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1

Angiotensin II and ischemic preconditioning synergize to improve mitochondrial function while showing additive effects on ventricular postischemic recovery.  

PubMed

Recent studies indicate that the cardioprotective effects of ischemic preconditioning (IPC) against sustained ischemia/reperfusion can be replicated by angiotensin II (Ang II). However, it is not clear whether IPC and Ang II-induced preconditioning (APC) act through similar mechanisms or synergize to enhance cardioprotection. In this study, Langendorff-perfused rat hearts were subjected to IPC, APC, or their combination (IPC/APC) followed by ischemia/reperfusion. IPC, and less potently APC, significantly increased the percent recoveries of the left ventricular developed pressure, the first derivative of developed pressure, and the rate pressure product compared with control. Furthermore, the postischemic recovery of the heart was significantly higher for IPC/APC compared with IPC or APC. The improvements in cardiac function by IPC, APC, and IPC/APC were associated with similar reductions in lactate dehydrogenase release and infarct size. However, a significant improvement in mitochondrial respiration was observed with IPC/APC. The postischemic recovery observed with APC and IPC/APC was inhibited by treatment with losartan, an Ang II type-1 receptor blocker, during the preconditioning phase but not by chelerythrine, a pan-PKC inhibitor. Both drugs, however, abolished the enhanced mitochondrial respiration by IPC/APC. Altogether, these results indicate that APC and IPC interact through mechanisms that enhance cardioprotection by affecting cardiac function and mitochondrial respiration. PMID:24705171

Nuñez, Rebeca E; Castro, Miriam; Javadov, Sabzali; Escobales, Nelson

2014-08-01

2

Unique Transcriptional Profile of Sustained Ligand-Activated Preconditioning in Pre- and Post-Ischemic Myocardium  

PubMed Central

Background Opioidergic SLP (sustained ligand-activated preconditioning) induced by 3–5 days of opioid receptor (OR) agonism induces persistent protection against ischemia-reperfusion (I-R) injury in young and aged hearts, and is mechanistically distinct from conventional preconditioning responses. We thus applied unbiased gene-array interrogation to identify molecular effects of SLP in pre- and post-ischemic myocardium. Methodology/Principal Findings Male C57Bl/6 mice were implanted with 75 mg morphine or placebo pellets for 5 days. Resultant SLP did not modify cardiac function, and markedly reduced dysfunction and injury in perfused hearts subjected to 25 min ischemia/45 min reperfusion. Microarray analysis identified 14 up- and 86 down-regulated genes in normoxic hearts from SLP mice (?1.3-fold change, FDR?5%). Induced genes encoded sarcomeric/contractile proteins (Myh7, Mybpc3,Myom2,Des), natriuretic peptides (Nppa,Nppb) and stress-signaling elements (Csda,Ptgds). Highly repressed genes primarily encoded chemokines (Ccl2,Ccl4,Ccl7,Ccl9,Ccl13,Ccl3l3,Cxcl3), cytokines (Il1b,Il6,Tnf) and other proteins involved in inflammation/immunity (C3,Cd74,Cd83, Cd86,Hla-dbq1,Hla-drb1,Saa1,Selp,Serpina3), together with endoplasmic stress proteins (known: Dnajb1,Herpud1,Socs3; putative: Il6, Gadd45g,Rcan1) and transcriptional controllers (Egr2,Egr3, Fos,Hmox1,Nfkbid). Biological themes modified thus related to inflammation/immunity, together with cellular/cardiovascular movement and development. SLP also modified the transcriptional response to I-R (46 genes uniquely altered post-ischemia), which may influence later infarction/remodeling. This included up-regulated determinants of cellular resistance to oxidant (Mgst3,Gstm1,Gstm2) and other forms of stress (Xirp1,Ankrd1,Clu), and repression of stress-response genes (Hspa1a,Hspd1,Hsp90aa,Hsph1,Serpinh1) and Txnip. Conclusions Protection via SLP is associated with transcriptional repression of inflammation/immunity, up-regulation of sarcomeric elements and natriuretic peptides, and modulation of cell stress, growth and development, while conventional protective molecules are unaltered. PMID:23991079

Ashton, Kevin J.; Tupicoff, Amanda; Williams-Pritchard, Grant; Kiessling, Can J.; See Hoe, Louise E.; Headrick, John P.; Peart, Jason N.

2013-01-01

3

Ischemic Preconditioning Decreases Mitochondrial Proton Leak and Reactive Oxygen Species Production in the Postischemic Heart  

PubMed Central

Background Proton leak (H+ leak) dissipates mitochondrial membrane potential (m??) through the reentry of protons into the mitochondrial matrix independent of ATP synthase. Changes in H+ leak may affect reactive oxygen species (ROS) production. We measured H+ leak and ROS production during ischemia-reperfusion and ischemic preconditioning (IPC) and examined how changing mitochondrial respiration affected m?? and ROS production. Materials/Methods Isolated rat hearts (n=6/group) were subjected to either Control-IR or IPC. Rate pressure product (RPP) was measured. Mitochondria were isolated at end reperfusion. Respiration was measured by polarography and titrated with increasing concentrations of malonate (0.5-2mM). m?? was measured using a tetraphenylphosphonium electrode. H+ leak is the respiratory rate required to maintain membrane potential at -150mV in the presence of oligomycin-A Mitochondrial complex III ROS production was measured by fluorometry using Amplex-Red. Results IPC improved recovery of RPP at end reperfusion (63±4% vs. 21±2% in Control-IR, p<0.05). Ischemia-reperfusion caused increased H+ leak (94±12 vs. 31±1 nanomoles O/mg protein/min in Non-Ischemic Control, p<0.05). IPC attenuates these increases (55±9 nanomoles O/mg protein/min, p< 0.05 vs. Control-IR). IPC reduced mitochondrial ROS production compared to Control-IR (31±2 vs. 40±3 nanomoles/mg protein/min, p<0.05). As mitochondrial respiration decreased, m?? and mitochondrial ROS production also decreased. ROS production remained lower in IPC than in Control-IR for all m?? and respiration rates. Conclusions Increasing H+ leak is not associated with increased ROS production. IPC decreases both the magnitude of H+ leak and ROS production after ischemia-reperfusion. PMID:21035133

Quarrie, Ricardo; Cramer, Brandon M.; Lee, Daniel S.; Steinbaugh, Gregory E.; Erdahl, Warren; Pfeiffer, Douglas R.; Zweier, Jay L.; Crestanello, Juan A.

2010-01-01

4

Plasmin Inhibitors Prevent Leukocyte Accumulation and Remodeling Events in the Postischemic Microvasculature  

PubMed Central

Clinical trials revealed beneficial effects of the broad-spectrum serine protease inhibitor aprotinin on the prevention of ischemia-reperfusion (I/R) injury. The underlying mechanisms remained largely unclear. Using in vivo microscopy on the cremaster muscle of male C57BL/6 mice, aprotinin as well as inhibitors of the serine protease plasmin including tranexamic acid and ?-aminocaproic acid were found to significantly diminish I/R-elicited intravascular firm adherence and (subsequent) transmigration of neutrophils. Remodeling of collagen IV within the postischemic perivenular basement membrane was almost completely abrogated in animals treated with plasmin inhibitors or aprotinin. In separate experiments, incubation with plasmin did not directly activate neutrophils. Extravascular, but not intravascular administration of plasmin caused a dose-dependent increase in numbers of firmly adherent and transmigrated neutrophils. Blockade of mast cell activation as well as inhibition of leukotriene synthesis or antagonism of the platelet-activating-factor receptor significantly reduced plasmin-dependent neutrophil responses. In conclusion, our data suggest that extravasated plasmin(ogen) mediates neutrophil recruitment in vivo via activation of perivascular mast cells and secondary generation of lipid mediators. Aprotinin as well as the plasmin inhibitors tranexamic acid and ?-aminocaproic acid interfere with this inflammatory cascade and effectively prevent postischemic neutrophil responses as well as remodeling events within the vessel wall. PMID:21364954

Reichel, Christoph A.; Lerchenberger, Max; Uhl, Bernd; Rehberg, Markus; Berberich, Nina; Zahler, Stefan; Wymann, Matthias P.; Krombach, Fritz

2011-01-01

5

Intraischemic but not postischemic hypothermia prevents non-selective hippocampal downregulation of AMPA and NMDA receptor gene expression after global ischemia.  

PubMed

Hypothermia may afford histological neuroprotection induced by ischemia by preventing aberrant Ca2+ influx through NMDA (N-methyl-D-aspartic acid) or Ca2+-permeable AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors. Expression of hippocampal GluR1A, GluR2B, GluR3C and NMDAR1 (NR1) subunits was investigated by in situ hybridization at 1 and 7 days after 10-min transient global ischemia in the presence and absence of intraischemic or postischemic brain hypothermia (30 degrees C). At 1 day, normothermic ischemia markedly suppressed the expression of GluR1A, GluR2B, and GluR3C receptor mRNAs to a similar degree in the vulnerable CA1. Less vulnerable CA3a-c subregions were also acutely downregulated. NR1 mRNA expression was reduced in CA1 but to a lesser extent than AMPA mRNAs. At 7 days after normothermic ischemia, a time of marked CA1 cell loss, all three AMPA transcripts were nearly absent in CA1 while a percentage (33.9+/-7.2%) of NR1 mRNA remained. Intraischemic hypothermia fully blocked the damage and non-selective mRNA downregulations at 1 and 7 days. By contrast, postischemic hypothermia postponed neurodegeneration but only partially rescued the expression of AMPA and NR1 mRNAs at 7 days and not at 1 day after the insult. Therefore, hippocampal AMPA receptor mRNAs decline at a relatively similar rate after normothermic global ischemia and cellular neuroprotection by intraischemic hypothermia occurred independently of altered subunit composition of AMPA receptors. Since decreases persist within resistant neurons under the postischemic condition, AMPA receptor-mediated Ca2+ currents probably do not contribute to selective vulnerability. PMID:11165369

Friedman, L K; Ginsberg, M D; Belayev, L; Busto, R; Alonso, O F; Lin, B; Globus, M Y

2001-01-31

6

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

7

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

8

Prevention of postischemic cardiac injury by the orally active iron chelator 1,2-dimethyl-3-hydroxy-4-pyridone (L1) and the antioxidant (+)-cyanidanol-3.  

PubMed

In this study, we investigated the role of oxygen-derived free radicals and iron in mediating myocardial injury during ischemia and reperfusion. Iron is of special interest because it may enhance tissue injury during ischemia and reperfusion by catalyzing the formation of highly reactive hydroxyl radicals (by modified Haber-Weiss or Fenton reactions). Rat hearts, perfused by the Langendorff method, were subjected to global ischemia (15 minutes at 37 degrees C) and reperfusion. The effects of two iron chelators, 1,2-dimethyl-3-hydroxy-4-pyridone (L1) and 5-hydroxy-2-hydroxymethyl-4-pyrone (kojic acid), and one antioxidant, (+)-cyanidanol-3, on contractile function, coronary flow, lactate dehydrogenase release, and lactate production were studied. The combination of these iron chelators is of special importance because L1 is known to prevent lipid peroxidation, induced by ADP/Fe3+ and NADPH in microsomes, in contrast to kojic acid. We found significant protection of contractile function (apex displacement) during reperfusion with 50 microM L1 and 20 microM (+)-cyanidanol-3 (p less than 0.01, n = 6), whereas no protection was found with 50 microM kojic acid (n = 6). Measurements of lactate dehydrogenase release during reperfusion showed a protective pattern similar to that found for heart contractile function, although 50 microM kojic acid also showed a significantly lower lactate dehydrogenase release during the first 10 minutes of reperfusion. No differences in coronary resistance or lactate release were found between the various groups. Our findings indicate that iron and oxygen-derived free radicals are important in the pathogenesis of postischemic reperfusion injury probably because of the formation of hydroxyl radicals.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2736747

van der Kraaij, A M; van Eijk, H G; Koster, J F

1989-07-01

9

Prevention of core cell damage in isolated islets of Langerhans by low temperature preconditioning  

PubMed Central

AIM: To study the core cell damage in isolated islets of Langerhans and its prevention by low temperature preconditioning (26 °C). METHODS: Islets were cultured at 37 °C for 7-14 d after isolation, and then at 26 °C for 2, 4 and 7 d before additional culture at 37 °C for another 7 d. Core cell damage in the isolated islets was monitored by video-microscopy and analyzed quantitatively by use of a computer-assisted image analysis system. The analysis included daily measurement of the diameter and the area of the isolated islets and the area of the core cell damage that developed in those islets over time during culture. Histology and TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay were used to characterize the cell damage and to monitor islet function. RESULTS: Microscopic analysis showed that during the 7 to 14 d of culture at 37 °C, core cell damage occurred in the larger islets with diameters >200 ?m, which included both necrotic and apoptotic cell death. Low temperature (26 °C) culture could prevent core cell damage of isolated islets. The 7-d culture procedure at 26 °C could inhibit most of the core cell (excluding diameters>300 ?m) damages when the islets were re-warmed at 37 °C. CONCLUSION: Our results indicate that core cell damage within isolated islets of Langerhans correlates with the size of islets. Low temperature (26 °C) culture can prevent core cell damage in isolated islets, and successfully precondition these islets for incubation at 37 °C. These novel findings may help to understand the pathophysiology of early loss of islet tissue after transplantation, and may provide a new strategy to improve graft function in the clinical setting of islet transplantation. PMID:15641143

Cui, Yun-Fu; Ma, Ming; Wang, Gui-Yu; Han, De-En; Vollmar, Brigitte; Menger, Michael D.

2005-01-01

10

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

11

Preconditioning, organ preservation, and postconditioning to prevent ischemia-reperfusion injury to the liver.  

PubMed

Ischemia and reperfusion lead to injury of the liver. Ischemia-reperfusion injury is inevitable in liver transplantation and trauma and, to a great extent, in liver resection. This article gives an overview of the mechanisms involved in this type of injury and summarizes protective and treatment strategies in clinical use today. Intervention is possible at different time points: during harvesting, during the period of preservation, and during implantation. Liver preconditioning and postconditioning can be applied in the transplant setting and for liver resection. Graft optimization is merely possible in the period between the harvest and the implantation. Given that there are 3 stages in which a surgeon can intervene against ischemia-reperfusion injury, we have structured the review as follows. The first section reviews the approaches using surgical interventions, such as ischemic preconditioning, as well as pharmacological applications. In the second section, static organ preservation and machine perfusion are addressed. Finally, the possibility of treating the recipient or postconditioning is discussed. PMID:19790166

de Rougemont, Olivier; Lehmann, Kuno; Clavien, Pierre-Alain

2009-10-01

12

Uncoupling protein 2 prevents neuronal death including that occurring during seizures: a mechanism for preconditioning.  

PubMed

The mitochondrial uncoupling protein (UCP2) is expressed in selected regions of the brain. Here we demonstrate that up-regulation of UCP2 is part of a neuroprotective set of responses to various cellular stresses in vitro and in vivo. PC12 cells, when transfected with UCP2, were protected against free radical-induced cell death. Seizure activity was associated with elevated UCP2 levels and mitochondrial uncoupling activity. In transgenic mice that expressed UCP2 constitutively in the hippocampus before seizure induction, a robust reduction in cell death was seen. Because UCP2 increased mitochondrial number and ATP levels with a parallel decrease in free radical-induced damage, it is reasonable to suggest that mitochondrial UCPs precondition neurons by dissociating cellular energy production from that of free radicals to withstand the harmful effects of cellular stress occurring in a variety of neurodegenerative disorders, including epilepsy. PMID:12960023

Diano, Sabrina; Matthews, Russell T; Patrylo, Peter; Yang, Lichuan; Beal, M Flint; Barnstable, Colin J; Horvath, Tamas L

2003-11-01

13

Hypoxia Preconditioned Mesenchymal Stem Cells Prevent Cardiac Fibroblast Activation and Collagen Production via Leptin  

PubMed Central

Aims Activation of cardiac fibroblasts into myofibroblasts constitutes a key step in cardiac remodeling after myocardial infarction (MI), due to interstitial fibrosis. Mesenchymal stem cells (MSCs) have been shown to improve post-MI remodeling an effect that is enhanced by hypoxia preconditioning (HPC). Leptin has been shown to promote cardiac fibrosis. The expression of leptin is significantly increased in MSCs after HPC but it is unknown whether leptin contributes to MSC therapy or the fibrosis process. The objective of this study was to determine whether leptin secreted from MSCs modulates cardiac fibrosis. Methods Cardiac fibroblast (CF) activation was induced by hypoxia (0.5% O2). The effects of MSCs on fibroblast activation were analyzed by co-culturing MSCs with CFs, and detecting the expression of ?-SMA, SM22?, and collagen I?I in CFs by western blot, immunofluorescence and Sirius red staining. In vivo MSCs antifibrotic effects on left ventricular remodeling were investigated using an acute MI model involving permanent ligation of the left anterior descending coronary artery. Results Co-cultured MSCs decreased fibroblast activation and HPC enhanced the effects. Leptin deficit MSCs from Ob/Ob mice did not decrease fibroblast activation. Consistent with this, H-MSCs significantly inhibited cardiac fibrosis after MI and mediated decreased expression of TGF-?/Smad2 and MRTF-A in CFs. These effects were again absent in leptin-deficient MSCs. Conclusion Our data demonstrate that activation of cardiac fibroblast was inhibited by MSCs in a manner that was leptin-dependent. The mechanism may involve blocking TGF-?/Smad2 and MRTF-A signal pathways. PMID:25116394

Chen, Panpan; Wu, Rongrong; Zhu, Wei; Jiang, Zhi; Xu, Yinchuan; Chen, Han; Zhang, Zhaocai; Chen, Huiqiang; Zhang, Ling; Yu, Hong; Wang, Jian'an; Hu, Xinyang

2014-01-01

14

[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

15

Tandem action of exercise training and food restriction completely preserves ischemic preconditioning in the aging heart.  

PubMed

Ischemic preconditioning (IP) has been proposed as an endogenous form of protection against ischemia reperfusion injury. IP, however, does not prevent post-ischemic dysfunction in the aging heart but may be partially corrected by exercise training and food restriction. We investigated the role of exercise training combined with food restriction on restoring IP in the aging heart. Effects of IP against ischemia-reperfusion injury in isolated hearts from adult (A, 6 months old), sedentary 'ad libitum' fed (SL), trained ad libitum fed (TL), sedentary food-restricted (SR), trained- and food-restricted senescent rats (TR) (24 months old) were investigated. Norepinephrine release in coronary effluent was determined by high performance liquid cromatography. IP significantly improved final recovery of percent developed pressure in hearts from A (p<0.01) but not in those from SL (p=NS) vs unconditioned controls. Developed pressure recovery was partial in hearts from TL and SR (64.3 and 67.3%, respectively; p<0.05 vs controls) but it was total in those from TR (82.3%, p=NS vs A; p<0.05 vs hearts from TL and SR). Similarly, IP determined a similar increase of norepinephrine release in A (p<0.001) and in TR (p<0.001, p=NS vs adult). IP was abolished by depletion of myocardial norepinephrine stores by reserpine in all groups. Thus, IP reduces post-ischemic dysfunction in A but not in SL. Moreover, IP was preserved partially in TR and SR and totally in TR. Complete IP maybe due to full restoration of norepinephrine release in response to IP stimulus. PMID:15664731

Abete, P; Testa, G; Galizia, G; Mazzella, F; Della Morte, D; de Santis, D; Calabrese, C; Cacciatore, F; Gargiulo, G; Ferrara, N; Rengo, G; Sica, V; Napoli, C; Rengo, F

2005-01-01

16

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

NASA Astrophysics Data System (ADS)

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

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

2012-05-01

17

Increased perception of post-ischemic paresthesias in depressed subjects  

Microsoft Academic Search

A psychophysical assessment of sensory activity linked to unmyelinated and myelinated primary afferents was conducted by estimating the intensity of thermal and tactile post-ischemic paresthesias in 11 nontreated depressed subjects (Zung's index ?50) and 19 controls. Blood flow in the dominant forearm was arrested until ischemic pain tolerance was reached. Ischemic pain and post-ischemic paresthesias were numerically rated. The duration

H Suarez-Roca; L Piñerua-Shuhaibar; M. E Morales; W Maixner

2003-01-01

18

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

19

Influence of ischemic preconditioning on intracellular sodium, pH, and cellular energy status in isolated perfused heart.  

PubMed

The possible relationships between intracellular Na(+) (Na(i)(+)), bioenergetic status and intracellular pH (pH(i)) in the mechanism for ischemic preconditioning were studied using (23)Na and (31)P magnetic resonance spectroscopy in isolated Langendorff perfused rat heart. The ischemic preconditioning (three 5-min ischemic episodes followed by two 5-min and one 10-min period of reperfusion) prior to prolonged ischemia (20 min stop-flow) resulted in a decrease in ischemic acidosis and faster and complete recovery of cardiac function (ventricular developed pressure and heart rate) after 30 min of reperfusion. The response of Na(i) during ischemia in the preconditioned hearts was characterized by an increase in Na(i)(+) at the end of preconditioning and an accelerated decrease during the first few minutes of reperfusion. During post-ischemic reperfusion, bioenergetic parameters (PCr/P(i) and betaATP/P(i) ratios) were partly recovered without any significant difference between control and preconditioned hearts. The reduced acidosis during prolonged ischemia and the accelerated decrease in Na(i)(+) during reperfusion in the preconditioned hearts suggest activation of Na(+)/H(+) exchanger and other ion transport systems during preconditioning, which may protect the heart from intracellular acidosis during prolonged ischemia, and result in better recovery of mechanical function (LVDP and heart rate) during post-ischemic reperfusion. PMID:12094017

Babsky, Andriy; Hekmatyar, Shahryar; Wehrli, Suzanne; Doliba, Nicolai; Osbakken, Mary; Bansal, Navin

2002-07-01

20

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

21

Vascular progenitor cells and diabetes: role in postischemic neovascularisation.  

PubMed

Advances in the field of vascular biology lead to the identification of endothelial progenitor cells (EPC) and to the development of EPC-based cell therapy to induce new vessel formation in ischemic tissues and to accelerate re-endothelialisation of injured vessels in human and various animals models. However, recent studies have shown that age and other risk factors for cardiovascular diseases, such as diabetes, reduce the availability of EPC and impair their function to varying degrees, leading to reduction in postischemic vessel growth. This review focus on the cellular and molecular mechanisms governing EPC-related functions and analyzes the impact of diabetes in this setting. PMID:18358425

Silvestre, J-S

2008-02-01

22

Junctional protein regulation by sphingosine kinase 2 contributes to blood–brain barrier protection in hypoxic preconditioning-induced cerebral ischemic tolerance  

PubMed Central

Protection of the blood–brain barrier (BBB) is correlated with improved outcome in stroke. Sphingosine kinase (SphK)-directed production of sphingosine-1-phosphate, which we previously documented as being vital to preconditioning-induced stroke protection, mediates peripheral vascular integrity via junctional protein regulation. We used a hypoxic preconditioning (HPC) model in adult wild-type and SphK2-null mice to examine the isoform-specific role of SphK2 signaling for ischemic tolerance to transient middle cerebral artery occlusion and attendant BBB protection. Reductions in infarct volume and BBB permeability in HPC-treated mice were completely lost in SphK2-null mice. Hypoxic preconditioning-induced attenuation of postischemic BBB disruption in wild types, evidenced by reduced extravascular immunoglobulin G intensity, suggests direct protection of BBB integrity. Measurement of BBB junctional protein status in response to HPC revealed SphK2-dependent increases in triton-insoluble claudin-5 and VE-cadherin, which may serve to strengthen the BBB before stroke. Postischemic loss of VE-cadherin, occludin, and zona occludens-1 in SphK2-null mice with prior HPC suggests that SphK2-dependent protection of these adherens and tight junction proteins is compulsory for HPC to establish a vasculoprotective phenotype. Further elucidation of the mediators of this endogenous, HPC-activated lipid signaling pathway, and their role in protecting the ischemic BBB, may provide new therapeutic targets for cerebrovascular protection in stroke patients. PMID:22314269

Wacker, Bradley K; Freie, Angela B; Perfater, Jennifer L; Gidday, Jeffrey M

2012-01-01

23

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

24

Hypoxic preconditioning protects rat hearts against ischemia-reperfusion injury via the arachidonate12-lipoxygenase/transient receptor potential vanilloid 1 pathway.  

PubMed

Hypoxic preconditioning (HPC) protects rat hearts against ischemia-reperfusion (IR) injury. However, the role of transient receptor potential vanilloid 1 (TRPV1) in HPC-mediated cardioprotection remains unknown. TRPV1 is activated by endovanilloid 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], which is synthesized by arachidonate 12-lipoxygenase (ALOX12). Therefore, we examined whether HPC protects the myocardium against IR via the ALOX12/TRPV1 pathway. Compared to hearts of rats kept in room air, the hearts of rats kept in air with 10 % oxygen for 4 weeks had better post-ischemic recovery and less tissue damage when subjected to 30-min global ischemia and 4-h reflow in a Langendorff apparatus. Capsazepine, a specific TRPV1 blocker, administered 5 min before reperfusion markedly attenuated the effects of HPC, confirming that TRPV1 is a downstream effector in HPC-mediated cardioprotection. HPC resulted in the upregulation of ALOX12 and myocardial 12(S)-HETE, and prevented IR-induced 12(S)-HETE reduction. In addition, sarcolemmal ALOX12 expression in HPC hearts mainly co-localized with TRPV1 expression. Blockade of ALOX12 by cinnamyl-3,4-dihydroxy-?-cyanocinnamate or baicalein abrogated the effects of HPC, baicalein also decreased 12(S)-HETE expression. Mimicking HPC by given 12(S)-HETE or capsaicin to baicalien-treated hearts enhanced cardiac recovery during reperfusion. The cardiac protein kinase C (PKC) isoforms ?, ?, ?, and ? were preferentially expressed in the sarcolemmal membrane of HPC-treated hearts, indicating their high intrinsic activation state. Capsazepine or co-treatment with baicalein attenuated translocation of PKC?, PKC? and PKC?, but not that of PKC?. We conclude that HPC reduces heart susceptibly to IR via ALOX12/TRPV1/PKC pathway, as shown by increased 12(S)-HETE expression in HPC hearts. PMID:24816396

Lu, Ming-Jen; Chen, Yih-Sharng; Huang, Ho-Shiang; Ma, Ming-Chieh

2014-07-01

25

Assessment by radionuclide ventriculography of postischemic regional left ventricular dysfunction in patients with healed myocardial infarction or angina pectoris  

Microsoft Academic Search

Postischemic left ventricular (LV) dysfunction has been observed in experimental animal models after brief, complete coronary artery occlusion followed by reperfusion, but less relevant information is available for humans. The incidence and duration of postischemic LV dysfunction was examined by exercise radionuclide ventriculography in 50 patients with coronary artery disease. Cardiac imaging was performed at rest and was repeated during

Takuya Tamai; Tokuji Konishi; Mashio Nakamura; Naoki Isaka; Takeshi Nakano

2002-01-01

26

Estrogen replacement therapy in diabetic ovariectomized female rats potentiates postischemic leukocyte adhesion in cerebral venules via a RAGE-related process  

PubMed Central

In this study, we tested the hypothesis that the documented transformation of 17?-estradiol (E2) from a counterinflammatory hormone in nondiabetic (ND) rats to a proinflammatory agent in rats with diabetes mellitus (DM) is due to an enhanced contribution from the receptor for advanced glycation end products (RAGE). Rhodamine 6G-labeled leukocytes were observed through a closed cranial window in rats. In vivo pial venular leukocyte adherence and infiltration were measured over 10 h reperfusion after transient forebrain ischemia in DM (streptozotocin) versus ND intact, ovariectomized (OVX), and E2-replaced (for 7–10 days) OVX (OVE) females. The role of RAGE was examined in two ways: 1) RAGE knockdown via topical application of RAGE antisense versus missense oligodeoxynucleotide or 2) intracerebroventricular injection of the RAGE decoy inhibitor, soluble RAGE. Among diabetic rats, the lowest levels of cortical RAGE mRNA and immunoreactivity of the RAGE ligand, AGE, were seen in OVX females, with significantly higher levels exhibited in intact and OVE females. However, results from the analysis of cortical RAGE protein only partially tracked those findings. When comparing ND to DM rats, cortical AGE immunoreactivity was significantly lower in OVE and intact females but similar in OVX rats. In DM rats, the level of postischemic leukocyte adhesion and infiltration (highest to lowest) was OVE > intact >> untreated OVX. In NDs, adhesion was highest in the untreated OVX group. Leukocyte extravasation was observed at >6 h postischemia but only in diabetic OVE and intact females and in ND OVX (untreated) rats. Pretreatment with RAGE antisense-oligodeoxynucleotide or soluble RAGE attenuated postischemic leukocyte adhesion and prevented infiltration but only in the diabetic OVE and intact groups. These results indicate that the exacerbation of postischemic leukocyte adhesion by chronic E2 replacement therapy in diabetic OVX females involves a RAGE-related mechanism. Targeting RAGE may restore the neuroprotective effect of E2 replacement therapy in diabetic females. PMID:19820198

Xu, Hao-Liang; Vetri, Francesco; Lee, Hae-Kyung; Ye, Shuhua; Paisansathan, Chanannait; Mao, Lizhen; Tan, Fulong

2009-01-01

27

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

28

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

29

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

30

Inhibition of post-ischemic reperfusion injury of the kidney by diamine oxidase  

Microsoft Academic Search

To elucidate the role of histamine in the pathogenesis of post-ischemic reperfusion injury of tissues, the effect of diamine oxidase (DAO) was studied on the changes in renal functions induced by 30 min occlusion followed by reperfusion of the renal vessels of unilaterally nephrectomized rats. Kinetic analysis using radiolabeled albumin revealed that vascular permeability of the kidney increased markedly after

Hirobumi Kaneko; Shuichi Koshi; Takehisa Hiraoka; Yoshimasa Miyauchi; Nobuo Kitamura; Masayasu Inoue

31

Inhibition of post-ischemic reperfusion injury of the kidney by diamine oxidase  

Microsoft Academic Search

To elucidate the role of histamine in the pathogenesis of post-ischemic reperfusion injury of tissues, the effect of diamine oxidase (DAO) was studied on the changes in renal functions induced by 30 min occlusion followed by reperfusion of the renal vessels of unilaterally nephrectomized rats. Kinetic analysis using radiolabeled albumin revealed that vascular permeability of the kidney increased markedly after

Hirobumi Kaneko; Shuichi Koshi; Takehisa Hiraoka; Yoshimasa Miyauchi; Nobuo Kitamura; Masayasu Inoue

1998-01-01

32

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.

33

Catestatin Improves Post-Ischemic Left Ventricular Function and Decreases Ischemia/Reperfusion Injury in Heart  

PubMed Central

The Chromogranin A (CgA)-derived anti-hypertensive peptide catestatin (CST) antagonizes catecholamine secretion, and is a negative myocardial inotrope acting via a nitric oxide-dependent mechanism. It is not known whether CST contributes to ischemia/reperfusion injury or is a component of a cardioprotective response to limit injury. Here, we tested whether CST by virtue of its negative inotropic activity improves post-ischemic cardiac function and cardiomyocyte survival. Three groups of isolated perfused hearts from adult Wistar rats underwent 30-min ischemia and 120-min reperfusion (I/R, Group 1), or were post-conditioned by brief ischemic episodes (PostC, 5-cycles of 10-s I/R at the beginning of 120-min reperfusion, Group 2), or with exogenous CST (75 nM for 20 min, CST-Post, Group-3) at the onset of reperfusion. Perfusion pressure and left ventricular pressure (LVP) were monitored. Infarct size was evaluated with nitroblue-tetrazolium staining. The CST (5 nM) effects were also tested in simulated ischemia/reperfusion experiments on cardiomyocytes isolated from young-adult rats, evaluating cell survival with propidium iodide labeling. Infarct size was 61 ± 6% of risk area in hearts subjected to I/R only. PostC reduced infarct size to 34 ± 5%. Infarct size in CST-Post was 36 ± 3% of risk area (P < 0.05 respect to I/R). CST-Post reduced post-ischemic rise of diastolic LVP, an index of contracture, and significantly improved post-ischemic recovery of developed LVP. In isolated cardiomyocytes, CST increased the cell viability rate by about 65% after simulated ischemia/reperfusion. These results suggest a novel cardioprotective role for CST, which appears mainly due to a direct reduction of post-ischemic myocardial damages and dysfunction, rather than to an involvement of adrenergic terminals and/or endothelium. PMID:21104119

Penna, Claudia; Alloatti, Giuseppe; Gallo, Maria Pia; Cerra, Maria Carmela; Levi, Renzo; Tullio, Francesca; Bassino, Eleonora; Dolgetta, Serena; Pagliaro, Pasquale

2010-01-01

34

Laser thermal preconditioning enhances dermal wound repair  

Microsoft Academic Search

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 (lambda

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

2008-01-01

35

The Time of Maximum Post-Ischemic Hyperperfusion Indicates Infarct Growth Following Transient Experimental Ischemia  

PubMed Central

After recanalization, cerebral blood flow (CBF) can increase above baseline in cerebral ischemia. However, the significance of post-ischemic hyperperfusion for tissue recovery remains unclear. To analyze the course of post-ischemic hyperperfusion and its impact on vascular function, we used magnetic resonance imaging (MRI) with pulsed arterial spin labeling (pASL) and measured CBF quantitatively during and after a 60 minute transient middle cerebral artery occlusion (MCAO) in adult rats. We added a 5% CO2 - challenge to analyze vasoreactivity in the same animals. Results from MRI were compared to histological correlates of angiogenesis. We found that CBF in the ischemic area recovered within one day and reached values significantly above contralateral thereafter. The extent of hyperperfusion changed over time, which was related to final infarct size: early (day 1) maximal hyperperfusion was associated with smaller lesions, whereas a later (day 4) maximum indicated large lesions. Furthermore, after initial vasoparalysis within the ischemic area, vasoreactivity on day 14 was above baseline in a fraction of animals, along with a higher density of blood vessels in the ischemic border zone. These data provide further evidence that late post-ischemic hyperperfusion is a sequel of ischemic damage in regions that are likely to undergo infarction. However, it is transient and its resolution coincides with re-gaining of vascular structure and function. PMID:23741488

Wegener, Susanne; Artmann, Judith; Luft, Andreas R.; Buxton, Richard B.; Weller, Michael; Wong, Eric C.

2013-01-01

36

Chemogenetic silencing of neurons in retrosplenial cortex disrupts sensory preconditioning.  

PubMed

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; Bucci, David J

2014-08-13

37

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

38

Epsilon PKC Increases Brain Mitochondrial SIRT1 Protein Levels via Heat Shock Protein 90 following Ischemic Preconditioning in Rats  

PubMed Central

Ischemic preconditioning is a neuroprotective mechanism whereby a sublethal ischemic exposure is protective against a subsequent lethal ischemic attack. We previously demonstrated that SIRT1, a nuclear localized stress-activated deacetylase, is vital for ischemic preconditioning neuroprotection. However, a recent study demonstrated that SIRT1 can also localize to the mitochondria. Mitochondrial localized SIRT1 may allow for a direct protection of mitochondria following ischemic preconditioning. The objective of this study was to determine whether ischemic preconditioning increases brain mitochondrial SIRT1 protein levels and to determine the role of PKC? and HSP90 in targeting SIRT1 to the mitochondria. Here we report that preconditioning rats, with 2 min of global cerebral ischemia, induces a delayed increase in non-synaptic mitochondrial SIRT1 protein levels which was not observed in synaptic mitochondria. This increase in mitochondrial SIRT1 protein was found to occur only in neuronal cells and was mediated by PKC? activation. Inhibition of HSP90, a protein chaperone involved in mitochondrial protein import, prevented preconditioning induced increases in mitochondrial SIRT1 and PKC? protein. Our work provides new insights into a possible direct role of SIRT1 in modulating mitochondrial function under both normal and stress conditions, and to a possible role of mitochondrial SIRT1 in activating preconditioning induced ischemic tolerance. PMID:24058702

Thompson, John W.; Dave, Kunjan R.; Saul, Isabel; Narayanan, Srinivasan V.; Perez-Pinzon, Miguel A.

