12-01

162

Gadolinium chloride-induced improvement of postischemic hepatic perfusion after warm ischemia is associated with reduced hepatic endothelin secretion.  

PubMed

Selective Kupffer cell blockade by gadolinium chloride (GdCl(3)) pretreatment of liver donors previously proved to be effective in reducing ischemia/reperfusion injury in rat liver transplants. Physiological mechanisms of this effect have not been specified so far. Vasoactive peptides are involved in liver blood flow regulation. We tested the hypothesis, that hepatic hemodynamic effects of GdCl(3) pretreatment are mediated by intrahepatic endothelin-1 (ET) secretion in a standardized porcine model of warm liver ischemia and reperfusion. Standardized warm hepatic ischemia (45 min) was induced after laparotomy in intubation narcoses (ITN) by Pringle-maneuver in pigs (n = 12). Animals were either pretreated with GdCl(3) (20 mg/kg i.v.) or sodium chloride 0.9% (control group) in a randomized manner 24 h before investigation. Relaparotomy was performed at day 7. Before, during ischemia and until 6 h after liver reperfusion, transhepatic blood flow (portal venous + hepatic artery flow) was defined by ultrasonic flow probes and hepatic parenchymous microcirculation evaluated by implanted thermodiffusion electrodes. ET plasma concentrations were analyzed (commercial RIA) at all time points in the hepatic veins after selective canulation. GdCl(3) pretreatment of animals markedly improved hepatic macro- and microperfusion before and particularly after warm ischemia. Mean ET plasma concentrations in the hepatic vein were significantly lower before, 6 h and 7 days after ischemia, compared with controls. Kupffer cell destruction by GdCl(3) pretreatment improves hepatic micro- and macroperfusion after warm ischemia, thus indicating reduced ischemia/reperfusion injury. Documented reduction of postischemic liver blood flow impairment after GdCl(3) pretreatment could be mediated by a decreased hepatic ET secretion, as hemodynamic effects were associated with significantly reduced ET plasma levels in hepatic veins. PMID:15773963

Frankenberg, Moritz V; Weimann, Jörg; Fritz, Stefan; Fiedler, Jörn; Mehrabi, A; Büchler, Markus W; Kraus, Thomas W

2005-04-01

163

Cardiac hypertrophy in the newborn delays the maturation of fatty acid ?-oxidation and compromises postischemic functional recovery.  

PubMed

During the neonatal period, cardiac energy metabolism progresses from a fetal glycolytic profile towards one more dependent on mitochondrial oxidative metabolism. In this study, we identified the effects of cardiac hypertrophy on neonatal cardiac metabolic maturation and its impact on neonatal postischemic functional recovery. Seven-day-old rabbits were subjected to either a sham or a surgical procedure to induce a left-to-right shunt via an aortocaval fistula to cause RV volume-overload. At 3 wk of age, hearts were isolated from both groups and perfused as isolated, biventricular preparations to assess cardiac energy metabolism. Volume-overload resulted in cardiac hypertrophy (16% increase in cardiac mass, P < 0.05) without evidence of cardiac dysfunction in vivo or in vitro. Fatty acid oxidation rates were 60% lower (P < 0.05) in hypertrophied hearts than controls, whereas glycolysis increased 246% (P < 0.05). In contrast, glucose and lactate oxidation rates were unchanged. Overall ATP production rates were significantly lower in hypertrophied hearts, resulting in increased AMP-to-ATP ratios in both aerobic hearts and ischemia-reperfused hearts. The lowered energy generation of hypertrophied hearts depressed functional recovery from ischemia. Decreased fatty acid oxidation rates were accompanied by increased malonyl-CoA levels due to decreased malonyl-CoA decarboxylase activity/expression. Increased glycolysis in hypertrophied hearts was accompanied by a significant increase in hypoxia-inducible factor-1? expression, a key transcriptional regulator of glycolysis. Cardiac hypertrophy in the neonatal heart results in a reemergence of the fetal metabolic profile, which compromises ATP production in the rapidly maturing heart and impairs recovery of function following ischemia. PMID:22408020

Oka, Tatsujiro; Lam, Victoria H; Zhang, Liyan; Keung, Wendy; Cadete, Virgilio J J; Samokhvalov, Victor; Tanner, Brandon A; Beker, Donna L; Ussher, John R; Huqi, Alda; Jaswal, Jagdip S; Rebeyka, Ivan M; Lopaschuk, Gary D

2012-05-01

164

Inhibition of thyroid hormone receptor ?1 impairs post-ischemic cardiac performance after myocardial infarction in mice.  

PubMed

Thyroid hormone receptor ?1 (TR?1) is shown to be critical for the maturation of cardiomyocytes and for the cellular response to stress. TR?1 is altered during post ischemic cardiac remodeling but the physiological significance of this response is not fully understood. Thus, the present study explored the potential consequences of selective pharmacological inhibition of TR?1 on the mechanical performance of the post-infarcted heart. Acute myocardial infarction was induced in mice (AMI), while sham operated animals served as controls (SHAM). A group of mice was treated with debutyl-dronedarone (DBD), a selective TR?1 inhibitor (AMI-DBD). AMI resulted in low T3 levels in plasma and in down-regulation of TR?1 and TR?1 expression. Left ventricular ejection fraction (LVEF%) was significantly reduced in AMI [33 (SEM 2.1) vs 79(2.5) in SHAM, p < 0.05] and was further declined in AMI-DBD [22(1.1) vs 33(2.1), respectively, p < 0.05]. Cardiac mass was increased in AMI but not in AMI-DBD hearts, resulting in significant increase in wall tension index. This increase in wall stress was accompanied by marked activation of p38 MAPK, a kinase that is sensitive to mechanical stretch and exerts negative inotropic effect. Furthermore, AMI resulted in ?-myosin heavy chain overexpression and reduction in the ratio of SR(Ca)ATPase to phospholamban (PLB). The latter further declined in AMI-DBD mainly due to increased expression of PLB. AMI induces downregulation of thyroid hormone signaling and pharmacological inhibition of TR?1 further depresses post-ischemic cardiac function. p38 MAPK and PLB may, at least in part, be involved in this response. PMID:23532677

Mourouzis, Iordanis; Kostakou, Erietta; Galanopoulos, Georgios; Mantzouratou, Polixeni; Pantos, Constantinos

2013-07-01

165

Shape reanalysis and sensitivities utilizing preconditioned iterative boundary solvers  

NASA Technical Reports Server (NTRS)

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.

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

1992-01-01

166

Can preconditioning reduce laparoscopy-induced tissue injury?  

Microsoft Academic Search

Background: Pneumoperitoneum (P) created to facilitate laparoscopy (L) is associated with splanchnic perfusion, ischemia\\/reperfusion (I\\/R) injury, and oxidative stress. In this randomized controlled experimental study with blind outcome assessment, we evaluated the effect of preconditioning (PRE) on L-induced I\\/R injury. Methods: The subjects were 40 Sprague-Dawley male rats. P was created in all except controls, using carbondioxide (CO 2) insufflation

S. Yilmaz; T. Koken; C. Tokyol; A. Kahraman; G. Akbulut; M. Serteser; C. Polat; C. Gokce; O. Gokce

2003-01-01

167

Preconditioning effects of intermittent stream flow on leaf litter decomposition  

Microsoft Academic Search

Autumnal input of leaf litter is a pivotal energy source in most headwater streams. In temporary streams, however, water stress\\u000a may lead to a seasonal shift in leaf abscission. Leaves accumulate at the surface of the dry streambed or in residual pools\\u000a and are subject to physicochemical preconditioning before decomposition starts after flow recovery. In this study, we experimentally\\u000a tested

D. Dieter; D. von Schiller; E. M. García-Roger; M. M. Sánchez-Montoya; R. Gómez; J. Mora-Gómez; F. Sangiorgio; J. Gelbrecht; K. Tockner

168

Preconditioned Alternating Projection Algorithms for Maximum a Posteriori ECT Reconstruction  

PubMed Central

We propose a preconditioned alternating projection algorithm (PAPA) for solving the maximum a posteriori (MAP) emission computed tomography (ECT) reconstruction problem. Specifically, we formulate the reconstruction problem as a constrained convex optimization problem with the total variation (TV) regularization. We then characterize the solution of the constrained convex optimization problem and show that it satisfies a system of fixed-point equations defined in terms of two proximity operators raised from the convex functions that define the TV-norm and the constrain involved in the problem. The characterization (of the solution) via the proximity operators that define two projection operators naturally leads to an alternating projection algorithm for finding the solution. For efficient numerical computation, we introduce to the alternating projection algorithm a preconditioning matrix (the EM-preconditioner) for the dense system matrix involved in the optimization problem. We prove theoretically convergence of the preconditioned alternating projection algorithm. In numerical experiments, performance of our algorithms, with an appropriately selected preconditioning matrix, is compared with performance of the conventional MAP expectation-maximization (MAP-EM) algorithm with TV regularizer (EM-TV) and that of the recently developed nested EM-TV algorithm for ECT reconstruction. Based on the numerical experiments performed in this work, we observe that the alternating projection algorithm with the EM-preconditioner outperforms significantly the EM-TV in all aspects including the convergence speed, the noise in the reconstructed images and the image quality. It also outperforms the nested EM-TV in the convergence speed while providing comparable image quality. PMID:23271835

Krol, Andrzej; Li, Si; Shen, Lixin; Xu, Yuesheng

2012-01-01

169

Effect of preconditioning unconditioned stimulus experience on learned taste aversions  

Microsoft Academic Search

Reports results from a taste-aversion study using 25 male Long-Evans rats in which ethanol was the unconditioned stimulus (UCS) and from 6 studies ^h (N?=?172) ^H in which lithium chloride (LiCl) was the UCS: (a) Exposure to the UCS prior to conditioning retards subsequent acquisition of learned taste aversions. (b) A single preconditioning UCS exposure is sufficient to attenuate conditioning.

Dale S. Cannon; Robert F. Berman; Timothy B. Baker; Carol A. Atkinson

1975-01-01

170

Preconditioned alternating projection algorithms for maximum a posteriori ECT reconstruction  

NASA Astrophysics Data System (ADS)

We propose a preconditioned alternating projection algorithm (PAPA) for solving the maximum a posteriori (MAP) emission computed tomography (ECT) reconstruction problem. Specifically, we formulate the reconstruction problem as a constrained convex optimization problem with the total variation (TV) regularization. We then characterize the solution of the constrained convex optimization problem and show that it satisfies a system of fixed-point equations defined in terms of two proximity operators raised from the convex functions that define the TV-norm and the constraint involved in the problem. The characterization (of the solution) via the proximity operators that define two projection operators naturally leads to an alternating projection algorithm for finding the solution. For efficient numerical computation, we introduce to the alternating projection algorithm a preconditioning matrix (the EM-preconditioner) for the dense system matrix involved in the optimization problem. We prove theoretically convergence of the PAPA. In numerical experiments, performance of our algorithms, with an appropriately selected preconditioning matrix, is compared with performance of the conventional MAP expectation-maximization (MAP-EM) algorithm with TV regularizer (EM-TV) and that of the recently developed nested EM-TV algorithm for ECT reconstruction. Based on the numerical experiments performed in this work, we observe that the alternating projection algorithm with the EM-preconditioner outperforms significantly the EM-TV in all aspects including the convergence speed, the noise in the reconstructed images and the image quality. It also outperforms the nested EM-TV in the convergence speed while providing comparable image quality.

Krol, Andrzej; Li, Si; Shen, Lixin; Xu, Yuesheng

2012-11-01

171

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

PubMed

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

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

172

Tachycardia Preconditions Infarct Size in Dogs Role of Adenosine and Protein Kinase C  

Microsoft Academic Search

Background—Myocardial ischemic preconditioning is a well-known phenomenon, however there is scant information in regard to nonischemic preconditioning. Methods and Results—We studied in anesthetized dogs the preconditioning effect of tachycardia and the mediation of adenosine and protein kinase C in this process. In a control group the anterior descending coronary artery was occluded for 60 minutes and reperfused for 270 minutes.

Raul J. Domenech; Pilar Macho; Diego Velez; Gina Sanchez; Xueliang Liu; Naranjan Dhalla

173

Poly-IC preconditioning protects against cerebral and renal ischemia-reperfusion injury  

Microsoft Academic Search

Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which

Amy E B Packard; Jason C Hedges; Frances R Bahjat; Susan L Stevens; Michael J Conlin; Andres M Salazar; Mary P Stenzel-Poore

2012-01-01

174

A review of the Alberta certified preconditioned feeder program (1980-1987)  

PubMed Central

Data from the Alberta Certified Preconditioned Feeder Program (1980-1987) were reviewed retrospectively. Numbers of calves sold, price premiums realized, pre-and postsale performance, production and health performance of preconditioned and regular calves were examined. During the study period, the program showed marked expansion and consistently resulted in substantial premiums for preconditioned calves. Real net returns from efficient rates of gain, increased sale weights, better calf quality and improved health status (disease resistance) were realized at sale time. Feedlot data indicated that postsale morbidity and mortality were markedly reduced in groups of preconditioned calves. PMID:17423421

Schipper, Casey; Church, Terry; Harris, Brian

1989-01-01

175

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

SciTech Connect

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 +}.

Chiueh, C.C. [School of Pharmacy, Taipei Medical University, Taipei 110, Taiwan (China) and Laboratory of Clinical Science, NIMH, NIH, Bethesda, MD 20892-1264 (United States)]. E-mail: chiueh@tmu.edu.tw; Andoh, Tsugunobu [Department of Applied Pharmacology, Toyama Medical and Pharmaceutical University (Japan); Chock, P. Boon [Laboratory of Biochemistry, NHLBI, NIH, Bethesda, MD 20892-8012 (United States)

2005-09-01

176

Role of ischemic preconditioning in hepatic ischemia-reperfusion injury  

PubMed Central

Background Investigation into less traumatic method of vascular occlusion during liver resection is the actual problem in hepatic surgery because of high level of complications such as liver failure. In this connection, the goal of our study was to determine the optimal model of vascular clamping. The research showed that vascular occlusion with ischemic preconditioning in the mode 5/10/15 the most delicate technique. Methods Forty white giant rabbits were divided randomly into four groups (n=10 in each group). In group I we used continuous Pringle maneuver by 30 min. In group II we used intermittent Pringle maneuver: 15 min of clamping/5 min of unclamping (reperfusion)/15 min of clamping. In group III we used intermittent Pringle maneuver with ischemic precondition: 5 min of ischemia/5 min of reperfusion, 10 min of ischemia/5 min of reperfusion/15 min of ischemia. Group IV (control group) is without hepatic ischemia. All animals were performed a liver biopsy at the end of the surgery. Five rabbits from each group underwent re-laparotomy on day 3 after surgery with biopsy samples being taken for studying reparative processes in liver parenchyma. Results Results of morphometric analysis were the best to illustrate different level of liver injury in the groups. Thus, there were 95.5% damaged hepatocytes after vascular occlusion in hepatic preparations in group I, 70.3% damaged hepatocytes in group II, and 42.3% damaged hepatocytes in group III. There were 5.3% damaged hepatocytes in the control group. Conclusions Vascular occlusion with ischemic preconditioning in the mode 5/10/15 the most delicate technique that does not involve major structural injuries and functional disorders in the remnant liver. Thus, it is amenable to translation into clinical practice and may improve outcomes in liver resection with inflow vascular occlusion. PMID:25202694

Boyko, Valeriy V.; Tyshchenko, Oleksandr M.; Skoryi, Denys I.; Kozlova, Tatiana V.; Gorgol, Natalia I.; Volchenko, Igor V.

2014-01-01

177

A preconditioned fast decoupled power flow method for contingency screening  

SciTech Connect

This paper proposes an efficient method for contingency screening in power systems. Contingency analysis requires substantial amounts of computational time in evaluating data for controlling generating units or power flows. In this paper, the Tchebychev iteration (TI) method of an indirect method is presented for solving a set of linear equations of Fast Decoupled Power Flow (FDPF) in the contingency screening. Furthermore, the precondition technique is introduced to improve the convergence characteristics of the indirect method. The proposed method has been successfully applied to a 2,107 node system.

Mori, Hiroyuki; Tanaka, Hideya [Meiji Univ., Kawasaki (Japan). Dept. of Electrical Engineering; Kanno, Junya [Tokyo Electric Power Co. (Japan)

1995-12-31

178

A preconditioned fast decoupled power flow method for contingency screening  

SciTech Connect

This paper proposes an efficient method for contingency screening in power systems. Contingency analysis requires substantial amounts of computational time in evaluating data for controlling generating units or power flows. In this paper, the Tchebychev iteration (TI) method of an indirect method is presented for solving a set of linear equations of Fast Decoupled Power Flow (FDPF) in the contingency screening. Furthermore, the precondition technique is introduced to improve the convergence characteristics of the indirect method. The proposed method has been successfully applied to a 2107 node system.

Mori, Hiroyuki; Tanaka, Hideya [Meiji Univ., Kawasaki (Japan). Dept. of Electrical Engineering] [Meiji Univ., Kawasaki (Japan). Dept. of Electrical Engineering; Kanno, Junya [Tokyo Electric Power Co. (Japan)] [Tokyo Electric Power Co. (Japan)

1996-02-01

179

Preconditioning methods for ideal and multiphase fluid flows  

NASA Astrophysics Data System (ADS)

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.

Gupta, Ashish

180

Preconditioning of the Navier-Stokes equations with multiple constraints  

NASA Astrophysics Data System (ADS)

The Navier-Stokes equations represent a mathematical model of incompressible fluid flow. To obtain a unique solution, these need to be supplemented by a physically relevant set of boundary conditions (BCs). These BCs, such as natural outflow, no-slip, no-penetration, can be easily imposed within the finite element setting in the case of straight boundaries that are aligned with the Cartesian axes. When more general domains are considered, as in many realistic industrial applications, one practical way of imposing BCs is with Lagrange multipliers. This procedure leads to an augmented linear system at the discrete level. In this paper we discuss efficient preconditioning of such systems.

White, Raymon; Heil, Matthias; Mihajlovi?, Milan

2013-10-01

181

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...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...

2010-07-01

182

Ischemic Preconditioning of Renal Tissue: Identification of Early Up-Regulated Genes  

Microsoft Academic Search

Given the important effects of ischemic preconditioning (IPC) in minimizing tissue damage induced by sustained ischemia in several tissues, this study evaluated the effect of IPC in preserving renal function and identified up-regulated genes after 30 min of preconditioning. IPC induced by 2, 3 and 4 min of ischemia, intercalated by 5 min of reperfusion, induced a measurable protection of

Marcelo Damario Gomes; Douglas Vasconcelos Cancherini; Marise Amaral Rebouças Moreira; Nancy Amaral Rebouças

2003-01-01

183

HL-1 Myocytes Exhibit PKC and KATP Channel-Dependent Delta Opioid Preconditioning1,2  

E-print Network

HL-1 Myocytes Exhibit PKC and KATP Channel-Dependent Delta Opioid Preconditioning1,2 Elisabeth M. Opioid preconditioning protects the myocardium against ischemia/reperfusion (IR) injury. By enhancing cardiomyocyte viability, opioids can en- hance cardiac function and recovery from IR injury during acute cardiac

Wojcik, Edward J.

184

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

Code of Federal Regulations, 2011 CFR

...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...

2011-07-01

185

Ischemic preconditioning suppresses apoptosis of rabbit spinal neurocytes by inhibiting ASK1-14-3-3 dissociation.  

PubMed

The mechanism by which a brief episode of sublethal ischemia followed by reperfusion (ischemic preconditioning, IPC) prevents the lethal effects of subsequent periods of prolonged ischemia, are poorly understood. A completely randomized, controlled study was designed to study the effect of IPC using a rabbit model of ischemic spinal cord injury. Twenty-four white adult New England rabbits were randomly assigned to one of 3 groups (n=8 per group); the groups were assigned as follows: Group I: sham-operation group, Group II: ischemic reperfusion (I/R) group, and Group III: ischemic preconditioning group. Spinal cord ischemia was induced by introducing an infra renal aortic cross-clamp for 30min. Following injury, rabbits were subjected to 30min, 2h, or 8h of reperfusion in Group II. In Group III, subjects underwent three cycles, 5min each, of ischemia followed by 5min of reperfusion, before receiving 30min of ischemia. We previously reported that the association between ASK1 (apoptosis signal-regulating kinase 1) and 14-3-3 played an important role in regulating ischemia/reperfusion spinal cord injuries. To evaluate the effect of ischemic preconditioning in injured spinal cords, we examined alterations in spinal tissue morphology, activation of key members of the ASK1-mediated signaling pathway, and the association between ASK1 and 14-3-3. Changes in spinal cord morphology were observed with hematoxylin and eosin (H&E) staining and electron microscopy. The phosphorylation levels of ASK1, JNK, and p38 were assessed by immunoblot analysis. The association between ASK1 and 14-3-3 was analyzed by co-immunoprecipitation experiments. We observed that swelling of the neurocyte bodies and hemorrhage of the spinal cord were dramatically decreased in Group III compared to Group II. In addition, the degree of apoptosis among neurocytes was reduced in Group III compared to Group II. Finally, the phosphorylation of ASK1, JNK, p38 and the dissociation of ASK1 from 14-3-3 were dramatically decreased in Group III compared with Group II. These results indicate that ischemic preconditioning may have a protective affect against ASK1/14-3-3 dissociation-induced spinal cord injuries. PMID:18577421

Yang, Chengwei; Ren, Yongxin; Liu, Feng; Cai, Weihua; Zhang, Ning; Nagel, David J; Yin, Guoyong

2008-08-29

186

Ischemic tolerance in an in vivo model of glutamate preconditioning.  

PubMed

Ischemia initiates a complicated biochemical cascade of events that triggers neuronal death. This study focuses on glutamate-mediated neuronal tolerance to ischemia-reperfusion. We employed an animal model of lifelong excess release of glutamate, the glutamate dehydrogenase 1 transgenic (Tg) mouse, as a model of in vivo glutamate preconditioning. Nine- and twenty-two-month-old Tg and wild-type (wt) mice were subjected to 90 min of middle cerebral artery occlusion, followed by 24 hr of reperfusion. The Tg mice suffered significantly reduced infarction and edema volume compared with their wt counterparts. We further analyzed proteasomal activity, level of ubiquitin immunostaining, and microtubule-associated protein-2A (MAP2A) expression to understand the mechanism of neuroprotection observed in the Tg mice. We found that, in the absence of ischemia, the Tg mice exhibited higher activity of the 20S and 26S proteasomes, whereas there was no significant difference in the level of hippocampal ubiquitin immunostaining between wt and Tg mice. A surprising, significant increase was observed in MAP2A expression in neurons of the Tg hippocampus following ischemia-reperfusion compared with that in wt hippocampus. The results suggest that increased proteasome activity and MAP2A synthesis and transport might account for the effectiveness of glutamate preconditioning against ischemia-reperfusion. © 2014 Wiley Periodicals, Inc. PMID:25421886

Badawi, Yomna; Pal, Ranu; Hui, Dongwei; Michaelis, Elias K; Shi, Honglian

2015-04-01

187

Effect of Preconditioning and Soldering on Failures of Chip Tantalum Capacitors  

NASA Technical Reports Server (NTRS)

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.

Teverovsky, Alexander A.

2014-01-01

188

Hyperglycemia abolishes the protective effect of ischemic preconditioning in glomerular endothelial cells in vitro  

PubMed Central

In preclinical investigations, ischemic preconditioning (IPC) protects kidneys from ischemia/reperfusion injury. The direct effects of IPC on glomerular endothelial cells have not been studied in detail. Most investigations of IPC have focused on healthy cells and animals, and it remains unknown whether IPC is renoprotective in the setting of medical comorbidities such as diabetes. In this study, we determined the preventive potential of IPC in healthy glomerular endothelial cell monolayers, and compared these results to monolayers cultured under hyperglycemic conditions. We exposed glomerular endothelial monolayers to 1 h of IPC 24 h prior to oxygen–glucose deprivation (OGD), an in vitro model of ischemia/reperfusion injury. Glomerular endothelial monolayer integrity was assessed by measuring transendothelial electrical resistance, albumin flux, and cell survival. We found that IPC protected healthy but not hyperglycemic glomerular endothelial monolayers from ischemia/reperfusion injury. Furthermore, not only was the protective effect of IPC lost in the setting of hyperglycemia, but IPC was actually deleterious to the integrity of hyperglycemic glomerular endothelial cell monolayers. PMID:25804266

Schenning, Katie J; Anderson, Sharon; Alkayed, Nabil J; Hutchens, Michael P

2015-01-01

189

Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury  

PubMed Central

Ischemic preconditioning (IPC) or postconditioning (Ipost) is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3? pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3? pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3? pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3? pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries. PMID:21822424

Yin, Xia; Zheng, Yang; Zhai, Xujie; Zhao, Xin; Cai, Lu

2012-01-01

190

Phorbol ester, but not ischemic preconditioning, activates protein kinase D in the rat heart.  

PubMed

The signal transduction pathways that mediate the cardioprotective effects of ischemic preconditioning remain unclear. Here we have determined the role of a novel kinase, protein kinase D (PKD), in mediating preconditioning in the rat heart. Isolated rat hearts (n=6/group) were subjected to either: (i) 36 min aerobic perfusion (control); (ii) 20 min aerobic perfusion plus 3 min no-flow ischemia, 3 min reperfusion, 5 min no-flow ischemia, 5 min reperfusion (ischemic preconditioning); (iii) 20 min aerobic perfusion plus 200 nmol/l phorbol 12-myristate 13-acetate (PMA) given as a substitute for ischemic preconditioning. The left ventricle then was excised, homogenized and PKD immunoprecipitated from the homogenate. Activity of the purified kinase was determined following bincubation with [gamma32P]-ATP+/-syntide-2, a substrate for PKD. Significant PKD autophosphorylation and syntide-2 phosphorylation occurred in PMA-treated hearts, but not in control or preconditioned hearts. Additional studies confirmed that recovery of LVDP was greater and initiation of ischemic contracture and time-to-peak contracture were less, in ischemic preconditioned hearts compared with controls (P<0.05). Our results suggest that the early events that mediate ischemic preconditioning in the rat heart occur via a PKD-independent mechanism. PMID:9281458

Brooks, G; Goss, M W; Rozengurt, E; Galiñanes, M

1997-08-01

191

Remote ischemic preconditioning has a neutral effect on the incidence of kidney injury after coronary artery bypass graft surgery.  

PubMed

Acute kidney injury (AKI) is a frequent complication of cardiac surgery and usually occurs in patients with preexisting chronic kidney disease (CKD). Remote ischemic preconditioning (RIPC) may mitigate the renal ischemia-reperfusion injury associated with cardiac surgery and may be a preventive strategy for postsurgical AKI. We undertook a randomized controlled trial of RIPC to prevent AKI in 86 patients with CKD (estimated glomerular filtration rate under 60?ml/min per 1.73?m(2)) undergoing coronary artery bypass graft (CABG) surgery. Forty-three patients each were randomized to receive standard care with or without RIPC consisting of three 5-minute cycles of forearm ischemia followed by reperfusion. The primary end point was the development of AKI defined as an increase in serum creatinine concentration over 0.3?mg/dl within 48?h of surgery. Secondary end points included a comparison between the study and control groups of several serum biomarkers of renal injury including cystatin-C, neutrophil gelatinase-associated lipocalin (NGAL), and interleukin-18 (IL-18), and urinary biomarkers including NGAL, IL-18, and kidney injury molecule-1 measured at 6, 12, and 24?h after CABG, and the 72-h serum troponin T concentration area under the curve as a marker of myocardial injury. Clinical and operative characteristics were similar between the preconditioned and control groups. AKI developed in 12 patients in both groups within 48?h of CABG. There were no significant differences between the two groups in the concentrations of any of the serum or urinary biomarkers of renal or cardiac injury after CABG. Thus, RIPC induced by forearm ischemia-reperfusion had no effect on the frequency of AKI after CABG in patients with CKD. PMID:25075773

Gallagher, Sean M; Jones, Dan A; Kapur, Akhil; Wragg, Andrew; Harwood, Steve M; Mathur, Rohini; Archbold, R Andrew; Uppal, Rakesh; Yaqoob, Muhammad M

2015-02-01

192

Aerodynamic shape optimization using preconditioned conjugate gradient methods  

NASA Technical Reports Server (NTRS)

In an effort to further improve upon the latest advancements made in aerodynamic shape optimization procedures, a systematic study is performed to examine several current solution methodologies as applied to various aspects of the optimization procedure. It is demonstrated that preconditioned conjugate gradient-like methodologies dramatically decrease the computational efforts required for such procedures. The design problem investigated is the shape optimization of the upper and lower surfaces of an initially symmetric (NACA-012) airfoil in inviscid transonic flow and at zero degree angle-of-attack. The complete surface shape is represented using a Bezier-Bernstein polynomial. The present optimization method then automatically obtains supercritical airfoil shapes over a variety of freestream Mach numbers. Furthermore, the best optimization strategy examined resulted in a factor of 8 decrease in computational time as well as a factor of 4 decrease in memory over the most efficient strategies in current use.

Burgreen, Greg W.; Baysal, Oktay

1993-01-01

193

A frequency dependent preconditioned wavelet method for atmospheric tomography  

NASA Astrophysics Data System (ADS)

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.

Yudytskiy, Mykhaylo; Helin, Tapio; Ramlau, Ronny

2013-12-01

194

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

NASA Technical Reports Server (NTRS)

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.

Darmofal, David L.

1998-01-01

195

Can anaerobic performance be improved by remote ischemic preconditioning?  