2013-01-01

39

REGULARIZATION AND PRECONDITIONING OF KKT SYSTEMS ...  

E-print Network

Technical Report MS-07-004, August 31th, 2007. Abstract. .... We provide the spectral analysis of the preconditioned system and show that the condition number ...... More insight into these failures, first we note that the linear algebra phase is.

2007-08-30

40

40 CFR 1065.518 - Engine preconditioning.  

...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

41

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

42

Pediatric cerebral stroke: susceptibility-weighted imaging may predict post-ischemic malignant edema.  

PubMed

Susceptibility-weighted imaging (SWI) is an advanced MRI technique providing information on the blood oxygenation level. Deoxyhemoglobin is increased in hypoperfused tissue characterized by SWI-hypointensity, while high oxyhemoglobin concentration within hyperperfused tissue results in a SWI iso- or hyperintensity compared to healthy brain tissue. We describe a child with a stroke, where SWI in addition to excluding hemorrhage and delineating the thrombus proved invaluable in determining regions of hyperperfusion or luxury perfusion, which contributed further to the prognosis including an increased risk of developing post-ischemic malignant edema. PMID:24199819

Bosemani, Thangamadhan; Poretti, Andrea; Orman, Gunes; Meoded, Avner; Huisman, Thierry A G M

2013-10-01

43

Osmotic diuretics and hemodilution in postischemic renal failure.  

PubMed

In the acute phase of ischemic renal failure, the severe depression of the glomerular filtration rate (GFR) is due to obstruction of the tubules by cells and cell debris rejected from the proximal tubules, a blockade which can be prevented at least partly, by treatment with osmotic diuretics. The isosthenuria, the second typical sign in ischemic acute renal failure, probably derives from the medullary ischemia that results from an intracapillary trapping of red cells. This, in turn, is suggested to be caused by oxygen-derived free radicals, which via increasing the capillary macromolecular permeability result in a massive extravasation of plasma and hence in hemoconcentration. As expected from this hypothesis, scavengers may ameliorate both the trapping and the consequent medullary ischemia. Unfortunately, however, a therapy using both osmotic diuretics and scavengers fails to improve the long-term outcome. Hemodilution would seem more promising, since it will both prevent the medullary ischemia seen in the acute phase and substantially improve the long-term outcome. At a hematocrit of 0.30, rat kidneys exposed to 45-min ischemia will show a GFR 1 month after the insult of more than 50% of the normal GFR as against 15% in untreated animals. PMID:1509160

Wolgast, M; Bayati, A; Hellberg, O; Källskog, O; Nygren, K

1992-01-01

44

Enhanced recovery from acute renal failure by the postischemic infusion of adenine nucleotides and magnesium chloride in rats  

Microsoft Academic Search

Enhanced recovery from acute renal failure by the postischemic infusion of adenine nucleotides and magnesium chloride in rats. Although a number of manipulations prior to or during the initiation phase of an acute renal injury will modify the degree of functional impairment, agents administered after the acute insult usually have been ineffective. In the present study, adenine nucleotides (AMP, ADP,

Norman J Siegel; Wayne B Glazier; Irshad H Chaudry; Karen M Gaudio; Bernard Lytton; Arthur E Baue; Michael Kashgarian

1980-01-01

45

Effects of Delayed Intraischemic and Postischemic Hypothermia on a Focal Model of Transient Cerebral Ischemia in Rats  

Microsoft Academic Search

Background and Purpose—Intraischemic mild hypothermia has been shown to be neuroprotective in reducing cerebral infarction in transient focal ischemia. As a more clinical relevant issue, we investigated the effect of delayed intraischemic and postischemic hypothermia on cerebral infarction in a rat model of reversible focal ischemia. We also examined the effect of hypothermia on the inflammatory response after ischemia-reperfusion to

Nobuyuki Kawai; Masanobu Okauchi; Kuniaki Morisaki; Seigo Nagao

46

Steps to translate preconditioning from basic research to the clinic  

PubMed Central

Efforts to treat cardiovascular and cerebrovascular diseases often focus on the mitigation of ischemia-reperfusion (I/R) injury. Many treatments or “preconditioners” are known to provide substantial protection against the I/R injury when administered prior to the event. Brief periods of ischemia itself have been validated as a means to achieve neuroprotection in many experimental disease settings, in multiple organ systems, and in multiple species suggesting a common pathway leading to tolerance. In addition, pharmacological agents that act as potent preconditioners have been described. Experimental induction of neuroprotection using these various preconditioning paradigms has provided a unique window into the brain’s endogenous protective mechanisms. Moreover, preconditioning agents themselves hold significant promise as clinical-stage therapies for prevention of I/R injury. The aim of this article is to explore several key steps involved in the preclinical validation of preconditioning agents prior to the conduct of clinical studies in humans. Drug development is difficult, expensive and relies on multi-factorial analysis of data from diverse disciplines. Importantly, there is no single path for the preclinical development of a novel therapeutic and no proven strategy to ensure success in clinical translation. Rather, the conduct of a diverse array of robust preclinical studies reduces the risk of clinical failure by varying degrees depending upon the relevance of preclinical models and drug pharmacology to humans. A strong sense of urgency and high tolerance of failure are often required to achieve success in the development of novel treatment paradigms for complex human conditions. PMID:23504609

Bahjat, Frances R; Gesuete, Raffaella; Stenzel-Poore, Mary P

2012-01-01

47

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

48

Preconditioning the Helmholtz Equation for Rigid Ducts  

NASA Technical Reports Server (NTRS)

An innovative hyperbolic preconditioning technique is developed for the numerical solution of the Helmholtz equation which governs acoustic propagation in ducts. Two pseudo-time parameters are used to produce an explicit iterative finite difference scheme. This scheme eliminates the large matrix storage requirements normally associated with numerical solutions to the Helmholtz equation. The solution procedure is very fast when compared to other transient and steady methods. Optimization and an error analysis of the preconditioning factors are present. For validation, the method is applied to sound propagation in a 2D semi-infinite hard wall duct.

Baumeister, Kenneth J.; Kreider, Kevin L.

1998-01-01

49

Creatine kinase overexpression improves ATP kinetics and contractile function in postischemic myocardium  

PubMed Central

Reduced myofibrillar ATP availability during prolonged myocardial ischemia may limit post-ischemic mechanical function. Because creatine kinase (CK) is the prime energy reserve reaction of the heart and because it has been difficult to augment ATP synthesis during and after ischemia, we used mice that overexpress the myofibrillar isoform of creatine kinase (CKM) in cardiac-specific, conditional fashion to test the hypothesis that CKM overexpression increases ATP delivery in ischemic-reperfused hearts and improves functional recovery. Isolated, retrograde-perfused hearts from control and CKM mice were subjected to 25 min of global, no-flow ischemia and 40 min of reperfusion while cardiac function [rate pressure product (RPP)] was monitored. A combination of 31P-nuclear magnetic resonance experiments at 11.7T and biochemical assays was used to measure the myocardial rate of ATP synthesis via CK (CK flux) and intracellular pH (pHi). Baseline CK flux was severalfold higher in CKM hearts (8.1 ± 1.0 vs. 32.9 ± 3.8, mM/s, control vs. CKM; P < 0.001) with no differences in phosphocreatine concentration [PCr] and RPP. End-ischemic pHi was higher in CKM hearts than in control hearts (6.04 ± 0.12 vs. 6.37 ± 0.04, control vs. CKM; P < 0.05) with no differences in [PCr] and [ATP] between the two groups. Post-ischemic PCr (66.2 ± 1.3 vs. 99.1 ± 8.0, %preischemic levels; P < 0.01), CK flux (3.2 ± 0.4 vs. 14.0 ± 1.2 mM/s; P < 0.001) and functional recovery (13.7 ± 3.4 vs. 64.9 ± 13.2%preischemic RPP; P < 0.01) were significantly higher and lactate dehydrogenase release was lower in CKM than in control hearts. Thus augmenting cardiac CKM expression attenuates ischemic acidosis, reduces injury, and improves not only high-energy phosphate content and the rate of CK ATP synthesis in postischemic myocardium but also recovery of contractile function. PMID:22886411

Akki, Ashwin; Su, Jason; Yano, Toshiyuki; Gupta, Ashish; Wang, Yibin; Leppo, Michelle K.; Chacko, Vadappuram P.; Steenbergen, Charles

2012-01-01

50

Revealing Preconditions for Trustful Collaboration in CSCL  

ERIC Educational Resources Information Center

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

Gerdes, Anne

2010-01-01

51

Protein Kinase C Isoform Diversity in Preconditioning  

Microsoft Academic Search

Protein kinase C (PKC) appears to be a common intracellular effector and signal collector during cardiac preconditioning; however, it remains unknown whether agonists that activate different PKC isoforms are also linked to select aspects of myocardial protection. Using agonists that are known to activate unique combinations of PKC isoforms, we interogated the relationship between isoform activation and the different aspects

Daniel R. Meldrum; Joseph C. Cleveland; Xianzhong Meng; Brett C. Sheridan; Fabia Gamboni; Brian S. Cain; Alden H. Harken; Anirban Banerjee

1997-01-01

52

Original article Preconditioning treatment maintains taste characteristic  

E-print Network

fruits immediately after harvest and prior to cold storage at 20 °C for 24­48 h in special chambers aimed fruit during this 40-day cold- storage period. Preconditioned and control fruit were also segregated maintained their sensory characteristics longer than control fruit during this 40-day cold-storage period

Crisosto, Carlos H.

53

Preconditioned Parallel MLFMA Solution of Metamaterial Structures  

E-print Network

Preconditioned Parallel MLFMA Solution of Metamaterial Structures Levent Gürel, �zgür Ergül, Tahir, Bilkent, Ankara, Turkey E-mail: lgurel@bilkent.edu.tr Since metamaterials display unusual electromagnetic issue. The metamaterial structures considered in this study consist of split-ring resonators (SRRs

Gürel, Levent

54

Resveratrol and ischemic preconditioning in the brain.  

PubMed

Cardiovascular pathologies in the French are not prevalent despite high dietary saturated fat consumption. This is commonly referred to as the "French Paradox" attributing its anti-lipidemic effects to moderate consumption of red wine. Resveratrol, a phytoalexin found in red wine, is currently the focus of intense research both in the cardiovascular system and the brain. Current research suggests resveratrol may enhance prognosis of neurological disorders such as, Parkinson's, Huntington's, Alzheimer's diseases and stroke. The beneficial effects of resveratrol include: antioxidation, free radical scavenger, and modulation of neuronal energy homeostasis and glutamatergic receptors/ion channels. Resveratrol directly increases sirtuin 1 (SIRT1) activity, a NAD(+) (oxidized form of nicotinamide adenine dinucleotide)-dependent histone deacetylase related to increased lifespan in various species similar to calorie restriction. We recently demonstrated that brief resveratrol pretreatment conferred neuroprotection against cerebral ischemia via SIRT1 activation. This neuroprotective effect produced by resveratrol was similar to ischemic preconditioning-induced neuroprotection, which protects against lethal ischemic insults in the brain and other organ systems. Inhibition of SIRT1 abolished ischemic preconditioning-induced neuroprotection in CA1 region of the hippocampus. Since resveratrol and ischemic preconditioning-induced neuroprotection require activation of SIRT1, this common signaling pathway may provide targeted therapeutic treatment modalities as it relates to stroke and other brain pathologies. In this review, we will examine common signaling pathways, cellular targets of resveratrol, and ischemic preconditioning-induced neuroprotection as it relates to the brain. PMID:18537630

Raval, Ami P; Lin, Hung Wen; Dave, Kunjan R; Defazio, R Anthony; Della Morte, David; Kim, Eun Joo; Perez-Pinzon, Miguel A

2008-01-01

55

Preconditioning and tolerance against cerebral ischaemia  

PubMed Central

Neuroprotection and brain repair in patients after acute brain damage are still major unfulfilled medical needs. Pharmacological treatments are either ineffective or confounded by adverse effects. Consequently, endogenous mechanisms by which the brain protects itself against noxious stimuli and recovers from damage are being studied. Research on preconditioning, also known as induced tolerance, over the past decade has resulted in various promising strategies for the treatment of patients with acute brain injury. Several of these strategies are being tested in randomised clinical trials. Additionally, research into preconditioning has led to the idea of prophylactically inducing protection in patients such as those undergoing brain surgery and those with transient ischaemic attack or subarachnoid haemorrhage who are at high risk of brain injury in the near future. In this Review, we focus on the clinical issues relating to preconditioning and tolerance in the brain; specifically, we discuss the clinical situations that might benefit from such procedures. We also discuss whether preconditioning and tolerance occur naturally in the brain and assess the most promising candidate strategies that are being investigated. PMID:19296922

Dirnagl, Ulrich; Becker, Kyra; Meisel, Andreas

2009-01-01

56

Evidence against oxidant injury as a critical mediator of postischemic acute renal failure.  

PubMed

The purpose of this study is to confirm previous evidence for reactive oxygen species (ROS) as critical mediators of postischemic renal injury by documenting lipid peroxidation after ischemic-hypoxic insults and by demonstrating that antioxidants confer protection. Renal malondialdehyde (MDA) concentrations, an index of lipid peroxidation, were measured using uncorrected and tissue-chromagen-corrected methods in 1) cortical (C), outer medullary stripe (OMS), inner medullary (IM) whole renal tissues, and C and OMS mitochondria obtained 15 min after in vivo renal artery occlusion (RAO; x 45 min); 2) C, OMS, and IM whole tissues obtained 15 min after completing 45 min of ischemia in an isolated perfused kidney; and 3) isolated proximal tubular cell (PTC) suspensions after 45 min of hypoxia with 15 min of reoxygenation. Despite significant oxygen deprivation-induced injury in each of these systems, no significant rise in MDA concentrations could be documented, with the sole exception of the in vivo IM region (by uncorrected MDA assay only). The latter rise could be attributed to medullary vascular congestion causing a hemoglobin-induced artifact in the MDA assay. Sixty-minute in vivo RAO plus reflow also did not raise MDA. To validate the MDA assay 4.2 mM H2O2 was added to PTC. An abrupt fourfold rise in MDA resulted. Pretreatment of 30- and 45-min RAO rats with two antioxidants (allopurinol or superoxide dismutase) failed to confer functional or morphological protection. We conclude that ROS may not be critical consistent mediators of in vivo postischemic acute renal failure. PMID:3414803

Gamelin, L M; Zager, R A

1988-09-01

57

Retinoic Acid Signalling Is Activated in the Postischemic Heart and May Influence Remodelling  

PubMed Central

Background All-trans retinoic acid (atRA), an active derivative of vitamin A, regulates cell differentiation, proliferation and cardiac morphogenesis via transcriptional activation of retinoic acid receptors (RARs) acting on retinoic acid response elements (RARE).We hypothesized that the retinoic acid (RA) signalling pathway is activated in myocardial ischemia and postischemic remodelling. Methods and Findings Myocardial infarction was induced through ligating the left coronary artery in mice. In vivo cardiac activation of the RARs was measured by imaging RARE-luciferase reporter mice, and analysing expression of RAR target genes and proteins by real time RT-PCR and western blot. Endogenous retinoids in postinfarcted hearts were analysed by triple-stage liquid chromatography/tandem mass spectrometry. Cardiomyocytes (CM) and cardiofibroblasts (CF) were isolated from infarcted and sham operated RARE luciferase reporter hearts and monitored for RAR activity and expression of target genes. The effect of atRA on CF proliferation was evaluated by EdU incorporation. Myocardial infarction increased thoracic RAR activity in vivo (p<0.001), which was ascribed to the heart through ex vivo imaging (p?=?0.002) with the largest signal 1 week postinfarct. This was accompanied by increased cardiac gene and protein expression of the RAR target genes retinol binding protein 1 (p?=?0.01 for RNA, p?=?0,006 for protein) and aldehyde dehydrogenase 1A2 (p?=?0.04 for RNA, p?=?0,014 for protein), while gene expression of cytochrome P450 26B1 was downregulated (p?=?0.007). Concomitantly, retinol accumulated in the infarcted zone (p?=?0.02). CM and CF isolated from infarcted hearts had higher luminescence than those from sham operated hearts (p?=?0.02 and p?=?0.008). AtRA inhibited CF proliferation in vitro (p?=?0.02). Conclusion The RA signalling pathway is activated in postischemic hearts and may play a role in regulation of damage and repair during remodelling. PMID:23028599

Bilbija, Dusan; Haugen, Fred; Sagave, Julia; Baysa, Anton; Bastani, Nasser; Levy, Finn Olav; Sirsjö, Allan; Blomhoff, Rune; Valen, Guro

2012-01-01

58

Role of uncoupling protein 3 in ischemia-reperfusion injury, arrhythmias, and preconditioning  

PubMed Central

Overexpression of mitochondrial uncoupling proteins (UCPs) attenuates ischemia-reperfusion (I/R) injury in cultured cardiomyocytes. However, it is not known whether UCPs play an essential role in cardioprotection in the intact heart. This study evaluated the cardioprotective efficacy of UCPs against I/R injury and characterized the mechanism of UCP-mediated protection in addition to the role of UCPs in ischemic preconditioning (IPC). Cardiac UCP3 knockout (UCP3?/?) and wild-type (WT) mice hearts were subjected to ex vivo and in vivo models of I/R injury and IPC. Isolated UCP3?/? mouse hearts were retrogradely perfused and found to have poorer recovery of left ventricular function compared with WT hearts under I/R conditions. In vivo occlusion of the left coronary artery resulted in twofold larger infarcts in UCP3?/? mice compared with WT mice. Moreover, the incidence of in vivo I/R arrhythmias was higher in UCP3?/? mice. Myocardial energetics were significantly impaired with I/R, as reflected by a decreased ATP content and an increase in the AMP-to-ATP ratio. UCP3?/? hearts generated more reactive oxygen species (ROS) than WT hearts during I/R. Pretreatment of UCP3?/? hearts with the pharmacological uncoupling agent carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone improved postischemic functional recovery. Also the protective efficacy of IPC was abolished in UCP3?/? mice. We conclude that UCP3 plays a critical role in cardioprotection against I/R injury and the IPC phenomenon. There is increased myocardial vulnerability to I/R injury in hearts lacking UCP3. The mechanisms of UCP3-mediated cardioprotection include regulation of myocardial energetics and ROS generation by UCP3 during I/R. PMID:23457013

Ozcan, Cevher; Palmeri, Monica; Horvath, Tamas L.; Russell, Kerry S.

2013-01-01

59

Ischemic preconditioning attenuates of ischemia-induced degradation of spectrin and tau: implications for ischemic tolerance  

Microsoft Academic Search

Global ischemia selectively induces CA1 neuronal death in the hippocampus. Pretreatment with non-lethal ischemia (i.e. ischemic\\u000a preconditioning) prevents CA1 neuronal death induced by lethal ischemia. While ischemic tolerance is a well-known phenomenon,\\u000a the underlying molecular mechanisms are not fully understood. Cytoskeletal proteins including ?-spectrin, tau, and microtubule-associated\\u000a protein 2 (MAP-2) are indispensable for the maintenance of neuronal homeostasis. Here, we

Takayuki Nakajima; Syoichi Ochi; Chika Oda; Maki Ishii; Kazushige Ogawa

2011-01-01

60

Morphological changes in the kidneys of rats with postischemic acute renal failure after intrarenal administration of fetal mesenchymal stem cells from human bone marrow.  

PubMed

Chronic experiments on outbred albino rats were performed to compare the dynamics of histological signs for postischemic renal injury (90-min thermal ischemia) after intraparenchymal injection of cultured fetal MSC from human bone marrow. Functional indexes of the ischemic kidney were predetermined. In the early period after ischemia (day 4), administration of human bone marrow MSC was followed by the increase in blood flow in the microcirculatory bed and decrease in the degree of alteration in renal tubules. An increase in the area of zones with histological signs for normal function of tubules was accompanied by the improvement of biochemical indexes for renal function. In the delayed period, a protective effect of cell therapy was manifested in the prevention of death of renal tubules. Mild calcification of the necrotic tubular epithelium served as a marker of this process. Human bone marrow MSC were labeled with the fluorescent probe Calcein. These cells migrated from the site of injection, spread in the interstitium, and retained viability for 7 days. During this period, some cells were incorporated into the lumen of renal tubules. PMID:19526146

Kudryavtsev, Yu V; Kirpatovskii, V I; Plotnikov, E Yu; Kazachenko, A V; Marei, M V; Khryapenkova, T G; Zorov, D B; Sukhikh, G T

2009-01-01

61

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

62

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

63

Combined postischemic hypothermia and delayed MK-801 treatment attenuates neurobehavioral deficits associated with transient global ischemia in rats  

Microsoft Academic Search

The present study was designed to determine whether postischemic hypothermia, delayed MK-801 (dizocilpine) administration, or a combination of these treatments can provide lasting neurobehavioral protection following transient global ischemia in rats. Rats were subjected to 10 min of normothermic (37°C) ischemia induced by 2-vessel occlusion and hypotension (50 mmHg) or sham procedures. Ischemia was followed by either: (a) 3 h

E. J. Green; A. J. Pazos; W. D. Dietrich; P. M. McCabe; N. Schneiderman; B. Lin; R. Busto; M. Y.-T. Globus; M. D. Ginsberg

1995-01-01

64

LPS-Induced Delayed Preconditioning Is Mediated by Hsp90 and Involves the Heat Shock Response in Mouse Kidney  

PubMed Central

Introduction We and others demonstrated previously that preconditioning with endotoxin (LPS) protected from a subsequent lethal LPS challenge or from renal ischemia-reperfusion injury (IRI). LPS is effective in evoking the heat shock response, an ancient and essential cellular defense mechanism, which plays a role in resistance to, and recovery from diseases. Here, by using the pharmacological Hsp90 inhibitor novobiocin (NB), we investigated the role of Hsp90 and the heat shock response in LPS-induced delayed renal preconditioning. Methods Male C57BL/6 mice were treated with preconditioning (P: 2 mg/kg, ip.) and subsequent lethal (L: 10 mg/kg, ip.) doses of LPS alone or in combination with NB (100 mg/kg, ip.). Controls received saline (C) or NB. Results Preconditioning LPS conferred protection from a subsequent lethal LPS treatment. Importantly, the protective effect of LPS preconditioning was completely abolished by a concomitant treatment with NB. LPS induced a marked heat shock protein increase as demonstrated by Western blots of Hsp70 and Hsp90. NB alone also stimulated Hsp70 and Hsp90 mRNA but not protein expression. However, Hsp70 and Hsp90 protein induction in LPS-treated mice was abolished by a concomitant NB treatment, demonstrating a NB-induced impairment of the heat shock response to LPS preconditioning. Conclusion LPS-induced heat shock protein induction and tolerance to a subsequent lethal LPS treatment was prevented by the Hsp90 inhibitor, novobiocin. Our findings demonstrate a critical role of Hsp90 in LPS signaling, and a potential involvement of the heat shock response in LPS-induced preconditioning. PMID:24646925

Kaucsár, Tamás; Bodor, Csaba; Godó, Mária; Szalay, Csaba; Révész, Csaba; Németh, Zalán; Mózes, Miklós; Szénási, Gábor; Rosivall, László; S?ti, Csaba; Hamar, Péter

2014-01-01

65

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

66

Preconditioning Stem Cells for In Vivo Delivery  

PubMed Central

Abstract Stem cells have emerged as promising tools for the treatment of incurable neural and heart diseases and tissue damage. However, the survival of transplanted stem cells is reported to be low, reducing their therapeutic effects. The major causes of poor survival of stem cells in vivo are linked to anoikis, potential immune rejection, and oxidative damage mediating apoptosis. This review investigates novel methods and potential molecular mechanisms for stem cell preconditioning in vitro to increase their retention after transplantation in damaged tissues. Microenvironmental preconditioning (e.g., hypoxia, heat shock, and exposure to oxidative stress), aggregate formation, and hydrogel encapsulation have been revealed as promising strategies to reduce cell apoptosis in vivo while maintaining biological functions of the cells. Moreover, this review seeks to identify methods of optimizing cell dose preparation to enhance stem cell survival and therapeutic function after transplantation. PMID:25126478

Sart, Sébastien; Ma, Teng

2014-01-01

67

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

68

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

69

Hypoxic Preconditioning Alleviates Ethanol Neurotoxicity: the Involvement of Autophagy  

PubMed Central

Ethanol is a neuroteratogen and neurodegeneration is the most devastating consequence of developmental exposure to ethanol. A sublethal preconditioning has been proposed as a neuroprotective strategy against several central nervous system (CNS) neurodegenerative diseases. We have recently demonstrated that autophagy is a protective response to alleviate ethanol toxicity. A modest hypoxic preconditioning (1% oxygen) did not cause neurotoxicity but induced autophagy (Tzeng et al., 2010). We therefore hypothesize that the modest hypoxic preconditioning may offer a protection against ethanol-induced neurotoxicity. We showed here that the modest hypoxic preconditioning (1% oxygen) for 8 hours significantly alleviated ethanol-induced death of SH-SY5Y neuroblastoma cells. Under the normoxia condition, cell viability in ethanol-exposed cultures (316 mg/dl for 48 hrs) was 49 ± 6% of untreated controls; however, with hypoxic preconditioning, cell viability in the ethanol-exposed group increased to 78 ± 7% of the controls (p < 0.05; n = 3). Bafilomycin A1, an inhibitor of autophagosome and lysosome fusion, blocked hypoxic preconditioning-mediated protection. Similarly, inhibition of autophagic initiation by wortmannin also eliminated hypoxic preconditioning-mediated protection. In contrast, activation of autophagy by rapamycin further enhanced neuroprotection caused by hypoxic preconditioning. Taken together, the results confirm that autophagy is a protective response against ethanol neurotoxicity and the modest hypoxic preconditioning can offer neuroprotection by activating autophagic pathways. PMID:23568540

Wang, Haiping; Bower, Kimberly A.; Frank, Jacqueline A.; Xu, Mei; Luo, Jia

2013-01-01

70

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

71

Preconditioning and the limit to the incompressible flow equations  

NASA Technical Reports Server (NTRS)

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

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

1993-01-01

72

Footprint Analysis: A Shape Analysis that Discovers Preconditions  

E-print Network

Footprint Analysis: A Shape Analysis that Discovers Preconditions Cristiano Calcagno1 , Dino of London Abstract. Existing shape analysis algorithms infer descriptions of data structures at program points, starting from a given precondition. We describe an analysis that does not require any

Yang, Hongseok

73

Nonnegative Mixed-Norm Preconditioning for Microscopy Image Segmentation  

Microsoft Academic Search

Image segmentation in microscopy, especially in interference- based optical microscopy modalities, is notoriously challenging due to inherent optical artifacts. We propose a general algebraic framework for preconditioning microscopy images. It transforms an image that is un- suitable for direct analysis into an image that can be effortlessly seg- mented using global thresholding. We formulate preconditioning as the minimization of nonnegative-constrained

Kang Li; Takeo Kanade

2009-01-01

74

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

75

CD38 Exacerbates Focal Cytokine Production, Postischemic Inflammation and Brain Injury after Focal Cerebral Ischemia  

PubMed Central

Background Converging evidence suggests that inflammatory processes significantly influence brain injury and clinical impairment in ischemic stroke. Although early studies suggested a key role of lymphocytes, recent data has emphasized the orchestrating function of innate immunity, i.e., macrophages and microglia. The bifunctional receptor and ectoenzyme CD38 synthesizes calcium-mobilizing second messengers (e.g., cyclic ADP-ribose), which have been shown to be necessary for activation and migration of myeloid immune cells. Therefore, we investigated the dynamics of CD38 in stroke and the impact of CD38-deficiency on cytokine production, inflammation and cerebral damage in a mouse model of cerebral ischemia-reperfusion. Methodology/Principal Findings We show that the local expression of the chemokine MCP-1 was attenuated in CD38-deficient mice compared with wildtype mice after focal cerebral ischemia and reperfusion. In contrast, no significant induction of MCP-1 expression was observed in peripheral blood after 6 hours. Flow cytometry analysis revealed less infiltrating macrophages and lymphocytes in the ischemic hemisphere of CD38-deficient mice, whereas the amount of resident microglia was unaltered. An up-regulation of CD38 expression was observed in macrophages and CD8+ cells after focal cerebral ischemia in wildtype mice, whereas CD38 expression was unchanged in microglia. Finally, we demonstrate that CD38-deficiency decreases the cerebral ischemic injury and the persistent neurological deficit after three days of reperfusion in this murine temporary middle cerebral artery occlusion (tMCAO) model. Conclusion/Significance CD38 is differentially regulated following stroke and its deficiency attenuates the postischemic chemokine production, the immune cell infiltration and the cerebral injury after temporary ischemia and reperfusion. Therefore CD38 might prove a therapeutic target in ischemic stroke. PMID:21625615

Gelderblom, Mathias; Ludewig, Peter; Leypoldt, Frank; Koch-Nolte, Friedrich; Gerloff, Christian; Magnus, Tim

2011-01-01

76

Post-ischemic therapy with CGS-19755 (alone or in combination with hypothermia) in gerbils.  

PubMed

Hypothermia or a glutamate receptor antagonist may offer protection when used before or within seconds of an ischemic insult. In this experiment, we tested the efficacy of hypothermia (34 degrees C) versus CGS-19755 (a potent competitive N-methyl-D-aspartate (NMDA) receptor blocker) and their combination which was administered 0.5 h after a 5-min forebrain ischemic insult in gerbils. Morphological assessments were done in Group A at the end of 7 days while Group B was evaluated at 29 days. Each group had four sets of animals: saline treated controls; hypothermia treated; CGS-19755 treated; and a combination of CGS-19755 + hypothermia treated animals. Group A showed significant 'protection', i.e. minimal neuronal damage in the animals treated with hypothermia alone. Protection was evident in the cerebral cortex (P < 0.001), hippocampus CA1 (P < 0.01), and in the striatum (P < 0.05). There was no evidence of neuronal protection in the animals that had received either CGS-19755 alone or a combination of hypothermia and CGS-19755. In Group B (29 day assessment) the neuroprotective effects were not evident in any of the animals when compared to the controls. Behavioral testing with Morris water-maze testing showed no significant differences between the control and any of the treated animals. Our data suggests that 'post-ischemic' therapy with hypothermia may delay the effects of ischemia but does not offer significant long-term neuronal protection. Protection seen at 7 days is not evident at 29 days.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7659298

Shuaib, A; Waqar, T; Wishart, T; Kanthan, R

1995-05-19

77

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

78

Microvessel changes after post-ischemic benign and malignant hyperemia: experimental study in rats  

PubMed Central

Background The present investigation was designed to elucidate the use of dynamic contrast enhanced perfusion MR imaging (DCE pMRI) in characterizing hyperemia, including microvessel changes, and to examine whether DCE pMRI can predict benign or malignant hyperemia. Methods Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) by intraluminal suture placement. All rats were randomized to 4 groups: MCAO for 0.5 hours followed by saline treatment (10 ml/kg; group 1); MCAO for 3 hours followed by treatment with saline (group 2) or urokinase (25000 IU/kg; group 3); and MCAO for 6 hours followed by urokinase treatment (group 4). Relative cerebral blood volume (rCBV) and relative maximum slope of increase of the signal intensity time curve (rMSI) were quantitatively analyzed from MRI. Microvessel diameter and blood-brain barrier disruption obtained by laser scanning confocal microscopy (LSCM) as well as transmission electron microscopy (TEM) were obtained for correlative study. Results Benign hyperemia was noticed only in group 1; malignant hyperemia was seen in group 3. Although the rCBV of malignant hyperemia was slightly higher than in benign hyperemia (P > 0.05), the rMSI, on the other hand, was significantly lower (P < 0.05). Fluoro-isothiocyanate dextran (FITC-dextran) extravasations, marked glial end-foot process swelling, and significant vasodilatation were seen in malignant hyperemia, while no or mild leakage of FITC-dextran and slight glial end-foot process swelling occurred in benign hyperemia. Conclusion Our findings indicate that DCE pMRI can characterize post-ischemic hyperemia and correlates well with microvascular damage. PMID:20398382

2010-01-01

79

Losartan Improved Antioxidant Defense, Renal Function and Structure of Postischemic Hypertensive Kidney  

PubMed Central

Ischemic acute renal failure (ARF) is a highly complex disorder involving renal vasoconstriction, filtration failure, tubular obstruction, tubular backleak and generation of reactive oxygen species. Due to this complexity, the aim of our study was to explore effects of Angiotensin II type 1 receptor (AT1R) blockade on kidney structure and function, as well as oxidative stress in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. Experiments were performed on anaesthetized adult male SHR in the model of ARF with 40 minutes clamping the left renal artery. The right kidney was removed and 40 minutes renal ischemia was performed. Experimental groups received AT1R antagonist (Losartan) or vehicle (saline) in the femoral vein 5 minutes before, during and 175 minutes after the period of ischemia. Biochemical parameters were measured and kidney specimens were collected 24h after reperfusion. ARF significantly decreased creatinine and urea clearance, increased LDL and lipid peroxidation in plasma. Treatment with losartan induced a significant increase of creatinine and urea clearance, as well as HDL. Lipid peroxidation in plasma was decreased and catalase enzyme activity in erythrocytes was increased after losartan treatment. Losartan reduced cortico-medullary necrosis and tubular dilatation in the kidney. High expression of pro-apoptotic Bax protein in the injured kidney was downregulated after losartan treatment. Our results reveal that angiotensin II (via AT1R) mediates the most postischemic injuries in hypertensive kidney through oxidative stress enhancement. Therefore, blockade of AT1R may have beneficial effects in hypertensive patients who have developed ARF. PMID:24796787

Ivanov, Milan; Mihailovi?-Stanojevi?, Nevena; Gruji? Milanovi?, Jelica; Jovovi?, ?ur?ica; Markovi?-Lipkovski, Jasmina; ?irovi?, Sanja; Miloradovi?, Zoran

2014-01-01

80

Fetal asphyctic preconditioning modulates the acute cytokine response thereby protecting against perinatal asphyxia in neonatal rats  

PubMed Central

Background Perinatal asphyxia (PA) is a major cause of brain damage and neurodevelopmental impairment in infants. Recent investigations have shown that experimental sublethal fetal asphyxia (FA preconditioning) protects against a subsequent more severe asphyctic insult at birth. The molecular mechanisms of this protection have, however, not been elucidated. Evidence implicates that inflammatory cytokines play a protective role in the induction of ischemic tolerance in the adult brain. Accordingly, we hypothesize that FA preconditioning leads to changes in the fetal cytokine response, thereby protecting the newborn against a subsequent asphyctic insult. Methods In rats, FA preconditioning was induced at embryonic day 17 by clamping the uterine vasculature for 30 min. At term birth, global PA was induced by placing the uterine horns, containing the pups, in a saline bath for 19 min. We assessed, at different time points after FA and PA, mRNA and protein expression of several cytokines and related receptor mRNA levels in total hemispheres of fetal and neonatal brains. Additionally, we measured pSTAT3/STAT3 levels to investigate cellular responses to these cytokines. Results Prenatally, FA induced acute downregulation in IL-1?, TNF-? and IL-10 mRNA levels. At 96 h post FA, IL-6 mRNA and IL-10 protein expression were increased in FA brains compared with controls. Two hours after birth, all proinflammatory cytokines and pSTAT3/STAT3 levels decreased in pups that experienced FA and/or PA. Interestingly, IL-10 and IL-6 mRNA levels increased after PA. When pups were FA preconditioned, however, IL-10 and IL-6 mRNA levels were comparable to those in controls. Conclusions FA leads to prenatal changes in the neuroinflammatory response. This modulation of the cytokine response probably results in the protective inflammatory phenotype seen when combining FA and PA and may have significant implications for preventing post-asphyctic perinatal encephalopathy. PMID:23351591

2013-01-01

81

Hyperbaric oxygen preconditioning protects rats against CNS oxygen toxicity.  