PubMed

Remote ischemic preconditioning (RIPC) provides a substantial benefit for heart protection during surgery. Recent literature on RIPC reveals the potential to benefit the enhancement of sports performance as well. The aim of this study was to investigate the effect of RIPC on anaerobic performance. Seventeen healthy participants who practice regular physical activity participated in the project (9 women and 8 men, mean age 28 ± 8 years). The participants were randomly assigned to an RIPC intervention (four 5-minute cycles of ischemia reperfusion, followed by 5 minutes using a pressure cuff) or a SHAM intervention in a crossover design. After the intervention, the participants were tested for alactic anaerobic performance (6 seconds of effort) followed by a Wingate test (lactic system) on an electromagnetic cycle ergometer. The following parameters were evaluated: average power, peak power, the scale of perceived exertion, fatigue index (in watt per second), peak power (in Watt), time to reach peak power (in seconds), minimum power (in Watt), the average power-to-weight ratio (in watt per kilogram), and the maximum power-to-weight ratio (in watt per kilogram). The peak power for the Wingate test is 794 W for RIPC and 777 W for the control group (p = 0.208). The average power is 529 W (RIPC) vs. 520 W for controls (p = 0.079). Perceived effort for RIPC is 9/10 on the Borg scale vs. 10/10 for the control group (p = 0.123). Remote ischemic preconditioning does not offer any significant benefits for anaerobic performance. PMID:25068802

Lalonde, François; Curnier, Daniel Y

2015-01-01

196

Iterated preconditioned LSQR method for inverse problems on unstructured grids  

NASA Astrophysics Data System (ADS)

This article presents a method for solving large-scale linear inverse imaging problems regularized with a nonlinear, edge-preserving penalty term such as total variation or the Perona-Malik technique. Our method is aimed at problems defined on unstructured meshes, where such regularizers naturally arise in unfactorized form as a stiffness matrix of an anisotropic diffusion operator and factorization is prohibitively expensive. In the proposed scheme, the nonlinearity is handled with lagged diffusivity fixed point iteration, which involves solving a large-scale linear least squares problem in each iteration. Because the convergence of Krylov methods for problems with discontinuities is notoriously slow, we propose to accelerate it by means of priorconditioning (Bayesian preconditioning). priorconditioning is a technique that, through transformation to the standard form, embeds the information contained in the prior (Bayesian interpretation of a regularizer) directly into the forward operator and thence into the solution space. We derive a factorization-free preconditioned LSQR algorithm (MLSQR), allowing implicit application of the preconditioner through efficient schemes such as multigrid. The resulting method is also matrix-free i.e. the forward map can be defined through its action on a vector. We illustrate the performance of the method on two numerical examples. Simple 1D-deblurring problem serves to visualize the discussion throughout the paper. The effectiveness of the proposed numerical scheme is demonstrated on a three-dimensional problem in fluorescence diffuse optical tomography with total variation regularization derived algebraic multigrid preconditioner, which is the type of large scale, unstructured mesh problem, requiring matrix-free and factorization-free approaches that motivated the work here.

Arridge, S. R.; Betcke, M. M.; Harhanen, L.

2014-06-01

197

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

NASA Technical Reports Server (NTRS)

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.

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

1997-01-01

198

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

SciTech Connect

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.

Cai, Yunfeng, E-mail: yfcai@math.pku.edu.cn [LMAM and School of Mathematical Sciences, Peking University, Beijing 100871 (China) [LMAM and School of Mathematical Sciences, Peking University, Beijing 100871 (China); Department of Computer Science, University of California, Davis 95616 (United States); Bai, Zhaojun, E-mail: bai@cs.ucdavis.edu [Department of Computer Science and Department of Mathematics, University of California, Davis 95616 (United States)] [Department of Computer Science and Department of Mathematics, University of California, Davis 95616 (United States); Pask, John E., E-mail: pask1@llnl.gov [Condensed Matter and Materials Division, Lawrence Livermore National Laboratory, Livermore, CA 94550 (United States); Sukumar, N., E-mail: nsukumar@ucdavis.edu [Department of Civil and Environmental Engineering, University of California, Davis 95616 (United States)

2013-12-15

199

An efficient preconditioned iterative solution of fully-coupled elastohydrodynamic lubrication problems  

E-print Network

An efficient preconditioned iterative solution of fully-coupled elastohydrodynamic lubrication elastohydrodynamic lubrication line and point contact problems. The new blockwise preconditioner that is presented that both grow linearly with the number of unknowns. Keywords: elastohydrodynamic lubrication; finite

Jimack, Peter

200

Hypoxia preconditioning protection of corneal stromal cells requires HIF1? but not VEGF  

PubMed Central

Purpose Hypoxia preconditioning protects corneal stromal cells from stress-induced death. This study determined whether the transcription factor HIF-1? (Hypoxia Inducible Factor) is responsible and whether this is promulgated by VEGF (Vascular Endothelial Growth Factor). Methods Cultured bovine stromal cells were preconditioned with hypoxia in the presence of cadmium chloride, a chemical inhibitor of HIF-1?, and HIF-1? siRNA to test if HIF-1? activity is needed for hypoxia preconditioning protection from UV-irradiation induced cell death. TUNEL assay was used to detect cell apoptosis after UV-irradiation. RT-PCR and western blot were used to detect the presence of HIF-1? and VEGF in transcriptional and translational levels. Results During hypoxia (0.5% O2), 5 ?M cadmium chloride completely inhibited HIF-1? expression and reversed the protection by hypoxia preconditioning.  HIF-1? siRNA (15 nM) reduced HIF-1? expression by 90% and produced a complete loss of protection provided by hypoxia preconditioning.  Since VEGF is induced by hypoxia, can be HIF-1? dependent, and is often protective, we examined the changes in transcription of VEGF and its receptors after 4 h of hypoxia preconditioning.  VEGF and its receptors Flt-1 and Flk-1 are up-regulated after hypoxia preconditioning.  However, the transcription and translation of VEGF were paradoxically increased by siHIF-1?, suggesting that VEGF expression in stromal cells is not down-stream of HIF-1?. Conclusions These findings demonstrate that hypoxia preconditioning protection in corneal stromal cells requires HIF-1?, but that VEGF is not a component of the protection. PMID:19461932

Xing, Dongmei

2009-01-01

201

That Which Does Not Kill You Makes You Stronger: A Molecular Mechanism for Preconditioning  

NSDL National Science Digital Library

Preconditioning by sublethal stress can protect a cell from subsequent injury and apoptosis through a mechanism that has been unclear. Many such stresses stimulate the formation of stress granules: transient cytoplasmic foci that contain heat shock protein as well as translationally stalled mRNA and various mRNA-binding proteins. Recent research suggests that sequestration in stress granules of TRAF2, an adaptor protein that is required for tumor necrosis factor receptor 1 signaling, may underlie preconditioning by sublethal stresses.

Jonathan E. McDunn (Washington University School of Medicine; Cellular Injury and Adaptation Laboratory, Departments of Surgery and Genetics REV)

2005-07-05

202

The acetylation of RelA in Lys310 dictates the NF-?B-dependent response in post-ischemic injury  

Microsoft Academic Search

The activation of nuclear factor kappa B (NF-?B) p50\\/RelA is a key event in ischemic neuronal injury, as well as in brain ischemic tolerance. We tested whether epigenetic mechanisms affecting the acetylation state of RelA might discriminate between neuroprotective and neurotoxic activation of NF-?B during ischemia. NF-?B activation and RelA acetylation were investigated in cortices of mice subjected to preconditioning

A Lanzillotta; I Sarnico; R Ingrassia; F Boroni; C Branca; M Benarese; G Faraco; F Blasi; A Chiarugi; P Spano; M Pizzi

2010-01-01

203

Preconditioning improves function and recovery of single muscle fibers during severe hypoxia and reoxygenation.  

PubMed

Reperfusion following prolonged ischemia induces cellular damage in whole skeletal muscle models. Ischemic preconditioning attenuates the deleterious effects. We tested whether individual skeletal muscle fibers would be similarly affected by severe hypoxia and reoxygenation (H/R) in the absence of extracellular factors and whether cellular damage could be alleviated by hypoxic preconditioning. Force and free cytosolic Ca2+ ([Ca2+]c) were monitored in Xenopus single muscle fibers (n = 24) contracting tetanically at 0.2 Hz during 5 min of severe hypoxia and 5 min of reoxygenation. Twelve cells were preconditioned by a shorter bout of H/R 1 h before the experimental trial. In preconditioned cells, force relative to initial maximal values (P/P(o)) and relative peak [Ca2+]c fell (P < 0.05) during 5 min of hypoxia and recovered during reoxygenation. In contrast, P/P(o) and relative peak [Ca2+]c fell more during hypoxia (P < 0.05) and recovered less during reoxygenation (P < 0.05) in control cells. The ratio of force to [Ca2+]c was significantly higher in the preconditioned cells during severe hypoxia, suggesting that changes in [Ca2+]c were not solely responsible for the loss in force. We conclude that 1) isolated skeletal muscle fibers contracting in the absence of extracellular factors are susceptible to H/R injury associated with changes in Ca2+ handling; and 2) hypoxic preconditioning improves contractility, Ca2+ handling, and cell recovery during subsequent hypoxic insult. PMID:11401836

Kohin, S; Stary, C M; Howlett, R A; Hogan, M C

2001-07-01

204

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

NASA Technical Reports Server (NTRS)

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.

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

1996-01-01

205

Neuroprotective effect of ischemic preconditioning in focal cerebral infarction: relationship with upregulation of vascular endothelial growth factor  

PubMed Central

Neuroprotection by ischemic preconditioning has been confirmed by many studies, but the precise mechanism remains unclear. In the present study, we performed cerebral ischemic preconditioning in rats by simulating a transient ischemic attack twice (each a 20-minute occlusion of the middle cerebral artery) before inducing focal cerebral infarction (2 hour occlusion-reperfusion in the same artery). We also explored the mechanism underlying the neuroprotective effect of ischemic preconditioning. Seven days after occlusion-reperfusion, tetrazolium chloride staining and immunohistochemistry revealed that the infarct volume was significantly smaller in the group that underwent preconditioning than in the model group. Furthermore, vascular endothelial growth factor immunoreactivity was considerably greater in the hippocampal CA3 region of preconditioned rats than model rats. Our results suggest that the protective effects of ischemic preconditioning on focal cerebral infarction are associated with upregulation of vascular endothelial growth factor. PMID:25206770

Liu, Yong; Zhu, Suiqiang; Wang, Yunfu; Hu, Jingquan; Xu, Lili; Ding, Li; Liu, Guangjian

2014-01-01

206

Awareness in nine countries: A public health approach to suicide prevention  

Microsoft Academic Search

Suicide is an important public health problem, increasing worldwide, and on a yearly basis accounting for the death of more than one million people, with estimates as high as 10–20 times that many attempting to take their own life. Because successful suicide prevention depends upon recognition of symptoms of mental ill-health, awareness of these signs is a necessary precondition. The

Christina W. Hoven; Danuta Wasserman; Camilla Wasserman; Donald J. Mandell

2009-01-01

207

PROTECTION AGAINST ACETAMINOPHEN-INDUCED LIVER INJURY BY ALLOPURINOL IS DEPENDENT ON ALDEHYDE OXIDASE-MEDIATED LIVER PRECONDITIONING  

PubMed Central

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 18h or 1h prior to an APAP overdose. Administration of allopurinol 18h prior to APAP overdose resulted in an 88% reduction in liver injury (serum ALT) 6h after APAP; however, 1h 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) has been implicated in the progression of APAP toxicity. In our study we showed equivalent early JNK activation (2h) however late JNK activation (6h) 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) 18h or 1h 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 18h 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. PMID:24345528

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

2014-01-01

208

Preconditioning with Triiodothyronine Improves the Clinical Signs and Acute Tubular Necrosis Induced by Ischemia/Reperfusion in Rats  

PubMed Central

Background Renal ischemia/reperfusion (I/R) injury is manifested by acute renal failure (ARF) and acute tubular necrosis (ATN). The aim of this study was to evaluate the effectiveness of preconditioning with 3, 3, 5 triiodothyronine (T3) to prevent I/R renal injury. Methodology/Principal Findings The rats were divided into four groups: sham-operated, placebo-treated (SO-P), sham-operated T3- treated (SO- T3), I/R-injured placebo-treated (IR-P), and I/R-injured T3-treated (IR- T3) groups. At 24 h before ischemia, the animals received a single dose of T3 (100 ?g/kg). Renal function and plasma, urinary, and tissue variables were studied at 4, 24, and 48 h of reperfusion, including biochemical, oxidative stress, and inflammation variables, PARP-1 immunohistochemical expression, and ATN morphology. In comparison to the SO groups, the IR-P groups had higher plasma urea and creatinine levels and greater proteinuria (at all reperfusion times) and also showed: increased oxidative stress-related plasma, urinary, and tissue variables; higher plasma levels of IL6 (proinflammatory cytokine); increased glomerular and tubular nuclear PARP-1 expression; and a greater degree of ATN. The IR-T3 group showed a marked reduction in all of these variables, especially at 48 h of reperfusion. No significant differences were observed between SO-P and SO-T3 groups. Conclusions This study demonstrates that preconditioning rats with a single dose of T3 improves the clinical signs and ATN of renal I/R injury. These beneficial effects are accompanied by reductions in oxidative stress, inflammation, and renal PARP-1 expression, indicating that this sequence of factors plays an important role in the ATN induced by I/R injury. PMID:24086411

Ferreyra, Carla; Vargas, Félix; Rodríguez-Gómez, Isabel; Pérez-Abud, Rocío; O'Valle, Francisco; Osuna, Antonio

2013-01-01

209

Positive Indian Ocean Dipole events precondition southeast Australia bushfires  

NASA Astrophysics Data System (ADS)

The devastating “Black Saturday” bushfire inferno in the southeast Australian state of Victoria in early February 2009 and the “Ash Wednesday” bushfires in February 1983 were both preceded by a positive Indian Ocean Dipole (pIOD) event. Is there a systematic pIOD linkage beyond these two natural disasters? We show that out of 21 significant bushfires seasons since 1950, 11 were preceded by a pIOD. During Victoria's wet season, particularly spring, a pIOD contributes to lower rainfall and higher temperatures exacerbating the dry conditions and increasing the fuel load leading into summer. Consequently, pIODs are effective in preconditioning Victoria for bushfires, more so than El Niño events, as seen in the impact on soil moisture on interannual time scales and in multi-decadal changes since the 1950s. Given that the recent increase in pIOD occurrences is consistent with what is expected from global warming, an increased bushfire risk in the future is likely across southeast Australia.

Cai, W.; Cowan, T.; Raupach, M.

2009-10-01

210

Subconjunctival and/or intrastromal bevacizumab injections as preconditioning therapy to promote corneal graft survival.  

PubMed

The purpose of this study is to investigate whether subconjunctival and/or intrastromal Bevacizumab injections could help to prevent graft failure in high-risk keratoplasties. Twenty seven eyes of 27 patients, affected by high immune rejection risk and corneal neovascularization, were involved in this prospective interventional case-control series (case group: 14 eyes and control group: 13 eyes). Case group was submitted to a cycle of three subconjunctival and/or intrastromal injections of 5 mg/0.2 ml Bevacizumab. After a mean period of 6.36 months ± 3.38 SD from the last injection, all patients underwent keratoplasty. An adjunctive injection was performed intraoperatively at the end of the surgical procedure. Control group did not receive any Bevacizumab injection, but directly underwent keratoplasty. Each patient was submitted to a complete eye examination and corneal confocal microscopy. The absence of immune rejection signs in the graft, at clinical and confocal microscopy examination, was considered as main outcome measure. All cases showed less ocular inflammation and activity of vessels. No side effects were detected after the injection procedure. No corneal graft rejection was seen during the follow-up (mean 26.1 months ± 5.7 SD) in the case group. Six eyes of the control group showed graft rejection 3.8 months ± 1.4 SD after keratoplasty. As a conclusion, Bevacizumab injection may represent a preconditioning treatment to improve prognosis in high-risk corneal transplantation. The procedure seems to be safe and it may help to reduce the inflammatory stimulus that plays a key role in corneal graft rejection. PMID:24715230

Fasciani, Romina; Mosca, Luigi; Giannico, Maria Ilaria; Ambrogio, Simone Antonio; Balestrazzi, Emilio

2015-04-01

211

Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats  

PubMed Central

Because radiation-induced cellular damage is attributed primarily to harmful effects of free radicals, molecules with direct free radical scavenging properties are particularly promising as radioprotectors. It has been demonstrated that controlled ozone administration may promote an adaptation to oxidative stress, preventing the damage induced by reactive oxygen species. Thus, we hypothesized that ozone would ameliorate oxidative damage caused by total body irradiation (TBI) with a single dose of 6 Gy in rat liver and ileum tissues. Rats were randomly divided into groups as follows: control group; saline-treated and irradiated (IR) groups; and ozone oxidative preconditioning (OOP) and IR groups. Animals were exposed to TBI after a 5-day intraperitoneal pretreatment with either saline or ozone (1 mg/kg/day). They were decapitated at either 6 h or 72 h after TBI. Plasma, liver and ileum samples were obtained. Serum AST, ALT and TNF-? levels were elevated in the IR groups compared with the control group and were decreased after treatment with OOP. TBI resulted in a significant increase in the levels of MDA in the liver and ileal tissues and a decrease of SOD activities. The results demonstrated that the levels of MDA liver and ileal tissues in irradiated rats that were pretreated with ozone were significantly decreased, while SOD activities were significantly increased. OOP reversed all histopathological alterations induced by irradiation. In conclusion, data obtained from this study indicated that ozone could increase the endogenous antioxidant defense mechanism in rats and there by protect the animals from radiation-induced organ toxicity. PMID:22915786

Gultekin, Fatma Ayca; Bakkal, Bekir Hakan; Guven, Berrak; Tasdoven, Ilhan; Bektas, Sibel; Can, Murat; Comert, Mustafa

2013-01-01

212

Evaluation of thyroid hormone induced pharmacological preconditioning on cardiomyocyte protection against ischemic-reperfusion injury  

PubMed Central

Objectives: Ischemic preconditioning (IPC) has been demonstrated to make myocardium transiently more resistant to deleterious effect of prolonged ischemia. The opening of the mitochondrial permeability transition pore (mPTP) at the time of myocardial reperfusion is a critical determinant of cell death. L-thyroxine pre-treatment increases the tolerance of the heart to ischemia and produces cardioprotection similar to ischemic precondition. This study has been designed to investigate the mechanism involved in L-thyroxine-induced cardiomyocyte protection against ischemia-reperfusion (I/R) injury in rats. Materials and Methods: L-thyroxine (T4) was administered to Wistar rats (n=6) (25 ?g/100 g/day s.c.) for two weeks. Hearts from normal and L-thyroxine-treated rats were perfused in Langendorff's mode and subjected to 30 min of ischemia followed by 120 min of reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining and lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) was analyzed in coronary effluent. Results: IPC and pharmacological preconditioning (PPC) significantly decreased (P<0.05) myocardial infarct size, release of LDH and CK-MB in rat heart. Perfusion of atractyloside, an opener of mPTP, significantly (P<0.05) attenuated the cardioprotective effect of IPC and L-thyroxine-induced pharmacological preconditioning (PPC) in normal rat heart. Conclusion: The cardioprotective effect of L-thyroxine-induced preconditioning may be mediated through inhibition of mPTP opening during reperfusion phase. PMID:22345873

Kumar, Anil; Taliyan, Rajeev; Sharma, P.L.

2012-01-01

213

Oleanolic Acid Enhances the Beneficial Effects of Preconditioning on PC12 Cells  

PubMed Central

Preconditioning triggers endogenous protection against subsequent exposure to higher concentrations of a neurotoxin. In this study, we investigated whether exposure to oleanolic acid (OA) enhances the protective effects of preconditioning on PC12 cells exposed to 6-hydroxydopamine (6-OHDA). A concentration response curve was constructed using 6-OHDA (50, 150, 300, and 600??M). The experiment consisted of 6 groups: untreated, OA only, Group 1: cells treated with 6-OHDA (50??M) for 1 hour, Group 2: cells treated with 6-OHDA (150??M) for 1 hour, Group 3: cells treated with 6-OHDA (50??M) for 30 minutes followed 6 hours later by treatment with 6-OHDA (150??M) for 30 minutes, and Group 4: cells treated as in group 3 but also received OA immediately after the second 6-OHDA treatment. Cell viability and apoptotic ratio were assessed using the MTT and Annexin V staining tests, respectively. In preconditioned cells, we found that cell viability remained high following exposure to 6-OHDA (150??M). OA treatment enhanced the protective effects of preconditioning. Similarly, with the annexin V apoptosis test, preconditioning protected the cell and this was enhanced by OA. Therefore, preexposure of PC12 cells to low 6-OHDA concentration can protect against subsequent toxic insults of 6-OHDA and OA enhances this protection. PMID:25478286

Daniels, Willie M. U.; Mabandla, Musa V.

2014-01-01

214

Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool  

PubMed Central

Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool. Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol. Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor, ?-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunction in vitro. Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus. PMID:25404991

Wang, Weiwei; Zhang, Hao; Xue, Guo; Zhang, Weihua; Wang, Lina; Lu, Fanghao; Li, Hongzhu; Bai, Shuzhi; Lin, Yan; Lou, Yu; Xu, Changqing; Zhao, Yajun

2014-01-01

215

Ischemic preconditioning reduces ischemic brain injury by suppressing nuclear factor kappa B expression and neuronal apoptosis?  

PubMed Central

Ischemic stroke induces a series of complex pathophysiological events including blood-brain barrier disruption, inflammatory response and neuronal apoptosis. Previous studies demonstrate that ischemic preconditioning attenuates ischemic brain damage via inhibiting blood-brain barrier disruption and the inflammatory response. Rats underwent transient (15 minutes) occlusion of the bilateral common carotid artery with 48 hours of reperfusion, and were subjected to permanent middle cerebral artery occlusion. This study explored whether ischemic preconditioning could reduce ischemic brain injury and relevant molecular mechanisms by inhibiting neuronal apoptosis. Results found that at 72 hours following cerebral ischemia, myeloperoxidase activity was enhanced, malondialdehyde levels increased, and neurological function was obviously damaged. Simultaneously, neuronal apoptosis increased, and nuclear factor-?B and cleaved caspase-3 expression was significantly increased in ischemic brain tissues. Ischemic preconditioning reduced the cerebral ischemia-induced inflammatory response, lipid peroxidation, and neurological function injury. In addition, ischemic preconditioning decreased nuclear factor-?B p65 and cleaved caspase-3 expression. These results suggested that ischemic preconditioning plays a protective effect against ischemic brain injury by suppressing the inflammatory response, reducing lipid peroxidation, and neuronal apoptosis via inhibition of nuclear factor-?B and cleaved caspase-3 expression. PMID:25206708

Shi, Songsheng; Yang, Weizhong; Tu, Xiankun; Chen, Chunmei; Wang, Chunhua

2013-01-01

216

Preconditioning Mesenchymal Stem Cells With Caspase Inhibition and Hyperoxia Prior to Hypoxia Exposure Increases Cell Proliferation  

PubMed Central

Myocardial infarction is a leading cause of mortality and morbidity worldwide. Occlusion of a coronary artery produces ischemia and myocardial necrosis that leads to left ventricular (LV) remodeling, dysfunction, and heart failure. Stem cell therapy may decrease infarct size and improve LV function; the hypoxic environment, however, following a myocardial infarction may result in apoptosis, which in turn decreases survival of transplanted stem cells. Therefore, the effects of preconditioned mesenchymal stem cells (MSC) with hyperoxia (100% oxygen), Z-VAD-FMK pan-caspase inhibitor (CI), or both in a hypoxic environment in order to mimic conditions seen in cardiac tissue post-myocardial infarction were studied in vitro. MSCs preconditioned with hyperoxia or CI significantly decreased apoptosis as suggested by TUNEL assay and Annexin V analysis using fluorescence assisted cell sorting. These effects were more profound when both, hyperoxia and CI, were used. Additionally, gene and protein expression of caspases 1, 3, 6, 7, and 9 were down-regulated significantly in MSCs preconditioned with hyperoxia, CI, or both, while the survival markers Akt1, NF-?B, and Bcl-2 were significantly increased in preconditioned MSCs. These changes ultimately resulted in a significant increase in MSC proliferation in hypoxic environment as determined by BrdU assays compared to MSCs without preconditioning. These effects may prove to be of great clinical significance when transplanting stem cells into the hypoxic myocardium of post-myocardial infarction patients in order to attenuate LV remodeling and improve LV function. PMID:23794477

Saini, Uksha; Gumina, Richard J.; Wolfe, Brian; Kuppusamy, M. Lakshmi; Kuppusamy, Periannan; Boudoulas, Konstantinos Dean

2014-01-01

217

Preventing Pneumoconiosis  

MedlinePLUS

... email. » Register for ENews Home > Lung Disease > Pneumoconiosis, Coal Workers Pneumoconiosis Preventing Pneumoconiosis Can Pneumoconiosis be Prevented? ... way to prevent pneumoconiosis is by not inhaling coal dust. The Occupational Safety & Health Administration (OSHA) (part ...

218

Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy  

PubMed Central

Pathological cardiac hypertrophy, a common response of the heart to a variety of cardiovascular diseases, is typically associated with myocytes remodeling and fibrotic replacement, cardiac dysfunction. Exercise preconditioning (EP) increases the myocardial mechanical load and enhances tolerance of cardiac ischemia-reperfusion injury (IRI), however, is less reported in pathological cardiac hypertrophy. To determine the effect of EP in pathological cardiac hypertrophy, Male 10-wk-old Sprague-Dawley rats (n=30) were subjected to 4 weeks of EP followed by 4-8 weeks of pressure overload (transverse aortic constriction, TAC) to induce pathological remodeling. TAC in untrained controls (n=30) led to pathological cardiac hypertrophy, depressed systolic function. We observed that left ventricular wall thickness in end diastole, heart size, heart weight-to-body weight ratio, heart weight-to-tibia length ratio, cross-sectional area of cardiomyocytes and the reactivation of fetal genes (atrial natriuretic peptide and brain natriuretic peptide) were markedly increased, meanwhile left ventricular internal dimension at end-diastole, systolic function were significantly decreased by TAC at 4 wks after operation (P < 0.01), all of which were effectively inhibited by EP treatment (P < 0.05), but the differences of these parameters were decreased at 8 wks after operation. Furthermore, EP treatment inhibited degradation of I?B?, and decreased NF-?B p65 subunit levels in the nuclear fraction, and then reduced IL2 levels in the myocardium of rats subject to TAC. EP can effectively attenuate pathological cardiac hypertrophic responses induced by TAC possibly through inhibition of degradation of I?B and blockade of the NF-?B signaling pathway in the early stage of pathological cardiac hypertrophy. PMID:25755743

Xu, Tongyi; Tang, Hao; Zhang, Ben; Cai, Chengliang; Liu, Xiaohong; Han, Qingqi; Zou, Liangjian

2015-01-01

219

Analysis and modeling of neural processes underlying sensory preconditioning.  

PubMed

Sensory preconditioning (SPC) is a procedure to demonstrate learning to associate between relatively neutral sensory stimuli in the absence of an external reinforcing stimulus, the underlying neural mechanisms of which have remained obscure. We address basic questions about neural processes underlying SPC, including whether neurons that mediate reward or punishment signals in reinforcement learning participate in association between neutral sensory stimuli. In crickets, we have suggested that octopaminergic (OA-ergic) or dopaminergic (DA-ergic) neurons participate in memory acquisition and retrieval in appetitive or aversive conditioning, respectively. Crickets that had been trained to associate an odor (CS2) with a visual pattern (CS1) (phase 1) and then to associate CS1 with water reward or quinine punishment (phase 2) exhibited a significantly increased or decreased preference for CS2 that had never been paired with the US, demonstrating successful SPC. Injection of an OA or DA receptor antagonist at different phases of the SPC training and testing showed that OA-ergic or DA-ergic neurons do not participate in learning of CS2-CS1 association in phase 1, but that OA-ergic neurons participate in learning in phase 2 and memory retrieval after appetitive SPC training. We also obtained evidence suggesting that association between CS2 and US, which should underlie conditioned response of crickets to CS2, is formed in phase 2, contrary to the standard theory of SPC assuming that it occurs in the final test. We propose models of SPC to account for these findings, by extending our model of classical conditioning. PMID:23380289

Matsumoto, Yukihisa; Hirashima, Daisuke; Mizunami, Makoto

2013-03-01

220

Glaciations in response to climate variations preconditioned by evolving topography.  

PubMed

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

Pedersen, Vivi Kathrine; Egholm, David Lundbek

2013-01-10

221

Limb ischemic preconditioning attenuates cerebral ischemic injury in rat model.  

PubMed

Ischemic brain injury is not uncommon after open-heart surgery with cardiopulmonary bypass and seriously undermines the patients' life quality. Therefore, potential protective effects of limb ischemic preconditioning (LIP) on subsequent ischemic injury of the brain were investigated by evaluating anti-inflammatory effects and apoptosis of pyramidal neurons in the CA1 hippocampus. One hundred and eight Sprague-Dawley rats were divided into the middle cerebral artery occlusion (MCAO) group (n=54) and the LIP group (n=54). A thread was used to occlude the middle cerebral artery in the MCAO group and the LIP group animals were pretreated with LIP followed by MCAO. In the two groups, nine samples were collected at each time-point of 0, 6, 12, 24, 48 and 72 h after MCAO to detect IL-6 and IL-17 and their mRNA levels. Neurological severity scores (NSS) were examined before the animals were sacrificed. Compared with the LIP group, cerebral histopathological changes in the MCAO group were most distinct and significantly more infiltrated inflammatory and apoptotic neuronal cells were observed at 24, 48 and 72 h post-surgery. IL-17 and IL-6 mRNA levels analyzed by quantitative real-time polymerase chain reaction (PCR) (qRT-PCR) were significantly reduced in the LIP group compared with the MCAO group at the 12, 24 and 48 h time-points. A significant reduction in IL-17 expression level was determined by enzyme-linked immunosorbent assay (ELISA) in the LIP group at 12, 24 and 48 h, while IL-6 was significantly reduced at the 24 and 48 h time-points. The NSSs were not significantly different between the groups. Therefore, in a MCAO rat model, we have proved that LIP pretreatment can protect the brain from infarction after ischemic injury and induce ischemic tolerance, potentially, by reducing IL-17 to provide anti-inflammatory effects and attenuate apoptosis of hippocampal neuronal cells. PMID:24002779

Wang, W; Yu, X D; Mo, X; Zhang, H B; Zhu, D M

2014-05-01

222

GDNF preconditioning can overcome Schwann cell phenotypic memory.  