PubMed

We examined the hypothesis that repeated exposure to non-convulsive hyperbaric oxygen (HBO) as preconditioning provides protection against central nervous system oxygen toxicity (CNS-OT). Four groups of rats were used in the study. Rats in the control and the negative control (Ctl-) groups were kept in normobaric air. Two groups of rats were preconditioned to non-convulsive HBO at 202 kPa for 1h once every other day for a total of three sessions. Twenty-four hours after preconditioning, one of the preconditioned groups and the control rats were exposed to convulsive HBO at 608 kPa, and latency to CNS-OT was measured. Ctl- rats and the second preconditioned group (PrC-) were not subjected to convulsive HBO exposure. Tissues harvested from the hippocampus and frontal cortex were evaluated for enzymatic activity and nitrotyrosine levels. In the group exposed to convulsive oxygen at 608 kPa, latency to CNS-OT increased from 12.8 to 22.4 min following preconditioning. A significant decrease in the activity of glutathione reductase and glucose-6-phosphate dehydrogenase, and a significant increase in glutathione peroxidase activity, was observed in the hippocampus of preconditioned rats. Nitrotyrosine levels were significantly lower in the preconditioned animals, the highest level being observed in the control rats. In the cortex of the preconditioned rats, a significant increase was observed in glutathione S-transferase and glutathione peroxidase activity. Repeated exposure to non-convulsive HBO provides protection against CNS-OT. The protective mechanism involves alterations in the enzymatic activity of the antioxidant system and lower levels of peroxynitrite, mainly in the hippocampus. PMID:24675062

Arieli, Yehuda; Kotler, Doron; Eynan, Mirit; Hochman, Ayala

2014-06-15

82

Integration of multiple memories in sensory preconditioning.  

PubMed

The present study demonstrates that humans' response to a single stimulus (S1) is determined by what follows S1's associates. The experiment used a sensory preconditioning (SPC) design where S1 was associated with both S2 and S3 on separate trials before establishing relationships between these latter stimuli with an outcome or its absence in a second phase. When S2 and S3 were associated with the same consequence, either an outcome or its absence, strong consequence-based responding to S1 was observed in a reaction time test. Participants responded quickly to indicate that the outcome was, or was not, predicted by S1. When S2 predicted the outcome and S3 did not, SPC was weaker although participants were not slower to respond to S1. Implications on the understanding of the mechanisms that allow for the response to S1 to emerge are discussed. PMID:25290440

Craddock, Paul; Renaux, Charlotte; Lefèvre, Françoise; Nelson, James Byron; Molet, Mikael

2014-10-01

83

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

E-print Network

cortical cultures and in the postischemic brain Il-Doo Kim a,1 , Chae-Moon Lim a,1 , Jung-Bin Kim a , Hye RNAs (siRNA) or plasmid encoding short-hairpin RNAs (shRNAs). shRNAs are synthesized from the plasmids

Park, Jong-Sang

84

40 CFR 1065.516 - Sample system decontamination and preconditioning.  

...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

85

PRECONDITIONING AND PARALLEL IMPLEMENTATION OF IMPLICIT RUNGE-KUTTA METHODS.  

E-print Network

iterative methods, nonlinear equations, ordinary differential equations, parallelism, preconditioning) methods applied to systems of differential equations is to solve the underlying systems of nonlinear equations of IRK methods. A detailed presentation of the new preconditioner i

Jay, Laurent O.

86

Distributed Kalman filtering compared to Fourier domain preconditioned conjugate gradient  

E-print Network

Distributed Kalman filtering compared to Fourier domain preconditioned conjugate gradient for laser of the tomography problem. The second algorithm is the distributed Kalman filter (DKF) developed by Massioni et al

Greer, Julia R.

87

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

88

Ischemic preconditioning of rat livers against cold storage-reperfusion injury: Role of nonparenchymal cells and the phenomenon of heterologous preconditioning  

Microsoft Academic Search

Brief periods of ischemia followed by reperfusion render tissues resistant against subsequent prolonged ischemia, a phenomenon called ischemic preconditioning. The effect of ischemic preconditioning on liver transplantation was investigated in relation to sinusoidal endothelial cell injury and Kupffer-cell activation, which are prominent features of storage and reperfusion injury leading to liver graft failure. Rat livers were preconditioned by 5 or

Masahiro Arai; Ronald G. Thurman; John J. Lemasters

2001-01-01

89

Protection of cardiac mitochondria by diazoxide and protein kinase C: Implications for ischemic preconditioning  

PubMed Central

Mitochondrial ATP-sensitive K (mitoKATP) channels play a central role in protecting the heart from injury in ischemic preconditioning. In isolated mitochondria exposed to elevated extramitochondrial Ca, Pi, and anoxia to simulate ischemic conditions, the selective mitoKATP channel agonist diazoxide (25–50 ?M) potently reduced mitochondrial injury by preventing both the mitochondrial permeability transition (MPT) and cytochrome c loss from the intermembrane space. Both effects were blocked completely by the selective mitoKATP antagonist 5-hydroxydecanoate. The protective effect against Ca-induced MPT was most evident under conditions in which the ability of electron transport to support membrane potential (??m) was decreased and inner membrane leakiness was increased moderately. Under these conditions, mitoKATP channel activity strongly regulated ??m, and diazoxide prevented MPT by inhibiting the driving force for Ca uptake. Phorbol 12-myristate 13-acetate mimicked the protective effects of diazoxide, unless 5-hydroxydecanoate was present, indicating that protein kinase C activation also protects mitochondria by activating mitoKATP channels. Because ??m recovery ultimately is required for heart functional recovery, these results may explain how mitoKATP channel activation mimics ischemic preconditioning by protecting mitochondria as they pass through a critical vulnerability window during ischemia/reperfusion. PMID:11867760

Korge, Paavo; Honda, Henry M.; Weiss, James N.

2002-01-01

90

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

91

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

92

Effects of dietary polyunsaturated fatty acids and hepatic steatosis on the functioning of isolated working rat heart under normoxic conditions and during post-ischemic reperfusion  

Microsoft Academic Search

The purpose of this study was to modify the amount of 22:4 n-6, 22:5 n-6 and 20:5 n-3 in cardiac phospholipids and to evaluate the influence of these changes on the functioning of working rat hearts and mitochondrial energy metabolism under normoxic conditions and during postischemic reperfusion. The animals were fed one of these four diets: (i) 10% sunflower seed

Luc Demaison; Daniel Moreau; Catherine Vergely-Vandriesse; Stéphane Grégoire; Martine Degois; Luc Rochette

2001-01-01

93

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

94

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

95

Multigrid Preconditioning for the Overlap Operator in Lattice QCD  

E-print Network

The overlap operator is a lattice discretization of the Dirac operator of quantum chromodynamics, the fundamental physical theory of the strong interaction between the quarks. As opposed to other discretizations it preserves the important physical property of chiral symmetry, at the expense of requiring much more effort when solving systems with this operator. We present a preconditioning technique based on another lattice discretization, the Wilson-Dirac operator. The mathematical analysis precisely describes the effect of this preconditioning in the case that the Wilson-Dirac operator is normal. Although this is not exactly the case in realistic settings, we show that current smearing techniques indeed drive the Wilson-Dirac operator towards normality, thus providing a motivation why our preconditioner works well in computational practice. Results of numerical experiments in physically relevant settings show that our preconditioning yields accelerations of up to one order of magnitude.

James Brannick; Andreas Frommer; Karsten Kahl; Björn Leder; Matthias Rottmann; Artur Strebel

2014-10-27

96

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

97

Impact of hypoglycemic agents on myocardial ischemic preconditioning.  

PubMed

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

2014-06-15

98

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

99

Remote preconditioning, perconditioning, and postconditioning: a comparative study of their cardioprotective properties in rat models  

PubMed Central

OBJECTIVE: Ischemia reperfusion injury is partly responsible for the high mortality associated with induced myocardial injury and the reduction in the full benefit of myocardial reperfusion. Remote ischemic preconditioning, perconditioning, and postconditioning have all been shown to be cardioprotective. However, it is still unknown which one is the most beneficial. To examine this issue, we used adult male Wistar rat ischemia reperfusion models to compare the cardioprotective effect of these three approaches applied on double-sided hind limbs. METHODS: The rats were randomly distributed to the following five groups: sham, ischemia reperfusion, remote preconditioning, remote perconditioning, and remote post-conditioning. The ischemia/reperfusion model was established by sternotomy followed by a 30-min ligation of the left coronary artery and a subsequent 3-h reperfusion. Remote conditioning was induced with three 5-min ischemia/5-min reperfusion cycles of the double-sided hind limbs using a tourniquet. RESULTS: A lower early reperfusion arrhythmia score (1.50±0.97) was found in the rats treated with remote perconditioning compared to those in the ischemia reperfusion group (2.33±0.71). Meanwhile, reduced infarct size was also observed (15.27±5.19% in remote perconditioning, 14.53±3.45% in remote preconditioning, and 19.84±5.85% in remote post-conditioning vs. 34.47±7.13% in ischemia reperfusion, p<0.05), as well as higher expression levels of the apoptosis-relevant protein Bcl-2/Bax following global (ischemia/reperfusion) injury in in vivo rat heart models (1.255±0.053 in remote perconditioning, 1.463±0.290 in remote preconditioning, and 1.461±0.541 in remote post-conditioning vs. 1.003±0.159 in ischemia reperfusion, p<0.05). CONCLUSION: Three remote conditioning strategies implemented with episodes of double-sided hind limb ischemia/reperfusion have similar therapeutic potential for cardiac ischemia/reperfusion injury, and remote perconditioning has a greater ability to prevent reperfusion arrhythmia. PMID:23525325

Zhu, Shui-Bo; Liu, Yong; Zhu, Yu; Yin, Gui-Lin; Wang, Rong-Ping; Zhang, Yu; Zhu, Jian; Jiang, Wei

2013-01-01

100

Lipoxin A4 Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats  

PubMed Central

This study aims to investigate the pre- and postconditioning effects of lipoxin A4 (LXA4) on myocardial damage caused by ischemia/reperfusion (I/R) injury. Seventy-two rats were divided into 6 groups: sham groups (C1 and C2), I/R groups (I/R1 and I/R2), and I/R plus LXA4 preconditioning and postconditioning groups (LX1 and LX2). The serum levels of IL-1?, IL-6, IL-8, IL-10, TNF-?, and cardiac troponin I (cTnI) were measured. The content and the activity of Na+-K+-ATPase as well as the superoxide dismutase (SOD), and malondialdehyde (MDA) levels were determined. Along with the examination of myocardium ultrastructure and ventricular arrhythmia scores (VAS), connexin 43 (Cx43) expression were also detected. Lower levels of IL-1?, IL-6, IL-8, TNF-?, cTnI, MDA content, and VAS and higher levels of IL-10, SOD activity, Na+-K+-ATPase content and activity, and Cx43 expression appeared in LX groups than I/R groups. Besides, H&E staining, TEM examination as well as analysis of gene, and protein confirmed that LXA4 preconditioning was more effective than postconditioning in preventing arrhythmogenesis via the upregulation of Cx43. That is, LXA4 postconditioning had better protective effect on Na+-K+-ATPase and myocardial ultrastructure. PMID:23956501

Zhao, Qifeng; Shao, Lan; Hu, Xingti; Wu, Guowei; Du, Jie; Xia, Jie; Qiu, Huixian

2013-01-01

101

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

102

Fourier analysis of finite element preconditioned collocation schemes  

NASA Technical Reports Server (NTRS)

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

Deville, Michel O.; Mund, Ernest H.

1990-01-01

103

Recent Progress in Parallel Schur Complement Preconditioning for Computational Fluid  

NASA Technical Reports Server (NTRS)

We consider preconditioning methods for nonself-adjoint advective-diffusive systems based on a nonoverlapping Schur complement procedure for arbitrary triangulated domains. The triangulation is first partitioned using the METIS multi-level $k$-way partitioning code. This partitioning of the triangulation induces a natural 2x2 partitioning of the demoralization matrix. By considering various inverse approximations of the 2x2 system we have developed a family of robust preconditioning techniques. The performance of these approximations will be discussed and numerous examples shown to illustrate the efficiency of the technique.

Barth, Tim; Kwak, Dochan (Technical Monitor)

1997-01-01

104

Time-reversal Waveform Preconditioning for Clutter Rejection T. Varslot,a  

E-print Network

Time-reversal Waveform Preconditioning for Clutter Rejection T. Varslot,a B. Yazici,a C.-E Yarman preconditioning scheme for optimal clutter rejection in radar imaging is presented. Waveform preconditioning for clutter rejection achieves efficient use of power and computational resources by distributing power

Yazici, Birsen

105

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

106

Influence of diabetic state and that of different sulfonylureas on the size of myocardial infarction with and without ischemic preconditioning in rabbits.  

PubMed

The sensitivity of the myocardium to ischemia and the level of protection achieved by ischemic preconditioning is shaped by the joint influence of several mechanisms in diabetes mellitus. In vivo studies were made in alloxan diabetic and non-diabetic control rabbits to assess if the effects of preconditioning and sulfonylurea pretreatment with either glibenclamide or glimepiride (0.05-0.2-0.6 micromol kg (-1)) influence the extent of the infarcted area caused by one hour ligature of the left coronary artery. For our study, we defined preconditioning as 2 minutes of ischemia followed by 2 minutes of reperfusion, which was repeated 3 times. The interrelationship of the diabetic pathophysiological state, and sulfonylurea treatment during ischemic preconditioning were studied by comparing the infarcted areas and the rate of infarction to risk areas in left ventricular slices using computer planimetry. In healthy control rabbits preconditioning reduced infarcted area (29.6 +/- 3.0% vs. 48.8 +/- 2.8% p < 0.0005), while in diabetic rabbits this protection did not occur (53.3 +/- 7.3% vs. 56.6 +/- 4.4% NS). Glibenclamide in all of applied doses prevented the protective effect in control animals (infarction/ risk area: HP: 0.47 +/- 0.04 vs. HP Glib-0.05 : 0.69+/-0.06 p< 0.004 vs. HP Glib-0.2 : 0.72+/-0.09 p< 0.002 vs. HP Glib-0.6 : 0.75 +/- 0.04 p< 0.001). In contrast, in diabetic rabbits low dose of glibenclamide contributed to the same development of preconditioning. However the highest dose of glibenclamide (infarction/risk area: DP Glib-0.6 : 0.77 +/- 0.17 vs. DP Glib-0.05 : 0.55 < 0.03 p < 0.047) and the consequences of the diabetic state blocked the salutary effect. Glimepiride had no considerable influence on the protective effect, either in control nor in diabetic animals. Glibenclamide and glimepiride, presumably due to their different sulfonylurea receptor affinity in the heart, resulted in different influence on preconditioning in healthy control animals. Glibenclamide treatment seemed to be more harmful when less K (+)ATP channels were activated. The accomplishment of myocardial preconditioning in diabetes mellitus is claimed to be determined by the interaction of both metabolically influenced K (+)ATP channel activity and the dose of sulfonylurea. PMID:12148084

Nieszner, E; Posa, I; Kocsis, E; Pogátsa, G; Préda, I; Koltai, M Z

2002-08-01

107

Hydrogen Sulfide Preconditioning Protects Rat Liver against Ischemia/Reperfusion Injury by Activating Akt-GSK-3? Signaling and Inhibiting Mitochondrial Permeability Transition  

PubMed Central

Hydrogen sulfide (H2S) is the third most common endogenously produced gaseous signaling molecule, but its impact on hepatic ischemia/reperfusion (I/R) injury, especially on mitochondrial function, remains unclear. In this study, rats were randomized into Sham, I/R, ischemia preconditioning (IPC) or sodium hydrosulfide (NaHS, an H2S donor) preconditioning groups. To establish a model of segmental (70%) warm hepatic ischemia, the hepatic artery, left portal vein and median liver lobes were occluded for 60 min and then unclamped to allow reperfusion. Preconditioning with 12.5, 25 or 50 ?mol/kg NaHS prior to the I/R insult significantly increased serum H2S levels, and, similar to IPC, NaHS preconditioning decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the plasma and prevented hepatocytes from undergoing I/R-induced necrosis. Moreover, a sub-toxic dose of NaHS (25 ?mol/kg) did not disrupt the systemic hemodynamics but dramatically inhibited mitochondrial permeability transition pore (MPTP) opening and thus prevented mitochondrial-related cell death and apoptosis. Mechanistic studies revealed that NaHS preconditioning markedly increased the expression of phosphorylated protein kinase B (p-Akt), phosphorylated glycogen synthase kinase-3 beta (p-GSK-3?) and B-cell lymphoma-2 (Bcl-2) and decreased the release of mitochondrial cytochrome c and cleaved caspase-3/9 levels. Therefore, NaHS administration prior to hepatic I/R ameliorates mitochondrial and hepatocellular damage through the inhibition of MPTP opening and the activation of Akt-GSK-3? signaling. Furthermore, this study provides experimental evidence for the clinical use of H2S to reduce liver damage after perioperative I/R injury. PMID:24058562

Zhang, Hao; Xu, Fengying; Zou, Zui; Liu, Meng; Wang, Quanxing; Miao, Mingyong; Shi, Xueyin

2013-01-01

108

Minimal preconditioning effects observed for inflation tests of planar tissues.  

PubMed

The purpose of this study is to investigate the effects of preconditioning on the deformation response of planar tissues measured by inflation tests. The inflation response of test specimens, including the bovine cornea, bovine and porcine sclera, and human skin, exhibited a negligible evolving deformation response when subjected to repeated pressure loading with recovery periods between cycles. Tissues obtained complete recovery to the reference state, and strain contours across the entire specimen were nearly identical at the maximum pressure of each load cycle. This repeatability was obtained regardless of strain history. These results suggest that negligible permanent change was induced in the microstructure by inflation testing. Additionally, we present data illustrating that a lack of a recovery period can result in an evolving deformation response to repeated loading that is commonly attributed to preconditioning. These results suggest that the commonly observed effects of preconditioning may be avoided by experimental design for planar tissues characterized by long collagen fibers arranged in the plane of the tissue. Specifically, if the test is designed to fully fix the specimen boundary during loading, adequate recovery periods are allowed after each load cycle, and loads are limited to avoid damage, preconditioning effects may be avoided for planar tissues. PMID:23897279

Tonge, Theresa K; Murienne, Barbara J; Coudrillier, Baptiste; Alexander, Stephen; Rothkopf, William; Nguyen, Thao D

2013-11-01

109

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

110

Preconditioning the Differential Emission Measure (Te) Inverse Problem  

NASA Astrophysics Data System (ADS)

In an inverse problem of any kind, poor conditioning of the inverse operator decreases the numerical stability of any unregularized solution in the presence of data noise. In this paper we show that the numerical stability of the differential emission measure (DEM) inverse problem can be considerably improved by judicious choice of the integral operator. Specifically, we formulate a combinatorial optimization problem where, in a preconditioning step, a subset of spectral lines is selected in such a way as to minimize explicitly the condition number of the discretized integral operator. We tackle this large combinatorial optimization problem using a genetic algorithm. We apply this preconditioning technique to a synthetic data set comprising of solar UV/EUV emission lines in the SOHO SUMER/CDS wavelength range. Following which we test the same hypothesis on lines observed by the Harvard S-055 EUV spectroheliometer. On performing the inversion we see that the temperature distribution in the emitting region of the solar atmosphere is recovered with considerably better stability and smaller error bars when our preconditioning technique is used, in both synthetic and ``real'' cases, even though this involves the analysis of fewer spectral lines than in the ``All-lines'' approach. The preconditioning step leads to regularized inversions that compare favorably to inversions by singular value decomposition, while providing greater flexibility in the incorporation of physically and/or observationally based constraints in the line selection process.

McIntosh, S. W.; Charbonneau, P.; Brown, J. C.

2000-02-01

111

40 CFR 86.232-94 - Vehicle preconditioning.  

Code of Federal Regulations, 2013 CFR

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

2013-07-01

112

40 CFR 86.232-94 - Vehicle preconditioning.  

Code of Federal Regulations, 2011 CFR

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

2011-07-01

113

40 CFR 86.232-94 - Vehicle preconditioning.  

Code of Federal Regulations, 2010 CFR

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

2010-07-01

114

40 CFR 86.232-94 - Vehicle preconditioning.  

Code of Federal Regulations, 2012 CFR

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

2012-07-01

115

Multilevel Preconditioning for Partition of Unity Methods -Some Analytic Concepts  

E-print Network

basis functions", "web splines", "generalized finite elements" or " smoothed particle hydrodynamics (see e.g. [11]) centering on atomic decompositions related to PUM. While most of the numerical workMultilevel Preconditioning for Partition of Unity Methods - Some Analytic Concepts W. Dahmen, S

116

Ischemic preconditioning accelerates the fatty acid oxidation of rat hearts  

Microsoft Academic Search

BackgroundIschemic preconditioning (IPC) reduced myocardial ATP depletion during sustained ischemia and has a powerful protective effect on the myocardium. The purpose of the present study was to clarify the effects of IPC on myocardial accumulation of fatty acid (FA) tracer and its intracellular metabolism.

Akira Matsuki; Takashi Nozawa; Akihiko Igawa; Norio Igarashi; Teruo Nakadate; Nozomu Fujii; Hiroshi Inoue

2009-01-01

117

33 CFR 183.320 - Preconditioning for tests.  

Code of Federal Regulations, 2011 CFR

...Outboard Boats Rated for Engines of 2 Horsepower or Less General § 183.320 Preconditioning...column 6 of Table 4 for the maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2011-07-01

118

33 CFR 183.220 - Preconditioning for tests.  

Code of Federal Regulations, 2012 CFR

...Boats Rated for Engines of More Than 2 Horsepower General § 183.220 Preconditioning...shown in Column 6 of Table 4 for maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2012-07-01

119

33 CFR 183.320 - Preconditioning for tests.  

Code of Federal Regulations, 2010 CFR

...Outboard Boats Rated for Engines of 2 Horsepower or Less General § 183.320 Preconditioning...column 6 of Table 4 for the maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2010-07-01

120

33 CFR 183.220 - Preconditioning for tests.  

Code of Federal Regulations, 2011 CFR

...Boats Rated for Engines of More Than 2 Horsepower General § 183.220 Preconditioning...shown in Column 6 of Table 4 for maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2011-07-01

121

33 CFR 183.320 - Preconditioning for tests.  

...Outboard Boats Rated for Engines of 2 Horsepower or Less General § 183.320 Preconditioning...column 6 of Table 4 for the maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2014-07-01

122

33 CFR 183.220 - Preconditioning for tests.  

Code of Federal Regulations, 2013 CFR

...Boats Rated for Engines of More Than 2 Horsepower General § 183.220 Preconditioning...shown in Column 6 of Table 4 for maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2013-07-01

123

33 CFR 183.320 - Preconditioning for tests.  

Code of Federal Regulations, 2013 CFR

...Outboard Boats Rated for Engines of 2 Horsepower or Less General § 183.320 Preconditioning...column 6 of Table 4 for the maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2013-07-01

124

33 CFR 183.220 - Preconditioning for tests.  

...Boats Rated for Engines of More Than 2 Horsepower General § 183.220 Preconditioning...shown in Column 6 of Table 4 for maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2014-07-01

125

33 CFR 183.320 - Preconditioning for tests.  

Code of Federal Regulations, 2012 CFR

...Outboard Boats Rated for Engines of 2 Horsepower or Less General § 183.320 Preconditioning...column 6 of Table 4 for the maximum horsepower marked on the boat; less the persons...purpose depends upon the maximum rated horsepower of the boat being tested and is...

2012-07-01

126

Preconditions of Change in Schools (FISK). Project Number 6051.  

ERIC Educational Resources Information Center

Preliminary results of this study of the preconditions for pedagogical change in Swedish schools indicate that national curricular emphases have changed, but that accompanying changes in teaching methods may conceal wide variation in content and import. The study's objective was to identify the factors conducive or hostile to change in the…

Svingby, Gunilla

1981-01-01

127

Approximate Schur Complement Preconditioning of the Lowest Order Nodal Discretizations  

E-print Network

Approximate Schur Complement Preconditioning of the Lowest Order Nodal Discretizations J. David moments, making the nodal discretization naturally compatible with the various homogenization techniques\\Gamma 1 2 and \\Deltay j = y j+ 1 2 \\Gamma y j \\Gamma 1 2 . 1.1 The Nodal Discretization Common to all

128

Two-level Overlapping Schwarz Preconditioning of Nodal Discontinuous  

E-print Network

Two-level Overlapping Schwarz Preconditioning of Nodal Discontinuous Galerkin Discretizations method for solving unstructured nodal discontinuous Galerkin discretizations of the indefinite Helmholtz in the subdomain solves as the order of the elements increases. In this paper, we detail the discretization

Olson, Luke

129

Acute Superoxide Radical Scavenging Reduces Blood Pressure but Does Not Influence Kidney Function in Hypertensive Rats with Postischemic Kidney Injury  

PubMed Central

Acute kidney injury (AKI) is associated with significant morbidity and mortality in hypertensive surroundings. We investigated superoxide radical molecules influence on systemic haemodynamic and kidney function in spontaneously hypertensive rats (SHR) with induced postischemic AKI. Experiment was performed in anesthetized adult male SHR. The right kidney was removed, and left renal artery was subjected to ischemia by clamping for 40 minutes. The treated group received synthetic superoxide dismutase mimetic TEMPOL in the femoral vein 5 minutes before, during, and 175 minutes after the period of reperfusion, while the control AKI group received the vehicle via the same route. All parameters were measured 24?h after renal reperfusion. TEMPOL treatment significantly decreased mean arterial pressure and total peripheral resistance (P < 0.05) compared to AKI control. It also increased cardiac output and catalase activity (P < 0.05). Lipid peroxidation and renal vascular resistance were decreased in TEMPOL (P < 0.05). Plasma creatinine and kidney morphological parameters were unchanged among TEMPOL treated and control groups. Our study shows that superoxide radicals participate in haemodynamic control, but acute superoxide scavenging is ineffective in glomerular and tubular improvement, probably due to hypertension-induced strong endothelial dysfunction which neutralizes beneficial effects of O2? scavenging. PMID:25050356

Miloradovi?, Zoran; Ivanov, Milan; Mihailovi?-Stanojevi?, Nevena; Gruji? Milanovi?, Jelica; Jovovi?, ?ur?ica; Vaji?, Una-Jovana; Markovi?-Lipkovski, Jasmina

2014-01-01

130

Mechanisms of neuroprotection during ischemic preconditioning: lessons from anoxic tolerance.  

PubMed

Different physiological adaptations for anoxia resistance have been described in the animal kingdom. These adaptations are particularly important in organs that are highly susceptible to energy deprivation such as the heart and brain. Among vertebrates, turtles are one of the species that are highly tolerant to anoxia. In mammals however, insults such as anoxia, ischemia and hypoglycemia, all cause major histopathological events to the brain. However, in mammals even ischemic or anoxic tolerance is found when a sublethal ischemic/anoxic insult is induced sometime before a lethal ischemic/anoxic insult is induced. This phenomenon is defined as ischemic preconditioning. Better understanding of the mechanisms inducing both anoxic tolerance in turtles or ischemic preconditioning in mammals may provide novel therapeutic interventions that may aide mammalian brain to resist the ravages of cerebral ischemia. In this review, we will summarize some of the mechanisms implemented in both models of tolerance, emphasizing physiological and biochemical similarities. PMID:17045830

Perez-Pinzon, Miguel A

2007-06-01

131

Parallel Domain Decomposition Preconditioning for Computational Fluid Dynamics  

NASA Technical Reports Server (NTRS)

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

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

1998-01-01

132

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

133

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

134

Imaging of MMP activity in postischemic cardiac remodeling using radiolabeled MMP-2/9 activatable peptide probes.  

PubMed

The noninvasive imaging of matrix metalloproteinases (MMPs) activity in postischemic myocardial tissue holds great promise to predict cardiac function post-myocardial infarction. Consequently, development of MMP specific molecular imaging probes for noninvasive visualization and quantification of MMP activity is of great interest. A novel MMP imaging strategy is based on activatable cell-penetrating peptide probes (ACPP) that are sensitive to the proteolytic activity of MMP-2 and -9. The MMP-mediated activation of these ACPPs drives probe accumulation at the target site. The aim of this study was the development and characterization of radiolabeled MMP-2/9 sensitive ACPPs to assess MMP activity in myocardial remodeling in vivo. Specifically, a short and long-circulating MMP activatable cell-penetrating imaging probe (ACPP and Alb-ACPP, respectively; the latter is an ACPP modified with an albumin binding ligand that prolongs blood clearance) were successfully synthesized and radiolabeled. Subsequently, their biodistributions were determined in vivo in a Swiss mouse model of myocardial infarction. Both peptide probes showed a significantly higher uptake in infarcted myocardium compared to remote myocardium. The biodistribution for dual-isotope radiolabeled probes, which allowed us to discriminate between uncleaved ACPP and activated ACPP, showed increased retention of activated ACPP and activated Alb-ACPP in infarcted myocardium compared to remote myocardium. The enhanced retention correlated to gelatinase levels determined by gelatin zymography, whereas no correlation was found for the negative control: an MMP-2/9 insensitive non-ACPP. In conclusion, radiolabeled MMP sensitive ACPP probes enable to assess MMP activity in the course of remodeling post-myocardial infarction in vivo. Future research should evaluate the feasibility and the predictive value of the ACPP strategy for assessing MMP activity as a main player in postinfarction myocardial remodeling in vivo. PMID:24641497

van Duijnhoven, Sander M J; Robillard, Marc S; Hermann, Sven; Kuhlmann, Michael T; Schäfers, Michael; Nicolay, Klaas; Grüll, Holger

2014-05-01

135

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

136

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

137

Islet preconditioning via multimodal microfluidic modulation of intermittent hypoxia  

PubMed Central

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

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

2012-01-01

138

Cardioprotection acquired through exercise: the role of ischemic preconditioning.  

PubMed

A great bulk of evidence supports the concept that regular exercise training can reduce the incidence of coronary events and increase survival chances after myocardial infarction. These exercise-induced beneficial effects on the myocardium are reached by means of the reduction of several risk factors relating to cardiovascular disease, such as high cholesterol, hypertension, obesity etc. Furthermore, it has been demonstrated that exercise can reproduce the "ischemic preconditioning" (IP), which refers to the capacity of short periods of ischemia to render the myocardium more resistant to subsequent ischemic insult and to limit infarct size during prolonged ischemia. However, IP is a complex phenomenon which, along with infarct size reduction, can also provide protection against arrhythmia and myocardial stunning due to ischemia-reperfusion. Several clues demonstrate that preconditioning may be directly induced by exercise, thus inducing a protective phenotype at the heart level without the necessity of causing ischemia. Exercise appears to act as a physiological stress that induces beneficial myocardial adaptive responses at cellular level. The purpose of the present paper is to review the latest data on the role played by exercise in triggering myocardial preconditioning. PMID:24720421

Marongiu, Elisabetta; Crisafulli, Antonio

2014-11-01

139

The ERK1/2 Signaling Pathway Is Involved in Sulfur Dioxide Preconditioning-Induced Protection against Cardiac Dysfunction in Isolated Perfused Rat Heart Subjected to Myocardial Ischemia/Reperfusion  

PubMed Central

Ischemia/reperfusion injury (IRI) occurs frequently during reperfusion of ischemic myocardium, and preconditioning has been regarded as one of the best strategies to prevent myocardial injury during the ischemia/reperfusion process. Our previous studies indicated that a small dose of sulfur dioxide (SO2) used as preconditioning exerts cardioprotection. However, the mechanisms underlying the cardioprotection remain unclear. The present study was designed to examine if the extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway mediated protection against cardiac dysfunction after SO2 preconditioning in isolated rat hearts subjected to ischemia/reperfusion (I/R). Langendorff heart perfusion was performed in vitro, where 56 male Wistar rats were randomly divided into seven groups: control group, 5 ?mol/L SO2 group (S5), 2-(2-Amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) + 5 ?mol/L SO2 (PD98059 + S5) group, PD98059 group, I/R group, 5 ?mol/L SO2 + I/R (S5 + I/R) group and PD98059 + 5 ?mol/L SO2 + I/R (PD98059 + S5 + I/R) group. Cardiac function and myocardial phosphorylated ERK1/2 protein were measured. We found that I/R in isolated rat heart resulted in cardiac dysfunction with a significant increase in phosphorylated ERK1/2 protein. SO2 preconditioning markedly suppressed phosphorylated ERK1/2 protein and improved cardiac function in isolated rat heart with I/R (p < 0.05). However, pre-treatment with PD98059 could prevent the above effects of SO2 preconditioning. In conclusion, SO2 preconditioning protected against cardiac dysfunction in isolated rat heart subjected to I/R via suppression of the over-activation of the ERK1/2 signaling pathway. PMID:24217229

Huang, Pan; Sun, Yan; Yang, Jinyan; Chen, Siyao; Liu, Angie Dong; Holmberg, Lukas; Huang, Xiaomei; Tang, Chaoshu; Du, Junbao; Jin, Hongfang

2013-01-01

140

Remote Ischemic Preconditioning Protects against Liver Ischemia-Reperfusion Injury via Heme Oxygenase-1-Induced Autophagy  

PubMed Central

Background Growing evidence has linked autophagy to a protective role of preconditioning in liver ischemia/reperfusion (IR). Heme oxygenase-1 (HO-1) is essential in limiting inflammation and preventing the apoptotic response to IR. We previously demonstrated that HO-1 is up-regulated in liver graft after remote ischemic preconditioning (RIPC). The aim of this study was to confirm that RIPC protects against IR via HO-1-mediated autophagy. Methods RIPC was performed with regional ischemia of limbs before liver ischemia, and HO-1 activity was inhibited pre-operation. Autophagy was assessed by the expression of light chain 3-II (LC3-II). The HO-1/extracellular signal-related kinase (ERK)/p38/mitogen-activated protein kinase (MAPK) pathway was detected in an autophagy model and mineral oil-induced IR in vitro. Results In liver IR, the expression of LC3-II peaked 12–24 h after IR, and the ultrastructure revealed abundant autophagosomes in hepatocytes after IR. Autophagy was inhibited when HO-1 was inactivated, which we believe resulted in the aggravation of liver IR injury (IRI) in vivo. Hemin-induced autophagy also protected rat hepatocytes from IRI in vitro, which was abrogated by HO-1 siRNA. Phosphorylation of p38-MAPK and ERK1/2 was up-regulated in hemin-pretreated liver cells and down-regulated after treatment with HO-1 siRNA. Conclusions RIPC may protect the liver from IRI by induction of HO-1/p38-MAPK-dependent autophagy. PMID:24914543

Xiong, Xuanxuan; Xu, Yonghua; Zhang, Hai; Huang, Changjun; Tian, Yuan; Jiao, Chengyu; Wang, Xuehao; Li, Xiangcheng

2014-01-01

141

Activation of K2P channel–TREK1 mediates the neuroprotection induced by sevoflurane preconditioning  

PubMed Central

Background Preconditioning with volatile anaesthetic agents induces tolerance to focal cerebral ischaemia, although the underlying mechanisms have not been clearly defined. The present study analyses whether TREK-1, a two-pore domain K+ channel and target for volatile anaesthetics, plays a role in mediating neuroprotection by sevoflurane. Methods Differentiated SH-SY5Y cells were preconditioning with sevoflurane and challenged by oxygen–glucose deprivation (OGD). Cell viability and expression of caspase-3 and TREK-1 were evaluated. Rats that were preconditioned with sevoflurane were subjected to middle cerebral artery occlusion (MCAO), and the expression of TREK-1 protein and mRNA was analysed. Neurological scores were evaluated and infarction volume was examined. Results Sevoflurane preconditioning reduced cell death in differentiated SH-SY5Y cells challenged by OGD. Sevoflurane preconditioning reduced infarct volume and improved neurological outcome in rats subjected to MCAO. Sevoflurane preconditioning increased levels of TREK-1 mRNA and protein. Knockdown of TREK-1 significantly attenuated sevoflurane preconditioning-induced neuroprotective effects in vitro and in vivo. Conclusions Sevoflurane preconditioning-induced neuroprotective effects against transient cerebral ischaemic injuries involve TREK-1 channels. These results suggest a novel mechanism for sevoflurane preconditioning-induced tolerance to focal cerebral ischaemia. PMID:24154701

Tong, L.; Cai, M.; Huang, Y.; Zhang, H.; Su, B.; Li, Z.; Dong, H.