PubMed

While it is known that Schwann cells (SCs) provide cues to enhance regeneration following peripheral nerve injury, the effect of SC phenotypic memory (muscle or cutaneous nerve-derived) on enhancing axonal regeneration and functional recovery has been unclear in the literature. In particular, differences between muscle and cutaneous nerve-derived SC may encourage specific motor or sensory axonal guidance in cell/tissue transplantation therapies. Thus, the goal of this study was to determine whether phenotypically matched combinations of neurons and SCs stimulate greater axonal extension compared to mismatched combinations (i.e. motor neurons/muscle nerve-derived SCs vs. motor neurons/cutaneous nerve-derived SCs). Additionally, the effect of glial cell line-derived neurotrophic factor (GDNF) treatment on SC-neuron interaction was also evaluated. In order to examine these interactions, microfluidic devices were used to assess the effects of soluble factors secreted from SCs on neurons. Unlike traditional co-culture methods, the devices allow for easier quantification of single neurite extension over long periods of time, as well as easy cell and media sampling of pure populations for biochemical analyses. Results demonstrated longer neurite growth when neurons are cultured with phenotype matched SCs, suggesting that SCs are capable of retaining phenotypic memory despite a prolonged absence of axonal contact. Furthermore, the negative effect of mismatched cultures can be overcome when mismatched SCs are preconditioned with GDNF. These results suggest that treatment of SCs with GDNF could enhance their ability to promote regeneration through mismatched grafts frequently used in clinical settings. PMID:25496841

Marquardt, Laura M; Sakiyama-Elbert, Shelly E

2015-03-01

223

Preconditioning with Endoplasmic Reticulum Stress Ameliorates Endothelial Cell Inflammation  

PubMed Central

Endoplasmic Reticulum (ER) stress, caused by disturbance in ER homeostasis, has been implicated in several pathological conditions such as ischemic injury, neurodegenerative disorders, metabolic diseases and more recently in inflammatory conditions. Our present study aims at understanding the role of ER stress in endothelial cell (EC) inflammation, a critical event in the pathogenesis of acute lung injury (ALI). We found that preconditioning human pulmonary artery endothelial cells (HPAEC) to ER stress either by depleting ER chaperone and signaling regulator BiP using siRNA, or specifically cleaving (inactivating) BiP using subtilase cytotoxin (SubAB), alleviates EC inflammation. The two approaches adopted to abrogate BiP function induced ATF4 protein expression and the phosphorylation of eIF2?, both markers of ER stress, which in turn resulted in blunting the activation of NF-?B, and restoring endothelial barrier integrity. Pretreatment of HPAEC with BiP siRNA inhibited thrombin-induced I?B? degradation and its resulting downstream signaling pathway involving NF-?B nuclear translocation, DNA binding, phosphorylation at serine536, transcriptional activation and subsequent expression of adhesion molecules. However, TNF?-mediated NF-?B signaling was unaffected upon BiP knockdown. In an alternative approach, SubAB-mediated inactivation of NF-?B was independent of I?B? degradation. Mechanistic analysis revealed that pretreatment of EC with SubAB interfered with the binding of the liberated NF-?B to the DNA, thereby resulting in reduced expression of adhesion molecules, cytokines and chemokines. In addition, both knockdown and inactivation of BiP stimulated actin cytoskeletal reorganization resulting in restoration of endothelial permeability. Together our studies indicate that BiP plays a central role in EC inflammation and injury via its action on NF-?B activation and regulation of vascular permeability. PMID:25356743

Leonard, Antony; Paton, Adrienne W.; El-Quadi, Monaliza; Paton, James C.; Fazal, Fabeha

2014-01-01

224

Preconditioning with endoplasmic reticulum stress ameliorates endothelial cell inflammation.  

PubMed

Endoplasmic Reticulum (ER) stress, caused by disturbance in ER homeostasis, has been implicated in several pathological conditions such as ischemic injury, neurodegenerative disorders, metabolic diseases and more recently in inflammatory conditions. Our present study aims at understanding the role of ER stress in endothelial cell (EC) inflammation, a critical event in the pathogenesis of acute lung injury (ALI). We found that preconditioning human pulmonary artery endothelial cells (HPAEC) to ER stress either by depleting ER chaperone and signaling regulator BiP using siRNA, or specifically cleaving (inactivating) BiP using subtilase cytotoxin (SubAB), alleviates EC inflammation. The two approaches adopted to abrogate BiP function induced ATF4 protein expression and the phosphorylation of eIF2?, both markers of ER stress, which in turn resulted in blunting the activation of NF-?B, and restoring endothelial barrier integrity. Pretreatment of HPAEC with BiP siRNA inhibited thrombin-induced I?B? degradation and its resulting downstream signaling pathway involving NF-?B nuclear translocation, DNA binding, phosphorylation at serine536, transcriptional activation and subsequent expression of adhesion molecules. However, TNF?-mediated NF-?B signaling was unaffected upon BiP knockdown. In an alternative approach, SubAB-mediated inactivation of NF-?B was independent of I?B? degradation. Mechanistic analysis revealed that pretreatment of EC with SubAB interfered with the binding of the liberated NF-?B to the DNA, thereby resulting in reduced expression of adhesion molecules, cytokines and chemokines. In addition, both knockdown and inactivation of BiP stimulated actin cytoskeletal reorganization resulting in restoration of endothelial permeability. Together our studies indicate that BiP plays a central role in EC inflammation and injury via its action on NF-?B activation and regulation of vascular permeability. PMID:25356743

Leonard, Antony; Paton, Adrienne W; El-Quadi, Monaliza; Paton, James C; Fazal, Fabeha

2014-01-01

225

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

PubMed Central

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

Kunst, G; Klein, A A

2015-01-01

226

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

NASA Technical Reports Server (NTRS)

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.

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

1999-01-01

227

Scheduling and Pre-Conditioning in Multi-User MIMO TDD Systems  

E-print Network

The downlink transmission in multi-user multiple-input multiple-output (MIMO) systems has been extensively studied from both communication-theoretic and information-theoretic perspectives. Most of these papers assume perfect/imperfect channel knowledge. In general, the problem of channel estimation is studied separately. However, in interference-limited communication systems with high mobility, the problem of channel estimation is tightly coupled with the problem of maximizing throughput of the system. In this paper, scheduling and pre-conditioning in the presence of reciprocal time-division duplex (TDD) training are considered. In the case of homogeneous users, a scheduling scheme is proposed and an improved lower bound on the sum capacity is derived. The problem of choosing training sequence length to maximize net throughput of the system is also studied. In the case of heterogeneous users, a modified pre-conditioning method is proposed and an optimized pre-conditioning matrix is derived. This method is com...

Jose, Jubin; Whiting, Phil; Vishwanath, Sriram

2007-01-01

228

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

PubMed Central

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

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

2015-01-01

229

Minocycline-preconditioned neural stem cells enhance neuroprotection after ischemic stroke in rats.  

PubMed

Transplantation of neural stem cells (NSCs) offers a novel therapeutic strategy for stroke; however, massive grafted cell death following transplantation, possibly due to a hostile host brain environment, lessens the effectiveness of this approach. Here, we have investigated whether reprogramming NSCs with minocycline, a broadly used antibiotic also known to possess cytoprotective properties, enhances survival of grafted cells and promotes neuroprotection in ischemic stroke. NSCs harvested from the subventricular zone of fetal rats were preconditioned with minocycline in vitro and transplanted into rat brains 6 h after transient middle cerebral artery occlusion. Histological and behavioral tests were examined from days 0-28 after stroke. For in vitro experiments, NSCs were subjected to oxygen-glucose deprivation and reoxygenation. Cell viability and antioxidant gene expression were analyzed. Minocycline preconditioning protected the grafted NSCs from ischemic reperfusion injury via upregulation of Nrf2 and Nrf2-regulated antioxidant genes. Additionally, preconditioning with minocycline induced the NSCs to release paracrine factors, including brain-derived neurotrophic factor, nerve growth factor, glial cell-derived neurotrophic factor, and vascular endothelial growth factor. Moreover, transplantation of the minocycline-preconditioned NSCs significantly attenuated infarct size and improved neurological performance, compared with non-preconditioned NSCs. Minocycline-induced neuroprotection was abolished by transfecting the NSCs with Nrf2-small interfering RNA before transplantation. Thus, preconditioning with minocycline, which reprograms NSCs to tolerate oxidative stress after ischemic reperfusion injury and express higher levels of paracrine factors through Nrf2 up-regulation, is a simple and safe approach to enhance the effectiveness of transplantation therapy in ischemic stroke. PMID:22399769

Sakata, Hiroyuki; Niizuma, Kuniyasu; Yoshioka, Hideyuki; Kim, Gab Seok; Jung, Joo Eun; Katsu, Masataka; Narasimhan, Purnima; Maier, Carolina M; Nishiyama, Yasuhiro; Chan, Pak H

2012-03-01

230

Fluid Shear Stress Pre-Conditioning Promotes Endothelial Morphogenesis of Embryonic Stem Cells Within Embryoid Bodies  

PubMed Central

Pluripotent embryonic stem cells (ESCs) are capable of differentiating into all mesoderm-derived cell lineages, including endothelial, hematopoietic, and cardiac cell types. Common strategies to direct mesoderm differentiation of ESCs rely on exposing the cells to a series of biochemical and biophysical cues at different stages of differentiation to promote maturation toward specific cell phenotypes. Shear forces that mimic cardiovascular physiological forces can evoke a myriad of responses in somatic and stem cell populations, and have, thus, been studied as a means to direct stem cell differentiation. However, elucidating the effects of shear pre-conditioning on the subsequent vascular differentiation and morphogenesis of ESCs has yet to be examined. In this study, ESC monolayers were subjected to physiological shear (5?dyn/cm2) or static conditions for 2 days on collagen IV-coated substrates before initiating embryoid body (EB) differentiation. Immediately after the pre-conditioning period, shear pre-conditioned and statically cultured ESCs exhibited similar morphologies and largely retained a pluripotent phenotype; however, ESCs exposed to fluid shear expressed increased levels of endothelial marker genes Flk-1 (?3-fold), VE-cadherin (?3-fold), and PECAM (?2-fold), compared with statically cultured ESCs. After 7 days of EB culture, ?70% of EBs formed from shear pre-conditioned ESCs expressed significantly higher levels of endothelial marker genes compared with EBs formed from statically cultured ESCs. Interestingly, unlike EBs formed from statically cultured ESCs, EBs formed from fluid shear stress pre-conditioned ESCs exhibited a centrally localized region of VE-cadherin+ cells that persisted for at least 10 days of differentiation. These results demonstrate that fluid shear stress pre-conditioning not only promotes ESC endothelial gene expression but also subsequently impacts the organization of endothelial cells within EBs. Together, these studies highlight a novel approach to promote in vitro morphogenesis of developmental vasculogenic models and potentially promote pre-vascularization of tissue-engineered constructs derived from pluripotent stem cells. PMID:24138406

Nsiah, Barbara A.; Ahsan, Tabassum; Griffiths, Sarah; Cooke, Marissa; Nerem, Robert M.

2014-01-01

231

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

NASA Technical Reports Server (NTRS)

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.

Godfrey, Andrew G.

1993-01-01

232

Isoflurane's Effect on Protein Conformation as a Proposed Mechanism for Preconditioning  

PubMed Central

Persistent alteration of protein conformation due to interaction with isoflurane may be a novel molecular aspect of preconditioning. We preincubated human serum albumin with isoflurane, dialyzed to release agent, and assessed protein conformation. Susceptibility to chemical modification by methylglyoxal and nitrophenylacetate was also examined. Isoflurane had a persistent effect on protein conformation. An increase in the susceptibility of surface residues to chemical modification attended this change in conformation. Modification of isoflurane-treated HSA included intra- and intersubunit cross-linking that may be a consequence of anesthetic-induced changes in multimeric subpopulations. This irreversible effect of isoflurane may represent a mechanism for preconditioning. PMID:21918721

Baker, Michelle R.; Benton, Sean K.; Theisen, Christopher S.; McClintick, Chad A.; Fibuch, Eugene E.; Seidler, Norbert W.

2011-01-01

233

Preconditioned methods for solving the incompressible and low speed compressible equations  

NASA Technical Reports Server (NTRS)

Acceleration methods are presented for solving the steady state incompressible equations. These systems are preconditioned by introducing artificial time derivatives which allow for a faster convergence to the steady state. The compressible equations in conservation form with slow flow are also considered. Two arbitrary functions, alpha and beta, are introduced in the general preconditioning. An analysis of this system is presented and an optimal value for beta is determined given a constant, alpha. It is further shown that the resultant incompressible equations form a symmetric hyperbolic system and so are well posed. Several generalizations to the compressible equations are presented which generalize previous results.

Turkel, E.

1986-01-01

234

Preconditioning electromyographic data for an upper extremity model using neural networks  

NASA Technical Reports Server (NTRS)

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.

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

1994-01-01

235

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

Code of Federal Regulations, 2010 CFR

...concentration of CO plus CO2 falls below 6 percent or the vehicle's...preconditioning mode. (B) In park or neutral for the idle mode...concentration of CO plus CO2 must be greater than or equal to 6 percent...If the dynamometer speed falls outside the limits for...

2010-07-01

236

AN ODYSSEY INTO LOCAL REFINEMENT AND MULTILEVEL PRECONDITIONING III: IMPLEMENTATION AND NUMERICAL  

E-print Network

implementations are performed in both C and MATLAB using the Finite Element ToolKit (FEtk), an open source finite element software package. We finish the paper with a sequence of numerical experiments illustrating words. finite element methods, local mesh refinement, multilevel preconditioning, BPX, red and red

237

Spectral Two-Step Preconditioning of Multilevel Fast Multipole Algorithm for the Fast Monostatic RCS Calculation  

Microsoft Academic Search

A new spectral two-step preconditioning of multilevel fast multipole algorithm (MLFMA) is proposed to solve large dense linear systems with multiple right-hand sides arising in monostatic radar cross section (RCS) calculations. The first system is solved with a deflated generalized minimal residual (GMRES) method and the eigenvector information is generated at the same time. Based on this eigenvector information, a

Ping-Liang Rui; Ru-Shan Chen; Dao-Xiang Wang; Edward Kai-Ning Yung

2007-01-01

238

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

PubMed Central

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

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

239

PURDUE EXTENSIONManagingYour Beef Herd: Highlighting Key Determinants of Success in Preconditioning PURDUE EXTENSION  

E-print Network

cattle. PC calves have re- duced morbidity and mortality in the feedlot and tend to have improved gain from a bunk and drink from a fountain/tank. Many PC programs encompass a beef quality assurance ­ commonly known as BQA ­ component. Preconditioning Advantages Nearly every study shows that the cattle

240

POLYNOMIAL PRECONDITIONED GMRES AND GMRES-DR QUAN LIU, RONALD B. MORGAN, AND WALTER WILCOX  

E-print Network

1 POLYNOMIAL PRECONDITIONED GMRES AND GMRES-DR QUAN LIU, RONALD B. MORGAN, AND WALTER WILCOX-7328 (Ronald Morgan@baylor.edu). §Department of Physics, Baylor University, Waco, TX 76798-7316. (Walter Wilcox@baylor.edu). 1 #12;2 Q. LIU, R. B. MORGAN and W. WILCOX with deflated restarting (GMRES-DR) [27] which both

Morgan, Ron

241

Ischemic Preconditioning Attenuates Portal Venous Plasma Concentrations of Purines following Warm Liver Ischemia in Man  

Microsoft Academic Search

Background\\/Aims: Degradation of adenine nucleotides to adenosine has been suggested to play a critical role in ischemic preconditioning (IPC). Thus, we questioned in patients undergoing partial hepatectomy whether (i) IPC will increase plasma purine catabolites and whether (ii) formation of purines in response to vascular clamping (Pringle maneuver) can be attenuated by prior IPC. Methods: 75 patients were randomly assigned

A. Choukèr; A. Martignoni; R. J. Schauer; H. G. Rau; A. Volk; O. Heizmann; M. Dugas; K. Messmer; K. Peter; M. Thiel

2005-01-01

242

Angiogenesis contributes to the neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats.  

PubMed

Ischemic stroke is one of the leading causes of mortality and disability worldwide. Previous studies have indicated that hyperbaric oxygen preconditioning (HBO-PC) can induce neuroprotection against focal cerebral ischemia. However, the underlying mechanisms are still not fully understood, and the optimal regimen for preconditioning must be confirmed. In the present study, we designed eight preconditioning regimens and compared their neuroprotective effects. Hyperbaric oxygen preconditioning every other day for there sessions exhibited the best neuroprotective effect; the infarct volume was reduced by almost 50% at 48 h after middle cerebral artery occlusion. We also found that HBO-PC significantly increased the microvessel density and the CD31-positive cells in the penumbra at 72 h after stroke. These results indicate that angiogenesis is involved in the neuroprotection induced by HBO-PC. Moreover, we explored the roles of HIF-1? and angiogenic factors in the angiogenesis process induced by HBO-PC. The results from western blotting demostrated that protein expression of Ang-2 in the HBO-PC group was significantly increased. In conclusion, HBO-PC reduced brain injury and improved neurological function after focal cerebral ischemia, as partly mediated by the increased microvessel density in the penumbra, and this effect may result from the upregulation of Ang-2. PMID:25171223

Duan, Shanshan; Shao, Guiqiang; Yu, Ling; Ren, Chuancheng

2014-09-17

243

A preconditioned Krylov subspace approach to a tightly coupled aeromechanical system  

NASA Astrophysics Data System (ADS)

A tightly coupled approach is attempted to compute a modest fluid-structure interaction for high subsonic flow through a converging nozzle with deformable walls. A globally convergent Newton statement and a matrix-free GMRES linear equation solver are used to linearize and solve the coupled system of equations without explicitly forming the left hand side jacobian matrix associated with the Newton method. A variable forcing function term is successfully incorporated into the Newton statement to balance inner (linear) and outer (nonlinear) iterations. The fluid-structure system is solved for comparison purposes using a loosely coupled approach. Residual convergence stagnated in the tightly coupled system approach but converged successfully in the loosely coupled approach using the same coding for domain calculations. A novel approach using time derivative preconditioning is incorporated to speed convergence of the GMRES linear equation solver. No algebraic preconditioning is used. The fluid flow equations showed significant improvements using the time derivative preconditioning method but the error term generated in the structural equations overwhelmed the physical solution increment. The Taylor Weak Statement derivation of the finite element form of the fluid flow equations with time derivative preconditioning shows a strong connection to the Streamwise Upwind Petrov Galerkin (SUPG) method. This connection is exploited to develop a theoretical basis for the damping term and the time scale parameter common to the SUPG method.

Kilpatrick, Kevin Larry

244

A dispersion minimizing finite difference scheme and preconditioned solver for the 3D Helmholtz equation  

NASA Astrophysics Data System (ADS)

In this paper, a new 27-point finite difference method is presented for solving the 3D Helmholtz equation with perfectly matched layer (PML), which is a second order scheme and pointwise consistent with the equation. An error analysis is made between the numerical wavenumber and the exact wavenumber, and a refined choice strategy based on minimizing the numerical dispersion is proposed for choosing weight parameters. A full-coarsening multigrid-based preconditioned Bi-CGSTAB method is developed for solving the linear system stemming from the Helmholtz equation with PML by the finite difference scheme. The shifted-Laplacian is extended to precondition the 3D Helmholtz equation, and a spectral analysis is given. The discrete preconditioned system is solved by the Bi-CGSTAB method, with a multigrid method used to invert the preconditioner approximately. Full-coarsening multigrid is employed, and a new matrix-based prolongation operator is constructed accordingly. Numerical results are presented to demonstrate the efficiency of both the new 27-point finite difference scheme with refined parameters, and the preconditioned Bi-CGSTAB method with the 3D full-coarsening multigrid.

Chen, Zhongying; Cheng, Dongsheng; Wu, Tingting

2012-10-01

245

Hypoxia-inducible factor 1 is required for remote ischemic preconditioning of the heart.  

PubMed

Both preclinical and clinical studies suggest that brief cycles of ischemia and reperfusion in the arm or leg may protect the heart against injury following prolonged coronary artery occlusion and reperfusion, a phenomenon known as remote ischemic preconditioning. Recent studies in mice indicate that increased plasma interleukin-10 (IL-10) levels play an important role in remote ischemic preconditioning induced by clamping the femoral artery for 5 min followed by 5 min of reperfusion for a total of three cycles. In this study, we demonstrate that remote ischemic preconditioning increases plasma IL-10 levels and decreases myocardial infarct size in wild-type mice but not in littermates that are heterozygous for a knockout allele at the locus encoding hypoxia-inducible factor (HIF) 1?. Injection of a recombinant adenovirus encoding a constitutively active form of HIF-1? into mouse hind limb muscle was sufficient to increase plasma IL-10 levels and decrease myocardial infarct size. Exposure of C2C12 mouse myocytes to cyclic hypoxia and reoxygenation rapidly increased levels of IL-10 mRNA, which was blocked by administration of the HIF-1 inhibitor acriflavine or by expression of short hairpin RNA targeting HIF-1? or HIF-1?. Chromatin immunoprecipitation assays demonstrated that binding of HIF-1 to the Il10 gene was induced when myocytes were subjected to cyclic hypoxia and reoxygenation. Taken together, these data indicate that HIF-1 activates Il10 gene transcription and is required for remote ischemic preconditioning. PMID:24101519

Cai, Zheqing; Luo, Weibo; Zhan, Huiwang; Semenza, Gregg L

2013-10-22

246

Histone preconditioning protects against obstructive jaundice-induced liver injury in rats  

PubMed Central

A major consequence of obstructive jaundice (OJ) in clinical practice is the development of severe liver injury, and at present, no effective treatments have been developed to protect against it. Preconditioning with damage-associated molecular pattern (DAMP) molecules has been demonstrated to protect multiple organs from injury, and histones have been recently identified as DAMP molecules. The aim of the present study was to investigate the protective effect of histone preconditioning against OJ-induced liver injury in rats and the involvement of Toll-like receptors. Rats were administered histone proteins (200 ?g/kg; 1 ml) or physiological saline (1 ml) intraperitoneally 24 h prior to being subjected to bile duct ligation (BDL). The serum levels of liver enzymes and bilirubin, as well as the histopathology were analyzed. The mRNA expression of interleukin-6 (IL-6) in the liver tissue was analyzed using quantitative polymerase chain reaction. BDL in the control group caused severe OJ-induced liver injury, as indicated by the significantly elevated levels of liver enzymes and mRNA levels of IL-6, and confirmed by histopathological alterations. However, histone preconditioning significantly ameliorated the OJ-induced liver injury caused by BDL, as shown by an improvement in the levels of liver enzymes, a suppression of IL-6 production, as well as histopathological alterations. Therefore, these results suggested that histone preconditioning is able to protect against OJ-induced liver injury in rats. PMID:24944590

ZHOU, YOU-XING; NI, YONG; LIU, YI-BING; LIU, XIAOHONG

2014-01-01

247

Preconditioning indefinite systems in interior point methods for large scale linear optimisation  

Microsoft Academic Search

We discuss the use of preconditioned conjugate gradients (CG) method for solving the reduced KKT systems arising in interior point algorithms for linear programming. The (indefinite) augmented system form of this linear system has a number of advantages, notably a higher degree of sparsity than the (positive definite) normal equations form. Therefore, we use the CG method to solve the

Ghussoun Al-Jeiroudi; Jacek Gondzio; Julian Hall

2008-01-01

248

Ischemic Preconditioning Protects against Spinal Cord Ischemia-Reperfusion Injury in Rabbits by Attenuating  

E-print Network

Abstract: Ischemic preconditioning has been reported to protect against spinal cord ischemia-reperfusion (I-R) injury, but the underlying mechanisms are not fully understood. To investigate this, Japanese white rabbits underwent I-R (30 min aortic occlusion followed by reperfusion), ischemic preconditioning (three cycles of 5 min aortic occlusion plus 5 min reperfusion) followed by I-R, or sham surgery. At 4 and 24 h following reperfusion, neurological function was assessed using Tarlov scores, blood spinal cord barrier permeability was measured by Evan’s Blue extravasation, spinal cord edema was evaluated using the wet-dry method, and spinal cord expression of zonula occluden-1 (ZO-1), matrix metalloproteinase-9 (MMP-9), and tumor necrosis factor-? (TNF-?) were measured by Western blot and a real-time polymerase chain reaction. ZO-1 was also assessed using immunofluorescence. Spinal cord I-R injury reduced neurologic scores, and ischemic preconditioning treatment ameliorated this effect. Ischemic preconditioning inhibited I-R-induced increases in blood spinal cord barrier permeability and water content,

2013-01-01

249

Winter pre-conditioning of seabird phenology in the California Current  

Microsoft Academic Search

Climate change is predicted to affect the phasing and amplitude of upwelling in eastern boundary current marine ecosystems. Effects may be strongest during the spring or summer 'upwelling season,' but may also be influential during winter before the spring transition. We tested the hypothesis that wintertime environmental forcing 'pre-conditions' the ecosystem and affects the timing and success of breeding in

Isaac D. Schroeder; William J. Sydeman; Nandita Sarkar; Sarah Ann Thompson; Steven J. Bograd; Franklin B. Schwing

2009-01-01

250

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

SciTech Connect

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.

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

2010-12-01

251

Delayed Energy Protection of Ischemic Preconditioning on Hepatic Ischemia\\/Reperfusion Injury in Rats  

Microsoft Academic Search

Background: Hepatic ischemia\\/reperfusion (IR) injuries associated with hepatic resections are unresolved problems in the clinical practice. The aim of this study is to elucidate the effect of ischemic preconditioning (IPC) on the energy charge (EC) and related mechanisms at the late phase of hepatic IR injury. Methods: 30 Wistar rats were randomly divided into sham, IR and IPC groups. The

E. Ofluoglu; M. Kerem; H. Pasaoglu; N. Turkozkan; I. Seven; A. Bedirli; T. Utku Yilmaz

2006-01-01

252

An M-step preconditioned conjugate gradient method for parallel computation  

NASA Technical Reports Server (NTRS)

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.

Adams, L.

1983-01-01

253

Analysis of the retinal gene expression profile after hypoxic preconditioning identifies candidate genes for neuroprotection  

Microsoft Academic Search

BACKGROUND: Retinal degeneration is a main cause of blindness in humans. Neuroprotective therapies may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning 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

Markus Thiersch; Wolfgang Raffelsberger; Rico Frigg; Marijana Samardzija; Andreas Wenzel; Olivier Poch; Christian Grimm

2008-01-01

254

Evaluation of High-intensity and Low-intensity Preconditioning Systems  

E-print Network

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 were assigned to systems...

Orsak, Andrew Nathan

2012-02-14

255

Ischemic preconditioning is lost in aging hypertensive rat heart: Independent effects of aging and longstanding hypertension  

Microsoft Academic Search

Although in experimental hypertension the cardioprotective effects of ischemic preconditioning (PC) appear to be maintained, most studies have examined the short-term hypertension in juvenile animals. However, aging may be an additional factor that influences the effectiveness of PC. The aim of this study was to characterise the effects on PC of LVH and aging simultaneously. Hearts from spontaneously hypertensive rats

Zaileen Ebrahim; Derek M. Yellon; Gary F. Baxter

2007-01-01

256

C. Vuik, A. Segal , J.A. Meijerinky An e cient preconditioned CG method  

E-print Network

drilling for oil, is the presence of excess uid pressures within the rock layers of the subsurface. Knowledge of the excess pressure is valuable in the prediction of the presence of oil and gas in reservoirsC. Vuik, A. Segal , J.A. Meijerinky An e cient preconditioned CG method for the solution of layered

Vuik, Kees

257

Preconditioned lattice-Boltzmann method for steady flows Zhaoli Guo, T. S. Zhao,* and Yong Shi  

E-print Network

Department of Mechanical Engineering, The Hong Kong University of Science and Technology, Kowloon, Hong Kong Boltzmann (LB) method for steady incompressible flows. For steady flows, the macroscopic equations derived system. The proposed model can be viewed as an explicit solver for preconditioned compressible Navier

Zhao, Tianshou

258

Resistance of the myocardium to ischemia and the efficacy of ischemic preconditioning in experimental diabetes mellitus.  

PubMed

Data on the influences of diabetes mellitus on the severity of ischemic damage to the myocardium are contradictory. We report here experiments using a model based on in vivo myocardial infarcts resulting from coronary occlusion to study the resistance of the myocardium in rats with alloxan-induced insulin-dependent diabetes mellitus to prolonged ischemia, along with studies of the infarct-limiting efficacy of ischemic preconditioning. The results showed that after diabetes mellitus for six weeks, the relative size of infarcts was significantly less than in controls (39.8 +/- 8.8 and 62.3 +/- 6.6% of the size of the anatomical risk zone respectively, p < 0.01). In addition, animals with diabetes mellitus developed ischemic ventricular tachyarrhythmia significantly less often than controls. A single episode of ischemic preconditioning in animals with diabetes mellitus had a less marked infarct-limiting effect than the same procedure in controls. Thus, these data support the existence of an endogenous cardioprotective phenotype (metabolic preconditioning) in experimental diabetes. On the other hand, the efficacy of ischemic preconditioning was sharply decreased in diabetes. PMID:17505800

Galagudza, M M; Nekrasova, M K; Syrenskii, A V; Nifontov, E M

2007-06-01

259

A Preconditioned Newton-Krylov Method for Computing Stationary Pulse Solutions of Mode-locked Lasers  

E-print Network

-locked Lasers Jonathan R. Birge and Franz X. Kärtner Research Laboratory of Electronics and Department-locked laser cavity using a preconditioned matrix-implicit Newton-Krylov solver. Solutions are obtained two: (000.4430) Numerical approximation and analysis; (320.7090) Ultrafast lasers 1. Overview The effective

Polz, Martin

260

Cognitive Preconditions of Early Reading and Spelling: A Latent-Variable Approach with Longitudinal Data  

ERIC Educational Resources Information Center

The aim of the present study was to empirically disentangle the interdependencies of the impact of nonverbal intelligence, working memory capacities, and phonological processing skills on early reading decoding and spelling within a latent variable approach. In a sample of 127 children, these cognitive preconditions were assessed before the onset…

Preßler, Anna-Lena; Könen, Tanja; Hasselhorn, Marcus; Krajewski, Kristin

2014-01-01

261

Ischemic preconditioning and infarct mass: the effect of hypercholesterolemia and endothelial dysfunction.  