2014-01-01

142

Pyruvate-enriched resuscitation: metabolic support of post-ischemic hindlimb muscle in hypovolemic goats.  

PubMed

Tourniquet-imposed ischemia-reperfusion of extremities generates reactive oxygen and nitrogen species (RONS), which can disrupt intermediary metabolism and ATP production. This study tested the hypothesis that fluid resuscitation with pyruvate, a natural antioxidant and metabolic fuel, ameliorates the deleterious effects of ischemia-reperfusion on intermediary metabolism in skeletal muscle. Anesthetized male goats (?25 kg) were bled to a mean arterial pressure of 48 ± 1 mmHg and then subjected to 90 min hindlimb ischemia with a tourniquet and femoral crossclamp, followed by 4-h reperfusion. Lactated Ringers (LR) or pyruvate Ringers (PR) was infused intravenous for 90 min, from 30 min ischemia to 30 min reperfusion, to deliver 0.05 mmol kg(-1) min(-1) lactate or pyruvate. Time controls (TC) underwent neither hemorrhage nor hindlimb ischemia. Lipid peroxidation product 8-isoprostane, RONS-sensitive aconitase and creatine kinase activities, antioxidant superoxide dismutase activity, and phosphocreatine phosphorylation potential ([PCr]/[{Cr}{P(i)}]), an index of tissue energy state, were measured in reperfused gastrocnemius at 90 min resuscitation (n = 6 all groups) and 3.5 h post-resuscitation (n = 8 TC, 9 LR, 10 PR). PR more effectively than LR suppressed 8-isoprostane formation, prevented inactivation of aconitase and creatine kinase, doubled superoxide dismutase activity, and augmented [PCr]/([Cr][P(i)]). Pyruvate-enriched Ringer's is metabolically superior to Ringer's lactate for fluid resuscitation of tourniqueted muscle. PMID:24414481

Gurji, Hunaid A; White, Daniel W; Hoxha, Besim; Sun, Jie; Harbor, Jessica P; Schulz, Diana R; Williams, Arthur G; Olivencia-Yurvati, Albert H; Mallet, Robert T

2014-02-01

143

Beneficial Effect of Propranolol in a Histologically Appropriate Model of Postischemic Acute Renal Failure  

PubMed Central

Acute renal failure caused in the rabbit by clamping one renal pedicle for 1 hour and removing the opposite kidney produced a histologic picture very similar to that observed in “hypotensive” acute renal failure in man. Intravenous infusion of propranolol, a drug which prevents renin release, at 1 mg/kg for 70 minutes beginning at time of pedicle clamping resulted in significantly lower serum creatinine in this model (2.8 ± 0.2 mg% at 48 hours with propranolol versus 5.2 ± 0.8 mg% without). Renin stimulation by dehydration or feeding a low-salt diet enhanced the difference between treated and untreated groups (2.6 ± 0.4 mg% with propranolol versus 6.2 ± 1.8 mg% without, after dehydration; 3.5 ± 1.0 mg% with propranolol versus 7.6 ± 1.4 mg% without, after low-salt diet).Suppression of renin production by saline feeding eliminated propranolol's beneficial effect (5.6 ± 0.9 mg% with propranolol versus 4.0 ± 0.6 mg% without). In rabbits with a normal food and water intake, renal denervation using phenol also eliminated propranolol's effect (creatinine 8.6 ± 1.4 mg% with propranolol versus 8.6 ± 1.8 mg% without). In rabbits with intact kidneys, flow probe recording of renal blood flow showed a significantly higher blood flow immediately after unclamping in the propranolol-treated animals, and renal angiograms showed less vasoconstriction in this group after unclamping. In this model of acute renal failure, renal vasoconstriction plays an important role following the initial ischemic insult. Propranolol lessens the severity of this vasoconstriction and the resulting acute renal failure. Its probable action is interference with neurogenically stimulated renin release. ImagesFigure 10Figure 1Figure 2Figure 3Figure 4Figure 5Figure 6Figure 7Figure 8Figure 9 PMID:879269

Solez, Kim; D'Agostini, Robert J.; Stawowy, Lala; Freedman, Matthew T.; Scott, William W.; Siegelman, Stanley S.; Heptinstall, Robert H.

1977-01-01

144

Thioredoxin reduces post-ischemic myocardial apoptosis by reducing oxidative/nitrative stress  

PubMed Central

Background and purpose: Thioredoxin (Trx) is an oxidoreductase that prevents free radical-induced cell death in cultured cells. Here we assessed the mechanism(s) underlying the cardioprotective effects of Trx in vivo. Experimental approach: The effects of myocardial ischemia (30?min) and reperfusion were measured in mice, with assays of myocardial apoptosis, superoxide production, NOx and nitrotyrosine content, and myocardial infarct size. Recombinant human Trx (rhTrx, 0.7–20?mg?kg-1, i.p.) was given 10?min before reperfusion. Key results: Treatment with 2?mg?kg-1 rhTrx significantly decreased myocardial apoptosis and reduced infarct size (P<0.01). Nitrotyrosine content of cardiomyocytes was markedly reduced in rhTrx-treated animals (P<0.01). To further identify the mechanisms by which rhTrx may exert its anti-nitrative effect, iNOS expression and production of NOx and superoxide were determined. Treatment with rhTrx had no significant effect on iNOS expression or NOx content in the ischemic/reperfused heart. However, it markedly upregulated mSOD and reduced tissue superoxide content. To further establish a causative link between the anti- peroxynitrite effect and the cardioprotective effect of rhTrx, cultured adult cardiomyocytes were incubated with SIN-1, a peroxynitrite donor, (50??M for 3?h) resulting in a nitrotyrosine content comparable to that seen in the ischemic/reperfused heart and causing significant cardiomyocyte apoptosis (P<0.01). Treatment with rhTrx markedly decreased SIN-1 induced apoptosis (P<0.01). Conclusions and implications: These results demonstrate that Trx is a novel anti-apoptotic and cardioprotective molecule that exerts its cardioprotective effects by reducing ischemia/reperfusion-induced oxidative/nitrative stress. PMID:16921396

Tao, L; Gao, E; Hu, A; Coletti, C; Wang, Y; Christopher, T A; Lopez, B L; Koch, W; Ma, X L

2006-01-01

145

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

146

Preconditioning with Associated Blocking of Ca2+ Inflow Alleviates Hypoxia-Induced Damage to Pancreatic ?-Cells  

PubMed Central

Objective Beta cells of pancreatic islets are susceptible to functional deficits and damage by hypoxia. Here we aimed to characterize such effects and to test for and pharmacological means to alleviate a negative impact of hypoxia. Methods and Design Rat and human pancreatic islets were subjected to 5.5 h of hypoxia after which functional and viability parameters were measured subsequent to the hypoxic period and/or following a 22 h re-oxygenation period. Preconditioning with diazoxide or other agents was usually done during a 22 h period prior to hypoxia. Results Insulin contents decreased by 23% after 5.5 h of hypoxia and by 61% after a re-oxygenation period. Preconditioning with diazoxide time-dependently alleviated these hypoxia effects in rat and human islets. Hypoxia reduced proinsulin biosynthesis (3H-leucine incorporation into proinsulin) by 35%. Preconditioning counteracted this decrease by 91%. Preconditioning reduced hypoxia-induced necrosis by 40%, attenuated lowering of proteins of mitochondrial complexes I–IV and enhanced stimulation of HIF-1-alpha and phosphorylated AMPK proteins. Preconditioning by diazoxide was abolished by co-exposure to tolbutamide or elevated potassium (i.e. conditions which increase Ca2+ inflow). Preconditioning with nifedipine, a calcium channel blocker, partly reproduced effects of diazoxide. Both diazoxide and nifedipine moderately reduced basal glucose oxidation whereas glucose-induced oxygen consumption (tested with diazoxide) was unaffected. Preconditioning with diaxoxide enhanced insulin contents in transplants of rat islets to non-diabetic rats and lowered hyperglycemia vs. non-preconditioned islets in streptozotocin-diabetic rats. Preconditioning of human islet transplants lowered hyperglycemia in streptozotocin-diabetic nude mice. Conclusions 1) Prior blocking of Ca2+ inflow associates with lesser hypoxia-induced damage, 2) preconditioning affects basal mitochondrial metabolism and accelerates activation of hypoxia-reactive and potentially protective factors, 3) results indicate that preconditioning by K+-ATP-channel openers has therapeutic potential for islet transplantations. PMID:23935835

Ma, Zuheng; Moruzzi, Noah; Catrina, Sergiu-Bogdan; Hals, Ingrid; Oberholzer, José

2013-01-01

147

Energy metabolism in preconditioned and control myocardium: effect of total ischemia.  

PubMed

Myocardium which has been preconditioned by one or several brief episodes of ischemia has much slower energy utilization during a subsequent sustained episode of ischemia. Since preconditioned tissue also is 'stunned', the reduced energy utilization of preconditioned tissue may be due to reduced contractile effort. This study was done to assess whether differences in energy utilization persisted or disappeared under conditions of total ischemia, in vitro, when contractile activity was abolished in both control and preconditioned regions by hyperkalemic cardiac arrest. Preconditioned myocardium was produced in open-chest anesthetized dogs by exposing the circumflex bed to four 5-min episodes of ischemia each followed by 5 min of arterial reperfusion. Non-preconditioned anterior descending bed was used as control myocardium. Hearts were arrested with hyperkalemia after the last reperfusion period in order to reduce or eliminate the effects of contractile activity. Metabolite content was measured in sequential biopsies of the tissue. Large differences in the rate of energy metabolism of the two regions were noted during the first 15 minutes of ischemia. During this time, the preconditioned tissue utilized less glycogen, and produced less lactate, glucose-6-phosphate (G6P), glucose-1-phosphate (G1P), and alpha-glycerol phosphate (alpha GP), than did control myocardium. Moreover, there was a much smaller decrease in net tissue ATP in the preconditioned than in the control tissue. Thus, the decrease in the demand of preconditioned tissue for energy, which has been observed in vivo, persisted despite the elimination of differences in contractile effort between control and preconditioned myocardium. Although the cause of this decrease in energy demand in preconditioned myocardium remains unknown, the present results suggest that it is not due to concomitant stunning. PMID:1811060

Jennings, R B; Murry, C E; Reimer, K A

1991-12-01

148

Calcium preconditioning triggers neuroprotection in retinal ganglion cells  

PubMed Central

In the mammalian retina, excitotoxicity has been shown to be involved in apoptotic retinal ganglion cell (RGC) death and is associated with certain retinal disease states including glaucoma, diabetic retinopathy and retinal ischemia. Previous studies from this lab (Wehrwein et al., 2004) have demonstrated that acetylcholine (ACh) and nicotine protects against glutamate-induced excitotoxicity in isolated adult pig RGCs through nicotinic acetylcholine receptors (nAChRs). Activation of nAChRs in these RGCs triggers cell survival signaling pathways and inhibits apoptotic enzymes (Asomugha et al., 2010). However, the link between binding of nAChRs and activation of neuroprotective pathways is unknown. In this study, we examine the hypothesis that calcium permeation through nAChR channels is required for ACh-induced neuroprotection against glutamate-induced excitotoxicity in isolated pig RGCs. RGCs were isolated from other retinal tissue using a two step panning technique and cultured for 3 days under different conditions. In some studies, calcium imaging experiments were performed using the fluorescent calcium indicator, fluo-4, and demonstrated that calcium permeates the nAChR channels located on pig RGCs. In other studies, the extracellular calcium concentration was altered to determine the effect on nicotine-induced neuroprotection. Results support the hypothesis that calcium is required for nicotine-induced neuroprotection in isolated pig RGCs. Lastly, studies were performed to analyze the effects of preconditioning on glutamate-induced excitotoxicity and neuroprotection. In these studies, a preconditioning dose of calcium was introduced to cells using a variety of mechanisms before a large glutamate insult was applied to cells. Results from these studies support the hypothesis that preconditioning cells with a relatively low level of calcium before an excitotoxic insult leads to neuroprotection. In the future, these results could provide important information concerning therapeutic agents developed to combat various diseases involved with glutamate-induced excitotoxicity. PMID:21044663

Brandt, Sean K.; Weatherly, Monique E.; Ware, Lillian; Linn, David M.; Linn, Cindy L.

2010-01-01

149

Dexmedetomidine preconditioning ameliorates kidney ischemia-reperfusion injury.  

PubMed

Kidney ischemia-reperfusion (I/R) injury is a common cause of acute kidney injury. We tested whether dexmedetomidine (Dex), an alpha2 adrenoceptor (?2-AR) agonist, protects against kidney I/R injury. Sprague-Dawley rats were divided into four groups: (1) Sham-operated group; (2) I/R group (40 min ischemia followed by 24 h reperfusion); (3) I/R group + Dex (1 ?g/kg i.v. 60 min before the surgery), (4) I/R group + Dex (10 ?g/kg). The effects of Dex postconditiong (Dex 1 or 10 ?g/kg i.v. after reperfusion) as well as the effects of peripheral ?2-AR agonism with fadolmidine were also examined. Hemodynamic effects were monitored, renal function measured, and acute tubular damage along with monocyte/macrophage infiltration scored. Kidney protein kinase B, toll like receptor 4, light chain 3B, p38 mitogen-activated protein kinase (p38 MAPK), sirtuin 1, adenosine monophosphate kinase (AMPK), and endothelial nitric oxide synthase (eNOS) expressions were measured, and kidney transciptome profiles analyzed. Dex preconditioning, but not postconditioning, attenuated I/R injury-induced renal dysfunction, acute tubular necrosis and inflammatory response. Neither pre- nor postconditioning with fadolmidine protected kidneys. Dex decreased blood pressure more than fadolmidine, ameliorated I/R-induced impairment of autophagy and increased renal p38 and eNOS expressions. Dex downregulated 245 and upregulated 61 genes representing 17 enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, in particular, integrin pathway and CD44. Ingenuity analysis revealed inhibition of Rac and nuclear factor (erythroid-derived 2)-like 2 pathways, whereas aryl hydrocarbon receptor (AHR) pathway was activated. Dex preconditioning ameliorates kidney I/R injury and inflammatory response, at least in part, through p38-CD44-pathway and possibly also through ischemic preconditioning. PMID:25505591

Lempiäinen, Juha; Finckenberg, Piet; Mervaala, Elina E; Storvik, Markus; Kaivola, Juha; Lindstedt, Ken; Levijoki, Jouko; Mervaala, Eero M

2014-06-01

150

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

E-print Network

Transplantation of hypoxia preconditioned bone marrow mesenchymal stem cells enhances angiogenesis online 9 March 2012 Keywords: Hypoxic preconditioning Bone marrow mesenchymal stem cell Transplantation for promoting cell survival after transplantation. The present investigation examined the hypothesis

Hayar, Abdallah

151

41 CFR 102-72.68 - What preconditions must be satisfied before an Executive agency may exercise the delegated...  

Code of Federal Regulations, 2010 CFR

...preconditions must be satisfied before an Executive agency may exercise the delegated authority to perform an individual ancillary...preconditions must be satisfied before an Executive agency may exercise the delegated authority to perform an individual...

2010-07-01

152

41 CFR 102-72.68 - What preconditions must be satisfied before an Executive agency may exercise the delegated...  

Code of Federal Regulations, 2011 CFR

...preconditions must be satisfied before an Executive agency may exercise the delegated authority to perform an individual ancillary...preconditions must be satisfied before an Executive agency may exercise the delegated authority to perform an individual...

2011-01-01

153

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

154

Weighted graph based ordering techniques for preconditioned conjugate gradient methods  

NASA Technical Reports Server (NTRS)

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

Clift, Simon S.; Tang, Wei-Pai

1994-01-01

155

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

ERIC Educational Resources Information Center

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

Coureaud, Gerard; Tourat, Audrey; Ferreira, Guillaume

2013-01-01

156

Effect of Heat Preconditioning on the Uptake and Permeability of R123 in Brain Microvessel  

E-print Network

Effect of Heat Preconditioning on the Uptake and Permeability of R123 in Brain Microvessel Endothelial Cells during Mild Heat Treatment KA-YUN NG,1 CHEONG-WEON CHO,1 THOMAS K. HENTHORN,2 ROBERT L of this study was to assess the effect of mild heat and heat preconditioning on the uptake and permeability

Tullos, Desiree

157

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method  

E-print Network

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method Jos'e Luis Morales \\Lambda Jorge Nocedal y March 30, 1999 Abstract PREQN is a package of Fortran 7725047­A004. 1 #12; 1 Introduction In this paper we describe Fortran 77 subroutines for preconditioning

Nocedal, Jorge

158

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method  

E-print Network

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method Jose Luis Morales Jorge Nocedaly March 14, 2000 Abstract PREQN is a package of Fortran 77 subroutines-A004. 1 #12;1 Introduction In this paper we describe Fortran 77 subroutines for preconditioning

Nocedal, Jorge

159

WAVEFORM PRECONDITIONING FOR CLUTTER REJECTION IN MULTIPATH FOR SPARSE DISTRIBUTED APERTURES  

E-print Network

WAVEFORM PRECONDITIONING FOR CLUTTER REJECTION IN MULTIPATH FOR SPARSE DISTRIBUTED APERTURES T,The idea of preconditioning transmit waveforms e.g. ultrasound imaging, sonar imaging and microwave clutter the elements Ourapproachis motivatedby communicationtheory: the being atd Wavefor*sprondit for clutter radar

Yazici, Birsen

160

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

161

Stress preconditioning of spreading depression in the locust CNS.  

PubMed

Cortical spreading depression (CSD) is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG) of locusts. Using K(+) -sensitive microelectrodes, we measured extracellular K(+) concentration ([K(+)](o)) in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K(+) in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na(+)/K(+) ATPase impairment, K(+) injection) was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45 degrees C) and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K(+) that was not linked to changes in ATP levels or total Na(+)/K(+) ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin. PMID:18159249

Rodgers, Corinne I; Armstrong, Gary A B; Shoemaker, Kelly L; LaBrie, John D; Moyes, Christopher D; Robertson, R Meldrum

2007-01-01

162

Preconditioning donor with a combination of tacrolimus and rapamacyn to decrease ischaemia–reperfusion injury in a rat syngenic kidney transplantation model  

PubMed Central

Reperfusion injury remains one of the major problems in transplantation. Repair from ischaemic acute renal failure (ARF) involves stimulation of tubular epithelial cell proliferation. The aim of this exploratory study was to evaluate the effects of preconditioning donor animals with rapamycin and tacrolimus to prevent ischaemia–reperfusion (I/R) injury. Twelve hours before nephrectomy, the donor animals received immunosuppressive drugs. The animals were divided into four groups, as follows: group 1 control: no treatment; group 2: rapamycin (2 mg/kg); group 3 FK506 (0, 3 mg/kg); and group 4: FK506 (0, 3 mg/kg) plus rapamycin (2 mg/kg). The left kidney was removed and after 3 h of cold ischaemia, the graft was transplanted. Twenty-four hours after transplant, the kidney was recovered for histological analysis and cytokine expression. Preconditioning treatment with rapamycin or tacrolimus significantly reduced blood urea nitrogen and creatinine compared with control [blood urea nitrogen (BUN): P < 0·001 versus control and creatinine: P < 0·001 versus control]. A further decrease was observed when rapamycin was combined with tacrolimus. Acute tubular necrosis was decreased significantly in donors treated with immunosuppressants compared with the control group (P < 0·001 versus control). Moreover, the number of apoptotic nuclei in the control group was higher compared with the treated groups (P < 0·001 versus control). Surprisingly, only rapamycin preconditioning treatment increased anti-apoptotic Bcl2 levels (P < 0·001). Finally, inflammatory cytokines, such as tumour necrosis factor (TNF)-? and interleukin (IL)-6, showed lower levels in the graft of those animals that had been pretreated with rapamycin or tacrolimus. This exploratory study demonstrates that preconditioning donor animals with rapamycin or tacrolimus improves clinical outcomes and reduce necrosis and apoptosis in kidney I/R injury. PMID:22132896

Cicora, F; Roberti, J; Vasquez, D; Guerrieri, D; Lausada, N; Cicora, P; Palti, G; Chuluyan, E; Gonzalez, P; Stringa, P; Raimondi, C

2012-01-01

163

Mechanisms of the Beneficial Actions of Ischemic Preconditioning on Subcellular Remodeling in Ischemic-Reperfused Heart  

PubMed Central

Cardiac function is compromised by oxidative stress which occurs upon exposing the heart to ischemia reperfusion (I/R) for a prolonged period. The reactive oxygen species (ROS) that are generated during I/R incur extensive damage to the myocardium and result in subcellular organelle remodeling. The cardiac nucleus, glycocalyx, myofilaments, sarcoplasmic reticulum, sarcolemma, and mitochondria are affected by ROS during I/R injury. On the other hand, brief periods of ischemia followed by reperfusion, or ischemic preconditioning (IPC), have been shown to be cardioprotective against oxidative stress by attenuating the cellular damage and alterations of subcellular organelles caused by subsequent I/R injury. Endogenous defense mechanisms, such as antioxidant enzymes and heat shock proteins, are activated by IPC and thus prevent damage caused by oxidative stress. Although these cardioprotective effects of IPC against I/R injury are considered to be a consequence of changes in the redox state of cardiomyocytes, IPC is considered to promote the production of NO which may protect subcellular organelles from the deleterious actions of oxidative stress. The article is intended to focus on the I/R-induced oxidative damage to subcellular organelles and to highlight the cardioprotective effects of IPC. In addition, the actions of various endogenous cardioprotective interventions are discussed to illustrate that changes in the redox state due to IPC are cardioprotective against I/R injury to the heart. PMID:22043201

Müller, By Alison L; Dhalla, Naranjan S

2010-01-01

164

Cardiac Phosphoproteomics during Remote Ischemic Preconditioning: A Role for the Sarcomeric Z-Disk Proteins  

PubMed Central

Remote ischemic preconditioning (RIPC) induced by brief ischemia/reperfusion cycles of remote organ (e.g., limb) is cardioprotective. The myocardial cellular changes during RIPC responsible for this phenomenon are not currently known. The aim of this work was to identify the activation by phosphorylation of cardiac proteins following RIPC. To achieve our aim we used isobaric tandem mass tagging (TMT) and reverse phase nanoliquid chromatography tandem spectrometry using a Linear Trap Quadropole (LTQ) Orbitrap Velos mass spectrometer. Male C57/Bl6 mice were anesthetized by an intraperitoneal injection of Tribromoethanol. A cuff was placed around the hind limb and inflated at 200?mmHg to prevent blood flow as confirmed by Laser Doppler Flowmetry. RIPC was induced by 4 cycles of 5?min of limb ischemia followed by 5?min of reperfusion. Hearts were extracted for phosphoproteomics. We identified approximately 30 phosphoproteins that were differentially expressed in response to RIPC protocol. The levels of several phosphoproteins in the Z-disk of the sarcomere including phospho-myozenin-2 were significantly higher than control. This study describes and validates a novel approach to monitor the changes in the cardiac phosphoproteome following the cardioprotective intervention of RIPC and prior to index ischemia. The increased level of phosphorylated sarcomeric proteins suggests they may have a role in cardiac signaling during RIPC. PMID:24795895

Abdul-Ghani, Safa; Heesom, Kate J.; Angelini, Gianni D.; Suleiman, M-Saadeh

2014-01-01

165

Cardiac proteomic responses to ischemia-reperfusion injury and ischemic preconditioning.  

PubMed

Cardiac ischemia and ischemia-reperfusion (I/R) injury are major contributors to morbidity and mortality worldwide. Pathological mechanisms of I/R and the physiological mechanisms of ischemic preconditioning (IPC), which is an effective cardiac protective response, have been widely investigated in the last decade to search for means to prevent or treat this disease. Proteomics is a powerful analytical tool that has provided important information to identify target proteins and understand the underlying mechanisms of I/R and IPC. Here, we review the application of proteomics to I/R injury and IPC to discover target proteins. We analyze the functional meaning of the accumulated data on hundreds of proteins using various bioinformatics applications. In addition, we review exercise-induced proteomic alterations in the heart to understand the potential cardioprotective role of exercise against I/R injury. Further developments in the proteomic field that target specialized proteins will yield new insights for optimizing therapeutic targets and developing a wide range of therapeutic agents against ischemic heart disease. PMID:21501017

Kim, Hyoung Kyu; Thu, Vu Thi; Heo, Hye-Jin; Kim, Nari; Han, Jin

2011-04-01

166

Hypoxically preconditioned human peripheral blood mononuclear cells improve blood flow in hindlimb ischemia xenograft model.  

PubMed

Transplantation of peripheral blood mononuclear cells (PBMNCs) is a promising therapeutic approach for the treatment of hindlimb ischemia. However, insufficient angiogenesis in ischemic hindlimb after cell transplantation reduces the importance and practicality of this approach. Previously, we demonstrated using mouse models that hypoxic preconditioning augmented the cellular functions of rodent PBMNCs, such as increased cell adhesion capacity and accelerated neovascularization in ischemic hindlimb. To test the clinical application of this therapeutic strategy in this study, we investigated whether the protocol of hypoxic preconditioning, which was established in a condition of 2% O2 for 24 h, can be made available for human PBMNCs (hPBMNCs). In addition, we grafted preconditioned hPBMNCs in a hindlimb ischemia mouse model. Hypoxic preconditioning enhanced cell adhesion capacity and oxidative stress resistance in hPBMNCs. We also observed an up-regulation of platelet endothelial cell adhesion molecule-1 (PECAM-1) in hPBMNCs by hypoxic preconditioning. Furthermore, preconditioned hPBMNCs significantly recovered limb blood flow in ischemic mice after transplantation. These results indicate that our established preconditioning protocol is available for hPBMNCs to effectively reinforce multiple cellular functions. Taken together with our series of study, we believe that this simple but powerful therapeutic strategy will be helpful in curing patients with severe hindlimb ischemia. PMID:25360221

Kudo, Tomoaki; Kubo, Masayuki; Katsura, Shunsaku; Nishimoto, Arata; Ueno, Koji; Samura, Makoto; Fujii, Yasuhiko; Hosoyama, Tohru; Hamano, Kimikazu

2014-01-01

167

Effect of preconditioning on the viscoelastic response of primate patellar tendon.  

PubMed

Current techniques for anterior cruciate ligament reconstruction with patellar tendon (PT) allow a measurable tension to be applied to the graft at the time of fixation. The viscoelastic nature of the PT, however, ensures that relaxation will cause the graft tension to decrease over time. To better understand this process, a primate model was used to evaluate acute viscoelastic relaxation in the PT. Thirty-five patella-patellar tendon-tibia (P-PT-T) complexes were harvested from normal primate knees (Cynomolgus monkeys), and were divided into five groups for mechanical comparison. Specimens were subjected to two 10-min relaxation tests separated by a 1-30-min unloaded interval. The first test provided baseline relaxation data as well as serving as preconditioning for the second test. Results indicate that preconditioning significantly reduces the tension lost in a graft due to viscoelastic relaxation. The effect of preconditioning is reduced with increasing recovery time (the time between preconditioning and the second relaxation test), but the effect is still significant after 30 min of unloading. No differences were observed in the relaxation behavior of specimens that were cyclicly or isometrically preconditioned, nor were differences observed between irradiated and nonirradiated specimens. These results suggest that preconditioning can reduce acute tension loss in a graft due to viscoelastic relaxation and that simple isometric preconditioning is just as effective as cyclic stretching. PMID:8166908

Graf, B K; Vanderby, R; Ulm, M J; Rogalski, R P; Thielke, R J

1994-02-01

168

Hypoxic preconditioning increases survival and angiogenic potency of peripheral blood mononuclear cells via oxidative stress resistance.  

PubMed

Cell-based angiogenesis is a promising treatment for ischemic diseases; however, the survival of implanted cells is impaired by oxidative stress in the ischemic microenvironment. We tested the hypothesis that hypoxic preconditioning of implanted cells enhances their resistance against oxidative stress, increasing cell survival and angiogenic potency after implantation into ischemic tissue. Mouse peripheral blood mononuclear cells (PBMNCs) were collected and subjected to hypoxic preconditioning by culture for 24 h in 2% O(2) at 33 degrees C. Hypoxic preconditioning of PBMNCs increased the expression of various genes related to antioxidant and survival signals remarkably. Compared with cells cultured under normoxia, the hypoxia-preconditioned PBMNCs showed significantly lower reactive oxygen species (ROS) accumulation and higher cell survival under oxidative stress induced by LY-83583 (a superoxide generator). Three days after intramuscular implantation into the ischemic hindlimbs of mice, survival of the hypoxia-preconditioned PBMNCs was high, whereas that of the normoxia-cultured PBMNCs was relatively low. Furthermore, 28 days after treatment microvessel density and blood flow in the ischemic hindlimbs were significantly better in the mice implanted with hypoxia-preconditioned PBMNCs than in those implanted with normoxia-cultured PBMNCs. Hypoxic preconditioning increased the survival and angiogenic potency of PBMNCs, through oxidative stress resistance mechanisms. PMID:18156196

Kubo, Masayuki; Li, Tao-Sheng; Suzuki, Ryo; Shirasawa, Bungo; Morikage, Noriyasu; Ohshima, Mako; Qin, Shu-Lan; Hamano, Kimikazu

2008-02-01

169

In vivo hypoxic preconditioning protects from warm liver ischemic/reperfusion injury through the adenosine A2B receptor  

PubMed Central

BACKGROUND Liver ischemia(I)/reperfusion(R) injury(I) is a known risk factor for the postoperative outcome of patients undergoing liver surgery/transplantation. Attempts to protect from organ damage require multidisciplinary strategies and are of emerging interest in view of patients with higher age and ASA-status. Ischemic preconditioning has been successfully applied to prevent from IRI during liver resections/transplantation. Since even short periods of ischemia during preconditioning inevitably lead to hypoxia and formation of anti-inflammatory/ cytoprotective acting adenosine, we reasoned that short non-ischemic hypoxia also protects against hepatic IRI. METHODS Mice underwent hypoxic preconditioning(HPC) by breathing 10%-oxygen for 10 minutes, followed by 10 minutes of 21%-oxygen prior to left-liver-lobe-ischemia(45 min) and reperfusion(4 hrs). The interactions of hypoxia->adenosine->adenosine-receptors were tested by pharmacologic antagonism at adenosine receptor(AR) sites in wild type mice and in mice with genetic deletions at the A1-;A2A-;A2B- and A3-ARs. Hepatocellular damage, inflammation and metabolic effects were quantified by enzyme activities, cytokines, liver-myeloperoxidase(MPO), blood adenosine and tissue-adenosinemonophosphate(AMP), respectively. RESULTS Hepatoprotection by HPC was significant in wild type and A1-, A2A-and A3 AR-knock-out mice as quantified by lower ALT serum activities, cytokine levels, histological damage-scores, tissue-myeloperoxidase-concentrations and as well as preserved AMP-concentrations. Protection by HPC was blunted in mice pretreated with the A2B-AR-antagonist MRS1754 or in A2B-AR“knock-outs”. CONCLUSION Because liver protective effects of HPC are negated when the A2B receptor is non-functional, the "hypoxia->adenosine->A2B receptor" pathway plays a critical role in the prevention of warm ischemia reperfusion injury in vivo. Hypoxic activation of this pathway warrants use of selective A2B-AR-agonists or even intermittent hypoxia (e.g. in deceased organ donors) to protect from liver ischemia/reperfusion injury. PMID:23073466

Choukèr, Alexander; Ohta, Akio; Martignoni, André; Lukashev, Dmitriy; Zacharia, Lefteris C; Jackson, Edwin K; Schnermann, Jürgen; Ward, Jerrold M; Kaufmann, Ines; Klaunberg, Brenda; Sitkovsky, Michail V; Thiel, Manfred

2012-01-01

170

Preconditioned Mixed Spectral Element Methods for Elasticity and Stokes Problems  

NASA Technical Reports Server (NTRS)

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

Pavarino, Luca F.

1996-01-01

171

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

172

Is There A Place For Cerebral Preconditioning In The Clinic?  

PubMed Central

Preconditioning (PC) describes a phenomenon whereby a sub-injury inducing stress can protect against a later injurious stress. Great strides have been made in identifying the mechanisms of PC-induced protection in animal models of brain injury. While these may help elucidate potential therapeutic targets, there are questions over the clinical utility of cerebral PC, primarily because of questions over the need to give the PC stimulus prior to the injury, narrow therapeutic windows and safety. The object of this review is to address the question of whether there may indeed be a clinical use for cerebral PC and to discuss the deficiencies in our knowledge of PC that may hamper such clinical translation. PMID:20563278

Keep, Richard F.; Wang, Michael M.; Xiang, Jianming; Hua, Ya; Xi, Guohua

2010-01-01

173

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

174

A block inverse-free preconditioned Krylov subspace method for symmetric generalized eigenvalue problems  

NASA Astrophysics Data System (ADS)

The inverse-free preconditioned Krylov subspace method of Golub and Ye [G.H. Golub, Q. Ye, An inverse free preconditioned Krylov subspace method for symmetric generalized eigenvalue problems, SIAM J. Sci. Comp. 24 (2002) 312-334] is an efficient algorithm for computing a few extreme eigenvalues of the symmetric generalized eigenvalue problem. In this paper, we first present an analysis of the preconditioning strategy based on incomplete factorizations. We then extend the method by developing a block generalization for computing multiple or severely clustered eigenvalues and develop a robust black-box implementation. Numerical examples are given to illustrate the analysis and the efficiency of the block algorithm.

Quillen, Patrick; Ye, Qiang

2010-01-01

175

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

176

Solving large mixed linear models using preconditioned conjugate gradient iteration.  

PubMed

Continuous evaluation of dairy cattle with a random regression test-day model requires a fast solving method and algorithm. A new computing technique feasible in Jacobi and conjugate gradient based iterative methods using iteration on data is presented. In the new computing technique, the calculations in multiplication of a vector by a matrix were recorded to three steps instead of the commonly used two steps. The three-step method was implemented in a general mixed linear model program that used preconditioned conjugate gradient iteration. Performance of this program in comparison to other general solving programs was assessed via estimation of breeding values using univariate, multivariate, and random regression test-day models. Central processing unit time per iteration with the new three-step technique was, at best, one-third that needed with the old technique. Performance was best with the test-day model, which was the largest and most complex model used. The new program did well in comparison to other general software. Programs keeping the mixed model equations in random access memory required at least 20 and 435% more time to solve the univariate and multivariate animal models, respectively. Computations of the second best iteration on data took approximately three and five times longer for the animal and test-day models, respectively, than did the new program. Good performance was due to fast computing time per iteration and quick convergence to the final solutions. Use of preconditioned conjugate gradient based methods in solving large breeding value problems is supported by our findings. PMID:10629826

Strandén, I; Lidauer, M

1999-12-01

177

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

178

Anatomical Preconditions for Operative-Technical Errors in Right Trisectionectomy  

PubMed Central

Objective: Certain anatomical variations may represent preconditions for technical operation errors in right trisectionectomy. These variations include: the confluence of the common bile duct, the length of the left hepatic duct, the localization of the bile duct confluence for segments 2 and 3 of the umbilical portion of the left portal vein and the peculiarities of the afferent and efferent blood supply of these two segments. The aim of the present study is to identify and discuss such preconditions. Materials and Methods: The anatomical variations of the common bile duct confluence were analyzed by intraoperative cholangiography in 112 patients undergoing liver resections and in 32 preparations after left hepatectomy. The variations of the afferent and efferent blood supply were morphologically examined in 43 liver resections. Results: Seven types of anatomical variations of the common bile duct confluence were detected through intraoperative cholangiography, and three were extracted from the available literature. Three anatomical types (central, peripheral, and combined) of bile drainage from segment 4 were established. The mean distance between the bile duct confluence for segments 2 and 3 and the main hepatic duct confluence, i. e., the length of the left hepatic duct, was 3.68 cm. The anatomical peculiarities of the afferent and efferent arterial and venous supply of segments 2 and 3 were presented and discussed with respect to their roles in a safe right trisectionectomy. Conclusion: Surgeons’ sound knowledge of anatomical variations of the biliary tract and hepatic blood vessels coupled with increased experience and technique refinements could contribute to better outcomes in right trisectionectomy.