PubMed

In an experimental model of atherosclerosis we investigated whether rabbits fed an atherogenic diet (0.25% cholesterol, 3% coconut oil) develop endothelial dysfunction accompanied with increased infarct mass compared to normal fed rabbits and, whether hypercholesterolemia would interfere with the beneficial outcome of ischemic preconditioning observed in normal rabbits. After four weeks on either a normal or an atherogenic diet, New Zealand White rabbits (n=7 in each group) were subjected to 30 min of myocardial ischemia by occlusion of a branch of the left anterior descending coronary artery (LAD) followed by 2 hours of reperfusion (infarct studies). For ischemic preconditioning experiments, LAD was additionally occluded twice for 5 min followed by 10 min reperfusion before the long-lasting (30 min) ischemia. Infarct mass was evaluated by triphenyl-tetrazolium staining. Besides the assessment of aortic endothelium-dependent function and NO-release, aortic and cardiac vessels were inspected for atherosclerotic lesions. Total cholesterol serum levels in rabbits on an atherogenic diet were significantly higher (15.3+/-2.7 mmol/L) than those on a standard diet (0.65+/-0.08 mmol/L). The aortas and heart vessels were without any histological evidence of atherosclerosis, whereas endothelial dysfunction and significantly reduced calcium-ionophore stimulated endothelial NO-release were found in isolated aortic rings of hypercholesterolemic animals. Rabbits on a standard diet showed an infarct mass (related to the area at risk) of 41+/-33%, which was reduced to 21+/-2% by ischemic preconditioning (49% decrease, p<0.05). In rabbits on an atherogenic diet, infarct mass was significantly increased to 63+/-3% (52% increase versus standard diet). Interestingly, hypercholesterolemia did not affect the beneficial influence of ischemic preconditioning; infarct mass (21+/-3%, p<0.05 vs hypercholesterolemia) was similar to rabbits on a standard diet with ischemic preconditioning. Our results show that experimental hypercholesterolemia increases infarct mass in nonpreconditioned hearts but it does not interfere with the reduction of infarct mass elicited by preconditioning. This may suggest that NO produced by the endothelium is not a prime factor in the cardioprotective mechanism of preconditioning. PMID:10744357

Jung, O; Jung, W; Malinski, T; Wiemer, G; Schoelkens, B A; Linz, W

2000-02-01

262

Effects of ischemic preconditioning in a pig model of large-for-size liver transplantation  

PubMed Central

OBJECTIVE: In most cases of pediatric liver transplantation, the clinical scenario of large-for-size transplants can lead to hepatic dysfunction and a decreased blood supply to the liver graft. The objective of the present experimental investigation was to evaluate the effects of ischemic preconditioning on this clinical entity. METHODS: Eighteen pigs were divided into three groups and underwent liver transplantation: a control group, in which the weights of the donors were similar to those of the recipients, a large-for-size group, and a large-for-size + ischemic preconditioning group. Blood samples were collected from the recipients to evaluate the pH and the sodium, potassium, aspartate aminotransferase and alanine aminotransferase levels. In addition, hepatic tissue was sampled from the recipients for histological evaluation, immunohistochemical analyses to detect hepatocyte apoptosis and proliferation and molecular analyses to evaluate the gene expression of Bax (pro-apoptotic), Bcl-XL (anti-apoptotic), c-Fos and c-Jun (immediate-early genes), ischemia-reperfusion-related inflammatory cytokines (IL-1, TNF-alpha and IL-6, which is also a stimulator of hepatocyte regeneration), intracellular adhesion molecule, endothelial nitric oxide synthase (a mediator of the protective effect of ischemic preconditioning) and TGF-beta (a pro-fibrogenic cytokine). RESULTS: All animals developed acidosis. At 1 hour and 3 hours after reperfusion, the animals in the large-for-size and large-for-size + ischemic preconditioning groups had decreased serum levels of Na and increased serum levels of K and aspartate aminotransferase compared with the control group. The molecular analysis revealed higher expression of the Bax, TNF-alpha, I-CAM and TGF-beta genes in the large-for-size group compared with the control and large-for-size + ischemic preconditioning groups. Ischemic preconditioning was responsible for an increase in c-Fos, IL-1, IL-6 and e-NOS gene expression. CONCLUSION: Ischemia-reperfusion injury in this model of large-for-size liver transplantation could be partially attenuated by ischemic preconditioning. PMID:25789522

Leal, Antonio José Gonçalves; Tannuri, Ana Cristina Aoun; Belon, Alessandro Rodrigo; Guimarães, Raimundo Renato Nunes; Coelho, Maria Cecília Mendonça; de Oliveira Gonçalves, Josiane; Serafini, Suellen; de Melo, Evandro Sobroza; Tannuri, Uenis

2015-01-01

263

Preventing Suicide  

MedlinePLUS

... Stages & Populations Travelers' Health Workplace Safety & Health Features Media Sign up for Features Get Email Updates To ... Prevention National Action Alliance for Suicide Prevention Features Media Sign up for Features Get Email Updates To ...

264

HIV Prevention  

MedlinePLUS

... post-exposure prophylaxis. How can I prevent getting HIV from anal or vaginal sex? Choose less risky ... consistently and correctly. How can I prevent getting HIV from oral sex? Avoid having your partner ejaculate ...

265

Drowning Prevention  

MedlinePLUS

... Adult: 18-21 yrs. Healthy Living Nutrition Fitness Sports Oral Health Emotional Wellness Growing Healthy Safety & Prevention ... System Obesity Skin Treatments View all Injuries & Emergencies Sports Injuries Vaccine Preventable Diseases Diphtheria Haemophilus influenzae type ...

266

AMP-activated protein kinase (AMPK)-induced preconditioning in primary cortical neurons involves activation of MCL-1.  

PubMed

Neuronal preconditioning is a phenomenon where a previous exposure to a sub-lethal stress stimulus increases the resistance of neurons towards a second, normally lethal stress stimulus. Activation of the energy stress sensor, AMP-activated protein kinase (AMPK) has been shown to contribute to the protective effects of ischaemic and mitochondrial uncoupling-induced preconditioning in neurons, however, the molecular basis of AMPK-mediated preconditioning has been less well characterized. We investigated the effect of AMPK preconditioning using 5-aminoimidazole-4-carboxamide riboside (AICAR) in a model of NMDA-mediated excitotoxic injury in primary mouse cortical neurons. Activation of AMPK with low concentrations of AICAR (0.1 mM for 2 h) induced a transient increase in AMPK phosphorylation, protecting neurons against NMDA-induced excitotoxicity. Analysing potential targets of AMPK activation, demonstrated a marked increase in mRNA expression and protein levels of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) in AICAR-preconditioned neurons. Interestingly, over-expression of MCL-1 protected neurons against NMDA-induced excitotoxicity while MCL-1 gene silencing abolished the effect of AICAR preconditioning. Monitored intracellular Ca²? levels during NMDA excitation revealed that MCL-1 over-expressing neurons exhibited improved bioenergetics and markedly reduced Ca²? elevations, suggesting a potential mechanism through which MCL-1 confers neuroprotection. This study identifies MCL-1 as a key effector of AMPK-induced preconditioning in neurons. PMID:23199202

Anilkumar, Ujval; Weisová, Petronela; Düssmann, Heiko; Concannon, Caoimhín G; König, Hans-Georg; Prehn, Jochen H M

2013-03-01

267

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

PubMed Central

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

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

2015-01-01

268

Preconditioning of Mesenchymal Stem Cells by Sevoflurane to Improve Their Therapeutic Potential  

PubMed Central

Background Bone marrow mesenchymal stem cells (MSCs) have been found to produce beneficial effects on ischemia-reperfusion injury. However, most of the MSCs died when transplanted into the ischemic tissue, which severely limit their therapeutic potential. Methods Using an in vitro model of hypoxia and serum deprivation (H/SD), we investigated the hypothesis that sevoflurane preconditioning could protect MSCs against H/SD-induced apoptosis and improve their migration, proliferation, and therapeutic potential. The H/SD of MSCs and neuron-like PC12 cells were incubated in a serum-free medium and an oxygen concentration below 0.1% for 24 h. Sevoflurane preconditioning was performed through a 2-h incubation of MSCs in an airtight chamber filled with 2 vol% sevoflurane. Apoptosis of MSCs or neuron-like PC12 cells was assessed using Annexin V-FITC/propidium iodide (PI). Furthermore, the mitochondrial membrane potential was assessed using lipophilic cationic probe. The proliferation rate was evaluated through cell cycle analysis. Finally, HIF-1?, HIF-2?, VEGF and p-Akt/Akt levels were measured by western blot. Results Sevoflurane preconditioning minimized the MSCs apoptosis and loss of mitochondrial membrane potential. Furthermore, it increased the migration and expression of HIF-1?, HIF-2?, VEGF, and p-Akt/Akt, reduced by H/SD. In addition, neuron-like PC12 cells were more resistant to H/SD-induced apoptosis when they were co-cultured with sevoflurane preconditioning MSCs. Conclusion These findings suggest that sevoflurane preconditioning produces protective effects on survival and migration of MSCs against H/SD, as well as improving the therapeutic potential of MSCs. These beneficial effects might be mediated at least in part by upregulating HIF-1?, HIF-2?, VEGF, and p-Akt/Akt. PMID:24599264

Zhao, Xi; Zhang, Guangwei; Ma, Hong

2014-01-01

269

High?dose fasudil preconditioning and postconditioning attenuate myocardial ischemia?reperfusion injury in hypercholesterolemic rats.  

PubMed

Fasudil may induce preconditioning and postconditioning against myocardial ischemia?reperfusion injury in normal rats, however, their effectivenesses in hypercholesterolemia remains to be determined. The study aimed to investigate whether fasudil induces preconditioning and postconditioning in hypercholesterolemic rats and to determine the roles of the phosphoinositol 3?kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS) pathway and mitochondrial KATP (m?KATP) channels in this process. Isolated rat hearts underwent 30 min global ischemia and 120 min reperfusion. Low? (1 mg/kg) or high?dose (10 mg/kg) fasudil was administered 15 min prior to ischemia and at the initial onset of reperfusion. 5?Hydroxydecanoic acid (5HD), an m?KATP channel blocker, at 10 mg/kg was administered 5 min prior to reperfusion. Myocardial infarct size was estimated by 2,3,5?triphenyltetrazolium chloride (TTC) staining and lactate dehydrogenase (LDH) and creatine kinase?MB (CK?MB) were analyzed from coronary effluents. Phosphorylation of Akt and eNOS was measured by immunoblotting. High?dose fasudil?induced preconditioning and postconditioning significantly reduced infarct size and the release of LDH and CK?MB and increased the phosphorylation of Akt and eNOS compared with the control group, whereas low?dose fasudil did not exert these beneficial effects. In addition, the cardioprotection of high?dose fasudil?induced preconditioning and postconditioning are blocked by 5HD. Low?dose fasudil?induced preconditioning and postconditioning are abrogated by hypercholesterolemia, while high?dose fasudil restores the cardioprotection, which is involved in upregulation of the PI3K/Akt/eNOS pathway and inducing the opening of the m?KATP channel. PMID:24271017

Wu, Nan; Zhang, Xiaowen; Jia, Dalin

2014-02-01

270

Preconditioning actions of aldosterone through p38 signaling modulation in isolated rat hearts.  

PubMed

Although persistent excessive actions of aldosterone have unfavorable effects on the cardiovascular system, primarily via mineralocorticoid receptor (MR)-dependent pathways, the pathophysiological significance of aldosterone cascade activation in heart diseases has not yet been fully clarified. We herein examined the effects of short-term aldosterone stimulation at a physiological dose on cardiac function during ischemia-reperfusion injury (IRI). In order to study the effects of aldosterone preconditioning, male Wistar rat Langendorff hearts were perfused with 10(-9)?mol/l of aldosterone for 10?min before ischemia, and the response to IRI was assessed. Although aldosterone did not affect the baseline hemodynamic parameters, preconditioning actions of aldosterone significantly improved the recovery in left ventricular contractility and left ventricular end-diastolic pressure associated with a reduced activity of creatine phosphokinase released into the perfusate after ischemia-reperfusion. Notably, the MR inhibitor eplerenone did not abrogate these beneficial effects. Biochemical analyses revealed that p38MAPK phosphorylation was significantly increased during aldosterone preconditioning before ischemia, whereas its phosphorylation was substantially attenuated during sustained ischemia-reperfusion, compared with the results for in the non-preconditioned control hearts. This dual regulation of p38MAPK was not affected by eplerenone. The phosphorylation levels of other MAPKs were not altered by aldosterone preconditioning. In conclusion, the temporal induction of the aldosterone cascade, at a physiological dose, has favorable effects on cardiac functional recovery and injury following ischemia-reperfusion in a MR-independent manner. Phasic dynamism of p38MAPK activation may play a key role in the physiological compensatory pathway of aldosterone under severe cardiac pathological conditions. PMID:24895416

Yoshino, Takuya; Nagoshi, Tomohisa; Anzawa, Ryuko; Kashiwagi, Yusuke; Ito, Keiichi; Katoh, Daisuke; Fujisaki, Masami; Kayama, Yosuke; Date, Taro; Hongo, Kenichi; Yoshimura, Michihiro

2014-08-01

271

Neuronal K(ATP) channels mediate hypoxic preconditioning and reduce subsequent neonatal hypoxic-ischemic brain injury.  

PubMed

Neonatal hypoxic-ischemic brain injury and its related illness hypoxic-ischemic encephalopathy (HIE) are major causes of nervous system damage and neurological morbidity in children. Hypoxic preconditioning (HPC) is known to be neuroprotective in cerebral ischemic brain injury. K(ATP) channels are involved in ischemic preconditioning in the heart; however the involvement of neuronal K(ATP) channels in HPC in the brain has not been fully investigated. In this study, we investigated the role of HPC in hypoxia-ischemia (HI)-induced brain injury in postnatal seven-day-old (P7) CD1 mouse pups. Specifically, TTC (2,3,5-triphenyltetrazolium chloride) staining was used to assess the infarct volume, TUNEL (Terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling) to detect apoptotic cells, Western blots to evaluate protein level, and patch-clamp recordings to measure K(ATP) channel current activities. Behavioral tests were performed to assess the functional recovery after hypoxic-ischemic insults. We found that hypoxic preconditioning reduced infarct volume, decreased the number of TUNEL-positive cells, and improved neurobehavioral functional recovery in neonatal mice following hypoxic-ischemic insults. Pre-treatment with a K(ATP) channel blocker, tolbutamide, inhibited hypoxic preconditioning-induced neuroprotection and augmented neurodegeneration following hypoxic-ischemic injury. Pre-treatment with a K(ATP) channel opener, diazoxide, reduced infarct volume and mimicked hypoxic preconditioning-induced neuroprotection. Hypoxic preconditioning induced upregulation of the protein level of the Kir6.2 isoform and enhanced current activities of K(ATP) channels. Hypoxic preconditioning restored the HI-reduced PKC and pAkt levels, and reduced caspase-3 level, while tolbutamide inhibited the effects of hypoxic preconditioning. We conclude that K(ATP) channels are involved in hypoxic preconditioning-induced neuroprotection in neonatal hypoxic-ischemic brain injury. K(ATP) channel openers may therefore have therapeutic effects in neonatal hypoxic-ischemic brain injury. PMID:25448006

Sun, Hong-Shuo; Xu, Baofeng; Chen, Wenliang; Xiao, Aijiao; Turlova, Ekaterina; Alibraham, Ammar; Barszczyk, Andrew; Bae, Christine Y J; Quan, Yi; Liu, Baosong; Pei, Lin; Sun, Christopher L F; Deurloo, Marielle; Feng, Zhong-Ping

2015-01-01

272

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

PubMed

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

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

273

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

SciTech Connect

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.

Williams, C. David; McGill, Mitchell R.; Lebofsky, Margitta; Bajt, Mary Lynn; Jaeschke, Hartmut, E-mail: hjaeschke@kumc.edu

2014-02-01

274

All preconditioning-related G protein-coupled receptors can be demonstrated in the rabbit cardiomyocyte  

PubMed Central

G protein-coupled receptors for adenosine (A1, A3, A2A and A2B), bradykinin (B1) and opioids (?) are all involved in the mechanism of ischemic preconditioning. Although the heart is comprised of many tissue types it has been assumed that preconditioning’s protective signaling occurs in the cardiomyocyte. We critically tested that hypothesis by testing for the presence of each of these receptors in isolated adult rabbit ventricular myocytes that had been transfected with cyclic nucleotide-gated (CNG) ion channels. Because subsarcolemmal cAMP opens the CNG channels we could monitor cAMP levels within a single cardiomyocyte by measuring channel current with a patch pipette. The presence of a receptor would be confirmed if we could alter cAMP in the cell with a selective agonist to the receptor being studied. Superfusion with the ?-adrenergic Gs-coupled receptor agonist isoproterenol (50 nM) transiently increased cAMP levels, and, therefore, channel current. Pretreatment with selective agonists to A1 or A3 adenosine receptors (AR) that are Gi-coupled markedly attenuated the response to isoproterenol indicating inhibition of adenylyl cyclase by increased Gi activity. Agonists to bradykinin or ?-opioid receptors also attenuated isoproterenol’s response. A2AAR and A2BAR are Gs-coupled. The A2AAR–selective agonist CGS21680 increased current through CNG channels but only in the presence of phosphodiesterase (PDE) inhibitors indicating low surface receptor activity and high intracellular PDE activity. As we previously reported, BAY 60–6583, an A2BAR-selective agonist which mimics preconditioning’s protection in rabbit heart, neither increased nor decreased membrane current in transfected cardiomyocytes, suggesting absence or a markedly limited number of A2BAR in the sarcolemma. However, RT-PCR of purified cardiomyocytes yielded an A2BAR band implying that rabbit cardiomyocytes do indeed express A2BAR. These data reveal that all receptors reported to be involved in ischemic preconditioning do exist on or within the cardiomyocyte. PMID:21828281

Xin, Wenkuan; Yang, Xiulan; Rich, Thomas C.; Krieg, Thomas; Barrington, Robert; Cohen, Michael V.; Downey, James M.

2012-01-01

275

Detailed qualitative dynamic knowledge representation using a BioNetGen model of TLR-4 signaling and preconditioning  

E-print Network

and preconditioning Gary C. An a,*, James R. Faeder b a Department of Surgery, Division of Trauma/Critical Care pathways, was used to model the toll-like receptor 4 (TLR-4) signal transduction cascade. The informational

Faeder, Jim

276

Integrated Pharmacological Preconditioning and Memory of Cardioprotection: The Role of Protein Kinase C and Phosphatidylinositol 3-kinase  

Microsoft Academic Search

Abstract Although protein kinase C (PKC) and phosphatidylinositol 3 (PI3)-kinase are implicated in cardioprotective signal transduction mediated by ischemic preconditioning, their role in pharmacological preconditioning (PPC) has not been determined. Cultured neonatal rat cardiomyocytes,(CMCs) were subjected to simulated,ischemia for 2 hours followed by 15 minutes reoxygenation. CMCs underwent PPC with 50 µM adenosine, 50 µM diazoxide, and 50 µM S-nitroso-N-acetyl-penicillamine

Takayuki Okada; Hajime Otani; Yue Wu; Takamichi Uchiyama

2005-01-01

277

High-amplitude elastic solitary wave propagation in 1-D granular chains with preconditioned beads: Experiments and theoretical analysis  

NASA Astrophysics Data System (ADS)

Elastic solitary waves resulting from Hertzian contact in one-dimensional (1-D) granular chains have demonstrated promising properties for wave tailoring such as amplitude-dependent wave speed and acoustic band gap zones. However, as load increases, plasticity or other material nonlinearities significantly affect the contact behavior between particles and hence alter the elastic solitary wave formation. This restricts the possible exploitation of solitary wave properties to relatively low load levels (up to a few hundred Newtons). In this work, a method, which we term preconditioning, based on contact pre-yielding is implemented to increase the contact force elastic limit of metallic beads in contact and consequently enhance the ability of 1-D granular chains to sustain high-amplitude elastic solitary waves. Theoretical analyses of single particle deformation and of wave propagation in a 1-D chain under different preconditioning levels are presented, while a complementary experimental setup was developed to demonstrate such behavior in practice. The experimental results show that 1-D granular chains with preconditioned beads can sustain high amplitude (up to several kN peak force) solitary waves. The solitary wave speed is affected by both the wave amplitude and the preconditioning level, while the wave spatial wavelength is still close to 5 times the preconditioned bead size. Comparison between the theoretical and experimental results shows that the current theory can capture the effect of preconditioning level on the solitary wave speed.

Wang, Erheng; Manjunath, Mohith; Awasthi, Amnaya P.; Pal, Raj Kumar; Geubelle, Philippe H.; Lambros, John

2014-12-01

278

On Physics-Based Preconditioning of the Navier-Stokes Equations  

SciTech Connect

An new and more ecient all-speed flow algorithm is developed. The governing hy- drodynamic equations, in conservative form, are solved implicitly using Jacobian- free Newton-Krylov methods. To overcome numerical stiffness caused by the dis- parity between acoustic and advective modes, the governing hydrodynamic equa- tions are transformed to the primitive variable form in a preconditioning step. This transformation enables implicit treatment of distinct physics using traditional semi- implicit and physics-based splitting approaches without a loss of consistency be- tween the original and preconditioned systems. The resulting algorithm is capable of solving slow natural circulations (M ~ 10^-4) with signicant heat flux as well as the high-speed (M ~ 1) flows effciently by following dynamical time scales.

HyeongKae Park; Robert R. Nourgaliev; Richard C. Martineau; Dana A. Knoll

2009-12-01

279

Parallelization of the preconditioned IDR solver for modern multicore computer systems  

NASA Astrophysics Data System (ADS)

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).

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

2012-10-01

280

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

SciTech Connect

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.

Feng, Tao, E-mail: fengtao2@mail.ustc.edu.cn [School of Mathematical Sciences, University of Science and Technology of China, Hefei 230052 (China) [School of Mathematical Sciences, University of Science and Technology of China, Hefei 230052 (China); Graduate School of China Academy Engineering Physics, Beijing 100083 (China); An, Hengbin, E-mail: an_hengbin@iapcm.ac.cn [National Key Laboratory of Computational Physics, Institute of Applied Physics and Computational Mathematics, Beijing 100094 (China)] [National Key Laboratory of Computational Physics, Institute of Applied Physics and Computational Mathematics, Beijing 100094 (China); Yu, Xijun, E-mail: yuxj@iapcm.ac.cn [National Key Laboratory of Computational Physics, Institute of Applied Physics and Computational Mathematics, Beijing 100094 (China)] [National Key Laboratory of Computational Physics, Institute of Applied Physics and Computational Mathematics, Beijing 100094 (China); Li, Qin, E-mail: liqin@lsec.cc.ac.cn [Chinese Academy of Mathematics and Systems Science, Beijing 100190 (China)] [Chinese Academy of Mathematics and Systems Science, Beijing 100190 (China); Zhang, Rongpei, E-mail: zhangrongpei@163.com [Graduate School of China Academy Engineering Physics, Beijing 100083 (China)] [Graduate School of China Academy Engineering Physics, Beijing 100083 (China)

2013-03-01

281

Measurement of 1,2-diacylglycerol and ceramide in hearts subjected to ischemic preconditioning  

Microsoft Academic Search

An accumulation of recent evidence suggests that the mechanism in ischemic preconditioning (IPC) may involve the activation of protein kinase C (PKC) regulatory pathway. In this study, we examined whether the content of 1,2-diacylglycerol (1,2-DAG) and ceramide, which are intracellular second messengers regulating PKC activity, change during IPC in isolated perfused rat hearts, and whether the observed change in 1,2-DAG

Kichiro Murase; Kenji Okumura; Kazunori Hayashi; Hideo Matsui; Yukio Toki; Takayuki Ito; Tetsuo Hayakawa

2000-01-01

282

Ouabain triggers preconditioning through activation of the Na+,K+ATPase signaling cascade in rat hearts  

Microsoft Academic Search

Objective: Because ouabain activates several pathways that are critical to cardioprotective mechanisms such as ischemic preconditioning, we tested if this digitalis compound could protect the heart against ischemia-reperfusion injury through activation of the Na+,K+-ATPase\\/c-Src receptor complex. Methods and results: In Langendorff-perfused rat hearts, a short (4 min) administration of ouabain 10 ?M followed by an 8-minute washout before 30 min

Sandrine V. Pierre; Changjun Yang; Zhaokan Yuan; Jennifer Seminerio; Christian Mouas; Keith D. Garlid; Pierre Dos-Santos; Zijian Xie

2007-01-01

283

Endoplasmic reticulum stress-dependent activation of ATF3 mediates the late phase of ischemic preconditioning.  

PubMed

Ischemic preconditioning (PC) is an adaptive response to transient myocardial ischemia that protects the heart from subsequent ischemia/reperfusion (I/R) injury. However, the mechanisms underlying its cardioprotective effects remain unclear. Myocardium of adult male C57/BL6 mice, preconditioned by 6 cycles of 4 minute coronary occlusion and reperfusion, showed nuclear translocation of ATF3 and ATF6 and PERK phosphorylation 30 min after PC. The abundance of ER proteins, ATF3 and ATF4 was increased 24h after PC; however, there was no evidence of IRE-1 activation in WT or ER-stress activated indicator (ERAI) mice expressing XBP-1-Venus fusion protein. PC-induced nuclear translocation of ATF3 was attenuated in transgenic mice with cardiac-restricted overexpression of inducible ATF6. Ischemic PC increased the abundance of inducible nitric oxide synthase, cyclooxygenase-2, heme oxygenase-1 and aldose reductase to levels similar between WT and ATF3-null hearts; however, the increase in IL-6 and ICAM-1 was exaggerated in ATF3-null hearts. Genetic deletion of ATF3 did not increase infarct size in non-preconditioned hearts but abolished the cardioprotective effects of PC. Larger infarct size in preconditioned ATF3-null hearts was associated with greater neutrophil infiltration in the myocardium, but no ATF3-dependent changes in the total or relative abundance of inflammatory monocytes were observed. Ischemic PC activates the unfolded protein response (UPR) and the activation of ATF3 by ER stress is essential for the cardioprotective effects of late PC. PMID:25151953

Brooks, Alan C; Guo, Yiru; Singh, Mahavir; McCracken, James; Xuan, Yu-Ting; Srivastava, Sanjay; Bolli, Roberto; Bhatnagar, Aruni

2014-11-01

284

Cyclooxygenase2 mediates the cardioprotective effects of the late phase of ischemic preconditioning in conscious rabbits  

Microsoft Academic Search

We examined the role of cyclooxygenase-2 (COX-2) in the late phase of ischemic preconditioning (PC). A total of 176 conscious rabbits were used. Ischemic PC (six cycles of 4-min coronary occlusions\\/4-min reperfusions) resulted in a rapid increase in myocardial COX-2 mRNA levels (+231 ± 64% at 1 h; RNase protection assay) followed 24 h later by an increase in COX-2

Ken Shinmura; Xian-Liang Tang; Yang Wang; Yu-Ting Xuan; Si-Qi Liu; Hitoshi Takano; Aruni Bhatnagar; Roberto Bolli

2000-01-01

285

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum  

PubMed Central

Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse. PMID:19915665

Cadet, Jean Lud; McCoy, Michael T.; Cai, Ning Sheng; Krasnova, Irina N.; Ladenheim, Bruce; Beauvais, Genevieve; Wilson, Natascha; Wood, William; Becker, Kevin G.; Hodges, Amber B.

2009-01-01

286

Multiple scattering among vias in planar waveguides using preconditioned SMCG method  

Microsoft Academic Search

Full-wave modeling for cylindrical vias in planar waveguides is formulated using Foldy-Lax multiple scattering equations. Recently, a sparse-matrix canonical-grid method based on fast Fourier transform and an iterative algorithm was proposed to solve a large-scale via problem. In this paper, we further improve computational efficiency by a preconditioning scheme based on the dominant information contained in the near field. We

Chung-Chi Huang; Leung Tsang; Chi Hou Chan; Kung-Hau Ding

2004-01-01

287

Delayed Preconditioning-Mimetic Action of Nitroglycerin in Patients Undergoing Coronary Angioplasty  

Microsoft Academic Search

Background—Experimental studies suggest that the cardioprotective effects of the late phase of ischemic preconditioning (PC) can be mimicked pharmacologically. However, to date, no drug has been tested with respect to its ability to elicit a late PC effect in humans. As a consequence, clinical exploitation of the powerful anti-stunning and anti-infarct actions of late PC has been elusive thus far.

Massoud A. Leesar; Marcus F. Stoddard; Buddhadeb Dawn; Venu G. Jasti; Ronald Masden; Roberto Bolli

2010-01-01

288

Exercise-induced ischemic preconditioning detected by sequential exercise stress tests: a meta-analysis.  

PubMed

Exercise-induced ischemic preconditioning (IPC) can be assessed with the second exercise stress test during sequential testing. Exercise-induced IPC is defined as the time to 1 mm ST segment depression (STD), the rate-pressure product (RPP) at 1 mm STD, the maximal ST depression and the rate-pressure product at peak exercise. The purpose of this meta-analysis is to validate the parameters used to assess exercise-induced IPC in the scientific community. A literature search was performed using electronic database. The main key words were limited to human studies, which were (a) ischemic preconditioning, (b) warm-up phenomenon, and (c) exercise. Meta-analyses were performed on the study-specific mean difference between the clinical measures obtained in the two consecutive stress tests (second minus first test score). Random effect models were fitted with inverse variance weighting to provide greater weight to studies with larger sample size and more precise estimates. The search resulted in 309 articles of which 34 were included after revision (1053 patients). Results are: (a) time to 1 mm ST segment depression increased by 91 s (95% confidence interval (CI): 75-108), p < 0.001; (b) peak ST depression decreased by -0.38 mm (95% CI: -0.66 to -0.10), p < 0.01; and (c) rate-pressure product at 1 mm STD increased by 1.80 × 10(3)mmHg (95% CI: 1.0-2.0), p < 0.001. This is the first meta-analysis to set clinical parameters to assess the benefit of exercise-induced ischemic preconditioning in sequential stress testing. The results of this first meta-analysis on the sequential stress test confirm what is presented in the literature by independent studies on exercise-induced ischemic preconditioning. From now on, the results could be used in further research to set standardized parameters to assess the phenomenon. PMID:23983070

Lalonde, François; Poirier, Paul; Sylvestre, Marie-Pierre; Arvisais, Denis; Curnier, Daniel

2015-01-01

289

Human embryonic stem cell neural differentiation and enhanced cell survival promoted by hypoxic preconditioning  

Microsoft Academic Search

Transplantation of neural progenitors derived from human embryonic stem cells (hESCs) provides a potential therapy for ischemic stroke. However, poor graft survival within the host environment has hampered the benefits and applications of cell-based therapies. The present investigation tested a preconditioning strategy to enhance hESC tolerance, thereby improving graft survival and the therapeutic potential of hESC transplantation. UC06 hESCs underwent

K R Francis; L Wei

2010-01-01

290

PKC-dependent Preconditioning with Norepinephrine Protects Sarcoplasmic Reticulum Function in Rat Trabeculae Following Metabolic Inhibition  

Microsoft Academic Search

The authors have previously shown that norepinephrine (NE) pretreatment attenuates Ca2+overloading in cardiac rat trabeculae during metabolic inhibition, and improves contractile function during a subsequent recovery period. The present study investigated: (i) whether protection of sarcoplasmic reticulum (SR) function during metabolic inhibition (MI) is involved in the preconditioning-like effect of NE-pretreatment, and (ii) whether or not this process is PKC-dependent.

René J. P. Musters; Esther T. van der Meulen; Marian Zuidwijk; Alice Muller; Warner S. Simonides; Anirban Banerjee; Cornelis van Hardeveld

1999-01-01

291

Violence Prevention  

MedlinePLUS

... Mental Health and Social Services (continued) Percentage of Schools Providing Violence Prevention Services in One-on-One or Small- ... Healthy and Safe School Environment • 30.6% of schools had or participated in a program to prevent gang violence. • The percentage of districts that required schools to ...

292

Completeness set proof of precondition and post-condition types of activity in any EPM  

NASA Astrophysics Data System (ADS)

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 precondition 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 precondition 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 precondition and its post-condition is presented. Lastly we prove that the activity type set in anyone EPM is completeness set by mathematical induction.

Yu, Qian; Li, Tong; Liu, JinZhuo; Zhang, Xuan; Yu, Yong

2013-12-01

293

Acute effect of ischemic preconditioning is detrimental to anaerobic performance in cyclists.  

PubMed

We verified the acute effect of ischemic preconditioning (IPC) in cyclists before high-intensity and short-duration activity. 15 amateur cyclists participated in a random crossover model on 2 different days [IPC or CONTROL (CON)]. Ischemic preconditioning consisted of 4 cycles of 5?min occlusion/5?min reperfusion in each thigh. After IPC or CON, volunteers performed a series of Wingate tests to evaluate anaerobic performance (maximal [Pmax] and medium [Pmed] power output, total anaerobic power, and fatigue index). Blood lactate concentrations were assessed at 6?min after each Wingate test. Ischemic preconditioning decreased Pmax (p<0.05), Pmed (p<0.01), and total anaerobic power (p<0.01) in the first Wingate, and decreased Pmed (p<0.01) and total anaerobic power (p<0.01) in the second Wingate (p<0.01). No significant differences were found in blood lactate or fatigue index between IPC and CON. In conclusion, our results indicate that IPC has a detrimental acute effect on anaerobic performance in amateur cyclists. Compared with positive results of previous studies, the effect of IPC seems to be dependent on the type of exercise. PMID:24863728

Paixão, R C; da Mota, G R; Marocolo, M

2014-10-01

294

Zinc preconditioning protects against neuronal apoptosis through the mitogen-activated protein kinase-mediated induction of heat shock protein 70.  