Kostov, Daniel V.; Kobakov, Georgi L.

2012-01-01

179

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

180

Loss of Potassium Homeostasis Underlies Hyperthermic Conduction Failure in Control and Preconditioned Locusts  

E-print Network

Loss of Potassium Homeostasis Underlies Hyperthermic Conduction Failure in Control homeostasis underlies hyperthermic conduction failure in control and preconditioned locusts. J Neurophysiol, neurons cease to function appropriately. Prior exposure to a heat stress (heat shock [HS]) can extend

Robertson, Meldrum

181

Age-related reduction of cerebral ischemic preconditioning: myth or reality?  

PubMed Central

Stroke is one of the leading causes of death in industrialized countries for people older than 65 years of age. The reasons are still unclear. A reduction of endogenous mechanisms against ischemic insults has been proposed to explain this phenomenon. The “cerebral” ischemic preconditioning mechanism is characterized by a brief episode of ischemia that renders the brain more resistant against subsequent longer ischemic events. This ischemic tolerance has been shown in numerous experimental models of cerebral ischemia. This protective mechanism seems to be reduced with aging both in experimental and clinical studies. Alterations of mediators released and/or intracellular pathways may be responsible for age-related ischemic preconditioning reduction. Agents able to mimic the “cerebral” preconditioning effect may represent a new powerful tool for the treatment of acute ischemic stroke in the elderly. In this article, animal and human cerebral ischemic preconditioning, its age-related difference, and its potential therapeutical applications are discussed. PMID:24204128

Della-Morte, David; Cacciatore, Francesco; Salsano, Elisa; Pirozzi, Gilda; Genio, Maria Teresa Del; D’Antonio, Iole; Gargiulo, Gaetano; Palmirotta, Raffaele; Guadagni, Fiorella; Rundek, Tatjana; Abete, Pasquale

2013-01-01

182

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

183

Toll-like receptor 9: a new target of ischemic preconditioning in the brain  

Microsoft Academic Search

Preconditioning with lipopolysaccharide (LPS), a toll-like receptor 4 (TLR4) ligand, provides neuroprotection against subsequent cerebral ischemic brain injury, through a tumor necrosis factor (TNF)?-dependent process. Here, we report the first evidence that another TLR, TLR9, can induce neuroprotection. We show that the TLR9 ligand CpG oligodeoxynucleotide (ODN) can serve as a potent preconditioning stimulus and provide protection against ischemic brain

Susan L Stevens; Thomas M P Ciesielski; Brenda J Marsh; Tao Yang; Delfina S Homen; Jo-Lynn Boule; Nikola S Lessov; Roger P Simon; Mary P Stenzel-Poore

2008-01-01

184

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); J. Perren Cobb (Washington University School of Medicine;Cellular Injury and Adaptation Laboratory, Departments of Surgery and Genetics REV)

2005-07-05

185

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

186

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

187

Ischemic preconditioning reduces infarct size in swine myocardium.  

PubMed

We evaluated the hypothesis that stunning swine myocardium with brief ischemia reduces oxygen demand in the stunned region and increases tolerance of myocardium to longer periods of ischemia. Wall function was quantified with ultrasonic crystals aligned to measure wall thickening, and stunning was achieved with two cycles of left anterior descending coronary artery (LAD) occlusion (10 minutes) and reperfusion (30 minutes), after which the LAD was occluded for 60 minutes and reperfused for 90 minutes. Infarct size (as a percent of risk region) was then determined by incubating myocardium with para-nitro blue tetrazolium. Regional oxygen demand was measured as myocardial oxygen consumption before the 60-minute LAD occlusion in the stunned region; tracer microspheres were used to determine blood flow, and blood from the anterior interventricular vein and left atrium was used to calculate oxygen saturations. After the second reperfusion period, wall thickening in the stunned region was reduced to 1.4 +/- 2.4% compared with 36.7 +/- 2.5% (mean +/- SEM) before ischemia (p less than 0.001). Regional myocardial oxygen consumption after stunning (3.1 +/- 0.7 ml O2/min/100 g) was no different from regional myocardial oxygen consumption before stunning (3.7 +/- 0.6 ml O2/min/100 g). In the nine pigs "preconditioned" by stunning, infarct size was 10.4 +/- 6.3% of the risk region compared with 48.0 +/- 12.7% in the six control pigs subjected to 60 minutes of ischemia without prior stunning (p less than 0.005). The risk regions were similar (14.4 +/- 1.5% vs. 14.6 +/- 1.9% of the left ventricle, preconditioned vs. control pigs, respectively). We conclude that stunning swine myocardium with two cycles of a 10-minute LAD occlusion followed by reperfusion increases ischemic tolerance but that changes in regional demand in stunned myocardium do not predict the marked reduction in infarct size that follows a subsequent 60-minute period of ischemia. PMID:2317890

Schott, R J; Rohmann, S; Braun, E R; Schaper, W

1990-04-01

188

Antioxidant and lysosomotropic properties of acute D-propranolol underlies its cardioprotection of postischemic hearts from moderate iron-overloaded rats.  

PubMed

The benefits of acute D-propranolol (D-Pro, non-beta-adrenergic receptor blocker) pretreatment against enhanced ischemia/reperfusion (I/R) injury of hearts from moderate iron-overloaded rats were examined. Perfused hearts from iron-dextran-treated rats (450 mg/kg/week for 3 weeks, intraperitoneal administration) exhibited normal control function, despite iron treatment that elevated plasma iron and conjugated diene levels by 8.1-and 2.5-fold, respectively. However, these hearts were more susceptible to 25 mins of global I/R stress compared with non-loaded hearts; the coronary flow rate, aortic output, cardiac work, left ventricular systolic pressure, positive differential left ventricular pressure (dP/dt), and left ventricular developed pressure displayed 38%, 60%, 55%, 13%, 41%, and 15% lower recoveries, respectively, and a 6.5-fold increase in left ventricular end-diastolic pressure. Postischemic hearts from iron-loaded rats also exhibited 5.6-, 3.48-, 2.43-, and 3.45-fold increases in total effluent iron content, conjugated diene levels, lactate dehydrogenase (LDH) activity, and lysosomal N-acetyl-beta-glucosaminidase (NAGA) activity, respectively, compared with similarly stressed non-loaded hearts. A comparison of detection time profiles during reperfusion suggests that most of the oxidative injury (conjugated diene) in hearts from iron-loaded rats occurred at later times of reperfusion (8.5-15 mins), and this corresponded with heightened tissue iron and NAGA release. D-Pro (2 microM infused for 30 mins) pretreatment before ischemia protected all parameters compared with the untreated iron-loaded group; pressure indices improved 1.2- to 1.6-fold, flow parameters improved 1.70- to 2.96-fold, cardiac work improved 2.87-fold, and end-diastolic pressure was reduced 56%. D-Pro lowered total release of tissue iron, conjugated diene content, LDH activity, and NAGA activity 4.59-, 2.55-, 3.04-, and 4.14-fold, respectively, in the effluent of I/R hearts from the iron-loaded group. These findings suggest that the enhanced postischemic dysfunction and tissue injury of hearts from iron-loaded rats was caused by excessive iron-catalyzed free radical stress, and that the membrane antioxidant properties of D-Pro and its stabilization of sequestered lysosomal iron by D-Pro may contribute to the cardioprotective actions of D-Pro. PMID:16565443

Kramer, Jay H; Murthi, Sarah B; Wise, Robert M; Mak, I-Tong; Weglicki, William B

2006-04-01

189

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

190

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

191

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

PubMed

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) have 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

2014-02-01

192

Preconditioning with levosimendan before implantation of left ventricular assist devices.  

PubMed

In this retrospective study, we investigated the impact of preconditioning of the right ventricle with the calcium sensitizer levosimendan immediately before left ventricular assist device (LVAD) implantation on outcome and survival. Nine consecutive LVAD patients (seven suffering from dilative cardiomyopathy and two from ischemic cardiomyopathy) with echocardiographic and invasive evidence of right heart insufficiency received levosimendan with 0.1 ?g/kg body weight/min for 24 h before implantation of the assist device (seven HeartWare and two Jarvik 2000). Administration of levosimendan was safe and had not to be discontinued in any patient. We observed no relevant side effects. Twelve-month survival after implantation of the LVAD was 89% representing a superior outcome compared with the fifth INTERMACS registry data with 75% survival. Two temporary extracorporeal membrane-oxygenation implantations were necessary due to intraoperative right ventricular dysfunction. Only one patient died 5 weeks after LVAD implantation of multiorgan failure, five patients were successfully transplanted, and three patients underwent LVAD implantation for destination therapy. Levosimendan might improve clinical outcome and survival when used as pretreatment in patients with right heart insufficiency prior to LVAD implantation. However, we recommend a larger controlled trial in the future to confirm our preliminary results. PMID:24147881

Theiss, Hans D; Grabmaier, Ulrich; Kreissl, Nicole; Hagl, Christian; Steinbeck, Gerhard; Sodian, Ralf; Franz, Wolfgang-M; Kaczmarek, Ingo

2014-03-01

193

Remote ischemic preconditioning delays fatigue development during handgrip exercise.  

PubMed

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

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

2014-04-15

194

Effects of hypoxic preconditioning on synaptic ultrastructure in mice.  

PubMed

Hypoxic preconditioning (HPC) elicits resistance to more drastic subsequent insults, which potentially provide neuroprotective therapeutic strategy, but the underlying mechanisms remain to be fully elucidated. Here, we examined the effects of HPC on synaptic ultrastructure in olfactory bulb of mice. Mice underwent up to five cycles of repeated HPC treatments, and hypoxic tolerance was assessed with a standard gasp reflex assay. As expected, HPC induced an increase in tolerance time. To assess synaptic responses, Western blots were used to quantify protein levels of representative markers for glia, neuron, and synapse, and transmission electron microscopy was used to examine synaptic ultrastructure and mitochondrial density. HPC did not significantly alter the protein levels of astroglial marker (GFAP), neuron-specific markers (GAP43, Tuj-1, and OMP), synaptic number markers (synaptophysin and SNAP25) or the percentage of excitatory synapses versus inhibitory synapses. However, HPC significantly affected synaptic curvature and the percentage of synapses with presynaptic mitochondria, which showed concomitant change pattern. These findings demonstrate that HPC is associated with changes in synaptic ultrastructure. Synapse 69:7-14, 2015. © 2014 Wiley Periodicals, Inc. PMID:25155519

Liu, Yi; Sun, Zhishan; Sun, Shufeng; Duan, Yunxia; Shi, Jingfei; Qi, Zhifeng; Meng, Ran; Sun, Yongxin; Zeng, Xianwei; Chui, Dehua; Ji, Xunming

2015-01-01

195

Neuroprotection Induced In Vitro by Ischemic Preconditioning and Postconditioning: Modulation of Apoptosis and PI3K–Akt Pathways  

Microsoft Academic Search

Preconditioning and postconditioning are mild ischemic exposures before or after severe injurious ischemia, respectively,\\u000a that elicit endogenous neuroprotective responses. Molecular mechanisms of neuroprotection through preconditioning and postconditioning\\u000a are not completely understood. Here we optimized the in vitro oxygen and glucose deprivation (OGD) models of preconditioning and postconditioning in primary cortical neuron cultures that\\u000a allow the studies of the corresponding molecular

Shiv S. Prasad; Marsha Russell; Margeryta Nowakowska

2011-01-01

196

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

197

Hypercholesterolemia Abrogates Late Preconditioning via a Tetrahydrobiopterin-Dependent Mechanism in Conscious Rabbits  

PubMed Central

Background Although the late phase of ischemic preconditioning (PC) is known to confer cardioprotection in healthy animal models, it is unknown whether this phenomenon exists in the presence of hypercholesterolemia. The goal of this study was to determine whether the infarct-sparing effect of late PC is affected by hypercholesterolemia and, if so, whether a tetrahydrobiopterin (BH4)-dependent mechanism is responsible for the loss of late PC. Methods and Results Conscious rabbits fed a normal diet or a 1% cholesterol diet for 6 weeks were subjected to ischemic PC (six 4-minute coronary occlusion/4-minute reperfusion cycles) and, 24 hours later, underwent a 30-minute occlusion followed by 3 days of reperfusion. A total of 125 rabbits were used. In normocholesterolemic rabbits, ischemic PC reduced infarct size, an effect that was abrogated by administration of the BH4 synthesis inhibitor N-acetylserotonin (15 mg/kg IV) before the 30-minute occlusion. In hypercholesterolemic rabbits, however, ischemic PC failed to reduce infarct size. Myocardial BH4 levels in the ischemic zone increased 24 hours after ischemic PC in normocholesterolemic rabbits but not in hypercholesterolemic rabbits. In addition, in normocholesterolemic rabbits, pretreatment with N-acetylserotonin completely abolished the ischemic PC-induced increase in myocardial BH4 levels. Conclusions This study demonstrates that (1) hypercholesterolemia abrogates both the infarct-sparing effect of late PC and the concomitant upregulation of myocardial BH4, and (2) inhibition of myocardial BH4 synthesis in the absence of hypercholesterolemia is sufficient to abolish the infarct-sparing effect of late PC. The results support the concept that hypercholesterolemia abrogates late PC by preventing the upregulation of BH4, an essential cofactor for inducible nitric oxide synthase. PMID:16186416

Tang, Xian-Liang; Takano, Hitoshi; Xuan, Yu-Ting; Sato, Hiroshi; Kodani, Eitaro; Dawn, Buddhadeb; Zhu, Yanqing; Shirk, Gregg; Wu, Wen-Jian; Bolli, Roberto

2013-01-01

198

Ozone oxidative preconditioning inhibits renal fibrosis induced by ischemia and reperfusion injury in rats  

PubMed Central

Ischemia and reperfusion injury (IRI) is a crucial contributor to the development of renal fibrosis. Ozone has been proposed as a novel medical therapy for various conditions, including organ IRI. The aim of this study was to investigate whether ozone oxidative preconditioning (OzoneOP) has a beneficial effect in preventing the development of renal fibrosis following IRI. Sprague Dawley rats were subjected to 45 min of ischemia followed by 8 weeks of reperfusion. Prior to surgery, rats in the OzoneOP group were treated with ozone and those in the IRI and Sham groups were untreated. Blood samples were collected for the detection of blood urea nitrogen (BUN) and creatinine (Cr) levels. To assess tissue fibrosis, Masson’s trichrome staining was performed. Immunohistochemistry was also performed to determine the localization of ?-smooth muscle actin (?-SMA). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to analyze the expression of transforming growth factor (TGF)-?1, ?-SMA and Smad7. The levels of BUN and Cr did not significantly differ between groups. Rats pretreated with ozone showed markedly less interstitial fibrosis than untreated rats following IRI. In addition, immunohistochemistry revealed that ?-SMA expression was attenuated in the OzoneOP group compared with the IRI group. RT-qPCR and western blot analysis showed that OzoneOP inhibited the IRI-induced increases in ?-SMA and TGF-?1 expression levels, and that the IRI-induced reduction in the expression of Smad7 was inhibited in the OzoneOP group. The results indicate that OzoneOP has beneficial effects on ischemic renal fibrosis. OzoneOP may exert its protective effects by a mechanism involving modulation of the TGF-?1/Smad7 pathway. PMID:25371729

WANG, LEI; CHEN, HUI; LIU, XIU-HENG; CHEN, ZHI-YUAN; WENG, XIAO-DONG; QIU, TAO; LIU, LIN; ZHU, HENG-CHENG

2014-01-01

199

Ozone oxidative preconditioning inhibits renal fibrosis induced by ischemia and reperfusion injury in rats.  

PubMed

Ischemia and reperfusion injury (IRI) is a crucial contributor to the development of renal fibrosis. Ozone has been proposed as a novel medical therapy for various conditions, including organ IRI. The aim of this study was to investigate whether ozone oxidative preconditioning (OzoneOP) has a beneficial effect in preventing the development of renal fibrosis following IRI. Sprague Dawley rats were subjected to 45 min of ischemia followed by 8 weeks of reperfusion. Prior to surgery, rats in the OzoneOP group were treated with ozone and those in the IRI and Sham groups were untreated. Blood samples were collected for the detection of blood urea nitrogen (BUN) and creatinine (Cr) levels. To assess tissue fibrosis, Masson's trichrome staining was performed. Immunohistochemistry was also performed to determine the localization of ?-smooth muscle actin (?-SMA). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to analyze the expression of transforming growth factor (TGF)-?1, ?-SMA and Smad7. The levels of BUN and Cr did not significantly differ between groups. Rats pretreated with ozone showed markedly less interstitial fibrosis than untreated rats following IRI. In addition, immunohistochemistry revealed that ?-SMA expression was attenuated in the OzoneOP group compared with the IRI group. RT-qPCR and western blot analysis showed that OzoneOP inhibited the IRI-induced increases in ?-SMA and TGF-?1 expression levels, and that the IRI-induced reduction in the expression of Smad7 was inhibited in the OzoneOP group. The results indicate that OzoneOP has beneficial effects on ischemic renal fibrosis. OzoneOP may exert its protective effects by a mechanism involving modulation of the TGF-?1/Smad7 pathway. PMID:25371729

Wang, Lei; Chen, Hui; Liu, Xiu-Heng; Chen, Zhi-Yuan; Weng, Xiao-Dong; Qiu, Tao; Liu, Lin; Zhu, Heng-Cheng

2014-12-01

200

Glycine transporters type 1 inhibitor promotes brain preconditioning against NMDA-induced excitotoxicity.  

PubMed

Brain preconditioning is a protective mechanism, which can be activated by sub-lethal stimulation of the NMDA receptors (NMDAR) and be used to achieve neuroprotection against stroke and neurodegenerative diseases models. Inhibitors of glycine transporters type 1 modulate glutamatergic neurotransmission through NMDAR, suggesting an alternative therapeutic strategy of brain preconditioning. The aim of this work was to evaluate the effects of brain preconditioning induced by NFPS, a GlyT1 inhibitor, against NMDA-induced excitotoxicity in mice hippocampus, as well as to study its neurochemical mechanisms. C57BL/6 mice (male, 10-weeks-old) were preconditioned by intraperitoneal injection of NFPS at doses of 1.25, 2.5 or 5.0 mg/kg, 24 h before intrahippocampal injection of NMDA. Neuronal death was evaluated by fluoro jade C staining and neurochemical parameters were evaluated by gas chromatography-mass spectrometry, scintillation spectrometry and western blot. We observed that NFPS preconditioning reduced neuronal death in CA1 region of hippocampus submitted to NMDA-induced excitotoxicity. The amino acids (glycine and glutamate) uptake and content were increased in hippocampus of animals treated with NFPS 5.0 mg/kg, which were associated to an increased expression of type-2 glycine transporter (GlyT2) and glutamate transporters (EAAT1, EAAT2 and EAAT3). The expression of GlyT1 was reduced in animals treated with NFPS. Interestingly, the preconditioning reduced expression of GluN2B subunits of NMDAR, whereas did not change the expression of GluN1 or GluN2A in all tested doses. Our study suggests that NFPS preconditioning induces resistance against excitotoxicity, which is associated with neurochemical changes and reduction of GluN2B-containing NMDAR expression. PMID:25312280

Cunha Xavier Pinto, Mauro; Lima, Isabel Vieira de Assis; Pessoa da Costa, Flávia Lage; Rosa, Daniela Valadão; Mendes-Goulart, Vânia Aparecida; Resende, Rodrigo Ribeiro; Romano-Silva, Marco Aurélio; Pinheiro de Oliveira, Antônio Carlos; Gomez, Marcus Vinícius; Gomez, Renato Santiago

2015-02-01

201

Delayed treatment with NSC23766 in streptozotocin-induced diabetic rats ameliorates post-ischemic neuronal apoptosis through suppression of mitochondrial p53 translocation.  

PubMed

NSC23766, a specific inhibitor of Rac1, has recently been shown to protect against cerebral ischemic injury, although the effects of NSC23766 in a diabetic model have not been examined. Therefore, the aim of our study was to investigate if NSC23766 provided neuroprotection in streptozotocin-induced diabetic rats and to determine the potential mechanism through which NSC23766 works. Diabetic Sprague-Dawley rats were subjected to right middle cerebral artery occlusion (MCAO) for 90 min. NSC23766 (10 or 30 mg kg(-1)) or isotonic saline were administered intraperitoneally twice daily starting 24 h after cerebral ischemia, for three consecutive days. Cerebral infarct volume, neurological deficit scores, neuronal apoptosis, and the release of cytochrome c, as well as the generation of ROS and mitochondrial integrity, were evaluated 96 h after reperfusion. In addition, the mitochondrial translocation of p53 and the expression of p53-upregulated modulator of apoptosis (PUMA) in the mitochondria of the cerebral ischemic cortex were determined by western blotting. NSC23766 not only ameliorated post-ischemic neuronal apoptosis but also decreased cerebral ischemia-induced mitochondrial p53 translocation and the expression of PUMA in mitochondria in diabetic rats. Thus, our data indicate that NSC23766 has therapeutic potential against cerebral ischemic reperfusion injury and that NSC23766 significantly ameliorates neuronal apoptosis by suppressing mitochondrial p53 translocation in streptozotocin-induced diabetic rats. PMID:24953831

Liao, Juan; Ye, Zhi; Huang, Guoqing; Xu, Chang; Guo, Qulian; Wang, E

2014-10-01

202

Preventing the Preventable  

PubMed Central

Objectives Growing literature suggests that a significant proportion of rehospitalizations could be prevented if systems were put in place aimed at identifying and addressing some of the underlying issues that cause them. This article highlights key risk factors for unplanned rehospitalizations and illustrates a project that has successfully addressed many of the underlying issues that contribute to them. Primary Practice Setting(s) The study illustrated herein took place at an inner-city academic teaching hospital. Findings/Conclusions Proactively identifying patient-, clinician-, and system-associated barriers to successful discharge transitions is critical for effective transitions of care for patients leaving the hospital setting. This process represents a culture change, requires a multidisciplinary approach to care, and mandates clear delineation of roles and responsibilities in the process, with ultimate and clear process ownership being defined. With such steps in place in a system of care, it is reasonable to expect a reduction in preventable rehospitalizations. PMID:19474639

Greenwald, Jeffrey L.; Jack, Brian W.

2009-01-01

203

Preconditioning with acute and chronic lithium administration reduces ischemia/reperfusion injury mediated by cyclooxygenase not nitric oxide synthase pathway in isolated rat heart.  

PubMed

Lithium is widely used for the management of neuropsychiatric symptoms in bipolar disorders. A variety of hypotheses have been invoked to explain the mechanism of action of lithium. To determine if lithium exerts direct cardiac protection, in the present study perfused rat heart model was used. The mechanism of lithium-mediated cardioprotection was explored by combined use of lithium and nitro-L-arginine methyl ester (L-NAME, a non-selective nitric oxide synthase inhibitor) or indomethacin (a non-selective cyclooxygenase pathway inhibitor). Rat isolated hearts were used for Langendorff perfusion. Hearts were either non-preconditioned or preconditioned with acute lithium (3 mM) or chronic lithium (600 mg/l in tap water for 4 weeks, 0.265 +/- 0.023 mM in serum) before 30 min global ischemia followed by 90 min reperfusion. Within each of these protocols, hearts were divided into two groups; one group was exposed to L-NAME (0.1 mM) and another group was exposed to indomethacin (10 microM). Infarct size was measured by the triphenyltetrazolium chloride method. Left ventricular function was assessed by left ventricular developed pressure (LVDP), heart rate and coronary flow (CF). In our experiment acute and/or chronic administration of lithium before prolonged ischemia offered significant myoprotective effects in terms of infarct size reduction and improved cardiac function against ischemia/reperfusion injury. The effects of lithium pretreatment were prevented by the administration of indomethacin but not L-NAME. In conclusion, our results demonstrate that preconditioning with acute and/or chronic lithium administration improves recovery of the ventricular function and reduces infarct size via cyclooxygenase (COX) pathway in isolated rat heart. PMID:18789320

Faghihi, Mahdieh; Mirershadi, Fatemeh; Dehpour, Ahmad Reza; Bazargan, Maryam

2008-11-12

204

Gauss-Newton inspired preconditioned optimization in large deformation diffeomorphic metric mapping.  

PubMed

In this work, we propose a novel preconditioned optimization method in the paradigm of Large Deformation Diffeomorphic Metric Mapping (LDDMM). The preconditioned update scheme is formulated for the non-stationary and the stationary parameterizations of diffeomorphisms, yielding three different LDDMM methods. The preconditioning matrices are inspired in the Hessian approximation used in Gauss-Newton method. The derivatives are computed using Frechet differentials. Thus, optimization is performed in a Sobolev space, in contrast to optimization in L(2) commonly used in non-rigid registration literature. The proposed LDDMM methods have been evaluated and compared with their respective implementations of gradient descent optimization. Evaluation has been performed using real and simulated images from the Non-rigid Image Registration Evaluation Project (NIREP). The experiments conducted in this work reported that our preconditioned LDDMM methods achieved a performance similar or superior to well-established-in-literature gradient descent non-stationary LDDMM in the great majority of cases. Moreover, preconditioned optimization showed a substantial reduction in the execution time with an affordable increase of the memory usage per iteration. Additional experiments reported that optimization using Frechet differentials should be preferable to optimization using L(2) differentials. PMID:25254606

Hernandez, Monica

2014-10-21

205

Gauss–Newton inspired preconditioned optimization in large deformation diffeomorphic metric mapping  

NASA Astrophysics Data System (ADS)

In this work, we propose a novel preconditioned optimization method in the paradigm of Large Deformation Diffeomorphic Metric Mapping (LDDMM). The preconditioned update scheme is formulated for the non-stationary and the stationary parameterizations of diffeomorphisms, yielding three different LDDMM methods. The preconditioning matrices are inspired in the Hessian approximation used in Gauss–Newton method. The derivatives are computed using Frechet differentials. Thus, optimization is performed in a Sobolev space, in contrast to optimization in L2 commonly used in non-rigid registration literature. The proposed LDDMM methods have been evaluated and compared with their respective implementations of gradient descent optimization. Evaluation has been performed using real and simulated images from the Non-rigid Image Registration Evaluation Project (NIREP). The experiments conducted in this work reported that our preconditioned LDDMM methods achieved a performance similar or superior to well-established-in-literature gradient descent non-stationary LDDMM in the great majority of cases. Moreover, preconditioned optimization showed a substantial reduction in the execution time with an affordable increase of the memory usage per iteration. Additional experiments reported that optimization using Frechet differentials should be preferable to optimization using L2 differentials.

Hernandez, Monica

2014-10-01

206

Lysine deacetylation in ischaemic preconditioning: the role of SIRT1  

PubMed Central

Aims Acute ischaemic preconditioning (IPC) induces protection against cardiac ischaemia–reperfusion (IR) via post-translational modification of key proteins. Lysine (Lys) acetylation is an important regulator of protein function, but this type of modification has not been studied in the context of IPC. We investigated Lys acetylation in IPC and its upstream regulation by SIRT1. Methods and results Hearts from C57BL/6 mice were Langendorff-perfused and subjected to IPC and IR injury. Mice were exposed to IPC by in vivo coronary artery occlusion. An isolated cardiomyocyte model of IPC was also developed. Lys acetylation was measured by western blotting, and pharmacological modulators of Lys acetylation were tested. More Lys deacetylation was observed in IPC, in the Langendorff, in vivo, and cellular IPC models; this was concurrent with an increase in SIRT1 activity measured by p53 Lys379 deacetylation. IPC was not accompanied by changes in SIRT1 protein level, but evidence was obtained for SIRT1 modification by Small Ubiquitin-like Modifier (SUMOylation) in IPC. Furthermore, the specific SIRT1 inhibitor splitomicin reversed both IPC-mediated Lys deacetylation and IPC-induced cardioprotection. Inhibition of nicotinamide phosphoribosyltransferase (Nampt, an important enzyme which regulates SIRT1 activity by maintaining availability of the substrate NAD+) also blocked both IPC-induced deacetylation and cardioprotection. Conclusion Lys deacetylation occurs during IPC and an elevation in SIRT1 activity plays a role in this phenomenon. Inhibition of SIRT1, either directly or by restricting the availability of its substrate NAD+, inhibits IPC. Together these data suggest a role for SIRT1-mediated Lys deacetylation in the mechanism of acute IPC. PMID:20823277

Nadtochiy, Sergiy M.; Redman, Emily; Rahman, Irfan; Brookes, Paul S.

2011-01-01

207

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

208

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

209

Human Amniotic Fluid Stem Cell Preconditioning Improves Their Regenerative Potential  

PubMed Central

Human amniotic fluid stem (hAFS) cells, a novel class of broadly multipotent stem cells that share characteristics of both embryonic and adult stem cells, have been regarded as promising candidate for cell therapy. Taking advantage by the well-established murine model of acute kidney injury (AKI), we studied the proregenerative effect of hAFS cells in immunodeficient mice injected with the nephrotoxic drug cisplatin. Infusion of hAFS cells in cisplatin mice improved renal function and limited tubular damage, although not to control level, and prolonged animal survival. Human AFS cells engrafted injured kidney predominantly in peritubular region without acquiring tubular epithelial markers. Human AFS cells exerted antiapoptotic effect, activated Akt, and stimulated proliferation of tubular cells possibly via local release of factors, including interleukin-6, vascular endothelial growth factor, and stromal cell–derived factor-1, which we documented in vitro to be produced by hAFS cells. The therapeutic potential of hAFS cells was enhanced by cell pretreatment with glial cell line–derived neurotrophic factor (GDNF), which markedly ameliorated renal function and tubular injury by increasing stem cell homing to the tubulointerstitial compartment. By in vitro studies, GDNF increased hAFS cell production of growth factors, motility, and expression of receptors involved in cell homing and survival. These findings indicate that hAFS cells can promote functional recovery and contribute to renal regeneration in AKI mice via local production of mitogenic and prosurvival factors. The effects of hAFS cells can be remarkably enhanced by GDNF preconditioning. PMID:22066606

Rota, Cinzia; Imberti, Barbara; Pozzobon, Michela; Piccoli, Martina; De Coppi, Paolo; Atala, Anthony; Gagliardini, Elena; Xinaris, Christodoulos; Benedetti, Valentina; Fabricio, Aline S.C.; Squarcina, Elisa; Abbate, Mauro; Benigni, Ariela; Remuzzi, Giuseppe

2012-01-01

210

Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning  

PubMed Central

Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhanced morphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with outcome in injury-experienced kidney. PMID:25243156

Kim, Jee In; Park, Jeen-Woo

2014-01-01

211

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

NASA Technical Reports Server (NTRS)

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

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

1993-01-01

212

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

213

Mechanical preconditioning enables electrophysiologic coupling of skeletal myoblast cells to myocardium  

PubMed Central

Objective The effect of mechanical preconditioning on skeletal myoblasts in engineered tissue constructs was investigated to resolve issues associated with conduction block between skeletal myoblast cells and cardiomyocytes. Methods Murine skeletal myoblasts were used to generate engineered tissue constructs with or without application of mechanical strain. After in vitro myotube formation, engineered tissue constructs were co-cultured for 6 days with viable embryonic heart slices. With the use of sharp electrodes, electrical coupling between engineered tissue constructs and embryonic heart slices was assessed in the presence or absence of pharmacologic agents. Results The isolation and expansion procedure for skeletal myoblasts resulted in high yields of homogeneously desmin-positive (97.1% ± 0.1%) cells. Mechanical strain was exerted on myotubes within engineered tissue constructs during gelation of the matrix, generating preconditioned engineered tissue constructs. Electrical coupling between preconditioned engineered tissue constructs and embryonic heart slices was observed; however, no coupling was apparent when engineered tissue constructs were not subjected to mechanical strain. Coupling of cells from engineered tissue constructs to cells in embryonic heart slices showed slower conduction velocities than myocardial cells with the embryonic heart slices (preconditioned engineered tissue constructs vs embryonic heart slices: 0.04 ± 0.02 ms vs 0.10 ± 0.05 ms, P = .011), lower stimulation frequencies (preconditioned engineered tissue constructs vs maximum embryonic heart slices: 4.82 ± 1.42 Hz vs 10.58 ± 1.56 Hz; P = .0009), and higher sensitivities to the gap junction inhibitor (preconditioned engineered tissue constructs vs embryonic heart slices: 0.22 ± 0.07 mmol/L vs 0.93 ± 0.15 mmol/L; P = .0004). Conclusions We have generated skeletal myoblast–based transplantable grafts that electrically couple to myocardium. PMID:22980065

Treskes, Philipp; Cowan, Douglas B.; Stamm, Christof; Rubach, Martin; Adelmann, Roland; Wittwer, Thorsten; Wahlers, Thorsten

2015-01-01

214

Sphingosine kinase 2 mediates cerebral preconditioning and protects mouse brain against ischemic injury  

PubMed Central

Background and purpose Cerebral preconditioning provides insights into endogenous mechanisms that protect the brain from ischemic injury. Hypoxia and the anesthetic isoflurane are powerful preconditioning agents. Recent data show that sphingosine 1-phosphate (S1P) receptor stimulation improves outcome in rodent models of stroke. Endogenous S1P levels are controlled by the expression and activity of sphingosine kinases (SPK). We hypothesize that SPK up-regulation mediates preconditioning induced by isoflurane and hypoxia and reduces ischemic injury. Methods Male wild-type C57BL/J, SPK1?/? and SPK2?/? mice were exposed to isoflurane (IsoPC) or hypoxia preconditioning (HPC) before transient middle cerebral artery occlusion. Infarct volume and neurological outcome were measured 24 hours later. SPK inhibitors (SKI-II and ABC294640) were used to test the involvement of SPK2. Expressions of SPK1, SPK2 and HIF1? were determined. Primary cultures of mouse cortical neurons were exposed to isoflurane before glutamate- or hydrogen peroxide-induced cell death. Results IsoPC and HPC significantly reduced infarct volume and improved neurological outcome in wild-type and SPK1?/? mice, but not in SPK2?/? mice. Pretreatment with SKI-II or ABC294640 abolished the IsoPC-induced tolerance. Western blot showed a rapid and sustained increase in SPK2 level, whereas SPK1 level was similar between preconditioned mice and controls. HIF1? was up-regulated in wild-type IsoPC mice, but not in SPK2?/?. IsoPC protected primary neurons against cell death, which was abolished in ABC294640-treated cells. Conclusions Applying genetic and pharmacological approaches, we demonstrate that neuronal SPK2 isoform plays an important role in cerebral preconditioning. PMID:21980199

Yung, Lai Ming; Wei, Ying; Qin, Tao; Wang, Yumei; Smith, Charles; Waeber, Christian

2011-01-01

215

NMDA preconditioning attenuates cortical and hippocampal seizures induced by intracerebroventricular quinolinic acid infusion.  