PubMed

During brain ischemic preconditioning (PC), mild bursts of ischemia render neurons resistant to subsequent strong ischemic injuries. Previously, we reported that zinc plays a key role in PC-induced neuroprotection in vitro and in vivo. Zinc-triggered p75(NTR) induction transiently activates caspase-3, which cleaves poly(ADP-ribose) polymerase-1 (PARP-1). Subsequently, the PARP-1 over-activation-induced depletion of nicotinamide adenine dinucleotide (NAD(+))/adenosine triphosphate (ATP) after exposures to lethal doses of zinc or N-methyl-d-aspartate is significantly attenuated in cortical neuronal cultures. In the present study, zinc-mediated preconditioning (Zn PC) reduced apoptotic neuronal death that was caused by N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), etoposide, or staurosporine in mouse cortical cells. We focused on heat shock protein 70 (HSP70) because NAD(+)/ATP depletion does not directly cause apoptosis, and HSP70 can inhibit the activation of caspase-9 or caspase-3 by preventing apoptosome formation or cytochrome C release. Zn PC-mediated HSP70 induction was required for neuroprotection against neuronal apoptosis, and geldanamycin-induced HSP70 induction sufficiently blocked neuronal apoptotic cell death. Furthermore, Zn PC-mediated HSP70 induction was blocked by chemical inhibitors of extracellular signal-regulated kinase (ERK) or p38 mitogen-activated protein kinase (MAPK) signaling, but not c-Jun N-terminal protein kinase. Similarly, neuroprotection by Zn PC against TPEN-induced apoptosis was almost completely reversed by the blockade of ERK or p38 MAPK signaling. Our findings suggest that the ERK- or p38 MAPK-mediated induction of HSP70 plays a key role in inhibiting caspase-3 activation during Zn PC. PMID:25712525

Lee, Jeong-Min; Lee, Jong-Min; Kim, Ki-Ryeong; Im, Hana; Kim, Yang-Hee

2015-04-01

295

Ozone oxidative preconditioning is mediated by A1 adenosine receptors in a rat model of liver ischemia/ reperfusion.  

PubMed

The liver is damaged by sustained ischemia in liver transplantation, and the reperfusion after ischemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischemia/reperfusion (I/R) injury. The aim of this study was to investigate the role of A(1) adenosine receptor on the protective actions conferred by OzoneOP in hepatic I/R. By using a specific agonist and antagonist of the A(1) subtype receptor (2-chloro N6 cyclopentyladenosine, CCPA and 8-cyclopentyl-1,3-dipropylxanthine, DPCPX respectively), we studied the role of A(1) receptor in the protective effects of OzoneOP on the liver damage, nitiric oxide (NO) generation, adenosine deaminase activity and preservation of the cellular redox balance. Immunohistochemical analysis of nuclear factor-kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha) and heat shock protein-70 (HSP-70) was performed. OzoneOP prevented and/or ameliorated ischemic damage. CCPA showed a similar effect to OzoneOP + I/R group. A(1)AR antagonist DPCPX blocked the protective effect of OzoneOP. OzoneOP largely reduced the intensity of the p65 expression, diminished TNF-alpha production, and promoted a reduction in HSP-70 immunoreactivity. In summary, OzoneOP exerted protective effects against liver I/R injury through activation of A(1) adenosine receptors (A(1)AR). Adenosine and (.)NO produced by OzoneOP may play a role in the pathways of cellular signalling which promote preservation of the cellular redox balance, mitochondrial function, glutathione pools as well as the regulation of NF-kappaB and HSP-70. PMID:17927680

León Fernández, Olga S; Ajamieh, Hussam H; Berlanga, Jorge; Menéndez, Silvia; Viebahn-Hánsler, Renate; Re, Lamberto; Carmona, Anna M

2008-01-01

296

Preventing Falls  

MedlinePLUS

... of falling. Exercises that improve balance, such as tai chi, are helpful. Your local health or senior center ... to prevent falls. Do balance exercises, such as tai chi. These types of exercises can lower the chances ...

297

Plague Prevention  

MedlinePLUS

... message, please visit this page: About CDC.gov . Plague Plague Ecology & Transmission Symptoms Diagnosis & Treatment Maps & Statistics Info ... Clinicians Public Health Officials Veterinarians Prevention History of Plague Resources FAQ Related Links USGS National Wildlife Health ...

298

Preventing Falls  

MedlinePLUS

... gov/Go4Life l Find sample exercises to help prevent falls. l Print useful tools. l Share your exercise story. National Institute on Aging National Institutes of Health U.S. Department of Health & ...

299

Effect of Air Abrasion Preconditioning on Microleakage in Class V Restorations Under Cyclic Loading: An In-vitro Study  

PubMed Central

Background: Microleakage in class V Glass Ionomer Cement(GIC) or composite restorations at enamel or cementum margins has been cited as a reason for their failure. Air abrasion has been used to precondition tooth surface for increasing retention of such restorations. This study is done to evaluate the effect of preconditioning with air abrasion on microleakage in class V GIC and composite restorations. Materials and Methods: Class V cavities were prepared in 40 freshly extracted teeth. They were categorised into following four groups (n=10) depending on cavity preconditioning and restoration. Group I: 10% polyacrylic acid and GI (Ketac molar TM 3M ESPE); Group II: AA and GI; Group III: 35% Phosphoric acid and micro filled composite (MC) (Heliomolar, Ivoclar Vivadent); Group IV: AA and MC. Each group was further divided into subgroups A (no loading) & B (cyclic loading). Microleakage at occlusal and gingival margins was evaluated using methylene blue dye penetration method. Statistical analysis was done using Kruskal-wallis test and Mann-Whitney U test. Results: Microleakage at cementum margins was higher than at enamel margins in all the groups. Preconditioning with AA resulted in increased micro leakage. Conclusion: AA as a preconditioning agent was ineffective in producing superior tooth-restoration bonding. PMID:24995240

Dharmani, Charan Kamal Kaur; Singh, Shamsher; Logani, Ajay; Shah, Naseem

2014-01-01

300

Mitochondrial-Mediated Suppression of ROS Production Upon Exposure of Neurons to Lethal Stress: Mitochondrial Targeted Preconditioning  

PubMed Central

Preconditioning represents the condition where transient exposure of cells to an initiating event leads to protection against subsequent, potentially lethal stimuli. Recent studies have established that mitochondrial-centered mechanisms are important mediators in promoting development of the preconditioning response. However, many details concerning these mechanisms are unclear. The purpose of this review is to describe the initiating and subsequent intracellular events involving mitochondria which can lead to neuronal preconditioning. These mitochondrial specific targets include: 1) potassium channels located on the inner mitochondrial membrane; 2) respiratory chain enzymes; and 3) oxidative phosphorylation. Following activation of mitochondrial ATP-sensitive potassium (mitoKATP) channels and/or increased production of reactive oxygen species (ROS) following disruption of the respiratory chain or during energy substrate deprivation, morphological changes or signaling events involving protein kinases confer immediate or delayed preconditioning on neurons that will allow them to survive otherwise lethal insults. While the mechanisms involved are not known with certainty, the results of preconditioning are the enhanced viability, the attenuated influx of intracellular calcium, the reduced availability of ROS, suppression of apoptosis, and the maintenance of ATP levels during and following stress. PMID:18652858

Busija, David W.; Gaspar, Tamas; Domoki, Ferenc; Katakam, Prasad V.; Bari, Ferenc

2008-01-01

301

Preconditioned conjugate-gradient methods for low-speed flow calculations  

NASA Technical Reports Server (NTRS)

An investigation is conducted into the viability of using a generalized Conjugate Gradient-like method as an iterative solver to obtain steady-state solutions of very low-speed fluid flow problems. Low-speed flow at Mach 0.1 over a backward-facing step is chosen as a representative test problem. The unsteady form of the two dimensional, compressible Navier-Stokes equations is integrated in time using discrete time-steps. The Navier-Stokes equations are cast in an implicit, upwind finite-volume, flux split formulation. The new iterative solver is used to solve a linear system of equations at each step of the time-integration. Preconditioning techniques are used with the new solver to enhance the stability and convergence rate of the solver and are found to be critical to the overall success of the solver. A study of various preconditioners reveals that a preconditioner based on the Lower-Upper Successive Symmetric Over-Relaxation iterative scheme is more efficient than a preconditioner based on Incomplete L-U factorizations of the iteration matrix. The performance of the new preconditioned solver is compared with a conventional Line Gauss-Seidel Relaxation (LGSR) solver. Overall speed-up factors of 28 (in terms of global time-steps required to converge to a steady-state solution) and 20 (in terms of total CPU time on one processor of a CRAY-YMP) are found in favor of the new preconditioned solver, when compared with the LGSR solver.

Ajmani, Kumud; Ng, Wing-Fai; Liou, Meng-Sing

1993-01-01

302

Hyperbaric oxygen preconditioning promotes neovascularization of transplanted skin flaps in rats  

PubMed Central

To determine whether Hyperbaric oxygen preconditioning (HBO-PC) promotes neovascularization by increasing Stromal cell derived factor-1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) in transplanted skin flaps of rats. The epigastric pedicle skin flap was established in a rat model. Rats were randomly assigned to the following five groups: 1) sham-operated group (SH); 2) ischemia followed by reperfusion 3 days postoperatively group (IR3d); 3) ischemia followed by reperfusion 5 days postoperatively group (IR5d); 4) hyperbaric oxygen preconditioning and ischemia followed by reperfusion 3 days postoperatively group (HBO-PC3d); and 5) hyperbaric oxygen preconditioning and ischemia followed by reperfusion 5 days postoperatively group(HBO-PC5d). For the groups receiving HBO-PC, animals underwent 1 hour of HBO at 2.0 ATA in 100% O2 twice per day for 3 days consecutively prior to surgery. After perfusion, Laser Doppler perfusion imaging (LDPI) was performed, and skin flap tissue samples were harvested for histological evaluation and western blot analysis. Perfusion was significantly improved in the HBO-PC groups compared with the IR groups on postoperative 3 and 5. Microvessel density (MVD) was significantly increased by HBO-PC compared with IR groups postoperatively. Western blot analysis revealed that SDF-1 and CXCR4 expression in the HBO-PC groups was significantly increased compared with IR groups. HBO-PC promoted neovascularization via increasing expression levels of SDF-1 and CXCR4 in transplanted skin flaps of rats. PMID:25197344

Liu, Xuehua; Yang, Jing; Li, Zhuo; Yang, Lin; Wang, Cong; Gao, Chunjin; Liang, Fang

2014-01-01

303

Rosuvastatin induces delayed preconditioning against oxygen-glucose deprivation in cultured cortical neurons  

PubMed Central

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-preconditioned 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 preconditioning 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 preconditions 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

Domoki, Ferenc; Kis, Béla; Gáspár, Tamás; Snipes, James A.; Parks, John S.; Bari, Ferenc; Busija, David W.

2009-01-01

304

Augmentation of aerobic respiration and mitochondrial biogenesis in skeletal muscle by hypoxia preconditioning with cobalt chloride  

SciTech Connect

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 preconditioning 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 preconditioning 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 preconditioning. -- 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.

Saxena, Saurabh [Experimental Biology Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054 (India)] [Experimental Biology Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054 (India); Shukla, Dhananjay [Department of Biotechnology, Gitam University, Gandhi Nagar, Rushikonda, Visakhapatnam-530 045 Andhra Pradesh (India)] [Department of Biotechnology, Gitam University, Gandhi Nagar, Rushikonda, Visakhapatnam-530 045 Andhra Pradesh (India); Bansal, Anju, E-mail: anjubansaldipas@gmail.com [Experimental Biology Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054 (India)] [Experimental Biology Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054 (India)

2012-11-01

305

A Randomized Pilot Trial of Remote Ischemic Preconditioning in Heart Failure with Reduced Ejection Fraction  

PubMed Central

Background Remote ischemic preconditioning (RIPC) induced by transient limb ischemia confers multi-organ protection and improves exercise performance in the setting of tissue hypoxia. We aimed to evaluate the effect of RIPC on exercise capacity in heart failure patients. Methods We performed a randomized crossover trial of RIPC (4×5-minutes limb ischemia) compared to sham control in heart failure patients undergoing exercise testing. Patients were randomly allocated to either RIPC or sham prior to exercise, then crossed over and completed the alternate intervention with repeat testing. The primary outcome was peak VO2, RIPC versus sham. A mechanistic substudy was performed using dialysate from study patient blood samples obtained after sham and RIPC. This dialysate was used to test for a protective effect of RIPC in a mouse heart Langendorff model of infarction. Mouse heart infarct size with RIPC or sham dialysate exposure was also compared with historical control data. Results Twenty patients completed the study. RIPC was not associated with improvements in peak VO2 (15.6+/?4.2 vs 15.3+/?4.6 mL/kg/min; p?=?0.53, sham and RIPC, respectively). In our Langendorff sub-study, infarct size was similar between RIPC and sham dialysate groups from our study patients, but was smaller than expected compared to healthy controls (29.0%, 27.9% [sham, RIPC] vs 51.2% [controls]. We observed less preconditioning among the subgroup of patients with increased exercise performance following RIPC (p<0.04). Conclusion In this pilot study of RIPC in heart failure patients, RIPC was not associated with improvements in exercise capacity overall. However, the degree of effect of RIPC may be inversely related to the degree of baseline preconditioning. These data provide the basis for a larger randomized trial to test the potential benefits of RIPC in patients with heart failure. Trial Registration ClinicalTrials.gov +++++NCT01128790 PMID:25181050

McDonald, Michael A.; Braga, Juarez R.; Li, Jing; Manlhiot, Cedric; Ross, Heather J.; Redington, Andrew N.

2014-01-01

306

Limb ischemic preconditioning protects against contrast-induced acute kidney injury in rats via phosphorylation of GSK-3?.  

PubMed

Contrast-induced acute kidney injury (CI-AKI) resulting from the use of intravascular iodinated contrast media for diagnostic and interventional cardiovascular procedures is associated with substantial morbidity and mortality. Despite preventative measures intended to mitigate the risk of CI-AKI, there remains a need for a novel and effective therapeutic approach. Limb ischemic preconditioning (LIPC), where short-term ischemia/reperfusion is applied to an arm prior to administration of the contrast agent, has been shown in several trials to preserve renal function in patients at high risk for CI-AKI. However, the underlying mechanism by which this procedure provides renoprotection against contrast media insults is not known. Here, we explored the molecular mechanism(s) of LIPC-induced protection of the kidneys from CI-AKI, particularly the role of phosphorylated glycogen synthase kinase-3? (GSK-3?). We used a novel CI-AKI model consisting of 5/6 nephrectomized (NE) rats at 6 weeks after the ablative surgery. LIPC- or sham-treated rats were administered iohexol (10ml/kg, 3.5gI) via the tail vein. The results showed that LIPC protected the kidneys against iohexol-induced injury. This protective effect was accompanied by the attenuation of renal dysfunction, tubular damage, apoptosis, mitochondrial swelling, oxidative stress, and inflammation. Furthermore, LIPC-induced renoprotection was blocked via treatment with inhibitors of PI3K (wortmannin or LY294002), but not ERK (U0126 or PD98059). LIPC also increased the protein expression levels of phospho-Akt, phospho-GSK-3?, and nuclear Nrf2, and decreased the levels of nuclear NF-?B. A specific GSK-3? inhibitor (SB216763) mimicked this effect of LIPC, by inhibiting the opening of the mitochondrial permeability transition pore and reducing the levels of oxidative stress and inflammation via activation of Nrf2 and suppression of NF-?B. The above results demonstrate that LIPC induces protection against CI-AKI, making this procedure a promising strategy for preventing CI-AKI. In particular, this renoprotective effect involves the phosphorylation of GSK-3?. PMID:25451640

Liu, Tongqiang; Fang, Yi; Liu, Shaopeng; Yu, Xiaofang; Zhang, Hui; Liang, Mingyu; Ding, Xiaoqiang

2015-04-01

307

Graph Embedding Techniques for Bounding Condition Numbers of Incomplete Factor Preconditioning  

NASA Technical Reports Server (NTRS)

We extend graph embedding techniques for bounding the spectral condition number of preconditioned 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.

Guattery, Stephen

1997-01-01

308

Non-preconditioned conjugate gradient on cell and FPGA based hybrid supercomputer nodes  

SciTech Connect

This work presents a detailed implementation of a double precision, non-preconditioned, 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.

Dubois, David H [Los Alamos National Laboratory; Dubois, Andrew J [Los Alamos National Laboratory; Boorman, Thomas M [Los Alamos National Laboratory; Connor, Carolyn M [Los Alamos National Laboratory

2009-01-01

309

Non-preconditioned conjugate gradient on cell and FPCA-based hybrid supercomputer nodes  

SciTech Connect

This work presents a detailed implementation of a double precision, Non-Preconditioned, 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.

Dubois, David H [Los Alamos National Laboratory; Dubois, Andrew J [Los Alamos National Laboratory; Boorman, Thomas M [Los Alamos National Laboratory; Connor, Carolyn M [Los Alamos National Laboratory

2009-03-10

310

Results on the effect of orderings on SSOR and ILU preconditionings  

SciTech Connect

It is known that for SSOR and ILU preconditionings for solving systems of linear equations, orderings can have an enormous impact on robustness, convergence rate and parallelism. Unfortunately, it has been observed that there is an inverse relation between the convergence rate and the parallelism of typical orderings used in practice. This paper presents some numerical experiments with simple matrices to illustrate this behavior as well as a new theoretical result which sheds some light on this phenomenon and also gives an upper bound on the convergence rate of a number of preconditioners in popular use.

Joubert, W.; Knill, E.

1998-12-31

311

Time-dependent effects of pre-conditioning activation on muscle fiber conduction velocity and twitch torque.  

PubMed

In this study we investigate the range of interstimulus intervals influencing the recovery functions for conduction velocity (velocity recovery function, or VRF) and twitch torque (twitch torque recovery function, or TRF) of muscle fibers. We studied the tibialis anterior muscle of 8 healthy men by varying the time interval between a pair of stimuli in the range of 4-1000 ms, with (triplet) and without (doublet) a preconditioning stimulus. For triplet stimulations, the interval between the first and second stimulus or between the second and third stimulus was fixed, and the other interval was varied. VRF and TRF were influenced by a preconditioning stimulus only when it was delivered within 125 ms and 30 ms, respectively, before the doublet stimulation. The results provide evidence of the range of preconditioning intervals influencing the VRF and TRF; this is relevant for understanding the mechanisms of force generation and for standardizing compound action potential measurements. PMID:20665512

Kamavuako, Ernest Nlandu; Farina, Dario

2010-10-01

312

Sevoflurane Enhances Ethanol-Induced Cardiac Preconditioning Through Modulation of Protein Kinase C, Mitochondrial KATP Channels, and Nitric Oxide Synthase, in Guinea Pig Hearts  

Microsoft Academic Search

BACKGROUND: Volatile anesthetics and regular ethanol consumption induce cardio- protection mimicking ischemic preconditioning. We investigated whether sevoflu- rane enhances ethanol preconditioning and whether inhibition of protein kinase C (PKC) and mitochondrial KATP channels attenuated this enhanced cardioprotec- tion. The effects of regular ethanol consumption on expression of inducible (iNOS) and endothelial (eNOS) nitric oxide synthase were determined. METHODS: Isolated perfused

Kazuhiro Kaneda; Masami Miyamae; Shingo Sugioka; Chika Okusa; Yoshitaka Inamura; Naochika Domae; Junichiro Kotani; Vincent M. Figueredo

2008-01-01

313

Plagiarism Prevention  

ERIC Educational Resources Information Center

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 prevent

Probett, Christine

2011-01-01

314

Poison Prevention  

MedlinePLUS

... Strength Training for Young Athletes Infant CPR Anytime® (English/Spanish) Pediatric First Aid for Caregivers and Teachers (PedFACTs) Participant Manual Pediatric First Aid for Caregivers and Teachers (PedFACTs) Teaching Package Safety & Prevention Immunizations All Around At Home ...

315

Preventing Tragedy.  

ERIC Educational Resources Information Center

The Navajo supervisor in the Office of Environmental Health in New Mexico identifies diseases and their risk factors, administers an injury prevention 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…

One Feather, Sandra

2003-01-01

316

CANCER PREVENTION  

Cancer.gov

If you are a person with a disability and require any assistive device, services or other reasonable accommodation to participate in this activity, please contact the Office of Preventive Oncology at 301-496-8640 at least one week in advance of the lecture date to discuss your accommodation needs.

317

Evaluation of the effects of ischemic preconditioning on the hematological parameters of rats subjected to intestinal ischemia and reperfusion  

PubMed Central

OBJECTIVES: Intestinal ischemia/reperfusion often leads to acute lung injury and multiple organ failure. Ischemic preconditioning is protective in nature and reduces tissue injuries in animal and human models. Although hematimetric parameters are widely used as diagnostic tools, there is no report of the influence of intestinal ischemia/reperfusion and ischemic preconditioning on such parameters. We evaluated the hematological changes during ischemia/reperfusion and preconditioning in rats. METHODS: Forty healthy rats were divided into four groups: control, laparotomy, intestinal ischemia/reperfusion and ischemic preconditioning. The intestinal ischemia/reperfusion group received 45 min of superior mesenteric artery occlusion, while the ischemic preconditioning group received 10 min of short ischemia and reperfusion before 45 min of prolonged occlusion. A cell counter was used to analyze blood obtained from rats before and after the surgical procedures and the hematological results were compared among the groups. RESULTS: The results showed significant differences in hematimetric parameters among the groups. The parameters that showed significant differences included lymphocyte, white blood cells and granulocyte counts; hematocrit; mean corpuscular hemoglobin concentration; red cell deviation width; platelet count; mean platelet volume; plateletcrit and platelet distribution width. CONCLUSION: The most remarkable parameters were those related to leukocytes and platelets. Some of the data, including the lymphocyte and granulocytes counts, suggest that ischemic preconditioning attenuates the effect of intestinal ischemia/reperfusion on circulating blood cells. Our work contributes to a better understanding of the hematological responses after intestinal ischemia/reperfusion and IPC, and the present findings may also be used as predictive values. PMID:25672431

Tahir, Muhammad; Arshid, Samina; Heimbecker, Ana Maria C; Castro, Mariana S; de Souza Montero, Edna Frasson; Fontes, Belchor; Fontes, Wagner

2015-01-01

318

(S)-ZJM-289 preconditioning induces a late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation.  

PubMed

(S)-ZJM-289, a novel nitric oxide (NO)-releasing derivative of 3-n-butylphthalide, induces the neuroprotection in a rat model of focal cerebral ischemia/reperfusion (I/R). However, much is unknown about the late phase effect in the neuroprotection of (S)-ZJM-289 preconditioning. The purpose of this study is to explore the late phase neuroprotection of (S)-ZJM-289 preconditioning, as well as underlying mechanisms involved. Preconditioning with 40-160 mg/kg, (S)-ZJM-289 significantly reduces brain damage after I/R. (S)-ZJM-289 preconditioning is effective when applied 1-3 days before I/R. Moreover, the degrees of neuroprotection offered by (S)-ZJM-289 preconditioning and ischemic preconditioning are virtually identical. (S)-ZJM-289 preconditioning also protects primary cultured cortical neurons against oxygen-glucose deprivation and recovery-induced cytotoxicity in vitro. (S)-ZJM-289 preconditioning significantly increases the generation of NO, but has no effect on the nitric oxide synthase activities. Additionally, (S)-ZJM-289 preconditioning promotes the dissociation between nuclear-factor-E2-related factor (Nrf2) and kelch-like ECH-associated protein 1, and induces Nrf2 nuclear localization. The neuroprotection of (S)-ZJM-289 preconditioning is blocked by Nrf2-siRNA in vitro. (S)-ZJM-289 preconditioning up-regulates antioxidant enzymes against nervous injury. (S)-ZJM-289 preconditioning significantly activates extracellular regulated protein kinases (ERK) and inhibits c-Jun N-terminal kinases signaling cascade. The neuroprotection is abolished by the ERK inhibitor PD98059 in vitro. Subsequently, (S)-ZJM-289 preconditioning increases the levels of anti-apoptotic protein B cell lymphoma 2 (Bcl-2) and inhibited the translocation of Bcl-2 associated X to the mitochondria, thus attenuating the release of cytochrome c from the mitochondria and the activation of downstream caspase. These results suggest that (S)-ZJM-289 preconditioning exerts the late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation. PMID:24277159

Zhang, Chao; Zhang, Zhenzhen; Zhao, Qian; Wang, Xuliang; Ji, Hui; Zhang, Yihua

2014-07-01

319

Lipopolysaccharide Preconditioning Protects Hepatocytes from Ischemia/Reperfusion Injury (IRI) through Inhibiting ATF4-CHOP Pathway in Mice  

PubMed Central

Background Low-dose lipopolysaccharide (LPS) preconditioning-induced liver protection has been demonstrated during ischemia-reperfusion injury (IRI) in several organs but has not been sufficiently elucidated underlying causal mechanism. This study investigated the role of low-dose LPS preconditioning on ATF4-CHOP pathway as well as the effects of the pathway on tissue injury and inflammation in a mouse model of liver partial-warm IRI. Methods LPS (100 µg/kg/d) was injected intraperitoneally two days before ischemia. Hepatic injury was evaluated based on serum alanine aminotransferase levels, histopathology, and caspase-3 activity. The ATF4-CHOP pathway and its related apoptotic molecules were investigated after reperfusion. The role of LPS preconditioning on apoptosis and ATF4-CHOP pathway was examined in vitro. Moreover, the effects of the ATF4-CHOP pathway on apoptosis, Caspase-12, and Caspase-3 were determined with ATF4 small interfering RNA (siRNA). Inflammatory cytokine expression was also checked after reperfusion. Inflammatory cytokines and related signaling pathways were analyzed in vitro in macrophages treated by LPS preconditioning or ATF4 siRNA. Results LPS preconditioning significantly attenuated liver injury after IRI. As demonstrated by in vitro experiments, LPS preconditioning significantly reduced the upregulation of the ATF4-CHOP pathway and inhibited Caspase-12 and Caspase-3 activation after IRI. Later experiments showed that ATF4 knockdown significantly suppressed CHOP, cleaved caspase-12 and caspase-3 expression, as well as inhibited hepatocellular apoptosis. In addition, in mice pretreated with LPS, TNF-? and IL-6 were inhibited after reperfusion, whereas IL-10 was upregulated. Similarly, low-dose LPS significantly inhibited TNF-?, IL-6, ATF4-CHOP pathway, NF-?B pathway, and ERK1/2 in high-dose LPS-stimulated macrophages, whereas IL-10 and cytokine signaling (SOCS)-3 suppressor were induced. Importantly, ATF4 siRNA is consistent with results of LPS preconditioning in macrophages. Conclusions This work is the first time to provide evidence for LPS preconditioning protects hepatocytes from IRI through inhibiting ATF4-CHOP pathway, which may be critical to reducing related apoptosis molecules and modulating innate inflammation. PMID:23750267

Qian, Xiaofeng; Lu, Ling; Wang, Ping; Wu, Zhengshan; Zhai, Yuan; Zhang, Feng; Li, Guoqiang; Wang, Xuehao

2013-01-01

320

The epidemiology of bovine respiratory disease: What is the evidence for preventive measures?  

PubMed Central

Bovine respiratory disease (BRD) is the most common and costly disease of beef cattle in North America. Despite extensive research, industry practices are often more informed by dogma than by fact. Frequently advocated interventions, including vaccination, various processing procedures, and nutritional manipulation, have limited impact on morbidity and mortality. Evidence for use of oral antimicrobials, either in feed or water, appears to be equivocal. In contrast, preconditioning and metaphylaxis have significant scientific evidence of efficacy, with weaning prior to sale potentially being the most important component of preconditioning. The inability to reach more definitive conclusions in preventing BRD may be attributable to difficulties in investigating the disease. Study challenges include potential for extensive confounding, tremendous variability, the multi-factorial nature of the disease, and inadequate methods for diagnosis. PMID:21358927

Taylor, Jared D.; Fulton, Robert W.; Lehenbauer, Terry W.; Step, Douglas L.; Confer, Anthony W.

2010-01-01

321

Effect of ischemic and pharmacological preconditioning of lower limb muscle tissue on tissue oxygenation measured by near-infrared spectroscopy – a pilot study  

PubMed Central

Background Ischemic or volatile anesthetic preconditioning is defined as tissue protection from impending ischemic cell damage by repetitive short periods of tissue exposure to ischemia or volatile anesthetics. Objective of this study was to elucidate, if ischemic preconditioning and pharmacological preconditioning with sevoflurane have effects on muscle tissue oxygen saturation in patients undergoing surgical revascularization of the lower limb. Methods In this prospective randomized pilot study ischemic and pharmacological (sevoflurane) preconditioning was performed in 40 patients with lower limb arterial occlusive disease undergoing surgical revascularization. Sevoflurane preconditioning was performed in one group (N?=?20) by repetitive application of sevoflurane for six minutes interspersed by six minutes of washout. Thereafter, ischemic preconditioning was performed in all patients (N?=?40) by repetitive clamping of the femoral artery for six minutes interspersed by six minutes of reperfusion. The effect of both procedures on leg muscle tissue oxygen saturation (rSO2) was measured by near-infrared spectroscopy during both procedures and during surgery and reperfusion (INVOS® 5100C Oxymeter with Small Adult SomaSensor® SAFB-SM, Somanetics, Troy, Michigan, USA). Results Repetitive clamping and reperfusion of the femoral artery resulted in significant cyclic decrease and increase of muscle rSO2 (p?preconditioning with sevoflurane resulted in a faster and higher increase of rSO2 during postoperative reperfusion (Maximal 111% baseline?±?20 versus 103% baseline?±?14, p?=?0.008) consistent with an additional effect of pharmacological preconditioning on leg perfusion. Conclusions Ischemic preconditioning of lower limb muscle tissue and pharmacological preconditioning with sevoflurane have an effect on tissue oxygenation in patients with lower limb occlusive arterial disease. Trial registration The trial has been registrated at http://www.ClinicalTrial.gov, Trial Number: NCT02038062 at 14 January 2014. PMID:25132803

2014-01-01

322

Effect of ischemic preconditioning on injuries caused by ischemia and reperfusion in rat intestine.  

PubMed

To study whether ischemic preconditioning (IPC) attenuated intestinal dysfunction caused by ischemia (I) and reperfusion (R), rats were underwent 60 minutes of I which was produced by occlusion of the superior mesenteric artery, and/or 120 minutes R. The IPC group had the I procedure previously stimulated for 5 minutes and the R for 10 minutes. IPC and sham groups were injected with saline solution (SS) via the femoral vein 5 minutes before the I and R, and for R. After I or I/R, 2-cm jejunal segments were mounted in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Compared with the sham group, jejunal contractions were similar in the IPC + I and the IPC + I/R groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS groups, but not in the IPC groups. These results suggested that ischemic preconditioning attenuated intestinal dysfunction caused by I and I/R. PMID:23026580

Taha, M O; Miranda-Ferreira, R; Chang, A C R; Rodrigues, A M; Fonseca, I S; Toral, L B; Cardoso, M R; Simões, M J; Oliveira-Junior, I S; Monteiro, H P; Fagundes, D J; Taha, N S A; Caricati-Neto, A

2012-10-01

323

Strategies to promote donor cell survival: combining preconditioning approach with stem cell transplantation  

PubMed Central

Stem cell transplantation has emerged as a potential modality in cardiovascular therapeutics due to their inherent characteristics of self-renewal, unlimited capacity for proliferation and ability to cross lineage restrictions and adopt different phenotypes. Constrained by extensive death in the unfriendly milieu of ischemic myocardium, the results of heart cell therapy in experimental animal models as well as clinical studies have been less than optimal. Several factors which play a role in early cell death after engraftment in the ischemic myocardium include; absence of survival factors in the transplanted heart, disruption of cell-cell interaction coupled with loss of survival signals from matrix attachments, insufficient vascular supply and elaboration of inflammatory cytokines resulting from ischemia and/or cell death. This article reviews various signaling pathways involved in triggering highly complex forms of cell death and provides critical appreciation of different novel anti-death strategies developed from the knowledge gained from using an ischemic preconditioning approach. The use of pharmacological preconditioning for up-regulation of pro-survival proteins and cardiogenic markers in the transplanted stem cells will be discussed. PMID:18561945

Haider, Husnain Kh; Ashraf, Muhammad

2008-01-01

324

Remote ischemic preconditioning for myocardial protection: update on mechanisms and clinical relevance.  

PubMed

Ischemic heart disease is the leading cause of death for both men and women worldwide, accruing 7.4 million deaths in 2012. There has been a continued search for better cardioprotective modalities that would reduce myocardial ischemia-reperfusion injury. Among these attempts, a more convenient model of ischemic preconditioning, known as remote ischemic preconditioning (RIPC) was first introduced in 1993 by Przyklenk and colleagues who reported that brief regional occlusion-reperfusion episodes in one vascular bed of the heart render protection to remote myocardial tissue. Subsequently, major advances in myocardial RIPC came with the use of skeletal muscle as the ischemic stimulus. To date, numerous studies have revealed that RIPC applied to the kidney, liver, mesentery, and skeletal muscle, have all exhibited cardioprotective effects. The main purpose of this review article is to summarize the new advances in understanding the molecular mechanisms of RIPC during the past 5 years, including those related to capsaicin-activated C sensory fibers, hypoxia-inducible factor 1?, connexin 43, extracellular vesicles, microRNA-144, microRNA-1, and nitrite. In addition, we have discussed results from several recent human clinical trials with RIPC. Taken together, the emerging clinical evidence supports the concept that the effectiveness of RIPC paired with its low-cost and non-invasive features makes it an ideal treatment before reperfusion after sustained ischemia. More carefully designed studies are warranted to fully exploit the clinical benefits of RIPC and its potential implications in patients with cardiovascular disease. PMID:25552250

Gill, Rabia; Kuriakose, Robin; Gertz, Zachary M; Salloum, Fadi N; Xi, Lei; Kukreja, Rakesh C

2015-04-01

325

Preconditioning crush increases the survival rate of motor neurons after spinal root avulsion  

PubMed Central

In a previous study, heat shock protein 27 was persistently upregulated in ventral motor neurons following nerve root avulsion or crush. Here, we examined whether the upregulation of heat shock protein 27 would increase the survival rate of motor neurons. Rats were divided into two groups: an avulsion-only group (avulsion of the L4 lumbar nerve root only) and a crush-avulsion group (the L4 lumbar nerve root was crushed 1 week prior to the avulsion). Immunofluorescent staining revealed that the survival rate of motor neurons was significantly greater in the crush-avulsion group than in the avulsion-only group, and this difference remained for at least 5 weeks after avulsion. The higher neuronal survival rate may be explained by the upregulation of heat shock protein 27 expression in motor neurons in the crush-avulsion group. Furthermore, preconditioning crush greatly attenuated the expression of nitric oxide synthase in the motor neurons. Our findings indicate that the neuroprotective action of preconditioning crush is mediated through the upregulation of heat shock protein 27 expression and the attenuation of neuronal nitric oxide synthase upregulation following avulsion. PMID:25206852

Li, Lin; Zuo, Yizhi; He, Jianwen

2014-01-01

326

Remote ischemic preconditioning to reduce contrast-induced nephropathy: study protocol for a randomized controlled trial  

PubMed Central

Background Despite the increasing use of pre- and posthydration protocols and low-osmolar instead of high-osmolar iodine-containing contrast media, the incidence of contrast-induced nephropathy (CIN) is still significant. There is evidence that contrast media cause ischemia-reperfusion injury of the medulla. Remote ischemic preconditioning (RIPC) is a non-invasive, safe, and low-cost method to reduce ischemia-reperfusion injury. Methods The RIPCIN study is a multicenter, single-blinded, randomized controlled trial in which 76 patients at risk of CIN will receive standard hydration combined with RIPC or hydration with sham preconditioning. RIPC will be applied by four cycles of 5 min ischemia and 5 min reperfusion of the forearm by inflating a blood pressure cuff at 50 mmHg above the actual systolic pressure. The primary outcome measure will be the change in serum creatinine from baseline to 48 to 72 h after contrast administration. Discussion A recent pilot study reported that RIPC reduced the incidence of CIN after coronary angioplasty. The unusual high incidence of CIN in this study is of concern and limits its generalizability. Therefore, we propose a randomized controlled trial to study whether RIPC reduces contrast-induced kidney injury in patients at risk for CIN according to the Dutch guidelines. Trial registration Current Controlled Trials ISRCTN76496973 PMID:24721127

2014-01-01

327

Enhanced matrix spectroscopy: The preconditioned Green-function block Lanczos algorithm  

NASA Astrophysics Data System (ADS)

We present herein the results of a doubly filtered block Lanczos code, which effectively uses shifted simultaneous inverse iteration to make a block tridiagonal representation of H, a Hamiltonian matrix. The first filter preconditions the starting block of Lanczos vectors through one or more applications of p(E), the preconditioning operator. This block is then used to seed the Lanczos recursion, driven with the Green-function filter G(E)=(EI-H)-1. Each set of successively generated Lanczos vectors is orthogonalized against all previous ones. These steps allow us to converge eigenvalues near E, in the interior region of the eigenspectrum, with extreme accuracy. Degenerate eigenvalues are reported; ``ghost'' eigenvalues (multiple copies of eigenvalues that have already converged) are avoided. For a set number of Lanczos recursions, the use of a preconditioner effectively doubles the number of converged eigenvalues than are resolved without its use. The computation time is increased almost imperceptibly. The 2eg<--ag torsional transition for the water trimer, (H2O)3, is examined in an application of our method. We resolve the quantities needed for this calculation is less than one-fifth the time required to directly diagonalize the matrices, with no loss of accuracy.

Minehardt, Todd J.; Adcock, J. David; Wyatt, Robert E.

1997-10-01

328

Exercise-Induced Ischemic Preconditioning and the Potential Application to Cardiac Rehabilitation: A SYSTEMATIC REVIEW.  

PubMed

Exercise-induced ischemic preconditioning (IPC) can be assessed by the results of the second of sequential exercise tests. Exercise-induced IPC is quantified by using the time to 1-mm ST-segment depression, the rate-pressure product at 1-mm ST-segment depression, the maximal ST-segment depression, and the rate-pressure product at the peak of exercise. Few studies reported whether exercise-induced IPC could be used in cardiovascular rehabilitation. A systematic review of the literature limited to human studies was performed using electronic databases, and the main key words were ischemic preconditioning, warm-up phenomenon, and exercise. After careful review, 38 articles were included in the systematic review. This review summarizes the molecular pathways of IPC and describes the first window of protection induced by sequential exercise tests, as well as the effect of medication on exercise-induced IPC. A section on the exercise protocol, mode of exercise, and intensity provides understanding as to what is needed for clinicians to induce IPC with sequential stress tests. The final section of the review is a discussion of the potential use of exercise-induced IPC in a cardiovascular rehabilitation setting. Even if exercise-induced IPC is a well-documented phenomenon, additional studies are needed in order to more fully understand its use in rehabilitation. PMID:25622217

Lalonde, François; Poirier, Paul; Arvisais, Denis; Curnier, Daniel

2015-01-01

329

Large Scale Topology Optimization Using Preconditioned Krylov Subspace Recycling and Continuous Approximation of Material Distribution  

NASA Astrophysics Data System (ADS)

Large-scale topology optimization problems demand the solution of a large number of linear systems arising in the finite element analysis. These systems can be solved efficiently by special iterative solvers. Because the linear systems in the sequence of optimization steps change slowly from one step to the next, we can significantly reduce the number of iterations and the runtime of the linear solver by recycling selected search spaces from previous linear systems, and by using preconditioning and scaling techniques. We also provide a new implementation of the 8-node brick (B8) element for the continuous approximation of material distribution (CAMD) approach to improve designs of functionally graded materials. Specifically, we develop a B8/B8 implementation in which the element shape functions are used for the approximation of both displacements and material density at nodal locations. Finally, we evaluate the effectiveness of several solver and preconditioning strategies, and we investigate large-scale examples, including functionally graded materials, which are solved with a special version of the SIMP (solid isotropic material with penalization) model. The effectiveness of the solver is demonstrated by means of a topology optimization problem in a functionally graded material with 1.6 million unknowns on a fast PC.

de Sturler, Eric; Le, Chau; Wang, Shun; Paulino, Glaucio

2008-02-01

330

The Role and Dynamics of ?-Catenin in Precondition Induced Neuroprotection after Traumatic Brain Injury  

PubMed Central

Preconditioning via heat acclimation (34°C 30 d) results in neuroprotection from traumatic brain injury due to constitutive as well as dynamic changes triggered by the trauma. Among these changes is Akt phosphorylation, which decreases apoptosis and induces HIF1?. In the present study we investigated the Akt downstream GSK3?/? -catenin pathway and focused on post injury alternations of ? catenin and its impact on the cellular response in preconditioned heat acclimated mice. We found that the reduction in motor disability is accompanied with attenuation of depressive like behavior in heat acclimated mice that correlates with the GSK3? phosphorylation state. Concomitantly, a robust ? catenin phosphorylation is not followed by its degradation, or by reduced nuclear accumulation. Enhanced tyrosine phosphorylation of ? catenin in the injured area weakens the ? catenin-N cadherin complex. Membrane ? catenin is transiently reduced in heat acclimated mice and its recovery 7 days post TBI is accompanied by induction of the synaptic marker synaptophysin. We suggest a set of cellular events following traumatic brain injury in heat acclimated mice that causes ? catenin to participate in cell-cell adhesion alternations rather than in Wnt signaling. These events may contribute to synaptogenesis and the improved motor and cognitive abilities seen heat acclimated mice after traumatic brain injury. PMID:24124534

Umschweif, Gali; Alexandrovich, Alexander G.; Trembovler, Victoria; Horowitz, Michal; Shohami, Esther

2013-01-01

331

Obesity Prevention  

Microsoft Academic Search

On the surface, weight maintenance may seem easier than weight loss because of the lower demand in terms of the number of\\u000a calories to be reduced in the diet or added in energy expenditure through physical activity. However, the literature to date\\u000a suggests that this reasoning may be deceptive. The prevention of obesity in childhood is particularly complex. Ultimately,\\u000a to

Shiriki K. Kumanyika; Stephen R. Daniels

332

Cell transplantation after oxidative hepatic preconditioning with radiation and ischemia-reperfusion leads to extensive liver repopulation  

NASA Astrophysics Data System (ADS)

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 preconditioned with whole liver radiation and warm ischemia-reperfusion followed by intrasplenic transplantation of syngeneic F344 rat hepatocytes. The preconditioning 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 preconditioned with ischemia-reperfusion alone. Animals treated with radiation alone showed some transplanted cell proliferation. In contrast, the liver of animals preconditioned 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.

Malhi, Harmeet; Gorla, Giridhar R.; Irani, Adil N.; Annamaneni, Pallavi; Gupta, Sanjeev

2002-10-01

333

Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72  

PubMed Central

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 preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise preconditioning 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 preconditioning is a promising strategy for facilitating functional recovery from SCI. PMID:25334068

Chang, Cheng-Kuei; Chou, Willy; Lin, Hung-Jung; Huang, Yi-Ching; Tang, Ling-Yu; Lin, Mao-Tsun; Chang, Ching-Ping

2014-01-01

334

From Real Friend to Imagined Foe: The Medieval Roots of Anti-Semitism as a Precondition for the Holocaust  

Microsoft Academic Search

This study examines the medieval roots of European anti-Semitism as a precondition for the Holocaust. The twelfth century saw an important transition from Jews being viewed as the adherents of a competing religion to dangerous, inhuman threats to the broader Christian society for the first time. Northern France is used as a case study, examining several Jewish, Christian, and secular

Christopher Tuckwood

2010-01-01

335

From Real Friend to Imagined Foe: The Medieval Roots of Anti-Semitism as a Precondition for the Holocaust  

Microsoft Academic Search

:This study examines the medieval roots of European anti-Semitism as a precondition for the Holocaust. The twelfth century saw an important transition from Jews being viewed as the adherents of a competing religion to dangerous, inhuman threats to the broader Christian society for the first time. Northern France is used as a case study, examining several Jewish, Christian, and secular

Christopher Tuckwood

2010-01-01

336

Two examples of the impact of partitioning with Chaco and Metis on the convergence of additive Schwarz-preconditioned FGMRES  

SciTech Connect

Algebraic graph partitioning packages that require no geometric or physical information are often used to partition sparse linear systems for solution on parallel computers using Krylov-space iterative methods with domain decomposition-type preconditioning methods. The authors show through a couple of examples that this can have a substantial impact on the convergence of the iterative methods.

DeLong, M.

1997-09-29

337

TARGETED DELETION OF INDUCIBLE HEAT SHOCK PROTEIN 70 ABROGATES THE LATE INFARCT-SPARING EFFECT OF MYOCARDIAL ISCHEMIC PRECONDITIONING  

EPA Science Inventory

Abstract submitted for 82nd annual meeting of the American Association for Thoracic Surgery, May 4-8, 2002 in Washington D.C. Targeted Deletion of Inducible Heat Shock Protein 70 Abrogates the Late Infarct-Sparing Effect of Myocardial Ischemic Preconditioning Craig...

338

Heat shock preconditioning protects against ER stress-induced apoptosis through the regulation of the BH3-only protein BIM.  

PubMed

A mild heat shock (HS) preconditioning and acquisition of thermotolerance protects cells against a variety of cytotoxic agents that otherwise induce apoptosis. Here we tested whether there is a molecular link between HS preconditioning and endoplasmic reticulum (ER) stress-induced apoptosis. ER stress results from a loss of ER lumen homeostasis, culminating in an accumulation of unfolded/misfolded proteins in the ER and activation of unfolded protein response (UPR). Unresolved, ER stress leads to activation of BH3-only proteins, mitochondrial membrane permeabilization, caspase activation and apoptotic cell death. HS preconditioning (1 h at 42 °C) induced a rapid increase in HSPA1 (HSP70) levels which remained elevated for at least 48 h post-HS. HS preconditioning significantly reduced BAX, caspase activation and apoptosis in cell cultures treated with the ER stress-inducing agents thapsigargin (TG) and tunicamycin (TM). HS-mediated protection was found to be due to regulation of the BH3-only protein BIM. Further, overexpression of HSPA1 could not mimic the effect of HS on BIM expression, suggesting that other HS factors may play a role in inhibiting ER stress-induced apoptosis by regulating BIM. PMID:25349785

Kennedy, Donna; Mnich, Katarzyna; Samali, Afshin

2014-01-01

339

Fatigue preconditioning increases fatigue resistance in mouse flexor digitorum brevis muscles with non-functioning KATP channels  

PubMed Central

The objective of this study was to determine how an initial fatigue bout (FAT1 at 37°C) affects free myoplasmic Ca2+ concentration and force ([Ca2+]i/force) during a subsequent fatigue bout (FAT2) in mouse flexor digitorum brevis (FDB). During FAT1, both tetanic [Ca2+]i/force decreased; however, they decreased to significantly lower levels when FAT1 was carried out in the presence of glibenclamide, a sarcolemmal KATP (sKATP) channel blocker. Glibenclamide also elicited greater increases in unstimulated [Ca2+]i/force, which occurred when fibres failed to fully relax between contractions during FAT1. Finally, glibenclamide impaired force recovery after FAT1. The decreases in tetanic [Ca2+]i/force and increases in unstimulated [Ca2+]i/force were slower during FAT2 elicited 60 min after FAT1. Under control conditions, the effects were small with very few significant differences. In the presence of glibenclamide, on the other hand, the differences between FAT1 and FAT2 were very large. Unexpectedly, the differences in unstimulated and tetanic [Ca2+]i/force between control and glibenclamide conditions observed during FAT1 were no longer observed during FAT2. The lack of differences was not related to a failure of glibenclamide to block KATP channels during FAT2 because the effects of FAT1 on FAT2 were also observed using Kir6.2?/? mouse FDB, which lack sKATP channel activity. The differences in [Ca2+]i/force between FAT1 and FAT2 could be observed with FAT1 duration of just 30 s and a FAT1–FAT2 interval of at least 30 min. A modulation of factors involved in ischaemic pre-conditioning, i.e. A1-adenosine receptors, sKATP and mitochondrial KATP (mKATP) channels, PKC and reactive oxygen species, during FAT1 had no effect on FAT2 fatigue kinetics. It is concluded that a preceding fatigue bout triggers an acute physiological process that prevents the contractile dysfunction induced by non-functioning KATP channels. PMID:20855438

Boudreault, Louise; Cifelli, Carlo; Bourassa, François; Scott, Kyle; Renaud, Jean-Marc

2010-01-01

340

Fatigue preconditioning increases fatigue resistance in mouse flexor digitorum brevis muscles with non-functioning K(ATP) channels.  

PubMed

The objective of this study was to determine how an initial fatigue bout (FAT1 at 37°C) affects free myoplasmic Ca(2+) concentration and force ([Ca(2+)](i)/force) during a subsequent fatigue bout (FAT2) in mouse flexor digitorum brevis (FDB). During FAT1, both tetanic [Ca(2+)](i)/force decreased; however, they decreased to significantly lower levels when FAT1 was carried out in the presence of glibenclamide, a sarcolemmal K(ATP) (sK(ATP)) channel blocker. Glibenclamide also elicited greater increases in unstimulated [Ca(2+)](i)/force, which occurred when fibres failed to fully relax between contractions during FAT1. Finally, glibenclamide impaired force recovery after FAT1. The decreases in tetanic [Ca(2+)](i)/force and increases in unstimulated [Ca(2+)](i)/force were slower during FAT2 elicited 60 min after FAT1. Under control conditions, the effects were small with very few significant differences. In the presence of glibenclamide, on the other hand, the differences between FAT1 and FAT2 were very large. Unexpectedly, the differences in unstimulated and tetanic [Ca(2+)](i)/force between control and glibenclamide conditions observed during FAT1 were no longer observed during FAT2. The lack of differences was not related to a failure of glibenclamide to block K(ATP) channels during FAT2 because the effects of FAT1 on FAT2 were also observed using Kir6.2(-/-) mouse FDB, which lack sK(ATP) channel activity. The differences in [Ca(2+)](i)/force between FAT1 and FAT2 could be observed with FAT1 duration of just 30 s and a FAT1-FAT2 interval of at least 30 min. A modulation of factors involved in ischaemic pre-conditioning, i.e. A1-adenosine receptors, sK(ATP) and mitochondrial K(ATP) (mK(ATP)) channels, PKC and reactive oxygen species, during FAT1 had no effect on FAT2 fatigue kinetics. It is concluded that a preceding fatigue bout triggers an acute physiological process that prevents the contractile dysfunction induced by non-functioning K(ATP) channels. PMID:20855438

Boudreault, Louise; Cifelli, Carlo; Bourassa, François; Scott, Kyle; Renaud, Jean-Marc

2010-11-15

341

Preconditioning of brain slices against hypoxia induced injury by a Gynostemma pentaphyllum extract--stimulation of anti-oxidative enzyme expression.  

PubMed

A short period of hypoxia/hypoglycaemia (oxygen and glucose deprivation, OGD) induced by perfusion with O(2)/glucose-free medium caused immediate loss and incomplete restoration of evoked field potentials in the CA1 region of transverse hippocampus slices. OGD-dependent decrease in evoked field potentials can be prevented by a proceeding short OGD event (preconditioning). We report about a study investigating the effect of an ethanolic Gynostemma pentaphyllum extract on evoked field potentials when administered before the OGD episode. Using this procedure, the extract completely protected the cells of the slices from functional injury. In an astroglia rich cell culture the ethanolic Gynostemma pentaphyllum extract caused within 48 h of cultivation increased protein and activity levels of the anti-oxidative enzymes manganese superoxide dismutase (Mn-SOD) and glutathione peroxidase (GPx). Consequently, the cellular H(2)O(2) concentration remained at a low level. These data suggest that the Gynostemma pentaphyllum-mediated increase in antioxidative enzyme activities may contribute to the protection of transverse hippocampus slices from OGD induced functional injury. Our results demonstrate that the prophylactic administration of the ethanolic extract from Gynostemma pentaphyllum has a high potential to protect from ischemia/reperfusion injury. PMID:22516894

Schild, L; Cotte, T; Keilhoff, G; Brödemann, R

2012-06-15

342

Hypoxic Preconditioning Improves Survival of Cardiac Progenitor Cells: Role of Stromal Cell Derived Factor-1?–CXCR4 Axis  

PubMed Central

Background Cardiac progenitor cells (CPCs) have been shown to be suitable in stem cell therapy for resurrecting damaged myocardium, but poor retention of transplanted cells in the ischemic myocardium causes ineffective cell therapy. Hypoxic preconditioning of cells can increase the expression of CXCR4 and pro-survival genes to promote better cell survival; however, it is unknown whether hypoxia preconditioning will influence the survival and retention of CPCs via the SDF-1?/CXCR4 axis. Methods and Results CPCs were isolated from adult mouse hearts and purified by magnetic activated cell sorting using c-kit magnetic beads. These cells were cultured at various times in either normoxic or hypoxic conditions, and cell survival was analyzed using flow cytometry and the expression of hypoxia-inducible factor-1? (HIF-1?), CXCR4, phosphorylated Akt and Bcl-2 were measured by Western blot. Results showed that the expression of pro-survival genes significantly increased after hypoxia treatment, especially in cells cultured in hypoxic conditions for six hours. Upon completion of hypoxia preconditioning from c-kit+ CPCs for six hours, the anti-apoptosis, migration and cardiac repair potential were evaluated. Results showed a significant enhancement in anti-apoptosis and migration in vitro, and better survival and cardiac function after being transplanted into acute myocardial infarction (MI) mice in vivo. The beneficial effects induced by hypoxia preconditioning of c-kit+ CPCs could largely be blocked by the addition of CXCR4 selective antagonist AMD3100. Conclusions Hypoxic preconditioning may improve the survival and retention of c-kit+ CPCs in the ischemic heart tissue through activating the SDF-1?/CXCR4 axis and the downstream anti-apoptosis pathway. Strategies targeting this aspect may enhance the effectiveness of cell-based cardiac regenerative therapy. PMID:22815687

Yan, Fengdi; Yao, Yuyu; Chen, Lijuan; Li, Yefei; Sheng, Zulong; Ma, Genshan

2012-01-01

343

Matrix multiplication operations with data pre-conditioning in a high performance computing architecture  

DOEpatents

Mechanisms for performing matrix multiplication operations with data pre-conditioning 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.

Eichenberger, Alexandre E; Gschwind, Michael K; Gunnels, John A

2013-11-05

344

Fluid preconditioning for Newton–Krylov-based, fully implicit, electrostatic particle-in-cell simulations  

SciTech Connect

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 preconditioning 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.

Chen, G., E-mail: gchen@lanl.gov [Los Alamos National Laboratory, Los Alamos, NM 87545 (United States); Chacón, L. [Los Alamos National Laboratory, Los Alamos, NM 87545 (United States)] [Los Alamos National Laboratory, Los Alamos, NM 87545 (United States); Leibs, C.A. [University of Colorado Boulder, Boulder, CO 80309 (United States)] [University of Colorado Boulder, Boulder, CO 80309 (United States); Knoll, D.A. [Los Alamos National Laboratory, Los Alamos, NM 87545 (United States)] [Los Alamos National Laboratory, Los Alamos, NM 87545 (United States); Taitano, W. [University of New Mexico, Albuquerque, NM 87131 (United States)] [University of New Mexico, Albuquerque, NM 87131 (United States)

2014-02-01

345

Fluid preconditioning for Newton-Krylov-based, fully implicit, electrostatic particle-in-cell simulations  

NASA Astrophysics Data System (ADS)

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 preconditioning 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.

Chen, G.; Chacón, L.; Leibs, C. A.; Knoll, D. A.; Taitano, W.

2014-02-01

346

Measurements of 1,2-diacylglycerol and ceramide in hearts subjected to ischemic preconditioning.  

PubMed

An accumulation of recent evidence suggests that the mechanism in ischemic preconditioning (IPC) may involve the activation of protein kinase C (PKC) regulatory pathway. In this study, we examined whether the content of 1,2-diacylglycerol (1,2-DAG) and ceramide, which are intracellular second messengers regulating PKC activity, change during IPC in isolated perfused rat hearts, and whether the observed change in 1,2-DAG is accompanied with alteration in its fatty acid composition. Hearts subjected to IPC, consisting of 5-min transient global ischemia followed by 5-min reperfusion, presented a significant functional recovery during subsequent 40-min reperfusion following 40-min global ischemia compared with non-preconditioned hearts. An increase in 1,2-DAG content was observed in hearts subjected to 5-min transient ischemia compared with non-ischemic control hearts, however this was not seen in hearts harvested after 5-min reperfusion following 5-min ischemia. While fatty acid composition in 1,2-DAG was virtually unchanged in hearts subjected to 5-min ischemia, saturated 1,2-DAG decreased and monounsaturated/polyunsaturated 1,2-DAG increased in hearts reperfused for 5-min following 5-min ischemia compared with the non-ischemic control hearts. Ceramide mass did not change significantly, suggesting that the contribution of ceramide may be small in IPC. These data are in concert with the hypothesis that 1,2-DAG is a second messenger in IPC and the changes in fatty acid composition of 1,2-DAG may add new insight concerning signal transduction pathway in IPC. PMID:10794496

Murase, K; Okumura, K; Hayashi, K; Matsui, H; Toki, Y; Ito, T; Hayakawa, T

2000-01-01

347

Preconditioning somatothermal stimulation on Qimen (LR14) reduces hepatic ischemia/reperfusion injury in rats  

PubMed Central

Background In human beings or animals, ischemia/reperfusion (I/R) injury of the liver may occur in many clinical conditions, such as circulating shock, liver transplantation and surgery and several other pathological conditions. I/R injury has a complex pathophysiology resulting from a number of contributing factors. Therefore, it is difficult to achieve effective treatment or protection by individually targeting the mediators. This study aimed at studying the effects of local somatothermal stimulation preconditioning on the right Qimen (LR14) on hepatic I/R injury in rats. Methods Eighteen male Sprague-Dawley rats were randomly divided into three groups. The rats were preconditioned with thermal tolerance study, which included one dose of local somatothermal stimulation (LSTS) on right Qimen (LR14) at an interval of 12 h, followed by hepatic ischemia for 60 min and then reperfusion for 60 min. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) have been used to assess the liver functions, and liver tissues were taken for the measurements such as malondialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxidase dismutase (SOD), and myeloperoxidase (MPO). Results The results show that the plasma ALT and AST activities were higher in the I/R group than in the control group. In addition, the plasma ALT and AST activities decreased in the groups that received LSTS. The hepatic SOD levels reduced significantly by I/R injury. Moreover, the hepatic MPO activity significantly increased by I/R injury while it decreased in the groups given LSTS. Conclusions Our findings show that LSTS provides a protective effects on the liver from the I/R injury. Therefore, LSTS might offer an easy and inexpensive intervention for patients who have suffered from I/R of the liver especially in the process of hepatotomy and hepatic transplantation. PMID:24417801

2014-01-01

348

Myocardial ischemic preconditioning in rodents is dependent on poly (ADP-ribose) synthetase.  

PubMed Central

BACKGROUND: Activation of the nuclear enzyme poly (ADP-ribose) synthetase (PARS) in response to oxidant-mediated DNA injury has been shown to play an important role in the pathogenesis of reperfusion injury. Here we investigated the role of PARS in myocardial ischemic preconditioning (IPC). MATERIALS AND METHODS: Mice with or without genetic disruption of PARS and rats in the absence or presence of the PARS inhibitor 3-aminobenzamide underwent coronary occlusion and reperfusion with or without IPC. RESULTS: Both poly(ADP-ribose) synthetase (PARS) deficiency and ischemic preconditioning (IPC) induced protection from reperfusion injury, attenuated inflammatory mediator production, and reduced neutrophil infiltration when compared to the response in wild-type mice. Surprisingly, the protective effect of IPC not only disappeared in PARS-/- mice, but the degree of myocardial injury and inflammatory response was similar to the one seen in wild-type animals. Similarly, in the rat model of IPC, 3-aminobenzamide pretreatment blocked the beneficial effect of IPC. Myocardial NAD+ levels were maintained in the PARS-deficient mice during reperfusion, while depleted in the wild-type mice. The protection against reperfusion injury by IPC was also associated with partially preserved myocardial NAD+ levels, indicating that PARS activation is attenuated by IPC. This conclusion was further strengthened by poly(ADP-ribose) immunohistochemical measurements, demonstrating that IPC markedly inhibits PARS activation during reperfusion. CONCLUSIONS: The mode of IPC's action is related, at least in part, to an inhibition of PARS. This process may occur either by self-auto-ribosylation of PARS during IPC, and/or via the release of endogenous purines during IPC that inhibit PARS activation during reperfusion. PMID:11474134

Liaudet, L.; Yang, Z.; Al-Affar, E. B.; Szabó, C.