PubMed

Searching for new therapeutic strategies through modulation of glutamatergic transmission using effective neuroprotective agents is essential. Glutamatergic excitotoxicity is a common factor to neurodegenerative diseases and acute events such as cerebral ischemia, traumatic brain injury, and epilepsy. This study aimed to evaluate behavioral and electroencephalographic (EEG) responses of mice cerebral cortex and hippocampus to subconvulsant and convulsant application of NMDA and quinolinic acid (QA), respectively. Moreover, it aimed to evaluate if EEG responses may be related to the neuroprotective effects of NMDA. Mice were preconditioned with NMDA (75 mg/kg, i.p.) and EEG recordings were performed for 30 min. One day later, QA was injected (36.8 nmol/site) and EEG recordings were performed during 10 min. EEG analysis demonstrated NMDA preconditioning promotes spike-wave discharges (SWDs), but it does not display behavioral manifestation of seizures. Animals that were protected by NMDA preconditioning against QA-induced behavioral seizures, presented higher number of SWD after NMDA administration, in comparison to animals preconditioned with NMDA that did display behavioral seizures after QA infusion. No differences were observed in latency for the first seizure or duration of seizures. EEG recordings after QA infusion demonstrated there were no differences in the number of SWD, latency for the first seizure or duration of seizures in animals pretreated with saline or in animals preconditioned by NMDA that received QA. A negative correlation was identified between the number of NMDA-induced SWD and QA-induced seizures severity. These results suggest a higher activation during NMDA preconditioning diminishes mice probability to display behavioral seizures after QA infusion. PMID:23184648

Vandresen-Filho, Samuel; Hoeller, Alexandre A; Herculano, Bruno A; Duzzioni, Marcelo; Duarte, Filipe S; Piermartiri, Tetsadê C B; Boeck, Carina C; de Lima, Thereza C M; Marino-Neto, José; Tasca, Carla I

2013-07-01

216

Propulsion-related flowfields using the preconditioned Navier-Stokes equations  

NASA Astrophysics Data System (ADS)

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

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

1992-07-01

217

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

218

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

219

Peripheral Vascular Disease as Remote Ischemic Preconditioning for Acute Stroke  

PubMed Central

Obectives Remote ischemic preconditioning (RIPC) is a powerful endogenous mechanism whereby a brief period of ischemia is capable of protecting remote tissues from subsequent ischemic insult. While this phenomenon has been extensively studied in the heart and brain in animal models, little work has been done to explore the effects of RIPC in human patients with acute cerebral ischemia. This study investigates whether chronic peripheral hypoperfusion, in the form of pre-existing arterial peripheral vascular disease (PVD) that has not been surgically treated, is capable of inducing neuroprotective effects for acute ischemic stroke. Methods Individuals with PVD who had not undergone prior surgical treatment were identified from a registry of stroke patients. A control group within the same database was identified by matching patient’s demographics and risk factors. The two groups were compared in terms of outcome by NIH Stroke Scale (NIHSS), modified Rankin Scale (mRS), mortality, and volume of infarcted tissue at presentation and at discharge. Results The matching algorithm identified 26 pairs of PVD-control patients (9 pairs were female and 17 pairs were male). Age range was 20 to 93 years (mean 73). The PVD group was found to have significantly lower NIHSS scores at admission (NIHSS ? 4: PVD 47.1%, Control 4.35%, p < 0.003), significantly more favorable outcomes at discharge (mRS ? 2: PVD 30.8%, Control 3.84%, p < 0.012), and a significantly lower mortality rate (PVD 26.9%, Control 57.7% p=0.024). Mean acute stroke volume at admission and at discharge were significantly lower for the PVD group (Admission: PVD 39.6mL, Control 148.3mL, p < 0.005 and Discharge: PVD 111.7mL, Control 275mL, p < 0.001). Conclusion Chronic limb hypoperfusion induced by PVD can potentially produce a neuroprotective effect in acute ischemic stroke. This effect resembles the neuroprotection induced by RIPC in preclinical models. PMID:23958050

Connolly, Mark; Bilgin-Freiert, Arzu; Ellingson, Benjamin; Dusick, Joshua R.; Liebeskind, David; Saver, Jeff; Gonzalez, Nestor R.

2013-01-01

220

A labdane diterpene exerts ex vivo and in vivo cardioprotection against post-ischemic injury: Involvement of AKT-dependent mechanisms.  

PubMed

Therapeutic approaches to protect the heart from ischemia/reperfusion (I/R) injury are an area of intense research, as myocardial infarction is a major cause of mortality and morbidity. Diterpenes are bioactive natural products with great therapeutic potential. In the present study, we have investigated the in vivo cardioprotective effects of a labdane diterpene (DT1) against cardiac I/R injury and the molecular mechanisms involved. DT1 attenuates post-ischemic injury via an AKT-dependent activation of HIF-1?, survival pathways and inhibition of NF-?B signaling. Myocardial infarction (MI) was induced in Wistar rats occluding the left coronary artery (LCA) for 30min followed by 72h reperfusion. DT1 (5mg/kg) was intravenously administered at reperfusion. In addition, we investigated the mechanisms of cardioprotection in the Langendorff-perfused model. Cardioprotection was observed when DT1 was administered after myocardial injury. The molecular mechanisms involved the activation of the survival pathway PDK-1, AKT and AMPK, a reduced phosphorylation of PKD1/2 and sustained HIF-1? activity, leading to increased expression of anti-apoptotic proteins and decreased caspase-3 activation. Pharmacological inhibition of AKT following MI and prior to DT1 challenge significantly decreased the cardioprotection afforded by DT1 therapy at reperfusion. Cardiac function after MI was significantly improved after DT1-treatment, as evidenced by hemodynamic recovery and decreased myocardial infarct size. These findings demonstrate an efficient in vivo cardioprotection by diterpene DT1 against I/R when administered at reperfusion, opening new therapeutic strategies as adjunctive therapy for the pharmacological management of I/R injury. PMID:25557296

Cuadrado-Berrocal, Irene; Gómez-Gaviro, María V; Benito, Yolanda; Barrio, Alicia; Bermejo, Javier; Fernández-Santos, María Eugenia; Sánchez, Pedro L; Desco, Manuel; Fernández-Avilés, Francisco; Fernández-Velasco, María; Boscá, Lisardo; de Las Heras, Beatriz

2015-02-15

221

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

PubMed Central

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

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

2013-01-01

222

Preventing Falls  

MedlinePLUS

... there are simple ways you can prevent most falls. Stay physically active. Regular exercise makes you stronger. ... that may result from falling. Here are some fall prevention tips from Go4Life : l Have your eyes ...

223

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

E-print Network

approximation of the three dimensional integral equation with hypersingular operators. The preconditioner, hypersingular integral equation, iterative methods, preconditioning. The first author was supported in part preconditioners in the case of the p-version approximation of boundary integral equations with hypersingular

Guo, Benqi

224

CaMeL: Learning Method Preconditions for HTN Planning Okhtay Ilghami and Dana S. Nau  

E-print Network

CaMeL: Learning Method Preconditions for HTN Planning Okhtay Ilghami and Dana S. Nau Department, and a supervised learning algorithm, named CaMeL, based on this formalism. We present theo- retical results about CaMeL's soundness, completeness, and convergence properties. We also report experimental results

Nau, Dana S.

225

Project: (version of January 17, 2012) Preconditioned Boundary Element Methods for Electromagnetic  

E-print Network

Project: (version of January 17, 2012) Preconditioned Boundary Element Methods for Electromagnetic in September 2008 The project targets the scattering of time-harmonic electromagnetic waves at dielectric materials with different electromagnetic properties. The goal is to design fast numerical simulation methods

Hiptmair, Ralf

226

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

227

IEEE TRANSACTIONS ON SIGNAL PROCESSING 1 Double Preconditioning for Gabor Frames  

E-print Network

IEEE TRANSACTIONS ON SIGNAL PROCESSING 1 Double Preconditioning for Gabor Frames Peter Balazs contract HPRN-CT-2002-00285 (HASSIP). P. Balazs is with the Acoustics Research Institute of the Austrian Acad- emy of Sciences, Reichsratsstrasse 17, A-1010 Wien, Austria. (e-mail: Pe- ter.Balazs

Feichtinger, Hans Georg

228

Preconditioning” for feature selection and regression in high-dimensional problems  

Microsoft Academic Search

We consider regression problems where the number of predictors greatly exceeds the number of observations. We propose a method for variable selection that first estimates the regression function, yielding a “preconditioned” response variable. The primary method used for this initial regression is supervised principal components. Then we apply a standard procedure such as forward stepwise selection or the LASSO to

Debashis Paul; Eric Bair; Trevor Hastie; Robert Tibshirani

2008-01-01

229

Mechanisms involved in attenuated cardio-protective role of ischemic preconditioning in metabolic disorders.  

PubMed

Myocardial infarction is a pathological state which occurs due to severe abrogation of the blood supply (ischemia) to a part of heart, which can cause myocardial damage. The short intermittent cycles of sub-lethal ischemia and reperfusion has shown to improve the tolerance of the myocardium against subsequent prolonged ischemia/reperfusion (I/R)-induced injury, which is known as ischemic preconditioning (IPC). Although, IPC-induced cardioprotection is well demonstrated in various species, including human beings, accumulated evidence clearly suggests critical abrogation of the beneficial effects of IPC in diabetes mellitus, hyperlipidemia and hyperhomocysteinemia. Various factors are involved in the attenuation of the cardioprotective effect of preconditioning, such as the reduced release of calcitonin gene-related peptide (CGRP), the over-expression of glycogen synthase kinase-3? (GSK-3?) and phosphatase and tensin homolog (PTEN), impairment of mito-KATP channels, the consequent opening of mitochondrial permeability transition pore (MPTP), etc. In this review, we have critically discussed the various signaling pathways involved in abrogated preconditioning in chronic diabetes mellitus, hyperlipidemia and hyperhomocysteinemia. We have also focused on the involvement of PTEN in abrogated preconditioning and the significance of PTEN inhibitors. PMID:24947460

Rana, A; Goyal, N; Ahlawat, A; Jamwal, S; Reddy, Bvk; Sharma, S

2014-06-19

230

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

231

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

232

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method  

E-print Network

Algorithm PREQN: Fortran 77 Subroutines for Preconditioning the Conjugate Gradient Method Jos'e Luis Morales \\Lambda Jorge Nocedal y March 14, 2000 Abstract PREQN is a package of Fortran 77 grant DE­FG02­87ER25047­A004. 1 #12; 1 Introduction In this paper we describe Fortran 77 subroutines

Nocedal, Jorge

233

Protection of Ischemic Preconditioning on Renal Neural Function in Rats with Acute Renal Failure  

Microsoft Academic Search

We tested whether tolerance induced by ischemic preconditioning (IPC) in kidneys was related to renal nerves. Experimental acute renal failure (ARF) in a rat model was induced for 45 min of left renal arterial occlusion (RAO), followed by 6 or 24 h of reperfusion (ischemic reperfusion (I\\/R) group). The episode of IPC was four cycles of 4 min of RAO

Ming-Shiou Wu; Chiang-Ting Chien; Ming-Chieh Ma; Chau-Fong Chen

234

Metaphors and the market: Consequences and preconditions of agent and object metaphors in stock market commentary  

E-print Network

; Attribution; Prediction; Media; Trajectory Much recent research has sought clues about market behavior research takes this approach by focusing on metaphor in market commentary. We use the term ``metaphorMetaphors and the market: Consequences and preconditions of agent and object metaphors in stock

Qian, Ning

235

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

236

Jacobi-Davidson Methods and Preconditioning with Applications in Pole-zero Analysis  

E-print Network

Jacobi-Davidson Methods and Preconditioning with Applications in Pole-zero Analysis J. Rommes 1 , H. The application of Jacobi-Davidson style methods in electric circuit simulation will be discussed in comparison equation is used to improve the Jacobi-Davidson process, but also reveals some problems in the correction

Eindhoven, Technische Universiteit

237

The Application of Preconditioned Jacobi-Davidson Methods in Pole-zero  

E-print Network

The Application of Preconditioned Jacobi-Davidson Methods in Pole-zero Analysis J. Rommes 1 , C of Technology, The Netherlands Abstract. The application of Jacobi-Davidson style methods in electric circuit the Jacobi-Davidson process, but may also cause computational and stability problems when solving the correc

Eindhoven, Technische Universiteit

238

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

239

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

240

Postischemic Long-Term Treatment with Qiangli Tianma Duzhong Capsule Improves Brain Functional Recovery via the Improvement of Hemorrheology and the Inhibition of Platelet Aggregation in a Rat Model of Focal Cerebral Ischemia  

PubMed Central

Qiangli Tianma Duzhong capsule (TMDZ), a Chinese herbal drug, is clinically used to improve functional outcome in patients with ischemic stroke in China. This study was conducted to establish whether postischemic long-term treatment with TMDZ could reduce the loss of injured hemisphere and confer the improvements of neurological outcome in chronic survival of rats with 2?h middle cerebral artery occlusion (MCAO)/reperfusion brain injury and its primary mechanisms. We found that TMDZ (44.5, 89, or 178?mg/kg), administered per os 6?h after the onset of ischemia and for 28 consecutive days, significantly improved the behavior deficits, beginning on day 7, and further improved later. TMDZ treatment also markedly reduced the tissue loss of the injured hemisphere and improved histopathology. In the meantime, TMDZ treatment could improve hemorrheology and inhibit platelet aggregation. These results provide the first evidence that post-ischemic long-term treatment with TMDZ confers the improvements of neurological outcome and the loss of injured hemisphere in an animal ischemic stroke model, and its mechanisms might be associated with the improvements of hemorrheology and the inhibition of platelet aggregation. PMID:24319485

Hong, Li-Zhi; Gu, Wei-wei; Ni, Yong; Xu, Min; Yang, Lei; Liu, Yan-Li; Yang, Shi-Ling; Zhou, Qiang; Gao, Xiu-Mei; Zhang, Hui-Ling

2013-01-01

241

Alpha 1-adrenoceptor activation mediates the infarct size-limiting effect of ischemic preconditioning through augmentation of 5'-nucleotidase activity.  

PubMed Central

We have reported that ischemic preconditioning may limit infarct size by increasing 5'-nucleotidase activity. The present study tested whether alpha 1-adrenoceptor stimulation in ischemic preconditioning mediates the infarct size-limiting effect through augmentation of 5'-nucleotidase activity. The coronary artery was occluded four times for 5 min separated by 5 min of reperfusion (ischemic preconditioning) in 82 dogs. Then the coronary artery was occluded for 90 min followed by 6 h of reperfusion. Infarct size normalized by risk area was smaller after ischemic preconditioning than in the control group (40.6 +/- 2.3 vs 6.7 +/- 2.0%, P < 0.001), even though no difference existed in endomyocardial collateral flow during ischemia (8.7 +/- 1.0 vs 8.9 +/- 1.0 ml/100 g per min). Ectosolic and cytosolic 5'-nucleotidase activity was increased after ischemic preconditioning. However, prazosin blunted the infarct size-limiting effect of ischemic preconditioning (infarct size: 42.8 +/- 3.7%). Intermittent alpha 1-adrenoceptor stimulation by methoxamine mimicked the increase in 5'-nucleotidase activity and the infarct size-limiting effect, which were abolished by alpha, beta,-methyleneadenosine 5'-diphosphate. Identical results were obtained in the conscious model (n = 20). Therefore, we conclude that increases in ectosolic 5'-nucleotidase activity due to alpha 1-adrenoceptor activation may contribute to the infarct size-limiting effect of ischemic preconditioning. Images PMID:8182151

Kitakaze, M; Hori, M; Morioka, T; Minamino, T; Takashima, S; Sato, H; Shinozaki, Y; Chujo, M; Mori, H; Inoue, M

1994-01-01

242

Pre-conditioned mesenchymal stem cells ameliorate renal ischemic injury in rats by augmented survival and engraftment  

PubMed Central

Background Ischemia is the major cause of acute kidney injury (AKI), associated with high mortality and morbidity. Mesenchymal stem cells (MSCs) have multilineage differentiation potential and can be a potent therapeutic option for the cure of AKI. Methods MSCs were cultured in four groups SNAP (S-nitroso N-acetyl penicillamine), SNAP + Methylene Blue (MB), MB and a control for in vitro analysis. Cultured MSCs were pre-conditioned with either SNAP (100 ?M) or MB (1 ?M) or both for 6 hours. Renal ischemia was induced in four groups (as in in vitro study) of rats by clamping the left renal padicle for 45 minutes and then different pre-conditioned stem cells were transplanted. Results We report that pre-conditioning of MSCs with SNAP enhances their proliferation, survival and engraftment in ischemic kidney. Rat MSCs pre-conditioned with SNAP decreased cell apoptosis and increased proliferation and cytoprotective genes’ expression in vitro. Our in vivo data showed enhanced survival and engraftment, proliferation, reduction in fibrosis, significant improvement in renal function and higher expression of pro-survival and pro-angiogenic factors in ischemic renal tissue in SNAP pre-conditioned group of animals. Cytoprotective effects of SNAP pre-conditioning were abrogated by MB, an inhibitor of nitric oxide synthase (NOS) and guanylate cyclase. Conclusion The results of these studies demonstrate that SNAP pre-conditioning might be useful to enhance therapeutic potential of MSCs in attenuating renal ischemia reperfusion injury. PMID:23217165

2012-01-01

243

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

244

Baicalein preconditioning protects cardiomyocytes from ischemia-reperfusion injury via mitochondrial oxidant signaling.  

PubMed

Previous studies suggest baicalein, in addition to its antioxidant effects, protects against hypoxia/reoxygenation injury via its pro-oxidant properties. We hypothesize that a brief period of baicalein treatment prior to ischemia/reperfusion (I/R) may trigger preconditioning protection via a mitochondrial pro-oxidant mechanism. Using an established chick cardiomyocyte model of I/R, cells were preconditioned with baicalein (10 ?M) for 10 min followed by 10-min wash prior to I/R. Intracellular oxidants were measured using 2', 7'-dichlorofluorescin diacetate (DCFH/DA). Cell viability was assessed by propidium iodide and apoptosis determined by DNA fragmentation. Baicalein induced a transient but significant increase of DCF fluorescence within the 10-min preconditioning period, and led to significant reduction of cell death (38.9 ± 1.8% vs. 58.7 ± 1.2% in I/R control, n = 6, p < 0.001) and DNA fragmentation after I/R. Cotreatment with N-acetylcysteine (500 ?M), mitochondrial complex III electron transport chain inhibitor myxothiazol (1 ?M), mitochondrial KATP channel blocker 5-hydroxydecanoate-Na (5-HD, 500 ?M) or anion channel inhibitor 4', 4'-diisothiocyanato-stilbene-2, 2'-disulfonic acid (DIDS, 200 ?M) resulted in significant abrogation of oxidant increase during induction as well as the protection conferred by baicalein preconditioning. These results suggest that baicalein preconditioning exhibits significant anti-apoptotic protection against cardiomyocyte I/R injury by mitochondrial oxidant signaling, which was in part mediated by mitochondrial KATP channel and anion channel opening. PMID:23548122

Chang, Wei-Tien; Li, Jing; Vanden Hoek, Matthew S; Zhu, Xiangdong; Li, Chang-Qing; Huang, Hsien-Hao; Hsu, Chin-Wang; Zhong, Qiang; Li, Juan; Chen, Sy-Jou; Vanden Hoek, Terry L; Shao, Zuo-Hui

2013-01-01

245

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

246

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

247

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

248

The effects of hypoxic preconditioning on white matter damage following hypoxic-ischaemic injury in the neonatal rat brain.  

PubMed

Myelination is an essential process in human development that is carried out by oligodendrocytes in the central nervous system. Hypoxic-ischaemic (HI) brain injury can disrupt myelination by causing oxidative stress, inflammation and excitotoxicity, resulting in the loss of myelin as well as cells of the oligodendrocyte lineage. We have previously shown that hypoxic preconditioning (HP) can protect against HI injury, however, to date there have been no reports of its effects on white matter injury. Sprague-Dawley rat pups (postnatal day (P) 6) were placed into control and HP groups. On P7, pups were further separated into HI and sham surgery groups. HI pups underwent a unilateral common carotid artery occlusion and then exposed to 8% oxygen for 3h. Sham pups underwent the same procedure without occlusion and were maintained in room air. Brains were removed 5 days post-surgery for analysis. In HI-only pups there was a significant reduction in brain volume observed. Consequently, when HP was performed prior to HI, the loss of brain tissue was prevented. The number of early and late oligodendrocyte progenitors (preOLs) in the corpus callosum was unaffected by HI, however, HI reduced the amount of myelin basic protein, indicating that HI may inhibit the maturation of preOLs. Whilst HP did not affect preOL density, it was found to prevent the loss of myelin caused by HI. This indicates that HP may either protect myelin directly or possibly promote the maturation of preOLs to regenerate the lost or damaged myelin. PMID:25009121

Suryana, Eurwin; Jones, Nicole M

2014-10-01

249

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

PubMed Central

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

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

2014-01-01

250

Both Na+-K+ ATPase and Na +-H+ exchanger are immediately active upon post-ischemic reperfusion in isolated rat hearts.  

PubMed

Limited time resolution has hampered proper evaluation of changes in intracellular Na+ (Na+i) in whole hearts upon post-ischemic reperfusion. In isolated rat hearts perfused at 37 degrees C, we studied the contribution of the Na+-K+ ATPase and the Na+-H+ exchanger to control of Na+i during reperfusion using 23Na NMR and the shift reagent Tm(DOTP)5- with a time resolution of 5 s. To assess activities of the Na +-K+ ATPase and the Na+-H+ exchanger, 250 micro mol/l ouabain and/or 3 micro mol/l EIPA, respectively, was added to the perfusate during the first 5 min of reperfusion, following 20 min of ischemia. When used, ouabain was also present for 2 min prior to ischemia. Na+i increased during ouabain perfusion prior to ischemia (132+/-5 and 133+/-4% of the pre-ischemic control value after 2 min, in ouabain and ouabain+EIPA hearts, respectively; mean+/-s.e.m.; n=6 per group) resulting in higher end-ischemic values in ouabain and ouabain+EIPA hearts (249+/-9 and 267+/-17% of the pre-ischemic control value, respectively) than in control and EIPA hearts (207+/-21 and 199+/-10% of the pre-ischemic control value, respectively). In ouabain, hearts Na+i started to rise directly upon reperfusion and amounted to 117+/-6% of the end-ischemic value after 60 s of reperfusion. In control hearts, however, Na+i dropped immediately and was 87+/-5% of the end-ischemic value after 60 s, indicating that the Na+-K+ ATPase resumed function directly upon reperfusion. The initial steep increase of Na+i upon reperfusion in ouabain hearts, which diminished after approximately 40 s to the rate of increase observed during ischemia, was absent in ouabain + EIPA hearts. This indicates the existence, although masked by Na+-K+ ATPase activity, of a Na+-H + exchange mediated Na+ influx upon reperfusion. If only EIPA was present during reperfusion the initial decrease in Na+i was faster than in control hearts, corroborating this finding. PMID:9515010

Van Emous, J G; Schreur, J H; Ruigrok, T J; Van Echteld, C J

1998-02-01

251

Cardioprotective effects of nicorandil in rabbits anaesthetized with halothane: potentiation of ischaemic preconditioning via KATP channels.  

PubMed

1. The roles of ATP-sensitive K+ channels (KATP channels) in ischaemic or pharmacological preconditioning in the rabbit heart remain unclear. Infarct limitation by ischaemic preconditioning was abolished by the KATP channel blocker glibenclamide under ketamine/xylazine anaesthesia, but not under anaesthesia induced by pentobarbital. Infarct limitation by the KATP channel opener pinacidil was detected under ketamine/xylazine anaesthesia, but not under pentobarbital anaesthesia. Thus, these effects appear to be anaesthetic dependent. 2. In the present study, we examined whether nicorandil (a KATP channel opener nitrate) exhibits cardioprotective actions under halothane anaesthesia, another commonly used volatile anaesthetic. Control animals were subjected to 40 min coronary occlusion and 120 min reperfusion. Before 40 min ischaemia, the nicorandil group received nicorandil (100 microg/kg per min, i.v., for 10 min), the 5' preconditioning (PC) group received 5 min ischaemia/20 min reperfusion, the 2.5'PC group received 2.5 min preconditioning ischaemia/20 min reperfusion, the nicorandil +2.5'PC group received both nicorandil and 2.5 min ischaemia/20 min reperfusion, the nicorandil +2.5'PC + 5-hydroxydecanoate (5HD) group received both nicorandil and 2.5 min ischaemia/20 min reperfusion in the presence of 5-hydroxydecanoate (5HD; a KATP blocker) and the 5HD group received 5 mg/kg, i.v., 5HD alone. Myocardial infarct size in control (n = 7), nicorandil (n = 5), 5'PC (n = 8), 2.5'PC (n = 5), nicorandil + 2.5'PC (n = 5), nicorandil + 2.5'PC + 5HD (n = 5) and 5HD (n = 4) groups averaged 44.4 +/- 3.6, 41.7 +/- 5.7, 17.8 +/- 3.2,* 34.1 +/- 4.8, 21.3 +/- 4.2,* 39.1 +/- 5.6 and 38.9 +/- 5.0% of the area at risk, respectively (*P <0.05 vs control). 3. Thus, nicorandil alone did not have an infarct size-limiting effect in halothane-anaesthetized rabbits. However, the results suggest that even when nicorandil alone does not demonstrate a direct cardioprotective effect, it may enhance ischaemic preconditioning via KATP channels. Key words: ATP-sensitive K+ (KATP) channel, ischaemic preconditioning, myocardial infarction, nicorandil, rabbit. PMID:11022974

Nakae, I; Takaoka, A; Mitsunami, K; Yabe, T; Ito, M; Masayuki; Takahashi; Matsumoto, T; Omura, T; Yokohama, H; Kinoshita, M

2000-10-01

252

Hypoxia preconditioned mesenchymal stem cells improve vascular and skeletal muscle fiber regeneration after ischemia through a Wnt4 dependent pathway  

E-print Network

Hypoxia preconditioned mesenchymal stem cells improve vascular and skeletal muscle fiber.108 #12;2 Abstract Mesenchymal stem cells (MSC) are multipotent postnatal stem cells, involved cell mobilization and skeletal muscle fiber regeneration via a paracrine Wnt dependent mechanism

Paris-Sud XI, Université de

253

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

PubMed Central

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

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

2014-01-01

254

Preventive Medicine.  

ERIC Educational Resources Information Center

Argues the importance of regularly inspecting thermoplastic roofs to avoid costly repairs. Preventive measures such as access restriction and the use of protective mats and pads to prevent third-party accidents are discussed as is the importance of checking for drain blockages. (GR)

Jozwiak, Dick

1998-01-01

255

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 ...

256

A Note on Substructuring Preconditioning for Nonconforming Finite Element Approximations of Second Order Elliptic Problems  

NASA Technical Reports Server (NTRS)

In this paper an algebraic substructuring preconditioner is considered for nonconforming finite element approximations of second order elliptic problems in 3D domains with a piecewise constant diffusion coefficient. Using a substructuring idea and a block Gauss elimination, part of the unknowns is eliminated and the Schur complement obtained is preconditioned by a spectrally equivalent very sparse matrix. In the case of quasiuniform tetrahedral mesh an appropriate algebraic multigrid solver can be used to solve the problem with this matrix. Explicit estimates of condition numbers and implementation algorithms are established for the constructed preconditioner. It is shown that the condition number of the preconditioned matrix does not depend on either the mesh step size or the jump of the coefficient. Finally, numerical experiments are presented to illustrate the theory being developed.

Maliassov, Serguei

1996-01-01

257

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

258

Effect of outer magnetosphere pre-conditioning on the inner magnetosphere during a magnetic storm  

NASA Astrophysics Data System (ADS)

It has been suggested that the plasma sheet conditions prior to the main phase of a geomagnetic storm can have a significant effect on the storm development and the minimum Dst. In particular, northward IMF conditions leading up to the storm may load the plasma sheet with cold dense plasma and lead to stronger storms as opposed to those storms that lack a northward IMF phase before storm commencement. We use the OpenGGCM-RCM model to simulate storm events with northward IMF preconditioning before the storm commences. We will show in the simulation how a cold dense plasma sheet is formed in the mid-tail plasma sheet, how a super-dense plasma sheet develops near the inner magnetosphere boundary, and how this dense plasma affects the ring current and Dst index in the storm main phase. In order to quantify the effect we will present comparisons of simulations of the same storm with and without preconditioning by northward IMF.

Li, W.; Raeder, J.; Ge, Y.; Gilson, M. L.

2013-12-01

259

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

NASA Astrophysics Data System (ADS)