2001-01-01

349

Mitochondrial cyclophilin-D as a critical mediator of ischaemic preconditioning  

PubMed Central

Aims It has been suggested that mitochondrial reactive oxygen species (ROS), Akt and Erk1/2 and more recently the mitochondrial permeability transition pore (mPTP) may act as mediators of ischaemic preconditioning (IPC), although the actual interplay between these mediators is unclear. The aim of the present study is to determine whether the cyclophilin-D (CYPD) component of the mPTP is required by IPC to generate mitochondrial ROS and subsequently activate Akt and Erk1/2. Methods and results Mice lacking CYPD (CYPD?/?) and B6Sv129 wild-type (WT) mice were used throughout. We have demonstrated that under basal conditions, non-pathological mPTP opening occurs (indicated by the percent reduction in mitochondrial calcein fluorescence). This effect was greater in WT cardiomyocytes compared with CYPD?/? ones (53 ± 2% WT vs. 17 ± 3% CYPD?/?; P < 0.01) and was augmented by hypoxic preconditioning (HPC) (70 ± 9% WT vs. 56 ± 1% CYPD?/?; P < 0.01). HPC reduced cell death following simulated ischaemia–reperfusion injury in WT (23.2 ± 3.5% HPC vs. 43.7 ± 3.2% WT; P < 0.05) but not CYPD?/? cardiomyocytes (19.6 ± 1.4% HPC vs. 24.4 ± 2.6% control; P > 0.05). HPC generated mitochondrial ROS in WT (four-fold increase; P < 0.05) but not CYPD?/? cardiomyocytes. HPC induced significant Akt phosphorylation in WT cardiomyocytes (two-fold increase; P < 0.05), an effect which was abrogated by ciclosporin-A (a CYPD inhibitor) and N-2-mercaptopropionyl glycine (a ROS scavenger). Finally, in vivo IPC of adult murine hearts resulted in significant phosphorylation of Akt and Erk1/2 in WT but not CYPD?/? hearts. Conclusion The CYPD component of the mPTP is required by IPC to generate mitochondrial ROS and phosphorylate Akt and Erk1/2, major steps in the IPC signalling pathway. PMID:20400621

Hausenloy, Derek J.; Lim, Shiang Y.; Ong, Sang-Ging; Davidson, Sean M.; Yellon, Derek M.

2010-01-01

350

Insulin suppresses ischemic preconditioning-mediated cardioprotection through Akt-dependent mechanisms.  

PubMed

It is believed that the diabetic myocardium is refractory to cardioprotection by ischemic preconditioning (IPC) mainly because of impaired insulin signaling to phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB or Akt). However, human as well as animal studies have clearly showed that the hearts of type 2 diabetic humans and animals may exhibit increased signaling through PI3K-Akt but yet are resistant to cardioprotection by IPC or ischemic post-conditioning. Therefore, this study was designed to determine whether activation of insulin signaling prior to IPC is detrimental for cardioprotection and to assess the role of insulin receptors (IRs) and Akt in mediating this effect. Wild-type (WT) hearts, hearts lacking IRs or hearts expressing an active form of Akt (myrAkt1) were perfused ex vivo using a Langendorff preparation and were subjected to IPC (3cycles of 5min ischemia followed by 5min reflow before 30min no flow ischemia and then by 45min reperfusion) in the presence or absence of 1nmol/L insulin. Interestingly, whereas insulin was protective against I/R (30min no flow ischemia and 45min reperfusion), it completely abolished cardioprotection by IPC in WT hearts but not in mice lacking insulin receptors (IRs) in cardiomyocytes (CIRKO) or in all cardiac cells (TIRKO). The suppression of IPC-mediated cardioprotection was mediated through downstream signaling to Akt and Gsk3?. In addition, transgenic induction of Akt in the heart was sufficient to abrogate IPC even when insulin was absent, further confirming the involvement of Akt in insulin's suppression of cardioprotection by IPC. These data provide evidence that excessive insulin signaling to Akt is detrimental for cardioprotection by IPC and could explain the failure of the diabetic myocardium to precondition. PMID:23994159

Fullmer, Tanner M; Pei, Shaobo; Zhu, Yi; Sloan, Crystal; Manzanares, Robert; Henrie, Brandon; Pires, Karla M; Cox, James E; Abel, E Dale; Boudina, Sihem

2013-11-01

351

Osteopontin Mediates Hyperbaric Oxygen Preconditioning-Induced Neuroprotection Against Ischemic Stroke.  

PubMed

Neurosurgical operations may result in surgical injury which would lead to postoperative neurological deficits. Hyperbaric oxygen preconditioning (HBO-PC) may be beneficial for such people. However, the exact mechanism underlying HBO-PC is not well known yet. The aim of this study is to explore the role of osteopontin (OPN) in HBO-PC-induced neuroprotection. The study consisted of two experiments. In experiment 1, Sprague Dawley (SD) rats were divided into four groups: sham group, HBO-PC sham group, stroke group, and HBO-PC group (HBO-PC?+?stroke). The animals in the second experiment were randomly assigned to one of two groups: OPN small interfering (siRNA) group (HBO-PC?+?stroke?+?OPN siRNA) and control siRNA group (HBO-PC?+?stroke?+?negative control siRNA). Neurological outcome in HBO-PC group was better than that of stroke group. After OPN siRNA was administered, neurological function aggravated compared with control siRNA group. Brain morphology and structure seen by light microscopy was diminished in stroke group and OPN siRNA group, while fewer pathological injuries occurred in HBO-PC and control siRNA group. The infarct volume in HBO-PC group was the lowest, followed by OPN siRNA group and stroke group, respectively. Preconditioning with HBO promoted expression of OPN, which reduced the expression of interleukin (IL)-1?/nuclear factor-?-gene binding (NF?B) and augmented protein kinase B (Akt). OPN siRNA reversed these changes. OPN plays an important role in the neuroprotection elicited by HBO-PC. Pretreatment with HBO may be beneficial for people going to undertake brain surgery. PMID:25146847

Hu, Sheng-Li; Huang, Yu-Xing; Hu, Rong; Li, Fei; Feng, Hua

2014-08-23

352

Preconditioning of Model Biocarriers by Soluble Pollutants: A QCM-D Study.  

PubMed

Preconditioning of a biocarrier surface is the first step in triggering biofilm formation in attached-growth bioreactors. However, the quantification and control of this step as influenced by solution conditions and biocarrier properties have been rarely explored. In this paper, deposition behaviors of soluble pollutants on the model biocarriers polystyrene (PS) and polyamide (PA) were performed using a quartz crystal microbalance with dissipation monitoring (QCM-D). Three types of wastewater from municipal and industrial wastewater treatment plants and 12 synthetic wastewaters with different configurations of model macromolecules (bovine serum albumin and sodium alginate) and ionic compositions (Na(+) and Ca(2+)) were prepared. Results showed that high organic contents (protein and humic acid) in real wastewater increased deposition compared to the impact of ions on the two types of carriers. For synthetic wastewater, an interesting phenomenon was observed in that the presence of Ca(2+) can transform a thin and rigid adlayer into a denser and viscoelastic one on the surface of PS with low organic contents, yet a viscoelastic adlayer can directly form on PS and an increase in the ionic strength hinders deposition in the presence of high organic contents. The deposition of solutes on PA produces a thicker and viscoelastic adlayer that is strengthened an elevated concentration of organic materials. Additionally, a weakening effect of Ca(2+) on deposition was revealed under high ionic strength. This is the first demonstration of control strategies for preconditioning hydrophilic and hydrophobic biocarriers under different water quality conditions and has important implications for the design of a start-up process for biofilm formation in attached-growth bioreactors. PMID:25785553

Huang, Hui; Ding, Li-Li; Ren, Hong-Qiang; Geng, Jin-Ju; Xu, Ke; Zhang, Yan

2015-04-01

353

Cardiac preconditioning with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3  

PubMed Central

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 preconditioning. 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 preconditioning 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

Kelly-Laubscher, Roisin F; King, Jonathan C; Hacking, Damian; Somers, Sarin; Hastie, Samantha; Stewart, Tessa; Imamdin, Aqeela; Maarman, Gerald; Pedretti, Sarah; Lecour, Sandrine

2014-01-01

354

Threshold level of NF-kB activation in small bowel ischemic preconditioning procedure.  

PubMed

Ischemic preconditioning (IPC), which is obtained by exposure to brief periods of vascular occlusion, improves organ tolerance to prolonged ischemia. The aim of this study was to evaluate the threshold level of NF-kB activation in small intestine during an IPC procedure. Various intestinal IPC were performed on 20 Wistar rats in seven groups: group I (GI, nonpreconditioned); group II (GII, 1-minute ischemia and 1-minute reperfusion); group III (GIII, two cycles of 1-minute ischemia and 1-minute reperfusion); group IV (GIV, 2-minutes ischemia and 2-minutes reperfusion); group V (GV, two cycles of 2-minute ischemia and 2-minute reperfusion); group VI (GVI, 5-minute ischemia and 10-minute reperfusion); group VII (GVII, two cycles of 5-minute ischemia and 10-minute reperfusion). Bowel biopsies were collected after laparotomy (control) as well as at 30, 60, and 120 minutes following IPC. We determined the cytoplasmic and nuclear NF-kB by a chemiluminescence-based ELISA method. Our results showed low, constant NF-kB levels in GI. In the preconditioned groups (GII-GVII), NF-kB was significantly elevated at 30 minutes following IPC (P < .05 vs control). After 1 hour, NF-kB activity decreased to the control level. However, 2 hours after IPC both forms of NF-kB were elevated significantly again, which was independent of the number of IPC cycles (P < .05 vs control). Our experiments revealed that one cycle of 1-minute ischemia and 1-minute reperfusion is a critical threshold level for NF-kB activation during small bowel IPC. Longer and more IPC cycles did not result in further elevation of NF-kB activation. PMID:16908285

Ferencz, A; Rácz, B; Gasz, B; Kalmár-Nagy, K; Horváth, O P; Röth, E

2006-01-01

355

Intravenous pretreatment with emulsified isoflurane preconditioning protects kidneys against ischemia/reperfusion injury in rats  

PubMed Central

Background Emulsified isoflurane (EIso) is a novel intravenous general anesthetic, which can provide rapid anesthetic induction and recovery. EIso preconditioning 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 preconditioning against renal I/R injury in rats, which might be mediated by attenuating inflammation and increasing antioxidation ability. PMID:24739487

2014-01-01

356

Tumor cell hyperresistance to photodynamic killing arising from nitric oxide preconditioning  

NASA Astrophysics Data System (ADS)

Relatively little is known about how nitric oxide (NO) generated by tumor vascular cells or tumor cells themselves might affect the outcome of photodynamic therapy (PDT). Using a breast tumor epithelial line (COH-BR1) metabolically sensitized with protoporphyrin IX (PpIX) by pre-treating with 5-aminolevulinic acid (ALA), we have recently shown that NO from chemical donors can elicit both an immediate (NO-now) and delayed (NO-then) hyperresistance to photokilling. Cell death was mainly apoptotic when PpIX was confined to mitochondria, but mainly necrotic when it was allowed to diffuse to the cell periphery. We found that NO-now operates primarily by scavenging lipid-derived free radicals, whereas NO-then "preconditions" cells by some other mechanism. In addressing this, we have used a biologically relevant NO donor/tumor target model, viz. RAW 264.7 macrophages grown on microporous membrane inserts and COH-BR1 cells grown in culture plate wells. The RAW cells were activated with lipopolysaccharide, and 15 h later (when NO output was ~ 2 ?M/h) placed over the tumor cells for 20 h, after which the latter were ALA-treated and then irradiated. Prior exposure to activated RAW macrophages reduced tumor cell photokilling by >50 %. This effect was completely lost when the RAW cells were pre-treated with the nitric oxide synthase inhibitor L-NAME, confirming that NO was involved in the hyperresistance. Results from other experiments suggest that heme oxygenase-1 and ferritin play a role in the preconditioning effect described. These studies provide new insights into how NO might modulate PDT efficacy.

Niziolek-Kierecka, Magdalena; Korytowski, Witold; Girotti, Albert W.

2007-02-01

357

Preventing Genocide  

NSDL National Science Digital Library

The United States Holocaust Museum website contains a section on genocide which offers eyewitness accounts of victims of various genocides, a timeline that details the concept and law of genocide, and information about the peoples who are at risk of becoming victims of genocide in our own time. The "World is Witness" link, located on the left hand menu, takes visitors to a map of the areas at risk, "Field Updates", and a "Gallery" of photos of "Burundi", "Chad", "Rwanda", "Sudan", "Congo" and "Other Regions". Visitors can read the caption for the photograph by clicking on it. In the "Chad" gallery, there are drawings by children at refugee camps of attacks on their villages. In the "Rwanda" area there are many photos of the memorial site of the 1994 Rwandan genocide. The mass graves of those who were killed are also pictured, as well as the graves of those few who received individual burial plots. Lastly, the website offers the ability to "View and Download the Report" of the Genocide Prevention Task Force, which is co-chaired by Madeleine Albright.

358

Low level laser irradiation precondition to create friendly milieu of infarcted myocardium and enhance early survival of transplanted bone marrow cells  

PubMed Central

Abstract We suggested that low-level laser irradiation (LLLI) precondition prior to cell transplantation might remodel the hostile milieu of infarcted myocardium and subsequently enhance early survival and therapeutic potential of implanted bone marrow mesenchymal stem cells (BMSCs). Therefore, in this study we wanted to address: (1) whether LLLI pre-treatment change the local cardiac micro-environment after myocardial infarction (MI) and (2) whether the LLLI preconditions enhance early cell survival and thus improve therapeutic angiogenesis and heart function. MI was induced by left anterior descending artery ligation in female rats. A 635 nm, 5 mW diode laser was performed with energy density of 0.96 J/cm2 for 150 sec. for the purpose of myocardial precondition. Three weeks later, qualified rats were randomly received with LLLI precondition (n= 26) or without LLLI precondition (n= 27) for LLLI precondition study. Rats that received thoracotomy without coronary ligation were served as sham group (n= 24). In the cell survival study, rats were randomly divided into 4 groups: serum-free culture media injection (n= 8), LLLI precondition and culture media injection (n= 8), 2 million male BMSCs transplantation without LLLI pre-treatment (n= 26) and 2 million male BMSCs transplantation with LLLI precondition (n= 25) group, respectively. Vascular endothelial growth factor (VEGF), glucose-regulated protein 78 (GRP78), superoxide dismutase (SOD) and malondialdehyde (MDA) in the infarcted myocardium were evaluated by Western blotting, real-time PCR and colorimetry, respectively, at 1 hr, 1 day and 1 week after laser irradiation. Cell survival was assayed with quantitative real-time PCR to identify Y chromosome gene and apoptosis was assayed with transferase-mediated dUTP end labelling staining. Capillary density, myogenic differentiation and left ventricular function were tested by immunohistochemistry and echocardiography, respectively, at 1 week. After LLLI precondition, increased VEGF and GRP78 expression, as well as the enhanced SOD activity and inhibited MDA production, was observed. Compared with BMSC transplantation and culture media injection group, although there was no difference in the improved heart function and myogenic differentiation, LLLI precondition significantly enhanced early cell survival rate by 2-fold, decreased the apoptotic percentage of implanted BMSCs in infarcted myocardium and thus increased the number of newly formed capillaries. Taken together, LLLI precondition could be a novel non-invasive approach for intraoperative cell transplantation to enhance cell early survival and therapeutic potential. PMID:19725921

Zhang, Hao; Hou, Jian-feng; Shen, Ya; Wang, Wei; Wei, Ying-jie; Hu, Shengshou

2010-01-01

359

Hyperbaric oxygen preconditioning improves myocardial function, reduces length of intensive care stay, and limits complications post coronary artery bypass graft surgery  

Microsoft Academic Search

ObjectiveThe objective of this study was to determine whether preconditioning coronary artery disease (CAD) patients with HBO2 prior to first-time elective on-pump cardiopulmonary bypass (CPB) coronary artery bypass graft surgery (CABG) leads to improved myocardial left ventricular stroke work (LVSW) post CABG. The primary end point of this study was to demonstrate that preconditioning CAD patients with HBO2 prior to

Jeysen Zivan Yogaratnam; Gerard Laden; Levant Guvendik; Mike Cowen; Alex Cale; Steve Griffin

2010-01-01

360

A Quasi-Newton Preconditioned Newton–Krylov Method for Robust and Efficient Time-Domain Simulation of Integrated Circuits With Strong Parasitic Couplings  

Microsoft Academic Search

In this paper, the Newton-Krylov method is explored for robust and efficient time-domain simulation of integrated circuits with large amount of parasitic elements. Different from LU-factorization-based direct methods used in SPICE-like circuit simulators, the Newton-Krylov method uses a preconditioned Krylov-subspace iterative method for solving linearized-circuit equations. A key contribution of this paper is to introduce an effective quasi-Newton preconditioning scheme

Zhao Li; C.-J. Richard Shi

2006-01-01

361

Single Intracoronary Injection of Encapsulated Antagomir?92a Promotes Angiogenesis and Prevents Adverse Infarct Remodeling  

PubMed Central

Background Small and large preclinical animal models have shown that antagomir?92a?based therapy reduces early postischemic loss of function, but its effect on postinfarction remodeling is not known. In addition, the reported remote miR?92a inhibition in noncardiac organs prevents 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 prevent 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 prevented 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 prevents 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

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

2014-01-01

362

Mitochondrial respiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-D-aspartate.  

PubMed

Traumatic brain injury (TBI) induces glutamatergic excitotoxicity through N-methyl-D-aspartate (NMDA) receptors, affecting the integrity of the mitochondrial membrane. Studies have pointed to mitochondria as the master organelle in the preconditioning-triggered endogenous neuroprotective response. The present study is aimed at understanding energy metabolism in the brains of mice after preconditioning with NMDA and TBI. For this purpose, male albino CF-1 mice were pre-treated with NMDA (75 mg/kg) and subjected to brain trauma. Mitochondrial respiratory chain and creatine kinase activities were assessed at 6 or 24 h after trauma. The mice preconditioned and subjected to TBI exhibited augmented activities of complexes II and IV in the cerebral cortex and/or cerebellum. Creatine kinase activity was also augmented in the cerebral cortex after 24 h. We suggest that even though NMDA preconditioning and TBI have similar effects on enzyme activities, each manage their response via opposite mechanisms because the protective effects of preconditioning are unambiguous. In conclusion, NMDA preconditioning induces protection via an increase of enzymes in the mitochondria. PMID:24013757

Boeck, Carina R; Carbonera, Leatrice S; Milioli, Mônia E; Constantino, Leandra C; Garcez, Michelle L; Rezin, Gislaine T; Scaini, Giselli; Streck, Emilio L

2013-12-01

363

Expression profiling the microRNA response to epileptic preconditioning identifies miR184 as a modulator of seizure-induced neuronal death  

PubMed Central

Brief seizures (epileptic/seizure preconditioning) are capable of activating endogenous protective pathways in the brain which can temporarily generate a damage-refractory state against subsequent and otherwise harmful episodes of prolonged seizures (tolerance). Altered expression of microRNAs, a class of non-coding RNAs that function post-transcriptionally to regulate mRNA translation has recently been implicated in the molecular mechanism of epileptic tolerance. Here we characterized the effect of seizure preconditioning induced by low-dose systemic kainic acid on microRNA expression in the hippocampus of mice. Seizure preconditioning resulted in up-regulation of 25 mature microRNAs in the CA3 subfield of the mouse hippocampus, with the highest levels detected for miR-184. This finding was supported by real-time PCR and in situ hybridization showing increased neuronal miR-184 levels and a reduction in protein levels of a miR-184 target. Inhibiting miR-184 expression in vivo resulted in the emergence of neuronal death after preconditioning seizures and increased seizure-induced neuronal death following status epilepticus in previously preconditioned animals, without altered electrographic seizure durations. The present study suggests miRNA up-regulation after preconditioning may contribute to development of epileptic tolerance and identifies miR-184 as a novel contributor to neuronal survival following both mild and severe seizures. PMID:22771761

McKiernan, Ross C.; Jimenez-Mateos, Eva M.; Sano, Takanori; Bray, Isabella; Stallings, Raymond L.; Simon, Roger P.; Henshall, David C.

2012-01-01

364

Importance of the variability of hydrographic preconditioning for deep convection in the Gulf of Lion, NW Mediterranean  

NASA Astrophysics Data System (ADS)

We study the variability of hydrographic preconditioning defined as the heat and salt contents in the Ligurian Sea before convection. The stratification is found to reach a maximum in the intermediate layer in December, whose causes and consequences for the interannual variability of convection are investigated. Further study of the interannual variability and correlation tests between the properties of the deep water formed and the winter surface fluxes support the description of convection as a process that transfers the heat and salt contents from the top and intermediate layers to the deep layer. A proxy for the rate of transfer is given by the final convective mixed layer depth, that is shown to depend equally on the surface fluxes and on the preconditioning. In particular, it is found that deep convection in winter 2004-2005 would have happened even with normal winter conditions, due to low pre-winter stratification.

Grignon, L.; Smeed, D. A.; Bryden, H. L.; Schroeder, K.

2010-06-01

365

Short-term interaction between nitrate and ammonium uptake in Thalassiosira pseudonana : Effect of preconditioning nitrogen source and growth rate  

Microsoft Academic Search

The effect of preconditioning nitrogen source and growth rate on the interaction between nitrate and ammonium uptake was determined inThalassiosira pseudonana (Clone 3H). A new method, using cells on a filter (Parslow et al. 1985), allowed continuous measurement of uptake from 0.5 to 9 min after the addition of nitrate, ammonium, or both, with no variation in concentration during the

Q. Dortch; P. A. Thompson; P. J. Harrison

1991-01-01

366

Molecular Imaging-Assisted Optimization of Hsp70 Expression during Laser-Induced Thermal Preconditioning for Wound Repair Enhancement  

Microsoft Academic Search

Patients at risk for impaired healing may benefit from prophylactic measures aimed at improving wound repair. Several photonic devices claim to enhance repair by thermal and photochemical mechanisms. We hypothesized that laser-induced thermal preconditioning would enhance surgical wound healing that was correlated with hsp70 expression. Using a pulsed diode laser (?=1.85 ?m, ?p=2 ms, 50 Hz, H=7.64 mJ cm?2), the

Gerald J Wilmink; Susan R Opalenik; Joshua T Beckham; Alexander A Abraham; Lillian B Nanney; Anita Mahadevan-Jansen; Jeffrey M Davidson; E Duco Jansen

2009-01-01

367

Chemical composition and physical quality characteristics of Ghanaian cocoa beans as affected by pulp pre-conditioning and fermentation  

Microsoft Academic Search

Investigations were conducted to evaluate the effects of pod storage (as a means of pulp preconditioning) and fermentation\\u000a on the chemical composition and physical characteristics of Ghanaian cocoa beans. A 4?×?2 full factorial design with factors\\u000a as pod storage (0, 7, 14, 21 days) and cocoa treatment (fermented and unfermented) were conducted. Samples were analyzed for\\u000a their chemical composition (moisture, crude

Emmanuel Ohene Afoakwa; Jennifer Quao; Jemmy Takrama; Agnes Simpson Budu; Firibu Kwesi Saalia

368

Chemical preconditioning with 3-nitropropionic acid: Lack of induction of neuronal tolerance in gerbil hippocampus subjected to transient forebrain ischemia  

Microsoft Academic Search

Chemical preconditioning using the mitochondrial toxin, 3-nitropropionic acid (3-NP) has been reported to induce neuroprotection against subsequent global ischemia. To investigate the underlying mechanisms, Mongolian gerbils were pretreated with either vehicle or 3-NP at the dose of 3 or 10mg\\/kg, intraperitoneal, 3 days prior to a 5-min bilateral carotid artery occlusion followed by either 48h or 7 days of blood

P Garnier; N Bertrand; C Demougeot; A Prigent-Tessier; C Marie; A Beley

2002-01-01

369

Preconditioning effect of (S)-3,5-dihydroxyphenylglycine on ischemic injury in middle cerebral artery occluded Sprague-Dawley rats.  

PubMed

Glutamate receptors are the integral cellular components associated with excitotoxicity mechanism induced by the ischemic cascade events. Therefore the glutamate receptors have become the major molecular targets of neuroprotective agents in stroke researches. Recent studies have demonstrated that a Group I metabotropic glutamate receptor agonist, (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG) preconditioning elicits neuroprotection in the hippocampal slice cultures exposed to toxic level of N-methyl-d-aspartate (NMDA). We further investigated the preconditioning effects of (S)-3,5-DHPG on acute ischemic stroke rats. One 10 or 100?M of (S)-3,5-DHPG was administered intrathecally to Sprague-Dawley adult male rats, 2h prior to induction of acute ischemic stroke by middle cerebral artery occlusion (MCAO). After 24h, neurological deficits were evaluated by modified stroke severity scores and grid-walking test. All rats were sacrificed and infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride staining. The serum level of neuron-specific enolase (NSE) of each rat was analyzed by enzyme-linked immunosorbent assay (ELISA). One and 10?M of (S)-3,5-DHPG preconditioning in the stroke rats showed significant improvements in motor impairment (P<0.01), reduction in the infarct volume (P<0.01) and reduction in the NSE serum level (P<0.01) compared to the control stroke rats. We conclude that 1 and 10?M (S)-3,5-DHPG preconditioning induced protective effects against acute ischemic insult in vivo. PMID:25562631

Nik Ramli, Nik Nasihah; Omar, Nursyazwani; Husin, Andrean; Ismail, Zalina; Siran, Rosfaiizah

2015-02-19

370

An efficient parallel\\/unstructured-multigrid preconditioned implicit method for simulating 3D unsteady compressible flows with moving objects  

Microsoft Academic Search

This paper presents the development and validation of a new parallel unstructured multi-grid preconditioned implicit method for the simulation of three-dimensional (3D) unsteady compressible flows using a so-called immersed membrane method (IMM) [G.H. Xia, Y. Zhao, J.H. Yeo, An immersed membrane method for simulation of fluid–structure interaction in bio-fluid flows, in: 1st International BioEngineering Conference (IBEC 2004), 08–10 September 2004].

X. Lv; Yong Zhao; X. Y. Huang; G. H. Xia; Z. J. Wang

2006-01-01

371

An efficient parallel\\/unstructured-multigrid preconditioned implicit method for simulating 3D unsteady compressible flows with moving objects  

Microsoft Academic Search

This paper presents the development and validation of a new parallel unstructured multi-grid preconditioned implicit method for the simulation of three-dimensional (3D) unsteady compressible flows using a so-called immersed membrane method (IMM) [G.H. Xia, Y. Zhao, J.H. Yeo, An immersed membrane method for simulation of fluid structure interaction in bio-fluid flows, in: 1st International BioEngineering Conference (IBEC 2004), 08 10

X. Lv; Y. Zhao; X. Y. Huang; G. H. Xia; Z. J. Wang

2006-01-01

372

Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury.  

PubMed

Hyperbaric oxygen (HBO) therapy is an effective therapy for ischemia/reperfusion (I/R) injury of the brain, small intestine, testes and liver. However, the detailed molecular mechanisms underlying the effect of HBO therapy remain undetermined. In the current study, the hypothesis that preconditioning rats with HBO protects grafted skin flaps against subsequent I/R injury was investigated. In addition, the molecular mechanisms underlying HBO therapy were characterized by analyzing the roles of the following important inflammatory factors: High mobility group protein 1 (HMGB1) and nuclear factor-? B (NF-?B). A total of 40 rats were randomly divided into the following five groups: (i) Sham surgery (SH); (ii) ischemia followed by reperfusion 3 days following surgery (I/R3d); (iii) ischemia followed by reperfusion 5 days following surgery (I/R5d); (iv) HBO preconditioning (HBO-PC) and ischemia followed by reperfusion 3 days following surgery (HBO-PC+3d); and (v) HBO-PC and ischemia followed by reperfusion 5 days following surgery (HBO-PC+5d). For the surgical procedure, all pedicled skin flaps were first measured and elevated (9x6 cm). The feeding vessels of the skin flaps were subsequently clamped for 3 h and released to restore blood flow. The rats in the HBO-PC+3d and HBO-PC+5d groups received 1 h HBO for 3 and 5 consecutive days, respectively, prior to surgery. Following surgery, the rats were euthanized, and grafted tissues were collected for western blotting and immunohistochemistry. HBO-PC increased blood perfusion in epigastric skin flaps and attenuated I/R injury following skin flap graft. Additionally, the elevated expression of HMGB1 and NF-?B proteins during I/R injury was attenuated by HBO-PC treatment. HBO-PC may therefore be applied to reduce I/R injury and improve the survival rate of grafted skin flaps. The molecular mechanisms underlying the effect of HBO therapy are associated with the attenuation of inflammatory responses. PMID:24676940

Kang, Nan; Hai, Yong; Liang, Fang; Gao, Chun-Jin; Liu, Xue-Hua

2014-06-01

373

Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury  

PubMed Central

Hyperbaric oxygen (HBO) therapy is an effective therapy for ischemia/reperfusion (I/R) injury of the brain, small intestine, testes and liver. However, the detailed molecular mechanisms underlying the effect of HBO therapy remain undetermined. In the current study, the hypothesis that preconditioning rats with HBO protects grafted skin flaps against subsequent I/R injury was investigated. In addition, the molecular mechanisms underlying HBO therapy were characterized by analyzing the roles of the following important inflammatory factors: High mobility group protein 1 (HMGB1) and nuclear factor-? B (NF-?B). A total of 40 rats were randomly divided into the following five groups: (i) Sham surgery (SH); (ii) ischemia followed by reperfusion 3 days following surgery (I/R3d); (iii) ischemia followed by reperfusion 5 days following surgery (I/R5d); (iv) HBO preconditioning (HBO-PC) and ischemia followed by reperfusion 3 days following surgery (HBO-PC+3d); and (v) HBO-PC and ischemia followed by reperfusion 5 days following surgery (HBO-PC+5d). For the surgical procedure, all pedicled skin flaps were first measured and elevated (9×6 cm). The feeding vessels of the skin flaps were subsequently clamped for 3 h and released to restore blood flow. The rats in the HBO-PC+3d and HBO-PC+5d groups received 1 h HBO for 3 and 5 consecutive days, respectively, prior to surgery. Following surgery, the rats were euthanized, and grafted tissues were collected for western blotting and immunohistochemistry. HBO-PC increased blood perfusion in epigastric skin flaps and attenuated I/R injury following skin flap graft. Additionally, the elevated expression of HMGB1 and NF-?B proteins during I/R injury was attenuated by HBO-PC treatment. HBO-PC may therefore be applied to reduce I/R injury and improve the survival rate of grafted skin flaps. The molecular mechanisms underlying the effect of HBO therapy are associated with the attenuation of inflammatory responses. PMID:24676940

KANG, NAN; HAI, YONG; LIANG, FANG; GAO, CHUN-JIN; LIU, XUE-HUA

2014-01-01

374

Aldehyde dehydrogenase-2 inhibition blocks remote preconditioning in experimental and human models.  

PubMed

Mitochondrial aldehyde dehydrogenase-2 (ALDH-2) is involved in preconditioning pathways, but its role in remote ischaemic preconditioning (rIPC) is unknown. We investigated its role in animal and human models of rIPC. (i) In a rabbit model of myocardial infarction, rIPC alone reduced infarct size [69 ± 5.8 % (n = 11) to 40 ± 6.5 % (n = 12), P = 0.019]. However, rIPC protection was lost after pre-treatment with the ALDH-2 inhibitor cyanamide (62 ± 7.6 % controls, n = 10, versus 61 ± 6.9 % rIPC after cyanamide, n = 10, P > 0.05). (ii) In a forearm plethysmography model of endothelial ischaemia-reperfusion injury, 24 individuals of Asian ethnic origin underwent combined rIPC and ischaemia-reperfusion (IR). 11 had wild-type (WT) enzyme and 13 carried the Glu504Lys (ALDH2*2) polymorphism (rendering ALDH-2 functionally inactive). In WT individuals, rIPC protected against impairment of response to acetylcholine (P = 0.9), but rIPC failed to protect carriers of Glu504Lys polymorphism (P = 0.004). (iii) In a second model of endothelial IR injury, 12 individuals participated in a double-blind placebo-controlled crossover study, receiving the ALDH-2 inhibitor disulfiram 600 mg od or placebo for 48 h prior to assessment of flow-mediated dilation (FMD) before and after combined rIPC and IR. With placebo, rIPC was effective with no difference in FMD before and after IR (6.18 ± 1.03 % and 4.76 ± 0.93 % P = 0.1), but disulfiram inhibited rIPC with a reduction in FMD after IR (7.87 ± 1.27 % and 3.05 ± 0.53 %, P = 0.001). This study demonstrates that ALDH-2 is involved in the rIPC pathway in three distinct rabbit and human models. This has potential implications for future clinical studies of remote conditioning. PMID:23525499

Contractor, Hussain; Støttrup, Nicolaj B; Cunnington, Colin; Manlhiot, Cedric; Diesch, Jonathan; Ormerod, Julian O M; Jensen, Rebekka; Bøtker, Hans Erik; Redington, Andrew; Schmidt, Michael R; Ashrafian, Houman; Kharbanda, Rajesh K

2013-05-01

375

Nonlinear preconditioning for efficient and accurate interface capturing in simulation of multicomponent compressible flows  

NASA Astrophysics Data System (ADS)

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 preconditioned 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 preconditioned 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.

Shukla, Ratnesh K.

2014-11-01

376

p-ERK involvement in the neuroprotection exerted by ischemic preconditioning in rat hippocampus subjected to four vessel occlusion.  

PubMed

Global brain ischemia-reperfusion causes delayed cell death in hippocampal CA1 (cornus ammonis 1) pyramidal neurons after reperfusion. Ischemic tolerance evoked by preconditioning (IPC) represents a phenomenon of CNS adaptation to any subsequent ischemia. This paper was designed to describe changes in the mitogen-activated protein kinases (MAPK) protein pathways of the hippocampal area following by IPC. Ischemia was induced by a 4-vessels occlusion (4VO) and the rats were preconditioned by a non-injurious ischemia. Apoptotic markers were used to follow the degeneration process. Western blot and immunohistochemistry identified p-ERK (phosphorylated extracellular signal-regulated protein kinase) and p38 proteins in injured hippocampal areas. P-ERK quantification increased after IPC and reached the highest level at 24 hours after ischemia. Interestingly, neuroprotection induced by IPC lead to the opposite effect on MAPK/p38, where the level was lowest at 24 hours after ischemia. Taken together, the present study clearly demonstrates that p-ERK takes part in complex cascades triggered by IPC in the selectively vulnerable hippocampal region. In addition, paper describes a crosstalk between p-ERK and p-p38 which occurs after preconditioning maneuver in 4VO model of global ischemia. PMID:25554980

Kovalska, M; Kovalska, L; Mikuskova, K; Adamkov, M; Tatarkova, Z; Lehotsky, J

2014-12-01

377

Role of calcitonin gene-related peptide and kinins in post-ischemic intestinal reperfusion 1 1 Abbreviations: BK, bradykinin; CGRP, calcitonin gene-related peptide; CGRP 8–37, CGRP 1 receptor antagonist; EB, Evans blue; L-NAME, N-nitro-L-arginine-methyl ester; MBF, mesenteric blood flow; MBP, mean blood pressure; MVR, mesenteric vascular resistance; NKA, neurokinin A; NO, nitric oxide; SP, substance P; SR 140333, tachykinin NK 1 receptor antagonist; SR 141716A, anandamide CB 1 receptor antagonist  

Microsoft Academic Search

The involvement of kinins, calcitonin gene-related peptide (CGRP), and tachykinins during mesenteric post-ischemic reperfusion was studied in anesthetized rats by using antagonists for bradykinin (BK) B1, BK B2, CGRP1, or tachykinin NK1 receptor, or by capsaicin-induced desensitization. B1, B2, or CGRP1 receptor antagonists or desensitization attenuated the transient hypotension and plasma protein and leukocyte infiltration of intestinal wall observed during

Paolo Madeddu; Costanza Emanueli; Maria Bonaria Salis; Anna Franca Milia; Tiziana Stacca; Luisa Carta; Alessandra Pinna; Maria Deiana; Leonardo Gaspa

2001-01-01

378

Extended Ischemia Prevents HIF1? Degradation at Reoxygenation by Impairing Prolyl-hydroxylation  

PubMed Central

Hypoxia-inducible factor (HIF) is a heterodimeric transcription factor that activates the cellular response to hypoxia. The HIF1? subunit is constantly synthesized and degraded under normoxia, but degradation is rapidly inhibited when oxygen levels drop. Oxygen-dependent hydroxylation by prolyl-4-hydroxylases (PHD) mediates HIF1? proteasome degradation. Brain ischemia limits the availability not only of oxygen but also of glucose. We hypothesized that this circumstance could have a modulating effect on HIF. We assessed the separate involvement of oxygen and glucose in HIF1? regulation in differentiated neuroblastoma cells subjected to ischemia. We report higher transcriptional activity and HIF1? expression under oxygen deprivation in the presence of glucose (OD), than in its absence (oxygen and glucose deprivation, OGD). Unexpectedly, HIF1? was not degraded at reoxygenation after an episode of OGD. This was not due to impairment of proteasome function, but was associated with lower HIF1? hydroxylation. Krebs cycle metabolites fumarate and succinate are known inhibitors of PHD, while ?-ketoglutarate is a co-substrate of the reaction. Lack of HIF1? degradation in the presence of oxygen was accompanied by a very low ?-ketoglutarate/fumarate ratio. Furthermore, treatment with a fumarate analogue prevented HIF1? degradation under normoxia. In all, our data suggest that postischemic metabolic alterations in Krebs cycle metabolites impair HIF1? degradation in the presence of oxygen by decreasing its hydroxylation, and highlight the involvement of metabolic pathways in HIF1? regulation besides the well known effects of oxygen. PMID:20368331

Serra-Pérez, Anna; Planas, Anna M.; Núñez-O'Mara, Analía; Berra, Edurne; García-Villoria, Judit; Ribes, Antònia; Santalucía, Tomàs

2010-01-01

379

[Prevention of reperfusion-induced arrhythmia by Na+/H+ exchange block].  

PubMed

Using the isolated papillary muscle and rat hearts, perfused by Langendorf, the effects of the Na+/H+ exchange blocker, ethylisopropylamiloride (EIPA), on electrical activity and contractility, and induction of ischemic and reperfusion arrhythmias were studied. In the experiments with regional ischemia and reperfusion of an isolated heart (the ligation of the left anterior descending coronary artery for 10 minutes), EIPA (5 microM) effectively abolished reperfusion fibrillations, reducing the incidence of the long fibrillations from 60% (in the controls) to 8%, and increased nearly five-fold the time interval prior to their onset. Antiarrhythmic action of EIPA seems to be unconnected with the direct block of ionic channels, because 5 microM of this compound did not significantly change the action potential parameters, first derivative Vmax and the contractile response of the papillary muscle in normal conditions. The results obtained show a significant role of the postischemic activation of the Na+/H+ exchange in the initiation of reperfusion-induced arrhythmias and possible use of amiloride derivatives for their prevention. PMID:2542686

Vasilets, L A; Mokh, V P; Khodorov, B I

1989-02-01

380

Hyperbaric oxygen preconditioning protects cortical neurons against oxygen-glucose deprivation injury: role of peroxisome proliferator-activated receptor-gamma.  

PubMed

Ischemic stroke is one of the leading causes of mortality and disability worldwide. Our previous studies have shown that hyperbaric oxygen (HBO) preconditioning can afford significant neuroprotection against cerebral ischemia-reperfusion (I/R) injury in rats. However, it is still unknown whether HBO preconditioning can directly protect primary cultured cortical neurons against oxygen-glucose deprivation (OGD). Peroxisome proliferator-activated receptor-gamma (PPAR ?) plays a central role in the regulation of apoptosis, oxidative stress and inflammation as well as affords significant neuroprotection against cerebral I/R injury. 15-deoxy-?(12,14)-prostaglandin J(2) (15d-PGJ(2)) is an endogenous ligand with a high affinity for PPAR ?. Recently, some studies demonstrate that activation of PPAR ? mediates lipopolysaccharide and anesthetic preconditioning. In the present study, we firstly found that OGD exposure caused the significant damage of cultured cortical neurons evaluated by cell viability, lactate dehydrogenase (LDH) release and caspase-3 activity, which were significantly ameliorated by HBO preconditioning. Furthermore, HBO preconditioning significantly increased the levels of PPAR ? mRNA and protein, PPAR ? DNA binding activity, 15d-PGJ(2) and antioxidant enzymatic activities in primary cultured cortical neurons with OGD exposure. Moreover, PPAR ? antagonist GW9662 dose-dependently abolished the protection of HBO preconditioning in OGD-exposed neurons. GW9662 blocked the increase of PPAR ? DNA binding activity and antioxidant enzymatic activities, but did not influence the 15d-PGJ(2) level in OGD-exposed neurons with HBO preconditioning. However, the cyclooxygenase (COX)-2 inhibitor NS-398 blocked the production of 15d-PGJ(2) in OGD-exposed neurons with HBO preconditioning. In addition, 15d-PGJ(2) preconditioning could also protect cultured neurons against OGD injury. These results demonstrate that HBO preconditioning has directly beneficial effects on ODG-exposed cortical neurons by the activation of PPAR ? subsequent to the production of 15d-PGJ(2), which in turn increases the downstream antioxidant enzymatic activities. PMID:22444276

Zeng, Yi; Xie, Keliang; Dong, Hailong; Zhang, Haopeng; Wang, Feng; Li, Yan; Xiong, Lize

2012-05-01

381

Comparison of the responses to hypoxia, ischaemia and ischaemic preconditioning in wild marmot and laboratory rabbit hearts.  

PubMed

Marmots (Marmota flaviventris) are burrowing mammals that may be subjected to low levels of oxygen and high levels of carbon dioxide in their underground environment. Since marmots successfully deal with this physiological challenge, we hypothesized that the isolated perfused marmot heart would be damaged less and recover better from a bout of induced hypoxia or ischaemia than would the heart of a comparison animal, the New Zealand laboratory rabbit (Oryctolagus cuniculus). Isolated marmot and rabbit hearts were made hypoxic by a 30 min perfusion with an oxygen-deficient buffer. The hearts were then perfused with an oxygen-replete buffer and measurements of heart rate, left ventricular pressure and lactate dehydrogenase (LDH) release (an indicator of cell damage) were made over 5 or 10 min intervals for 30 min of hypoxia and 30 min of recovery. There were no species differences in the responses, except that the heart rate in marmots was about 50% of the rate in rabbits during the hypoxia part of the experiment. There was no evidence that the marmot hearts were damaged less or recovered better from hypoxia and reoxgenation than the rabbit hearts. Marmot and rabbit hearts were also subjected to 30 min of total ischaemia; measurements of heart rate, left ventricular pressure and LDH release were obtained during 30 min of reperfusion and compared with the pre-ischaemia values for these variables. There were no significant species differences. When the 30 min ischaemic period was preceded by a 5 min period of ischaemia and a 10 min reperfusion period (preconditioning), the rabbit hearts were protected by this brief ischaemic insult and recovered better than the hearts that had not been subjected to the preconditioning ischaemia. This was not true in the marmot hearts, however, as the preconditioning ischaemia did not promote a greater recovery over that in its absence. When preconditioned marmots hearts were compared with preconditioned rabbit hearts, there were no statistical differences in the responses. The hypothesis that marmot hearts would be damaged less and recover better from hypoxia and ischaemia was not supported by the experimental data. PMID:8867278

McKean, T; Mendenhall, W

1996-03-01

382

Electrophilic surface sites as precondition for the chemisorption of pyrrole on GaAs(001) surfaces  

NASA Astrophysics Data System (ADS)

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 precondition for the chemisorption of pyrrole on GaAs(001) surfaces.

Bruhn, Thomas; Fimland, Bjørn-Ove; Vogt, Patrick

2015-03-01

383

The protective effect of ozone oxidative preconditioning against hypoxia/reoxygenation injury in rat kidney cells.  

PubMed

Abstract Ozone (O3) has been viewed as a novel treatment for different diseases in these years and oxidative stress and apoptosis play a key role in the pathogenesis of kidney diseases including renal ischemia and reperfusion (I/R). In the present study, we investigated the role of ozone oxidative preconditioning (OzoneOP) in attenuating oxidative stress and apoptosis in a hypoxia/reoxygenation (H/R) injury model using rat kidney cells. We induced H/R injury in kidney cells treated with or without OzoneOP. Oxidative stress parameters such as superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH) were determined, as well as some apoptotic proteins. We observed that oxidative stress and apoptosis were increased in H/R group compared to OzoneOP group; however, these changes were significantly decreased by the treatment with OzoneOP. We concluded that OzoneOP can protect the kidney cells against H/R injury and its mechanism may be through the reduction of oxidative stress and apoptosis. PMID:25246346

Wang, Lei; Chen, Hui; Liu, Xiu-Heng; Chen, Zhi-Yuan; Weng, Xiao-Dong; Qiu, Tao; Liu, Lin

2014-10-01

384

T2CG1, a package of preconditioned conjugate gradient solvers for TOUGH2  

SciTech Connect

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 preconditioned 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.

Moridis, G.; Pruess, K.; Antunez, E. [Lawrence Berkeley Lab., CA (United States). Earth Sciences Div.

1994-03-01

385

Preconditioned domain decomposition scheme for three-dimensional aerodynamic sensitivity analysis  

NASA Technical Reports Server (NTRS)

A discrete sensitivity analysis algorithm had previously been developed and applied to two-dimensional aerodynamic optimization problems, where the computational domains were discretized by using single grids. The sparse, unsymmetric systems of linear equations resulting from this algorithm were solved by a direct matrix inversion matrix. However, for large two-dimensional problems and, practically, all three-dimensional problems, direct inversion methods become inapplicable, primarily due to the prohibitive computer storage needed. In an attempt to alleviate such hindrances, the sensitivity analysis with domain decomposition (SADD) scheme was developed. This scheme divides the computational domain into smaller and nonoverlapping subdomains (multiblock grids) that are solved separately. Then, the final solution is constructed from the subdomain solutions. As the number of grid points in the interface boundaries of the subdomains becomes large, the computer memory required to store the effective coefficient matrix of these interface points starts to increase. Presented in this Technical Note is a preconditioned iterative procedure to overcome this particular problem.

Eleshaky, Mohamed E.; Baysal, Oktay

1994-01-01

386

Hyperbaric oxygen preconditioning attenuates hemorrhagic transformation through increasing PPAR? in hyperglycemic MCAO rats.  

PubMed

Hyperbaric oxygen preconditioning (HBO-PC) has been demonstrated to attenuate hemorrhagic transformation (HT) after middle cerebral artery occlusion (MCAO) in hyperglycemic rats. However, the mechanisms remain to be illustrated. Recently, HBO-PC has been shown to activate peroxisome proliferator-activated receptor-gamma (PPAR?) by increasing 15d-PGJ2 in primary cultured neurons. We hypothesize that HBO-PC reduces HT by suppressing inflammation through increasing 15d-PGJ2 and activating PPAR? in hyperglycemic MCAO rats. HBO (2.5ATA) was administered for 1h daily for 5 consecutive days. The PPAR? inhibitor GW9662 was administered intraperitoneally to designated animals. Infarction volume, hemorrhage volume, neurological scores and mortality were analyzed. The levels of 15d-PGJ2, PPAR?, TNF-? and IL-1?, tight junction proteins as well as the activity of MMP-2 and MMP-9 were evaluated 24h after MCAO. HBO-PC reduced HT, improved neurological function, down-regulated inflammatory molecules and inhibited the activation of MMP-9 by increasing 15d-PGJ2 and PPAR? at 24h after MCAO. The results suggested that HBO-PC might be an alternative measure to decrease HT in ischemic stroke. PMID:25542160

Bian, Hetao; Hu, Qin; Liang, Xiping; Chen, Di; Li, Bo; Tang, Jiping; Zhang, John H

2015-03-01

387

A genetically engineered, nonthrombogenic cellular lining for LVADs: in vitro preconditioning before in vivo implantation.  

PubMed

Because of the clinical success of left ventricular assist devices (LVADs) used for short-term "bridge to transplant" and the limited availability of donor organs, heart assist devices are being considered for long-term implantation as an alternative to heart transplantation. In an effort to improve biocompatibility, our laboratory has developed a nonthrombogenic cellular lining from genetically engineered smooth muscle cells (GE-SMC) for the Thermocardiosystems Heartmate LVAD. Smooth muscle cells have been transduced with the gene for endothelial nitric oxide synthase (NOS III) and produce NO at concentrations that reduce platelet deposition and smooth muscle cell proliferation when tested in vitro. In this investigation, the adhesive capabilities of GE-SMC linings were examined. An in vitro circulatory loop was designed to expose cell lined LVADs to in vivo operating conditions. Cumulative cell loss from cell lined LVADs was less than 10% after 24 hours of flow. Using a protocol for "preconditioning" the cell lining within the mock circulatory loop, the first implantation of an LVAD containing a genetically engineered SMC lining was successfully implemented in a bovine model. Results from this 24 hour study indicate that the flow-conditioned cellular lining remained intact with no evidence of thromboembolization and only minimal changes in coagulation studies. PMID:10360718

Tock, C L; Bosley, J P; Parnis, S M; Clubb, F J; Macris, M P; Frazier, O H; Scott-Burden, T

1999-01-01

388

Cardiac effect of ischemic preconditioning and heparin following intestinal ischemia and reperfusion in rats.  

PubMed

To study the role of heparin and ischemic preconditioning (IPC) in cardiac injury after intestinal ischemia (I) and reperfusion (R), 54 rats underwent 60 minutes of I, which was produced by occlusion of the superior mesenteric artery, and/or 120 minutes of R. The IPC group had the I procedure stimulation for 5 minutes and R for 10 minutes. The control group was subjected to sham surgery only, and the other groups were injected with saline solution (SS; 0.1 mL) or heparin (100 IU/kg) via the inferior cava vein 5 minutes before I and 5 minutes before R and 55 minutes after the R begins in I-R groups. In all animals, cardiac samples were stained with hematoxylin and eosin for optical microscopy analysis, and other sample was processed for lipid peroxidation determination. In I-R groups, both heparin and IPC showed significant protection compared to the SS group; conversely, in animals subjected only to I, no protection was observed. Moreover, when heparin was associated with IPC, I-R protection was compromised and the ischemic injury increased. Data showed that IPC and heparin attenuated cardiac dysfunction caused by intestinal I and I-R, but when used in association did not show beneficial effects. PMID:25131053

Saurim, R; Koike, M K; Bonservizi, W G S; Felix, G A A; Silva, S M; Taha, M O; Montero, E F S

2014-01-01

389

Using hormetic strategies to improve ischemic preconditioning and postconditioning against stroke.  

PubMed

Both ischemic preconditioning (IPreC) and ischemic postconditioning (IPostC) trigger endogenous neuroprotective mechanisms in cerebral ischemia. IPreC is defined as a brief ischemia that protects against a subsequent severe ischemia, while IPostC refers to a series of brief cerebral blood vessel occlusions performed at reperfusion following an ischemic event. Hormesis describes a biphasic dose-response relationship in toxicology, where a low dose of toxicant stimulates and a high dose inhibits biological responses. In general, any minor stress will stimulate a biological system to generate an adaptive response; in most cases, if not all, such an adaptive response to a minor stress is beneficial to the biological system. Proponents of hormesis suggest that this effect is independent of any models, either in vivo or in vitro, from animal, plant, fungi, yeast, to bacteria, by any measurement of end points, survival ratio or time, growth, tissue repair, life span, cognition, learning and memory. In this review, we examine whether IPreC and IPostC are actually sub-forms of hormesis and whether quantitative hormetic strategies can be used to study IPreC and IPostC. By integrating the concepts of IPreC and IPostC with hormesis, we aim to broaden the avenues leading to clinical translation of IPreC and IPostC in stroke treatment. PMID:23750305

Zhao, Heng; Joo, Sungpil; Xie, Weiying; Ji, Xunming

2013-01-01

390

Impact of Ischemic Preconditioning on Outcome in Clinical Liver Surgery: A Systematic Review  

PubMed Central

Background. Ischemia-reperfusion injury is a major cause of post-liver-surgery complications. Ischemic preconditioning (IPC) has been demonstrated to protect against ischemia-reperfusion injury. Clinical studies have examined IPC in liver surgery but with conflicting results. This systematic review aimed to evaluate the effects of IPC on outcome in clinical liver surgery. Methods. An electronic search of OVID Medline and Embase databases was performed to identify studies that reported outcomes in patients undergoing liver surgery subjected to IPC. Basic descriptive statistics were used to summarise data from individual clinical studies. Results. 1093 articles were identified, of which 24 met the inclusion criteria. Seven topics were selected and analysed by subgroup. There were 10 studies in cadaveric liver transplantation, 2 in living-related liver transplantation, and 12 in liver resection. IPC decreases hepatocellular damage in liver surgery as determined by transaminases but does not translate to any significant clinical benefit in orthotopic liver transplant or liver resection. Conclusions. Available clinical evidence does not support routine use of IPC in liver surgery as it does not offer any apparent benefit in perioperative outcome. Further clinical studies will need to be carried out to determine the subset of patients that will benefit from IPC. PMID:25756045

Chu, Michael J. J.; Vather, Ryash; Hickey, Anthony J. R.; Phillips, Anthony R. J.; Bartlett, Adam S. J. R.

2015-01-01

391

Delayed neuronal preconditioning by NS1619 is independent of calcium activated potassium channels  

PubMed Central

1,3-Dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)-2H-benzimidazol-2-one (NS1619), a potent activator of the large conductance Ca2+ activated potassium (BKCa) channel, has been demonstrated to induce preconditioning (PC) in the heart. The aim of our study was to test the delayed PC effect of NS1619 in rat cortical neuronal cultures against oxygen-glucose deprivation, H2O2, or glutamate excitotoxicity. We also investigated its actions on reactive oxygen species (ROS) generation, and on mitochondrial and plasma membrane potentials. Furthermore, we tested the activation of the phosphoinositide 3-kinase (PI3K) signaling pathway, and the effect of NS1619 on caspase-3/7. NS1619 dose-dependently protected the cells against the toxic insults, and the protection was completely blocked by a superoxide dismutase mimetic and a PI3K antagonist, but not by BKCa channel inhibitors. Application of NS1619 increased ROS generation, depolarized isolated mitochondria, hyperpolarized the neuronal cell membrane, and activated the PI3K signaling cascade. However, only the effect on the cell membrane potential was antagonized by BKCa channel blockers. NS1619 inhibited the activation of capase-3/7. In summary, NS1619 is a potent inducer of delayed neuronal PC. However, the neuroprotective effect seems to be independent of cell membrane and mitochondrial BKCa channels. Rather it is the consequence of ROS generation, activation of the PI3K pathway, and inhibition of caspase activation. PMID:18182041

Gáspár, Tamás; Katakam, Prasad; Snipes, James A.; Kis, Béla; Domoki, Ferenc; Bari, Ferenc; Busija, David W.

2010-01-01

392

Preconditioned implicit solvers for the Navier-Stokes equations on distributed-memory machines  

NASA Technical Reports Server (NTRS)

The GMRES method is parallelized, and combined with local preconditioning to construct an implicit parallel solver to obtain steady-state solutions for the Navier-Stokes equations of fluid flow on distributed-memory machines. The new implicit parallel solver is designed to preserve the convergence rate of the equivalent 'serial' solver. A static domain-decomposition is used to partition the computational domain amongst the available processing nodes of the parallel machine. The SPMD (Single-Program Multiple-Data) programming model is combined with message-passing tools to develop the parallel code on a 32-node Intel Hypercube and a 512-node Intel Delta machine. The implicit parallel solver is validated for internal and external flow problems, and is found to compare identically with flow solutions obtained on a Cray Y-MP/8. A peak computational speed of 2300 MFlops/sec has been achieved on 512 nodes of the Intel Delta machine,k for a problem size of 1024 K equations (256 K grid points).

Ajmani, Kumud; Liou, Meng-Sing; Dyson, Rodger W.

1994-01-01

393

A preconditioned conjugate gradient method for computing eigenvector derivatives with distinct and repeated eigenvalues  

NASA Astrophysics Data System (ADS)

A preconditioned conjugate gradient method is proposed for computing eigenvector derivatives with distinct and repeated eigenvalues in the real symmetric eigensystems. In view of singular character of the coefficient matrices of the governing equations for particular solutions of eigenvector derivatives, a modified governing equation for the complementary part of the computed modal contribution excluding those of the repeated modes is introduced, and its coefficient matrix is symmetric and positive definite. The existing factored (shifted) stiffness matrix from an iterative eigensolution such as Lanczos or Subspace Iteration is then utilized as preconditioner. High accurate approximations to particular solutions of eigenvector derivatives can be provided with a few iterations. The present method can deal with both cases of simple and repeated eigenvalues in a unified manner, and can be integrated into a coupled eigensolver/derivative software module. It is especially suitable for the large sparse matrices that arise in industrial-size finite element models. Finally, two numerical examples are used to demonstrate the superior efficiency and fast convergence of the present method.

Wu, Baisheng; Yang, Shitong; Li, Zhengguang; Zheng, Shaopeng

2015-01-01

394

Discretization and Preconditioning Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes  

NASA Technical Reports Server (NTRS)

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 preconditioned 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.

Barth, Timothy J.; Kutler, Paul (Technical Monitor)

1998-01-01

395

Discretization and Preconditioning Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes  

NASA Technical Reports Server (NTRS)

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 preconditioned 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.

Barth, Timothy; Chancellor, Marisa K. (Technical Monitor)

1997-01-01

396

Effect of ischemic preconditioning on repeated sprint ability in team sport athletes.  

PubMed

This study investigated whether ischemic preconditioning (IPC) in a trained population affected repeated sprint performance. A secondary aim was to assess responses according to gender. Sixteen (nine females and seven males) well trained team sport athletes took part in a randomised crossover study design. Participants underwent an IPC and placebo treatment involving three periods of 5 min occlusion applied unilaterally (3 × 5 min occlusion to each leg) at either 220 mmHg or 50 mmHg. Each period of occlusion was followed by 5 min reperfusion. Following treatment 5 × 6 s maximal effort sprints were undertaken on a cycle ergometer against 7.5% body mass, each interspersed by 24 s recovery. Measured parameters included peak power, total power, percentage decrement, post-exercise blood lactate and ratings of perceived exertion. Nor within subject main effect for IPC was observed, neither was there an interaction effect with gender. Effect sizes were trivial (ES < 0.2) with the exception of a moderate (ES < 1.2) change in post-exercise blood lactate in the female cohort (1.6 ± 0.4 mmol(-1) lower following IPC). Results suggest no benefit to team sport players in utilising IPC as a means of enhancing repeated sprint performance. A lower blood lactate response in female participants following IPC may suggest improved blood flow through vasodilation. PMID:25517761

Gibson, Neil; Mahony, Ben; Tracey, Claire; Fawkner, Samantha; Murray, Andrew

2015-06-01

397

Neural correlates of sensory preconditioning: a preliminary fMRI investigation.  

PubMed

Sensory preconditioning (SPC; also known as behaviorally silent learning) consists of a combination of two neutral stimuli, none of which elicits an unconditional response. After one of them is later paired with an unconditional stimulus (US), the other neutral stimulus also yields a conditional response although it has never been paired with the US. In this study, an event-related functional magnetic resonance imaging (fMRI) paradigm was used to specify brain regions involved in SPC. The results demonstrated that SPC was associated with significant changes in activity of several regions, notably, the left amygdala, the left hippocampus, the bilateral thalamus, the bilateral medial globus pallidus, the bilateral cerebellum, the bilateral premotor cortex, and the bilateral middle frontal gyrus. This is a first effort to use fMRI to examine the effects of SPC on brain activation. Our data suggest that there is a distributed network of structures involved in SPC including both cortical and subcortical regions, therefore add to our understanding of the neural mechanisms underlying the ability to associative learning. PMID:23450811

Yu, Tao; Lang, Simone; Birbaumer, Niels; Kotchoubey, Boris

2014-04-01

398

Spinal neuronal NOS activation mediates intrathecal fentanyl preconditioning induced remote cardioprotection in rats.  

PubMed

Fentanyl has been widely used in anesthesia and analgesia, especially for cardiovascular surgeries. The aim of the study was to evaluate whether remote intrathecal fentanyl preconditioning (RFPC) provides cardioprotection and the role of spinal nitric oxide synthase (NOS) system in this effect. Fentanyl (0.3?g/kg) was administered intrathecally during RFPC by 3 cycles of 5-minute infusions interspersed with 5-minute infusion free periods. A non-specific nitric oxide synthase (NOS) inhibitor NG-nitro l-arginine methyl ester (l-NAME, 30nmol) and a selective nNOS inhibitor 7-nitroindazole (7-NI, 100nmol) were administered intrathecally 10min before RFPC, and were used to evaluate the involvement of the NOS system of the spinal cord. RFPC group markedly reduced the infarct size compared with control. However, the cardioprotection of RFPC could be abolished by pretreatment with l-NAME and 7-NI. RFPC merely increased the expression of nNOS and did not affect iNOS and eNOS expression. l-NAME reversed nNOS expression up-regulation induced by RFPC treatment. The present study demonstrated that RFPC effectively induced cardioprotection through activating the nNOS in the spinal cord. PMID:24462544

Lu, Yao; Hu, Jun; Zhang, Ye; Dong, Chunshan

2014-03-01

399

Electrophilic surface sites as precondition for the chemisorption of pyrrole on GaAs(001) surfaces.  

PubMed

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 precondition for the chemisorption of pyrrole on GaAs(001) surfaces. PMID:25770492

Bruhn, Thomas; Fimland, Bjørn-Ove; Vogt, Patrick

2015-03-14

400

Chickenpox Prevention and Treatment  

MedlinePLUS

... Multimedia Related Links Medline Plus Healthfinder.gov Shingles Prevention & Treatment Language: English Español (Spanish) Recommend on Facebook ... by Your Doctor Español: Prevención y tratamiento Prevention The best way to prevent chickenpox is to ...