Abstract Variations in large-scale atmospheric forcing influence upwelling dynamics and ecosystem productivity in the California Current System (CCS). In this paper, we characterize interannual variability of the North Pacific High over 40 years and investigate how variation in its amplitude and position affect upwelling and biology. We develop a winter upwelling "<span class="hlt">pre-conditioning</span>" index and demonstrate its utility to understanding biological processes. Variation in the winter NPH can be well described by its areal extent and maximum pressure, which in turn is predictive of winter upwelling. Our winter <span class="hlt">pre-conditioning</span> index explained 64% of the variation in biological responses (fish and seabirds). Understanding characteristics of the NPH in winter is therefore critical to predicting biological responses in the CCS.</p> <div class="credits"> <p class="dwt_author">Schroeder, Isaac D.; Black, Bryan A.; Sydeman, William J.; Bograd, Steven J.; Hazen, Elliott L.; Santora, Jarrod A.; Wells, Brian K.</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-02-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">260</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/19202436"> <span id="translatedtitle">Donor <span class="hlt">preconditioning</span> with a calcineurin inhibitor improves outcome in rat syngeneic kidney transplantation.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Ischemia-reperfusion injury (IRI) in the early posttransplant period affects immediate graft function and late allograft dysfunction. This study determines the influence of pharmacologic <span class="hlt">preconditioning</span> with a calcineurin inhibitor on IRI in a syngeneic F344 rat kidney transplant model. Donor rats were pretreated with one dose of cyclosporine (10 mg/kg) or tacrolimus (1 mg/kg) administered at 24 hr or 7 days before being subjected to 2 hr of cold ischemia and then transplanted. Pharmacologic <span class="hlt">preconditioning</span> significantly improved renal function, as assessed by serum creatinine and inulin clearance, and histologic score versus vehicle-treated rats. There were no differences between cyclosporine and tacrolimus in the measured outcomes. This renoprotective effect, although not complete, was seen with only one dose of calcineurin inhibitor, and the effect was sustained for at least 7 days before IRI. This approach may represent a viable pharmacologic intervention to decrease IRI at the time of organ transplantation. PMID:19202436</p> <div class="credits"> <p class="dwt_author">Shihab, Fuad S; Bennett, William M; Andoh, Takeshi F</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-02-15</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_12");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' 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id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_13");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' href="#">2</a> <a onClick='return showDiv("page_3");' href="#">3</a> <a onClick='return showDiv("page_4");' href="#">4</a> <a onClick='return showDiv("page_5");' href="#">5</a> <a onClick='return showDiv("page_6");' href="#">6</a> <a onClick='return showDiv("page_7");' href="#">7</a> <a onClick='return showDiv("page_8");' href="#">8</a> <a onClick='return showDiv("page_9");' href="#">9</a> <a onClick='return 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src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">261</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3731182"> <span id="translatedtitle">Effects of ischemic <span class="hlt">preconditioning</span> and iloprost on myocardial ischemia-reperfusion damage in rats</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">This study investigates the effects of cardiac ischemic <span class="hlt">preconditioning</span> and iloprost on reperfusion damage in rats with myocardial ischemia/reperfusion. 38 male Wistar Albino rats used in this study were divided into 5 groups. The control group (Group 1) (n=6), ischemia/reperfusion (IR) group (Group 2) (n=8), cardiac ischemic <span class="hlt">preconditioning</span> (CIP) group (Group 3) (n=8), iloprost (ILO) group (Group 4) (n=8), and cardiac ischemic <span class="hlt">preconditioning</span> + iloprost (CIP+ILO) group (Group 5) (n=8). Pre-ischemia, 15 minutes post-ischemia, 45 minutes post-reperfusion, mean blood pressure (MBP), and heart rates (HR) were recorded. The rate-pressure product (RPP) was calculated. Post-reperfusion plasma creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), troponin (cTn) vlaues, and infarct size/area at risk (IS/AAR) were calculated from myocardial tissue samples. Arrhythmia and ST segment elevations were evaluated during the ischemia and reperfusion stages. Although the MBP, HR, RPP values, biochemical parameters of CK-MB and LDH levels, IS/AAR rates, ST segment elevation values were found to be similar in CIP and CIP+ILO groups and the IR and ILO groups (p>0.05), CIP-containing group values had a positively meaningful difference (p<0.05) compared with the IR and ILO group. While mild-moderate findings of damage were observed in Group 3 and Group 5, severely findings of damage were releaved in Group 2 and Group 4. The arrhythmia score of the ILO group was meaningfully lower (F: 41.4, p<0.001) than the IR group. We can conclude that the effects of myocardial reperfusion damage can be reduced by cardiac ischemic <span class="hlt">preconditioning</span>, intravenous iloprost reduced the incidence of ventricular arrhythmia associated with reperfusion, and its use with CIP caused no additional changes. PMID:23936589</p> <div class="credits"> <p class="dwt_author">Ay, Yasin; Kara, Ibrahim; Aydin, Cemalettin; Ay, Nuray Kahraman; Teker, Melike Elif; Senol, Serkan; Inan, Bekir; Basel, Halil; Uysal, Omer; Zeybek, Rahmi</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">262</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.cs.odu.edu/~cscapes/csc07/talks/Schenk.pdf"> <span id="translatedtitle">An Inertia Revealing <span class="hlt">Preconditioning</span> Method For Large-Scale Nonconvex PDE-Constrained Optimization</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">We propose an inertia revealing <span class="hlt">preconditioning</span> approach for the solution of nonconvex PDE-constrained optimization problems. If interior methods with second-derivative information are used for these op- timization problems, a linearized Karush-Kuhn-Tucker system of the optimality conditions has to be solved. The main issue addressed is how to ensure that the Hessian is positive definite in the null-space of the constraints</p> <div class="credits"> <p class="dwt_author">Olaf Schenk</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">263</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/53679483"> <span id="translatedtitle">Multigrid <span class="hlt">preconditioned</span> conjugate-gradient method for large-scale wave-front reconstruction</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">We introduce a multigrid <span class="hlt">preconditioned</span> conjugate-gradient (MGCG) iterative scheme for computing open-loop wave-front reconstructors for extreme adaptive optics systems. We present numerical simulations for a 17-m class telescope with n=48756 sensor measurement grid points within the aperture, which indicate that our MGCG method has a rapid convergence rate for a wide range of subaperture average slope measurement signal-to-noise ratios. The</p> <div class="credits"> <p class="dwt_author">Luc Gilles; Curtis R. Vogel; Brent L. Ellerbroek</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">264</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23936589"> <span id="translatedtitle">Effects of ischemic <span class="hlt">preconditioning</span> and iloprost on myocardial ischemia-reperfusion damage in rats.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">This study investigates the effects of cardiac ischemic <span class="hlt">preconditioning</span> and iloprost on reperfusion damage in rats with myocardial ischemia/reperfusion. 38 male Wistar Albino rats used in this study were divided into 5 groups. The control group (Group 1) (n=6), ischemia/reperfusion (IR) group (Group 2) (n=8), cardiac ischemic <span class="hlt">preconditioning</span> (CIP) group (Group 3) (n=8), iloprost (ILO) group (Group 4) (n=8), and cardiac ischemic <span class="hlt">preconditioning</span> + iloprost (CIP+ILO) group (Group 5) (n=8). Pre-ischemia, 15 minutes post-ischemia, 45 minutes post-reperfusion, mean blood pressure (MBP), and heart rates (HR) were recorded. The rate-pressure product (RPP) was calculated. Post-reperfusion plasma creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), troponin (cTn) vlaues, and infarct size/area at risk (IS/AAR) were calculated from myocardial tissue samples. Arrhythmia and ST segment elevations were evaluated during the ischemia and reperfusion stages. Although the MBP, HR, RPP values, biochemical parameters of CK-MB and LDH levels, IS/AAR rates, ST segment elevation values were found to be similar in CIP and CIP+ILO groups and the IR and ILO groups (p>0.05), CIP-containing group values had a positively meaningful difference (p<0.05) compared with the IR and ILO group. While mild-moderate findings of damage were observed in Group 3 and Group 5, severely findings of damage were releaved in Group 2 and Group 4. The arrhythmia score of the ILO group was meaningfully lower (F: 41.4, p<0.001) than the IR group. We can conclude that the effects of myocardial reperfusion damage can be reduced by cardiac ischemic <span class="hlt">preconditioning</span>, intravenous iloprost reduced the incidence of ventricular arrhythmia associated with reperfusion, and its use with CIP caused no additional changes. PMID:23936589</p> <div class="credits"> <p class="dwt_author">Ay, Yasin; Kara, Ibrahim; Aydin, Cemalettin; Ay, Nuray Kahraman; Teker, Melike Elif; Senol, Serkan; Inan, Bekir; Basel, Halil; Uysal, Omer; Zeybek, Rahmi</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">265</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/29334734"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> of the distal tubular epithelium of the human kidney precedes nephrocalcinosis</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary"><span class="hlt">Preconditioning</span> of the distal tubular epithelium of the human kidney precedes nephrocalcinosis.BackgroundPreterm neonates and renal transplant patients frequently develop nephrocalcinosis. Experimental studies revealed that crystal retention in the distal nephron, a process that may lead to nephrocalcinosis, is limited to proliferating\\/regenerating tubular cells expressing hyaluronan and osteopontin at their luminal surface. Fetal and transplant kidneys contain proliferating and\\/or regenerating cells</p> <div class="credits"> <p class="dwt_author">ANJA VERHULST; MARINO ASSELMAN; STEPHANIE DE NAEYER; BENJAMIN A VERVAET; MICHAEL MENGEL; WILFRIED GWINNER; PATRICK C D'HAESE; CARL F VERKOELEN; MARC E DE BROE</p> <p class="dwt_publisher"></p> <p class="publishDate">2005-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">266</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://repository.tamu.edu/handle/1969.1/ETD-TAMU-1995-THESIS-H877"> <span id="translatedtitle">The effects of <span class="hlt">preconditioning</span> on the performance and profitability of feedyard cattle</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">participants was tremendous. Even though the majority of the cattle that were entered into the Ranch to Rail program made money that first year, it was evident that there were some differences in profitability between certain groups of calves from certain...THE EFFECTS OF <span class="hlt">PRECONDITIONING</span> ON THE PERFORMANCE AND PROFITABILITY OF FEEDYARD CATTLE A PROFESSIONAL PAPER by Douglas Paul Husfeld Submitted to Texas ABtM University in partial fulfillment of the requirements for the degree of MASTER...</p> <div class="credits"> <p class="dwt_author">Husfeld, Douglas Paul</p> <p class="dwt_publisher"></p> <p class="publishDate">1995-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">267</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/13309061"> <span id="translatedtitle">Flat MPI vs. Hybrid: Evaluation of Parallel Programming Models for <span class="hlt">Preconditioned</span> Iterative Solvers on</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">In this work, parallel <span class="hlt">preconditioning</span> methods based on ¿hierarchical interface decomposition (HID)¿ and hybrid parallel programming models were applied to finite-element based simulations of linear elasticity problems in media with heterogeneous material properties. Reverse Cuthill-McKee reordering with cyclic multicoloring (CM-RCM) was applied for parallelism through OpenMP. The developed code has been tested on the ¿T2K open supercomputer (Todai combined cluster)¿</p> <div class="credits"> <p class="dwt_author">Kengo Nakajima</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">268</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://jamaica.ee.pitt.edu/Archives/ProceedingArchives/Dac/Dac2001/papers/2001/dac01/pdffiles/34_3.pdf"> <span id="translatedtitle">Efficient large-scale power grid analysis based on <span class="hlt">preconditioned</span> krylov-subspace iterative methods</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">In this paper, we propose <span class="hlt">preconditioned</span> Krylov-subspace iterative methods to perform efficient DC and transient simulations for large-scale linear circuits with an emphasis on power delivery circuits. We also prove that a circuit with inductors can be simplified from MNA to NA format, and the matrix becomes an s.p.d matrix. This property makes it suitable for the conjugate gradient with</p> <div class="credits"> <p class="dwt_author">Tsung-Hao Chen; Charlie Chung-Ping Chen</p> <p class="dwt_publisher"></p> <p class="publishDate">2001-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">269</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/48047359"> <span id="translatedtitle">Heart-rate changes in asphyxic <span class="hlt">preconditioning</span> in rats depend on light-dark cycle</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Generally, it is assumed that heart-rhythm disorders during hypoxia result from the interplay between the autonomic nervous\\u000a system (ANS) and the direct effect of hypoxia on cardiorespiratory structures of the central nervous system and on the myocardium.\\u000a Circadian variability in the ANS may substantially influence the electrical stability of the myocardium, and thus it is associated\\u000a with the <span class="hlt">preconditioning</span> protective</p> <div class="credits"> <p class="dwt_author">Pavol Svorc; Ivana Bacova; Roman Benacka; Ruzena Galanova; Benjamin Lee Fulton</p> <p class="dwt_publisher"></p> <p class="publishDate">2011-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">270</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/50963167"> <span id="translatedtitle">Progress toward a stabilization and <span class="hlt">preconditioning</span> protocol for polycrystalline thin-film photovoltaic modules</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Cadmium telluride (CdTe) and copper indium gallium diselenide (CIGS) thin-film photovoltaic (PV) modules can exhibit substantial variation in measured performance depending on prior exposure history. We studied the metastable performance changes in these PV modules with the goal of establishing standard <span class="hlt">preconditioning</span> or stabilization exposure procedures to mitigate measured variations prior to current-voltage (IV) measurements. We present the results of</p> <div class="credits"> <p class="dwt_author">Joseph A. del Cueto; Chris A. Deline; Steve R. Rummel; Allan Anderberg</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">271</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23983070"> <span id="translatedtitle">Exercise-induced ischemic <span class="hlt">preconditioning</span> detected by sequential exercise stress tests: A meta-analysis.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Exercise-induced ischemic <span class="hlt">preconditioning</span> (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 <span class="hlt">preconditioning</span>, (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 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span>. From now on, the results could be used in further research to set standardized parameters to assess the phenomenon. PMID:23983070</p> <div class="credits"> <p class="dwt_author">Lalonde, François; Poirier, Paul; Sylvestre, Marie-Pierre; Arvisais, Denis; Curnier, Daniel</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">272</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/24939299"> <span id="translatedtitle">Human embryonic stem cell neural differentiation and enhanced cell survival promoted by hypoxic <span class="hlt">preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">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 <span class="hlt">preconditioning</span> strategy to enhance hESC tolerance, thereby improving graft survival and the therapeutic potential of hESC transplantation. UC06 hESCs underwent</p> <div class="credits"> <p class="dwt_author">K R Francis; L Wei</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">273</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/1502276"> <span id="translatedtitle">Multiple scattering among vias in planar waveguides using <span class="hlt">preconditioned</span> SMCG method</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">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 <span class="hlt">preconditioning</span> scheme based on the dominant information contained in the near field. We</p> <div class="credits"> <p class="dwt_author">Chung-Chi Huang; Leung Tsang; Chi Hou Chan; Kung-Hau Ding</p> <p class="dwt_publisher"></p> <p class="publishDate">2004-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">274</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23536200"> <span id="translatedtitle">Anti-caspase-3 <span class="hlt">preconditioning</span> increases proinsulin secretion and deteriorates posttransplant function of isolated human islets.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Human islet isolation is associated with adverse conditions inducing apoptosis and necrosis. The aim of the present study was to assess whether antiapoptotic <span class="hlt">preconditioning</span> can improve in vitro and posttransplant function of isolated human islets. A dose-finding study demonstrated that 200 ?mol/L of the caspase-3 inhibitor Ac-DEVD-CMK was most efficient to reduce the expression of activated caspase-3 in isolated human islets exposed to severe heat shock. Ac-DEVD-CMK-pretreated or sham-treated islets were transplanted into immunocompetent or immunodeficient diabetic mice and subjected to static glucose incubation to measure insulin and proinsulin secretion. Antiapoptotic pretreatment significantly deteriorated graft function resulting in elevated nonfasting serum glucose when compared to sham-treated islets transplanted into diabetic nude mice (p < 0.01) and into immunocompetent mice (p < 0.05). Ac-DEVD-CMK pretreatment did not significantly change basal and glucose-stimulated insulin release compared to sham-treated human islets but increased the proinsulin release at high glucose concentrations (20 mM) thus reducing the insulin-to-proinsulin ratio in <span class="hlt">preconditioned</span> islets (p < 0.05). This study demonstrates that the caspase-3 inhibitor Ac-DEVD-CMK interferes with proinsulin conversion in <span class="hlt">preconditioned</span> islets reducing their potency to cure diabetic mice. The mechanism behind this phenomenon is unclear so far but may be related to the ketone CMK linked to the Ac-DEVD molecule. Further studies are required to identify biocompatible caspase inhibitors suitable for islet <span class="hlt">preconditioning</span>. PMID:23536200</p> <div class="credits"> <p class="dwt_author">Brandhorst, Daniel; Brandhorst, Heide; Maataoui, Vidya; Maataoui, Adel; Johnson, Paul R V</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-06-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">275</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2013SPIE.9067E..1ZY"> <span id="translatedtitle">Completeness set proof of <span class="hlt">precondition</span> and post-condition types of activity in any EPM</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">Software evolution process model (EPM) is created in terms of a formal evolution process meta-model (EPMM) and semi-formal approach to modeling based on EPMM [1]. In order to better manage and control the software evolution process and make the best of existing software technology, the method to transform any EPM to its execution model based logic programming has been proposed. Completeness of conversion depends on completeness of the rules, that is, all the expressions of the original model are found the correspondence in the target model. Since transformation rules are proposed based on <span class="hlt">precondition</span> or post-condition types of activities in anyone EPM, this need to prove that activity type set in anyone EPM is completeness set. To this end, the <span class="hlt">precondition</span> and post-condition of activities in EPM are classified based on analyzing all expressions in EPMs and the semantics of the activity execution. Type completeness set of activity's <span class="hlt">precondition</span> and its post-condition is presented. Lastly we prove that the activity type set in anyone EPM is completeness set by mathematical induction.</p> <div class="credits"> <p class="dwt_author">Yu, Qian; Li, Tong; Liu, JinZhuo; Zhang, Xuan; Yu, Yong</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-12-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">276</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3868166"> <span id="translatedtitle">The role of remote ischemic <span class="hlt">preconditioning</span> in the treatment of atherosclerotic diseases</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background Remote ischemic <span class="hlt">preconditioning</span> (RIPC) is the application of a transient and brief ischemic stimulus to a distant site from the organ or tissue that is afterward exposed to injury ischemia, and has been found to reduce ischemia–reperfusion injury (IRI) in various animal models. RIPC appears to offer two distinct phases of endothelial IRI protection, which are presumably mediated through neuronal and humoral pathways. Methods We conducted a comprehensive literature review on the available published data about the potential effect of RIPC in patients undergoing IRI in one or more vital organs. Results Our search highlighted 24 randomized clinical trials about the effect of RIPC on variable clinical settings (abdominal aortic aneurysm repair, open heart surgery, percutaneous coronary intervention, living donor renal transplantation, coronary angiography, elective decompression surgery, carotid endarterectomy, recent stroke, or transient ischemic attack combined with intracranial carotid artery stenosis). Most of the trials focused on postoperative cardiac or renal function after RIPC with conflicting results. <span class="hlt">Preconditioning</span> protocols, age limits, comorbidities, and concomitant drug use varied significantly across trials, and therefore no firm conclusions can be drawn using the available data. However, no severe local adverse events were observed in any patient undergoing limb or arm <span class="hlt">preconditioning</span>. Conclusions RIPC is a safe and well-tolerated procedure that may constitute a potentially promising innovative treatment in atherosclerotic diseases. Large, multicenter, randomized clinical trials are required to determine an optimal protocol for the RIPC procedure, and to evaluate further the potential benefits of RIPC in human ischemic injury. PMID:24363964</p> <div class="credits"> <p class="dwt_author">Vasdekis, Spyros N; Athanasiadis, Dimitrios; Lazaris, Andreas; Martikos, Georgios; Katsanos, Aristeidis H; Tsivgoulis, Georgios; Machairas, Anastasios; Liakakos, Theodoros</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">277</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2008JCoPh.227.2366N"> <span id="translatedtitle">Effect of discretization order on <span class="hlt">preconditioning</span> and convergence of a high-order unstructured Newton-GMRES solver for the Euler equations</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">This article studies the effect of discretization order on <span class="hlt">preconditioning</span> and convergence of a high-order Newton-Krylov unstructured flow solver. The generalized minimal residual (GMRES) algorithm is used for inexactly solving the linear system arising from implicit time discretization of the governing equations. A first-order Jacobian is used as the <span class="hlt">preconditioning</span> matrix. The complete lower-upper factorization (LU) and an incomplete lower-upper factorization (ILU(4)) techniques are employed for <span class="hlt">preconditioning</span> of the resultant linear system. The solver performance and the conditioning of the <span class="hlt">preconditioned</span> linear system have been compared in detail for second, third, and fourth-order accuracy. The conditioning and eigenvalue spectrum of the <span class="hlt">preconditioned</span> system are examined to investigate the quality of <span class="hlt">preconditioning</span>.</p> <div class="credits"> <p class="dwt_author">Nejat, Amir; Ollivier-Gooch, Carl</p> <p class="dwt_publisher"></p> <p class="publishDate">2008-02-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">278</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.cdc.gov/Features/Shingles/"> <span id="translatedtitle"><span class="hlt">Prevent</span> Shingles</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... will develop chickenpox, not shingles. Disease of the Week App "Want to know more about shingles? Download CDC's mobile app now . See "Disease of the Week," highlighting disease facts and <span class="hlt">prevention</span> tips. Find "Shingles" ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">279</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.healthychildren.org/English/health-issues/injuries-emergencies/Pages/Choking-Prevention.aspx"> <span id="translatedtitle">Choking <span class="hlt">Prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... Safety (Audio) New Study Reinforces Need for Continued Infant Sleep Campaigns to <span class="hlt">Prevent</span> SIDS Implementing Safe Routes to School Is Effective in Reducing Pedestrian Injuries Healthy Children Radio: Fireworks (Audio) Children ... Health ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">280</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23652994"> <span id="translatedtitle">Hexokinase cellular trafficking in ischemia-reperfusion and ischemic <span class="hlt">preconditioning</span> is altered in type I diabetic heart.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Diabetes mellitus (DM) has been reported to alter the cardiac response to ischemia-reperfusion (IR). In addition, cardioprotection induced by ischemic <span class="hlt">preconditioning</span> (IPC) is often impaired in diabetes. We have previously shown that the subcellular localisation of the glycolytic enzyme hexokinase (HK) is causally related to IR injury and IPC protective potential. Especially the binding of HK to mitochondria and <span class="hlt">prevention</span> of HK solubilisation (HK detachment from mitochondria) during ischemia confers cardioprotection. It is unknown whether diabetes affects HK localisation during IR and IPC as compared to non-diabetes. In this study we hypothesize that DM alters cellular trafficking of hexokinase in response to IR and IPC, possibly explaining the altered response to IR and IPC in diabetic heart. Control (CON) and type I diabetic (DM) rat hearts (65 mg/kg streptozotocin, 4 weeks) were isolated and perfused in Langendorff-mode and subjected to 35 min I and 30 min R with or without IPC (3 times 5 min I). Cytosolic and mitochondrial fractions were obtained at (1) baseline, i.e. after IPC but before I, (2) 35 min I, (3) 5 min R and (4) 30 min R. DM improved rate-pressure product recovery (RPP; 71 ± 10 % baseline (DM) versus 9 ± 1 % baseline (CON) and decreased contracture (end-diastolic pressure: 24 ± 8 mmHg (DM) vs 77 ± 4 mmHg (CON)) after IR as compared to control, and was associated with <span class="hlt">prevention</span> of HK solubilisation at 35 min I. IPC improved cardiac function in CON but not in DM hearts. IPC in CON <span class="hlt">prevented</span> HK solubilisation at 35 min I and at 5 min R, with a trend for increased mitochondrial HK. In contrast, the non-effective IPC in DM was associated with solubilisation of HK and decreased mitochondrial HK at early reperfusion and a reciprocal behaviour at late reperfusion. We conclude that type I DM significantly altered cellular HK translocation patterns in the heart in response to IR and IPC, possibly explaining altered response to IR and IPC in diabetes. PMID:23652994</p> <div class="credits"> <p class="dwt_author">Gurel, Ebru; Ustunova, Savas; Kapucu, Aysegul; Yilmazer, Nadim; Eerbeek, Otto; Nederlof, Rianne; Hollmann, Markus W; Demirci-Tansel, Cihan; Zuurbier, Coert J</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-07-01</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_13");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> 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showDiv("page_16");' href="#" title="Next Page"> <img id="NextPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">281</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.springerlink.com/index/9hqd8ygc0jbpdwh8.pdf"> <span id="translatedtitle">Stroke <span class="hlt">prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Stroke <span class="hlt">prevention</span> is a crucial issue because (i) stroke is a frequent and severe disorder, and (ii) acute stroke therapies\\u000a that are effective at the individual level have only a little impact in term of public health. Stroke <span class="hlt">prevention</span> consists\\u000a of the combination of 3 strategies: an optimal management of vascular risk factors, associated when appropriate with antithrombotic\\u000a therapies, carotid</p> <div class="credits"> <p class="dwt_author">Didier Leys; Dominique Deplanque; Claire Mounier-Vehier; Marie-Anne Mackowiak-Cordoliani; Christian Lucas; Régis Bordet</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">282</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3543687"> <span id="translatedtitle">Modulation of cardiac Na+,K+-ATPase cell surface abundance by simulated ischemia-reperfusion and ouabain <span class="hlt">preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Na+,K+-ATPase and cell survival were investigated in a cellular model of ischemia-reperfusion (I/R)-induced injury and protection by ouabain-induced <span class="hlt">preconditioning</span> (OPC). Rat neonatal cardiac myocytes were subjected to 30 min of substrate and coverslip-induced ischemia followed by 30 min of simulated reperfusion. This significantly compromised cell viability as documented by lactate dehydrogenase release and Annexin V/propidium iodide staining. Total Na+,K+-ATPase ?1- and ?3-polypeptide expression remained unchanged, but cell surface biotinylation and immunostaining studies revealed that ?1-cell surface abundance was significantly decreased. Na+,K+-ATPase-activity in crude homogenates and 86Rb+ transport in live cells were both significantly decreased by about 30% after I/R. OPC, induced by a 4-min exposure to 10 ?M ouabain that ended 8 min before the beginning of ischemia, increased cell viability in a PKC?-dependent manner. This was comparable with the protective effect of OPC previously reported in intact heart preparations. OPC <span class="hlt">prevented</span> I/R-induced decrease of Na+,K+-ATPase activity and surface expression. This model also revealed that Na+,K+-ATPase-mediated 86Rb+ uptake was not restored to control levels in the OPC group, suggesting that the increased viability was not conferred by an increased Na+,K+-ATPase-mediated ion transport capacity at the cell membrane. Consistent with this observation, transient expression of an internalization-resistant mutant form of Na+,K+-ATPase ?1 known to have increased surface abundance without increased ion transport activity successfully reduced I/R-induced cell death. These results suggest that maintenance of Na+,K+-ATPase cell surface abundance is critical to myocyte survival after an ischemic attack and plays a role in OPC-induced protection. They further suggest that the protection conferred by increased surface expression of Na+,K+-ATPase may be independent of ion transport. PMID:23086991</p> <div class="credits"> <p class="dwt_author">Belliard, Aude; Sottejeau, Yoann; Duan, Qiming; Karabin, Jessa L.</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">283</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4057195"> <span id="translatedtitle">Pharmacological <span class="hlt">Preconditioning</span> with Vitamin C Attenuates Intestinal Injury via the Induction of Heme Oxygenase-1 after Hemorrhagic Shock in Rats</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Pre-induction of heme oxygenase (HO)-1, which is regarded as an effective method of “organ <span class="hlt">preconditioning</span>”, exerts beneficial effects during hemorrhagic shock (HS). However, the available HO-1 inducers exhibit disadvantages such as toxicity or complex technical requirements. Therefore, a safe and convenient HO-1 inducer would be promising and could be exploited in the treatment of foreseeable hemorrhaging, such as prior to major surgery. Here we investigated the effect of vitamin C (VitC), a common antioxidant, on intestinal HO-1 expression and examined whether VitC pretreatment <span class="hlt">prevented</span> HS related intestinal tissue injuries after HO-1 induction. First, we conducted an in vitro study and found that HO-1 expression in rat intestinal epithelial cells (IEC-6) was induced by non-toxic VitC in a time and concentration dependent manner, and the mechanism was related to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Next, we conducted an in vivo study and found that VitC induced intestinal HO-1 protein expression (mainly observed in the intestinal epithelial cells) and HO-1 activity in normal SD rats, and that these HO-1 levels were further enhanced by VitC in a rat model of HS. The HS related intestinal injuries, including histological damage, pro-inflammatory cytokine levels (tumor necrosis factor and interleukin-6), neutrophil infiltration and apoptosis decreased after VitC pretreatment, and this alleviating of organ injuries was abrogated after the inhibition of HO-1 activity by zinc protoporphyrin-IX. It was of note that VitC did little histological damage to the intestine of the sham rats. These data suggested that VitC might be applied as a safe inducer of intestinal HO-1 and that VitC pretreatment attenuated HS related intestinal injuries via the induction of HO-1. PMID:24927128</p> <div class="credits"> <p class="dwt_author">Chen, Ying; Ying, Yi-Lin; Ma, Li; Song, Xiao-Qin; Wang, Lu; Chen, Er-Zhen; Mao, En-Qiang</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">284</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/21699894"> <span id="translatedtitle">Is there a trigger role of peroxynitrite in the anti-arrhythmic effect of ischaemic <span class="hlt">preconditioning</span> and peroxynitrite infusion?</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">This study has examined whether peroxynitrite (PN), generated during the <span class="hlt">preconditioning</span> (PC) procedure or administered by brief intracoronary infusions, plays a trigger role in the anti-arrhythmic effects of <span class="hlt">preconditioning</span> and peroxynitrite in anaesthetized dogs. To achieve this we infused the peroxynitrite scavenger uric acid (UA; 0.2 mg/kg/min, i.v.) over a 30 min period, just prior to a 25 min occlusion of the left anterior descending coronary artery, in <span class="hlt">preconditioned</span> (UA+PC, n=8), peroxynitrite-treated (UA+PN, n=8) and in control (UAC; n=9) dogs. The effects were compared to those obtained from groups (PC, n=10; PN, n=10; C1, n=14) without uric acid administration. Severities of ischaemia (ST-segment elevation, inhomogeneity of electrical activation) and ventricular arrhythmias (VPBs, VT, VF), plasma nitrate/nitrite levels, as well as myocardial superoxide and nitrotyrosine productions were determined. Both <span class="hlt">preconditioning</span> and the infusion of peroxynitrite increased nitrotyrosine formation which was abolished by the simultaneous administration of urate. Despite this, the protective effects of <span class="hlt">preconditioning</span> (i.e. reductions in arrhythmias, superoxide and nitrotyrosine productions, as well as the increase in nitric oxide availability), occurring during the prolonged period of occlusion and reperfusion were still present. In contrast, urate completely abolished the protection resulted from peroxynitrite administration. This effect is most probably due to the fact that urate has already scavenged peroxynitrite during the infusion. Interestingly, urate itself, given prior to ischaemia and reperfusion, was also protective. We conclude that peroxynitrite in nanomolar concentrations can induce an anti-arrhythmic effect but peroxynitrite, generated during the <span class="hlt">preconditioning</span> stimulus, is not necessary for the <span class="hlt">preconditioning</span>-induced anti-arrhythmic protection. PMID:21699894</p> <div class="credits"> <p class="dwt_author">Juhász, László; Kiss, Attila; Nyeso, Edit; Kovács, Mária; Seprényi, György; Kaszaki, József; Végh, Agnes</p> <p class="dwt_publisher"></p> <p class="publishDate">2011-09-30</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">285</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4080061"> <span id="translatedtitle">Effect of Air Abrasion <span class="hlt">Preconditioning</span> on Microleakage in Class V Restorations Under Cyclic Loading: An In-vitro Study</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">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 <span class="hlt">precondition</span> tooth surface for increasing retention of such restorations. This study is done to evaluate the effect of <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> 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. <span class="hlt">Preconditioning</span> with AA resulted in increased micro leakage. Conclusion: AA as a <span class="hlt">preconditioning</span> agent was ineffective in producing superior tooth-restoration bonding. PMID:24995240</p> <div class="credits"> <p class="dwt_author">Dharmani, Charan Kamal Kaur; Singh, Shamsher; Logani, Ajay; Shah, Naseem</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">286</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25370861"> <span id="translatedtitle">Increased BDNF protein expression after ischemic or PKC epsilon <span class="hlt">preconditioning</span> promotes electrophysiologic changes that lead to neuroprotection.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Ischemic <span class="hlt">preconditioning</span> (IPC) via protein kinase C epsilon (PKC?) activation induces neuroprotection against lethal ischemia. Brain-derived neurotrophic factor (BDNF) is a pro-survival signaling molecule that modulates synaptic plasticity and neurogenesis. Interestingly, BDNF mRNA expression increases after IPC. In this study, we investigated whether IPC or pharmacological <span class="hlt">preconditioning</span> (PKC? activation) promoted BDNF-induced neuroprotection, if neuroprotection by IPC or PKC? activation altered neuronal excitability, and whether these changes were BDNF-mediated. We used both in vitro (hippocampal organotypic cultures and cortical neuronal-glial cocultures) and in vivo (acute hippocampal slices 48 hours after <span class="hlt">preconditioning</span>) models of IPC or PKC? activation. BDNF protein expression increased 24 to 48 hours after <span class="hlt">preconditioning</span>, where inhibition of the BDNF Trk receptors abolished neuroprotection against oxygen and glucose deprivation (OGD) in vitro. In addition, there was a significant decrease in neuronal firing frequency and increase in threshold potential 48 hours after <span class="hlt">preconditioning</span> in vivo, where this threshold modulation was dependent on BDNF activation of Trk receptors in excitatory cortical neurons. In addition, 48 hours after PKC? activation in vivo, the onset of anoxic depolarization during OGD was significantly delayed in hippocampal slices. Overall, these results suggest that after IPC or PKC? activation, there are BDNF-dependent electrophysiologic modifications that lead to neuroprotection. PMID:25370861</p> <div class="credits"> <p class="dwt_author">Neumann, Jake T; Thompson, John W; Raval, Ami P; Cohan, Charles H; Koronowski, Kevin B; Perez-Pinzon, Miguel A</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">287</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3835261"> <span id="translatedtitle">Conditional Knockout of Myocyte Focal Adhesion Kinase Abrogates Ischemic <span class="hlt">Preconditioning</span> in Adult Murine Hearts</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background Our laboratory has previously demonstrated the importance of a cytoskeletal?based survival signaling pathway using in vitro models of ischemia/reperfusion (IR). However, the importance of this pathway in mediating stress?elicited survival signaling in vivo is unknown. Methods and Results The essential cytoskeletal signaling pathway member focal adhesion kinase (FAK) was selectively deleted in adult cardiac myocytes using a tamoxifen?inducible Cre?Lox system (??MHC?MerCreMer). Polymerase chain reaction (PCR) and Western blot were performed to confirm FAK knockout (KO). All mice were subjected to a 40?minute coronary occlusion followed by 24 hours of reperfusion. Ischemic <span class="hlt">preconditioning</span> (IP) was performed using a standard protocol. Control groups included wild?type (WT) and tamoxifen?treated ??MHC?MerCreMer+/?/FAKWT/WT (experimental control) mice. Infarct size was expressed as a percentage of the risk region. In WT mice IP significantly enhanced the expression of activated/phosphorylated FAK by 36.3% compared to WT mice subjected to a sham experimental protocol (P?0.05; n=6 hearts [sham], n=4 hearts [IP]). IP significantly reduced infarct size in both WT and experimental control mice (43.7% versus 19.8%; P?0.001; 44.7% versus 17.5%; P?0.001, respectively). No difference in infarct size was observed between <span class="hlt">preconditioned</span> FAK KO and nonpreconditioned controls (37.1% versus 43.7% versus 44.7%; FAK KO versus WT versus experimental control; P=NS). IP elicited a 67.2%/88.8% increase in activated phosphatidylinositol?3?kinase (PI3K) p85/activated Akt expression in WT mice, but failed to enhance the expression of either in <span class="hlt">preconditioned</span> FAK KO mice. Conclusions Our results indicate that FAK is an essential mediator of IP?elicited cardioprotection and provide further support for the hypothesis that cytoskeletal?based signaling is an important component of stress?elicited survival signaling. PMID:24080910</p> <div class="credits"> <p class="dwt_author">Perricone, Adam J.; Bivona, Benjamin J.; Jackson, Fannie R.; Vander Heide, Richard S.</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">288</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3884906"> <span id="translatedtitle">Sevoflurane <span class="hlt">Preconditioning</span> Attenuates Myocardial Ischemia/Reperfusion Injury via Cav-3-Dependent COX-2 Inhibition</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background The inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury, via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane <span class="hlt">preconditioning</span>-mediated cardioprotection, and their precise underlying mechanisms of action, remain incompletely understood. Methods and Results Sevoflurane <span class="hlt">preconditioning</span> (SF-PreCon, consisting of 3 cycles of 15 minute-exposures to 2% sevoflurane prior to 30 minutes of MI) decreased MI/R injury in WT mice (caspase-3 activity ?29.1%, infarct size ?20.2%, and LVEDP ?33.8%). In cardiac-specific AMPK?2 dominant negative overexpression (AMPK-DN) mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity ?26.7%, infarct size ?16.7%, and LVEDP ?25.9%, P<0.01). In contrast, SF-PreCon failed to significantly protect Cav3-knockout (Cav3-KO) mice against MI/R injury (P>0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in WT (?43.6%) and AMPK-DN mice (?35.5%, P<0.01), but not in Cav3-KO mice. SF-PreCon did not affect NADPH oxidase expression, but significantly inhibited COX-2 expression in WT (?38.7%) and AMPK-DN mice (?35.8%), but not in Cav-3KO mice. Conclusions We demonstrate for the first time sevoflurane <span class="hlt">preconditioning</span> mediates cardioprotection against MI/R injury via Cav-3 dependent-COX-2 inhibition and anti-oxidative effects. PMID:24030395</p> <div class="credits"> <p class="dwt_author">Zhao, Jianli; Zhang, Yanqing; Wang, Feng; Jiao, Liyuan; Lau, Wayne Bond; Wang, Lili; Liu, Baojiang; Gao, Erhe; Koch, Walter J.; Ma, Xin-Liang; Wang, Yajing</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">289</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3846887"> <span id="translatedtitle">Bradykinin <span class="hlt">Preconditioning</span> Improves Therapeutic Potential of Human Endothelial Progenitor Cells in Infarcted Myocardium</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Objectives Stem cell <span class="hlt">preconditioning</span> (PC) is a powerful approach in reducing cell death after transplantation. We hypothesized that PC human endothelial progenitor cells (hEPCs) with bradykinin (BK) enhance cell survival, inhibit apoptosis and repair the infarcted myocardium. Methods The hEPCs were <span class="hlt">preconditioned</span> with or without BK. The hEPCs apoptosis induced by hypoxia along with serum deprivation was determined by annexin V-fluorescein isothiocyanate/ propidium iodide staining. Cleaved caspase-3, Akt and eNOS expressions were determined by Western blots. Caspase-3 activity and vascular endothelial growth factor (VEGF) levels were assessed in hEPCs. For in vivo studies, the survival and cardiomyocytes apoptosis of transplanted hEPCs were assessed using 1,1?-dioctadecyl-3,3,3?,3?-tetramethylindodi- carbocyanine,4-chlorobenzenesul-fonate salt labeled hEPCs and TUNEL staining. Infarct size and cardiac function were measured at 10 days after transplantation, and the survival of transplanted hEPCs were visualized using near-infrared optical imaging. Results In vitro data showed a marked suppression in cell apoptosis following BK PC. The PC reduced caspase-3 activation, increased the Akt, eNOS phosphorylation and VEGF levels. In vivo data in <span class="hlt">preconditioned</span> group showed a robust cell anti-apoptosis, reduction in infarct size, and significant improvement in cardiac function. The effects of BK PC were abrogated by the B2 receptor antagonist HOE140, the Akt and eNOS antagonists LY294002 and L-NAME, respectively. Conclusions The activation of B2 receptor-dependent PI3K/Akt/eNOS pathway by BK PC promotes VEGF secretion, hEPC survival and inhibits apoptosis, thereby improving cardiac function in vivo. The BK PC hEPC transplantation for stem cell-based therapies is a novel approach that has potential for clinical used. PMID:24312554</p> <div class="credits"> <p class="dwt_author">Li, Yefei; Yan, Fengdi; Huang, Jie; Ma, Genshan</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">290</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4152122"> <span id="translatedtitle">A Randomized Pilot Trial of Remote Ischemic <span class="hlt">Preconditioning</span> in Heart Failure with Reduced Ejection Fraction</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background Remote ischemic <span class="hlt">preconditioning</span> (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 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span>. 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</p> <div class="credits"> <p class="dwt_author">McDonald, Michael A.; Braga, Juarez R.; Li, Jing; Manlhiot, Cedric; Ross, Heather J.; Redington, Andrew N.</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">291</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=plagiarism&id=EJ924860"> <span id="translatedtitle">Plagiarism <span class="hlt">Prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">Plagiarism does exist at universities today. In some cases, students are naive with respect to understanding what plagiarism is and how to avoid it. In other cases, students blatantly disregard and disrespect the written work of others, claiming it as their own. Regardless, educators must be vigilant in their efforts to discourage and <span class="hlt">prevent</span>…</p> <div class="credits"> <p class="dwt_author">Probett, Christine</p> <p class="dwt_publisher"></p> <p class="publishDate">2011-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">292</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www3.cancer.gov/prevention/pob/fellowship/rimal_050907.doc"> <span id="translatedtitle">CANCER <span class="hlt">PREVENTION</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.cancer.gov">Cancer.gov</a></p> <p class="result-summary">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 <span class="hlt">Preventive</span> Oncology at 301-496-8640 at least one week in advance of the lecture date to discuss your accommodation needs.</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">293</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25451640"> <span id="translatedtitle">Limb ischemic <span class="hlt">preconditioning</span> protects against contrast-induced acute kidney injury in rats via phosphorylation of GSK-3?</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">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 <span class="hlt">preventative</span> measures intended to mitigate the risk of CI-AKI, there remains a need for a novel and effective therapeutic approach. Limb ischemic <span class="hlt">preconditioning</span> (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 <span class="hlt">preventing</span> CI-AKI. In particular, this renoprotective effect involves the phosphorylation of GSK-3?. PMID:25451640</p> <div class="credits"> <p class="dwt_author">Liu, Tongqiang; Fang, Yi; Liu, Shaopeng; Yu, Xiaofang; Zhang, Hui; Liang, Mingyu; Ding, Xiaoqiang</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-10-31</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">294</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/12216875"> <span id="translatedtitle">Multigrid <span class="hlt">preconditioned</span> conjugate-gradient method for large-scale wave-front reconstruction.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">We introduce a multigrid <span class="hlt">preconditioned</span> conjugate-gradient (MGCG) iterative scheme for computing open-loop wave-front reconstructors for extreme adaptive optics systems. We present numerical simulations for a 17-m class telescope with n = 48756 sensor measurement grid points within the aperture, which indicate that our MGCG method has a rapid convergence rate for a wide range of subaperture average slope measurement signal-to-noise ratios. The total computational cost is of order n log n. Hence our scheme provides for fast wave-front simulation and control in large-scale adaptive optics systems. PMID:12216875</p> <div class="credits"> <p class="dwt_author">Gilles, Luc; Vogel, Curtis R; Ellerbroek, Brent L</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-09-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">295</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/servlets/purl/956510"> <span id="translatedtitle">Non-<span class="hlt">preconditioned</span> conjugate gradient on cell and FPGA based hybrid supercomputer nodes</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">This work presents a detailed implementation of a double precision, non-<span class="hlt">preconditioned</span>, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{sup TM} in conjunction with x86 Opteron{sup TM} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.</p> <div class="credits"> <p class="dwt_author">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</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">296</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/servlets/purl/962335"> <span id="translatedtitle">Non-<span class="hlt">preconditioned</span> conjugate gradient on cell and FPCA-based hybrid supercomputer nodes</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">This work presents a detailed implementation of a double precision, Non-<span class="hlt">Preconditioned</span>, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{trademark} in conjunction with x86 Opteron{trademark} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.</p> <div class="credits"> <p class="dwt_author">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</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-03-10</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">297</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/11230995"> <span id="translatedtitle">Role of adenosine and glycogen in ischemic <span class="hlt">preconditioning</span> of rat hearts.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">We tested whether ischemic <span class="hlt">preconditioning</span> of the rat heart is mediated by reduced glycogenolysis during ischemia, an event triggered by adenosine A1 receptor activation. Rat hearts (n=40) were studied with [31P] and [13C] nuclear magnetic resonance (NMR) spectroscopy, using the Langendorff perfusion technique (5.5 mM [1-13C]glucose, 10 U/l insulin). In parallel experiments, hearts (n=43) were freeze-clamped at different time-points throughout the protocol. They were subjected to either ischemic <span class="hlt">preconditioning</span> (PC), PC in the presence of 50 microM adenosine receptor antagonist, 8-(p-sulfophenyl)-theophylline (SPT), or intermittent infusion of 0.25 microM adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine (CCPA). After 30 min ischemia and reperfusion, recovery of heart ratexpressure product was improved in hearts treated with <span class="hlt">preconditioning</span> (33+/-13%) or CCPA (58+/-14%) compared with the SPT and ischemic control (IC) groups, which both failed to recover (P<0.05). CCPA administration induced a 58% increase in pre-ischemic [13C]glycogen (P<0.05 vs. all groups). In the PC and SPT groups, [13C]glycogen decreased by 25 and 47%, respectively (P<0.05) due to the short bouts of ischemia, resulting in lower pre-ischemic glycogen compared to ischemic control and CCPA hearts (P<0.05). The rate of [13C]glycogen utilization during the first 15 min of ischemia (in micromol/min g wwt) was not statistically different between IC (0.42+/-0.03), PC (0.30+/-0.04), and CCPA (0.38+/-0.05) hearts, but was reduced in SPT hearts (0.24+/-0.05; P<0.05). Total glycogen depletion during 30-min ischemia was reduced in PC hearts (0.61 mg/g wwt) compared to IC (1.84 mg/g wwt) and CCPA (1.75 mg/g wwt) hearts; SPT did not block reduced glycogenolysis during ischemia in PC hearts (0.77 mg/g wwt vs. IC). This study adds further strong evidence that in rat hearts, adenosine is involved in ischemic <span class="hlt">preconditioning</span>. However, protection is unrelated to pre-ischemic glycogen levels and glycogenolysis during ischemia. PMID:11230995</p> <div class="credits"> <p class="dwt_author">de Jonge, R; de Jong, J W; Giacometti, D; Bradamante, S</p> <p class="dwt_publisher"></p> <p class="publishDate">2001-02-23</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">298</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23645192"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> with cations increases the attachment of Anoxybacillus flavithermus and Geobacillus species to stainless steel.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary"><span class="hlt">Preconditioning</span> of Anoxybacillus flavithermus E16 and Geobacillus sp. strain F75 with cations prior to attachment often significantly increased (P ? 0.05) the number of viable cells that attached to stainless steel (by up to 1.5 log CFU/cm(2)) compared with unconditioned bacteria. It is proposed that the transition of A. flavithermus and Geobacillus spp. from milk formulations to stainless steel product contact surfaces in milk powder manufacturing plants is mediated predominantly by bacterial physiological factors (e.g., surface-exposed adhesins) rather than the concentrations of cations in milk formulations surrounding bacteria. PMID:23645192</p> <div class="credits"> <p class="dwt_author">Somerton, Ben; Flint, Steve; Palmer, Jon; Brooks, John; Lindsay, Denise</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-07-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">299</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3697576"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> with Cations Increases the Attachment of Anoxybacillus flavithermus and Geobacillus Species to Stainless Steel</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary"><span class="hlt">Preconditioning</span> of Anoxybacillus flavithermus E16 and Geobacillus sp. strain F75 with cations prior to attachment often significantly increased (P ? 0.05) the number of viable cells that attached to stainless steel (by up to 1.5 log CFU/cm2) compared with unconditioned bacteria. It is proposed that the transition of A. flavithermus and Geobacillus spp. from milk formulations to stainless steel product contact surfaces in milk powder manufacturing plants is mediated predominantly by bacterial physiological factors (e.g., surface-exposed adhesins) rather than the concentrations of cations in milk formulations surrounding bacteria. PMID:23645192</p> <div class="credits"> <p class="dwt_author">Flint, Steve; Palmer, Jon; Brooks, John; Lindsay, Denise</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">300</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://ntrs.nasa.gov/search.jsp?R=19980000320&hterms=nods+number&qs=N%3D0%26Ntk%3DAll%26Ntx%3Dmode%2Bmatchall%26Ntt%3Dnods%2Bnumber"> <span id="translatedtitle">Graph Embedding Techniques for Bounding Condition Numbers of Incomplete Factor <span class="hlt">Preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p class="result-summary">We extend graph embedding techniques for bounding the spectral condition number of <span class="hlt">preconditioned</span> systems involving symmetric, irreducibly diagonally dominant M-matrices to systems where the preconditioner is not diagonally dominant. In particular, this allows us to bound the spectral condition number when the preconditioner is based on an incomplete factorization. We provide a review of previous techniques, describe our extension, and give examples both of a bound for a model problem, and of ways in which our techniques give intuitive way of looking at incomplete factor preconditioners.</p> <div class="credits"> <p class="dwt_author">Guattery, Stephen</p> <p class="dwt_publisher"></p> <p class="publishDate">1997-01-01</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_14");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" 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onClick='return showDiv("page_6");' href="#">6</a> <a onClick='return showDiv("page_7");' href="#">7</a> <a onClick='return showDiv("page_8");' href="#">8</a> <a onClick='return showDiv("page_9");' href="#">9</a> <a onClick='return showDiv("page_10");' href="#">10</a> <a onClick='return showDiv("page_11");' href="#">11</a> <a onClick='return showDiv("page_12");' href="#">12</a> <a onClick='return showDiv("page_13");' href="#">13</a> <a onClick='return showDiv("page_14");' href="#">14</a> <a onClick='return showDiv("page_15");' href="#">15</a> <a style="font-weight: bold;">16</a> <a onClick='return showDiv("page_17");' href="#">17</a> <a onClick='return showDiv("page_18");' href="#">18</a> <a onClick='return showDiv("page_19");' href="#">19</a> <a onClick='return showDiv("page_20");' href="#">20</a> <a onClick='return showDiv("page_21");' href="#">21</a> <a onClick='return showDiv("page_22");' href="#">22</a> <a onClick='return showDiv("page_23");' href="#">23</a> <a onClick='return showDiv("page_24");' href="#">24</a> <a onClick='return showDiv("page_25");' href="#">25</a> </span> </span> <a id="NextPageLink" onclick='return showDiv("page_17");' href="#" title="Next Page"> <img id="NextPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">301</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23664061"> <span id="translatedtitle">[Iliac aneurysm rupture during <span class="hlt">preconditioning</span> with levosimendan for coronary artery bypass graft].</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">We present the case of a 77 year-old patient scheduled for coronary artery bypass. During the infusion of levosimendan as <span class="hlt">preconditioning</span> for surgery, a rupture of right common iliac artery occurred. Surgery was delayed and an urgent aorto-bifemoral bypass was performed. We believe that the rupture of the artery was triggered by an increase in transmural pressure due to the inotropic effects of levosimendan in a dilated diseased vessel. To our knowledge, there are no cases of aneurysm rupture as a complication during levosimendan infusion, but the coincidence of events in time strongly suggests some kind of causal relationship. PMID:23664061</p> <div class="credits"> <p class="dwt_author">Román Fernández, A; López Álvarez, A; Corujeira Rivera, M C; Vilanova Vázquez, V; Carregal Rañó, A; Pereira Loureiro, M Á</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-03-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">302</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3587824"> <span id="translatedtitle">A functional role of the cyclin-dependent kinase inhibitor 1 (p21WAF1/CIP1) for neuronal <span class="hlt">preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Hypoxic <span class="hlt">preconditioning</span> is thought to rely on gene products regulated by hypoxia-inducible factor (HIF)-1. Here, we show that the HIF-1 target gene cyclin-dependent kinase inhibitor 1, p21WAF1/CIP1, is essential for neuroprotection by hypoxic/aglycemic or erythropoietin <span class="hlt">preconditioning</span> using wild-type and p21WAF1/CIP1-deficient neurons. Furthermore, overexpression of wild-type p21WAF1/CIP1 or phospho-mutants significantly increased cell death after hypoxia/aglycemia. Moreover, deferoxamine-induced endogenous tolerance did not involve p21WAF1/CIP1 expression in cortical neurons. Our data suggest that balanced expression and potentially posttranslational regulation of p21WAF1/CIP1 is required for hypoxic <span class="hlt">preconditioning</span>. PMID:23299246</p> <div class="credits"> <p class="dwt_author">Mergenthaler, Philipp; Muselmann, Claudia; Sünwoldt, Juliane; Isaev, Nickolay K; Wieloch, Tadeusz; Dirnagl, Ulrich; Meisel, Andreas; Ruscher, Karsten</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">303</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/24197755"> <span id="translatedtitle">The neuroprotective effects of isoflurane <span class="hlt">preconditioning</span> in a murine transient global cerebral ischemia-reperfusion model: the role of the Notch signaling pathway.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Inhalational anesthetic <span class="hlt">preconditioning</span> can induce neuroprotective effects, and the notch signaling pathway plays an important role in neural progenitor cell differentiation and the inflammatory response after central nervous system injury. This study evaluated whether the neuroprotective effect of isoflurane <span class="hlt">preconditioning</span> is mediated by the activation of the notch signaling pathway. Mice were divided into two groups consisting of those that did or did not receive <span class="hlt">preconditioning</span> with isoflurane. The expression levels of notch-1, notch intracellular domain (NICD), and hairy and enhancer of split (HES-1) were measured in mice subjected to transient global cerebral ischemia-reperfusion injury. The notch signaling inhibitor DAPT and conditional notch-RBP-J knockout mice were used to investigate the mechanisms of isoflurane <span class="hlt">preconditioning</span>-induced neuroprotection. Immunohistochemical staining, real-time polymerase chain reaction assays, and Western blotting were performed. Isoflurane <span class="hlt">preconditioning</span> induced neuroprotection against global cerebral ischemia. <span class="hlt">Preconditioning</span> up-regulated the expression of notch-1, HES-1, and NICD after ischemic-reperfusion. However, these molecules were down-regulated at 72 h after ischemic-reperfusion. The inhibition of notch signaling activity by DAPT significantly attenuated the isoflurane <span class="hlt">preconditioning</span>-induced neuroprotection, and similar results were obtained using notch knockout mice. Our results demonstrate that the neuroprotective effects of isoflurane <span class="hlt">preconditioning</span> are mediated by the pre-activation of the notch signaling pathway. PMID:24197755</p> <div class="credits"> <p class="dwt_author">Zhang, Hao-peng; Sun, Yan-yan; Chen, Xiao-mei; Yuan, Li-bang; Su, Bin-xiao; Ma, Rui; Zhao, Rui-ni; Dong, Hai-long; Xiong, Lize</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-03-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">304</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4321002"> <span id="translatedtitle">Evaluation of the effects of ischemic <span class="hlt">preconditioning</span> on the hematological parameters of rats subjected to intestinal ischemia and reperfusion</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">OBJECTIVES: Intestinal ischemia/reperfusion often leads to acute lung injury and multiple organ failure. Ischemic <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> on such parameters. We evaluated the hematological changes during ischemia/reperfusion and <span class="hlt">preconditioning</span> in rats. METHODS: Forty healthy rats were divided into four groups: control, laparotomy, intestinal ischemia/reperfusion and ischemic <span class="hlt">preconditioning</span>. The intestinal ischemia/reperfusion group received 45 min of superior mesenteric artery occlusion, while the ischemic <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> 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.</p> <div class="credits"> <p class="dwt_author">Tahir, Muhammad; Arshid, Samina; Heimbecker, Ana Maria C; Castro, Mariana S; de Souza Montero, Edna Frasson; Fontes, Belchor; Fontes, Wagner</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">305</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/24277159"> <span id="translatedtitle">(S)-ZJM-289 <span class="hlt">preconditioning</span> induces a late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">(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 <span class="hlt">preconditioning</span>. The purpose of this study is to explore the late phase neuroprotection of (S)-ZJM-289 <span class="hlt">preconditioning</span>, as well as underlying mechanisms involved. <span class="hlt">Preconditioning</span> with 40-160 mg/kg, (S)-ZJM-289 significantly reduces brain damage after I/R. (S)-ZJM-289 <span class="hlt">preconditioning</span> is effective when applied 1-3 days before I/R. Moreover, the degrees of neuroprotection offered by (S)-ZJM-289 <span class="hlt">preconditioning</span> and ischemic <span class="hlt">preconditioning</span> are virtually identical. (S)-ZJM-289 <span class="hlt">preconditioning</span> also protects primary cultured cortical neurons against oxygen-glucose deprivation and recovery-induced cytotoxicity in vitro. (S)-ZJM-289 <span class="hlt">preconditioning</span> significantly increases the generation of NO, but has no effect on the nitric oxide synthase activities. Additionally, (S)-ZJM-289 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> is blocked by Nrf2-siRNA in vitro. (S)-ZJM-289 <span class="hlt">preconditioning</span> up-regulates antioxidant enzymes against nervous injury. (S)-ZJM-289 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> exerts the late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation. PMID:24277159</p> <div class="credits"> <p class="dwt_author">Zhang, Chao; Zhang, Zhenzhen; Zhao, Qian; Wang, Xuliang; Ji, Hui; Zhang, Yihua</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-07-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">306</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/servlets/purl/936450"> <span id="translatedtitle">Overlapping Schwarz for Nonlinear Problems. An Element Agglomeration Nonlinear Additive Schwarz <span class="hlt">Preconditioned</span> Newton Method for Unstructured Finite Element Problems</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">This paper extends previous results on nonlinear Schwarz <span class="hlt">preconditioning</span> ([4]) to unstructured finite element elliptic problems exploiting now nonlocal (but small) subspaces. The non-local finite element subspaces are associated with subdomains obtained from a non-overlapping element partitioning of the original set of elements and are coarse outside the prescribed element subdomain. The coarsening is based on a modification of the agglomeration based AMGe method proposed in [8]. Then, the algebraic construction from [9] of the corresponding non-linear finite element subproblems is applied to generate the subspace based nonlinear preconditioner. The overall nonlinearly <span class="hlt">preconditioned</span> problem is solved by an inexact Newton method. Numerical illustration is also provided.</p> <div class="credits"> <p class="dwt_author">Cai, X C; Marcinkowski, L; Vassilevski, P S</p> <p class="dwt_publisher"></p> <p class="publishDate">2005-02-10</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">307</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/47817275"> <span id="translatedtitle">Obesity <span class="hlt">Prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">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 <span class="hlt">prevention</span> of obesity in childhood is particularly complex. Ultimately,\\u000a to</p> <div class="credits"> <p class="dwt_author">Shiriki K. Kumanyika; Stephen R. Daniels</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">308</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2998236"> <span id="translatedtitle">Non-crossing large-margin probability estimation and its application to robust SVM via <span class="hlt">preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Many large-margin classifiers such as the Support Vector Machine (SVM) sidestep estimating conditional class probabilities and target the discovery of classification boundaries directly. However, estimation of conditional class probabilities can be useful in many applications. Wang, Shen, and Liu (2008) bridged the gap by providing an interval estimator of the conditional class probability via bracketing. The interval estimator was achieved by applying different weights to positive and negative classes and training the corresponding weighted large-margin classifiers. They propose to estimate the weighted large-margin classifiers individually. However, empirically the individually estimated classification boundaries may suffer from crossing each other even though, theoretically, they should not. In this work, we propose a technique to ensure non-crossing of the estimated classification boundaries. Furthermore, we take advantage of the estimated conditional class probabilities to <span class="hlt">precondition</span> our training data. The standard SVM is then applied to the <span class="hlt">preconditioned</span> training data to achieve robustness. Simulations and real data are used to illustrate their finite sample performance. PMID:21151740</p> <div class="credits"> <p class="dwt_author">Wu, Yichao; Liu, Yufeng</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">309</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2670565"> <span id="translatedtitle">Strategies to promote donor cell survival: combining <span class="hlt">preconditioning</span> approach with stem cell transplantation</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">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 <span class="hlt">preconditioning</span> approach. The use of pharmacological <span class="hlt">preconditioning</span> for up-regulation of pro-survival proteins and cardiogenic markers in the transplanted stem cells will be discussed. PMID:18561945</p> <div class="credits"> <p class="dwt_author">Haider, Husnain Kh; Ashraf, Muhammad</p> <p class="dwt_publisher"></p> <p class="publishDate">2008-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">310</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25552250"> <span id="translatedtitle">Remote ischemic <span class="hlt">preconditioning</span> for myocardial protection: update on mechanisms and clinical relevance.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">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 <span class="hlt">preconditioning</span>, known as remote ischemic <span class="hlt">preconditioning</span> (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</p> <div class="credits"> <p class="dwt_author">Gill, Rabia; Kuriakose, Robin; Gertz, Zachary M; Salloum, Fadi N; Xi, Lei; Kukreja, Rakesh C</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-04-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">311</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3758789"> <span id="translatedtitle">Electroacupuncture <span class="hlt">preconditioning</span>-induced neuroprotection may be mediated by glutamate transporter type 2</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Electroacupuncture has been shown to induce a <span class="hlt">preconditioning</span> effect in the brain. The mechanisms for this protection are not fully elucidated. We hypothesize that this protection is mediated by excitatory amino acid transporters (EAATs) that have been shown to be neuroprotective. To test this hypothesis, two-month old male Sprague-Dawley rats and EAAT type 3 (EAAT3) knockout mice received or did not receive 30-min electroacupuncture once a day for 5 consecutive days. They were subjected to a 120-min middle cerebral arterial occlusion (MCAO) at 24 h after the last electroacupuncture. Neurological outcome was assessed 2 days after the MCAO. Brain tissues were harvested at 24 h after the last electroacupuncture for Western blotting. Rats subjected to electroacupuncture at the Baihui acupoint had smaller brain infarct volumes and better neurological deficit scores than control rats. Electroacupuncture increased EAAT type 2 (EAAT2) in the cerebral cortex, tended to increase EAAT3 in the hippocampus, and had no effect on EAAT type 1 expression. Dihydrokainate, an EAAT2 inhibitor, worsened the neurological outcome of rats with electroacupuncture pretreatment. Electroacupuncture pretreatment at the Baihui acupoint increased EAAT2 in the cerebral cortex and improved the neurological outcome of EAAT3 knockout mice. Together, our results suggest that EAAT2 may mediate the electroacupuncture <span class="hlt">preconditioning</span>-induced neuroprotection. PMID:23831620</p> <div class="credits"> <p class="dwt_author">Zhu, Xiaoling; Yin, Jinbo; Li, Liaoliao; Ma, Lei; Tan, Hongying; Deng, Jiao; Chen, Shaoyang; Zuo, Zhiyi</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">312</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/19878402"> <span id="translatedtitle">Allergy <span class="hlt">prevention</span>.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">The further increase of allergies in industrialized countries demands evidence-based measures of primary <span class="hlt">prevention</span>. The recommendations as published in the guideline of 2004 were updated and consented on the basis of a systematic literature search. Evidence from the period February 2003-May 2008 was searched in the electronic databases Cochrane and MEDLINE as well as in reference lists of recent reviews and by contacting experts. The retrieved citations were screened for relevance first by title and abstract and in a second step as full paper. Levels of evidence were assigned to each included study and the methodological quality of the studies was assessed as high or low. Finally the revised recommendations were formally consented (nominal group process) by representatives of relevant societies and organizations including a self-help group. Of originally 4556 hits, 217 studies (4 Cochrane Reviews, 14 meta-analyses, 19 randomized controlled trials, 135 cohort and 45 case-control studies) were included and critically appraised. Grossly unchanged remained the recommendations on avoiding environmental tobacco smoke, breast-feeding over 4 months (alternatively hypoallergenic formulas for children at risk), avoiding a mold-promoting indoor climate, vaccination according to current recommendations, and avoidance of furry pets (especially cats) in children at risk. The recommendation on reducing the house dust mite allergen exposure as a measure of primary <span class="hlt">prevention</span> was omitted and the impact of a delayed introduction of supplementary food was reduced. New recommendations were adopted concerning fish consumption (during pregnancy / breast-feeding and as supplementary food in the first year), avoidance of overweight, and reducing the exposure to indoor and outdoor air pollutants. The revision of this guideline on a profound evidence basis led to (1) a confirmation of existing recommendations, (2) substantial revisions, and (3) new recommendations. Thereby it is possible to give evidence-based and up-to-date recommendations on primary <span class="hlt">prevention</span> of allergies. PMID:19878402</p> <div class="credits"> <p class="dwt_author">Muche-Borowski, Cathleen; Kopp, Matthias; Reese, Imke; Sitter, Helmut; Werfel, Thomas; Schäfer, Torsten</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-09-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">313</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4270574"> <span id="translatedtitle">Hypoxic <span class="hlt">preconditioning</span> protects cardiomyocytes against hypoxia/reoxygenation injury through AMPK/eNOS/PGC-1? signaling pathway</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Objective: AMP-activated protein kinase (AMPK) is an important regulator of multiple cellular pathways in the setting of energetic stress. Whether AMPK plays a critical role in hypoxic <span class="hlt">preconditioning</span> (HPC), protecting cardiomyocytes against hypoxia reoxygenation (H/R) injury remains uncertain. Methods: H9c2 cells were <span class="hlt">preconditioned</span> by exposing to 10 min of hypoxia and 30 min of reoxygenation. Then, the <span class="hlt">preconditioned</span> and non-<span class="hlt">preconditioned</span> cardiomyocytes were exposed to 90 min of hypoxia followed by 120 min of reoxygenation. Results: HPC protected H9c2 cells against H/R injury, the AMPK inhibitor or eNOS inhibitor abolished the effect of HPC. Compared with H/R group, HPC significantly increased the expression of p-AMPK (Thr172). HPC also markedly increased p-eNOS (Ser1177) expression, which was abolished by AMPK inhibition. HPC significantly increased PGC-1? expression, which were nullified by AMPK inhibition or eNOS inhibition. HPC attenuated the oxidative stress by increasing the SOD activity and decreasing the MDA and ROS level, which were abolished by AMPK inhibition or eNOS inhibition. Interestingly, the AMPK activator metformin mimicked the effects of HPC in part. Conclusions: These results indicated that HPC protects H9c2 cells against H/R injury by reducing oxidative stress partly via AMPK/eNOS/PGC-1? signaling pathway. PMID:25550773</p> <div class="credits"> <p class="dwt_author">Hu, Liang; Zhou, Lu; Wu, Xiaowei; Liu, Chao; Fan, Yue; Li, Qingping</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">314</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=social+AND+work+AND+autism&pg=3&id=EJ928337"> <span id="translatedtitle">Educating Children on the Autism Spectrum: <span class="hlt">Preconditions</span> for Inclusion and Notions of "Best Autism Practice" in the Early Years</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">This article draws together findings from expert evidence and empirical studies to identify the <span class="hlt">preconditions</span> for developing inclusive learning environments for young children on the autism spectrum. It concludes that in order to develop "best practice", practitioners need to adapt interventions to the unique needs of the individual child, work in…</p> <div class="credits"> <p class="dwt_author">Guldberg, Karen</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">315</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4227258"> <span id="translatedtitle">Exercise <span class="hlt">Preconditioning</span> Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise <span class="hlt">preconditioning</span> in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise <span class="hlt">preconditioning</span> induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise <span class="hlt">preconditioning</span> promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise <span class="hlt">preconditioning</span> is a promising strategy for facilitating functional recovery from SCI. PMID:25334068</p> <div class="credits"> <p class="dwt_author">Chang, Cheng-Kuei; Chou, Willy; Lin, Hung-Jung; Huang, Yi-Ching; Tang, Ling-Yu; Lin, Mao-Tsun; Chang, Ching-Ping</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">316</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://oaspub.epa.gov/eims/eimsapi.dispdetail?deid=61821"> <span id="translatedtitle">TARGETED DELETION OF INDUCIBLE HEAT SHOCK PROTEIN 70 ABROGATES THE LATE INFARCT-SPARING EFFECT OF MYOCARDIAL ISCHEMIC <span class="hlt">PRECONDITIONING</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p class="result-summary">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 <span class="hlt">Preconditioning</span> Craig...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">317</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ccbb.pitt.edu/Faculty/Faeder/Publications/Reprints/An2008.pdf"> <span id="translatedtitle">Detailed qualitative dynamic knowledge representation using a BioNetGen model of TLR-4 signaling and <span class="hlt">preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">and <span class="hlt">preconditioning</span> Gary C. An a,*, James R. Faeder b a Department of Surgery, Division of Trauma/Critical Care LPS at 10, 100, 1000 and 10,000 and a secondary dose of LPS at 10,000 administered at 27 h</p> <div class="credits"> <p class="dwt_author">Faeder, Jim</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">318</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25334068"> <span id="translatedtitle">Exercise <span class="hlt">preconditioning</span> protects against spinal cord injury in rats by upregulating neuronal and astroglial heat shock protein 72.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise <span class="hlt">preconditioning</span> in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise <span class="hlt">preconditioning</span> induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise <span class="hlt">preconditioning</span> promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise <span class="hlt">preconditioning</span> is a promising strategy for facilitating functional recovery from SCI. PMID:25334068</p> <div class="credits"> <p class="dwt_author">Chang, Cheng-Kuei; Chou, Willy; Lin, Hung-Jung; Huang, Yi-Ching; Tang, Ling-Yu; Lin, Mao-Tsun; Chang, Ching-Ping</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">319</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/servlets/purl/578661"> <span id="translatedtitle">Two examples of the impact of partitioning with Chaco and Metis on the convergence of additive Schwarz-<span class="hlt">preconditioned</span> FGMRES</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">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 <span class="hlt">preconditioning</span> methods. The authors show through a couple of examples that this can have a substantial impact on the convergence of the iterative methods.</p> <div class="credits"> <p class="dwt_author">DeLong, M.</p> <p class="dwt_publisher"></p> <p class="publishDate">1997-09-29</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">320</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/32904167"> <span id="translatedtitle">Modification of the Hepatic Mitochondrial Proteome in Response to Ischemic <span class="hlt">Preconditioning</span> following Ischemia-Reperfusion Injury of the Rat Liver</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Background\\/Aim: Ischemic <span class="hlt">preconditioning</span> (IPC) may reduce hepatic ischemia-reperfusion (IR) injury, but efficacy of IPC on mitochondrial proteome is not demonstrated. We investigated how IPC modifies the mitochondrial proteome after IR injury. Methods: Rats were subjected to 25 min of portal triad crossclamping (IR group, n = 8). In the IPC group (n = 8), 10 min of temporal portal triad</p> <div class="credits"> <p class="dwt_author">R. Oshima; H. Nakano; M. Katayama; J. Sakurai; W. Wu; S. Koizumi; T. Asano; T. Watanabe; T. Asakura; T. Ohta; T. Otsubo</p> <p class="dwt_publisher"></p> <p class="publishDate">2008-01-01</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_15");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' href="#">2</a> <a onClick='return showDiv("page_3");' href="#">3</a> <a onClick='return showDiv("page_4");' 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class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_16");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' href="#">2</a> <a onClick='return showDiv("page_3");' href="#">3</a> <a onClick='return showDiv("page_4");' href="#">4</a> <a onClick='return showDiv("page_5");' href="#">5</a> <a onClick='return showDiv("page_6");' href="#">6</a> <a onClick='return showDiv("page_7");' href="#">7</a> <a onClick='return showDiv("page_8");' href="#">8</a> <a onClick='return showDiv("page_9");' href="#">9</a> <a onClick='return showDiv("page_10");' href="#">10</a> <a onClick='return showDiv("page_11");' href="#">11</a> <a onClick='return showDiv("page_12");' href="#">12</a> <a onClick='return showDiv("page_13");' href="#">13</a> <a onClick='return showDiv("page_14");' href="#">14</a> <a onClick='return showDiv("page_15");' href="#">15</a> <a onClick='return showDiv("page_16");' href="#">16</a> <a style="font-weight: bold;">17</a> <a onClick='return showDiv("page_18");' href="#">18</a> <a onClick='return showDiv("page_19");' href="#">19</a> <a onClick='return showDiv("page_20");' href="#">20</a> <a onClick='return showDiv("page_21");' href="#">21</a> <a onClick='return showDiv("page_22");' href="#">22</a> <a onClick='return showDiv("page_23");' href="#">23</a> <a onClick='return showDiv("page_24");' href="#">24</a> <a onClick='return showDiv("page_25");' href="#">25</a> </span> </span> <a id="NextPageLink" onclick='return showDiv("page_18");' href="#" title="Next Page"> <img id="NextPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">321</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2645802"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> mediated by sublethal oxygen–glucose deprivation-induced cyclooxygenase-2 expression via the signal transducers and activators of transcription 3 phosphorylation</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">The signal transducers and activators of transcription (STATs) were found to be essential for cardioprotection. However, their role in <span class="hlt">preconditioning</span> (PC) neuroprotection remains undefined. Previously, our studies showed that PC mediated a signaling cascade that involves activation of epsilon protein kinase C (?PKC), extracellular signal-regulated kinase (ERK1/2), and cyclooxygenase-2 (COX-2) pathways. However, the intermediate pathway by which ERK1/2 activates COX-2 was not defined. In this study, we investigated whether the PC-induced signaling pathway requires phosphorylation of STAT isoforms for COX-2 expression. To mimic PC or lethal ischemia, mixed cortical neuron/astrocyte cell cultures were subjected to 1 and/or 4 h of oxygen–glucose deprivation (OGD), respectively. The results indicated serine phosphorylation of STAT3 after PC or ?PKC activation. Inhibition of either ?PKC or ERK1/2 activation abolished PC-induced serine phosphorylation of STAT3. Additionally, inhibition of STAT3 <span class="hlt">prevented</span> PC-induced COX-2 expression and neuroprotection against OGD. Therefore, our findings suggest that PC signaling cascade involves STAT3 activation after ?PKC and ERK1/2 activation. Finally, we show that STAT3 activation mediates COX-2 expression and ischemic tolerance. PMID:18398416</p> <div class="credits"> <p class="dwt_author">Kim, Eun J; Raval, Ami P; Perez-Pinzon, Miguel A</p> <p class="dwt_publisher"></p> <p class="publishDate">2008-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">322</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25388675"> <span id="translatedtitle">CpG <span class="hlt">preconditioning</span> regulates miRNA expression that modulates genomic reprogramming associated with neuroprotection against ischemic injury.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Cytosine-phosphate-guanine (CpG) <span class="hlt">preconditioning</span> reprograms the genomic response to stroke to protect the brain against ischemic injury. The mechanisms underlying genomic reprogramming are incompletely understood. MicroRNAs (miRNAs) regulate gene expression; however, their role in modulating gene responses produced by CpG <span class="hlt">preconditioning</span> is unknown. We evaluated brain miRNA expression in response to CpG <span class="hlt">preconditioning</span> before and after stroke using microarray. Importantly, we have data from previous gene microarrays under the same conditions, which allowed integration of miRNA and gene expression data to specifically identify regulated miRNA gene targets. CpG <span class="hlt">preconditioning</span> did not significantly alter miRNA expression before stroke, indicating that miRNA regulation is not critical for the initiation of <span class="hlt">preconditioning</span>-induced neuroprotection. However, after stroke, differentially regulated miRNAs between CpG- and saline-treated animals associated with the upregulation of several neuroprotective genes, implicating these miRNAs in genomic reprogramming that increases neuroprotection. Statistical analysis revealed that the miRNA targets were enriched in the gene population regulated in the setting of stroke, implying that miRNAs likely orchestrate this gene expression. These data suggest that miRNAs regulate endogenous responses to stroke and that manipulation of these miRNAs may have the potential to acutely activate novel neuroprotective processes that reduce damage.Journal of Cerebral Blood Flow & Metabolism advance online publication, 12 November 2014; doi:10.1038/jcbfm.2014.193. PMID:25388675</p> <div class="credits"> <p class="dwt_author">Vartanian, Keri B; Mitchell, Hugh D; Stevens, Susan L; Conrad, Valerie K; McDermott, Jason E; Stenzel-Poore, Mary P</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-11-12</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">323</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3582752"> <span id="translatedtitle">Microarray Analyses of Genes Regulated by Isoflurane Anesthesia In Vivo: A Novel Approach to Identifying Potential <span class="hlt">Preconditioning</span> Mechanisms</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background While general anesthetics are recognized for their potential to render patients unconscious during surgery, exposure can also lead to long-term outcomes of both cellular damage and protection. As regards the latter, delayed anesthetic <span class="hlt">preconditioning</span> is an evolutionarily conserved physiological response that has the potential for protecting against ischemic injury in a number of tissues. While it is known that delayed <span class="hlt">preconditioning</span> requires de novo protein synthesis, knowledge of anesthetic-regulated genes is incomplete. In this study we used the conserved nature of <span class="hlt">preconditioning</span> to analyze differentially regulated genes in three different rat tissues. We hypothesized that by selecting those genes regulated in multiple tissues, we could develop a focused list of gene candidates potentially involved in delayed anesthetic <span class="hlt">preconditioning</span>. Methods Young adult male Sprague Dawley rats were anesthetized with a 2% isoflurane/98% air mixture for 90 min. Immediately after anesthetic exposure, animals were killed and liver, kidney and heart were removed and total RNA was isolated. Differential gene expression was determined using rat oligonucleotide gene arrays. Array data were analyzed to select for genes that were significantly regulated in multiple tissues. Results All three tissues showed differentially regulated genes in response to a clinically relevant exposure to isoflurane. Analysis of coordinately regulated genes yielded a focused list of 34 potential gene candidates with a range of ontologies including regulation of inflammation, modulation of apoptosis, regulation of ion gradients and maintenance of energy pathways. Conclusions We conclude that, through using an analysis approach focusing on coordinately regulated genes, we were able to generate a focused list of interesting gene candidates with potential to enable future <span class="hlt">preconditioning</span> studies. PMID:23400992</p> <div class="credits"> <p class="dwt_author">Edmands, Scott D; Hall, Adam C.; LaDow, Eva</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">324</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3481200"> <span id="translatedtitle">Poly-ICLC <span class="hlt">preconditioning</span> protects the blood-brain barrier against ischemic injury in vitro through type I interferon signaling</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary"><span class="hlt">Preconditioning</span> with a low dose of harmful stimulus prior to injury induces tolerance to a subsequent ischemic challenge resulting in neuroprotection against stroke. Experimental models of <span class="hlt">preconditioning</span> primarily focus on neurons as the cellular target of cerebral protection while less attention has been paid to the cerebrovascular compartment whose role in the pathogenesis of ischemic brain injury is crucial. We have shown that <span class="hlt">preconditioning</span> with polyinosinic polycytidylic acid (poly-ICLC) protects against cerebral ischemic damage. To delineate the mechanism of poly-ICLC protection, we investigated whether poly-ICLC <span class="hlt">preconditioning</span> preserves the function of the blood-brain-barrier (BBB) in response to ischemic injury. Using an in vitro BBB model, we found that poly-ICLC treatment prior to exposure to oxygen-glucose deprivation maintained the paracellular and transcellular transport across the endothelium and attenuated the drop in transendothelial electric resistance. We found that poly-ICLC treatment induced interferon (IFN) ? mRNA expression in astrocytes and microglia and that type I IFN signaling in brain microvascular endothelial cells was required for protection. Importantly, this implicates a potential mechanism underlying neuroprotection in our in vivo experimental stroke model where type I IFN signaling is required for poly-ICLC-induced neuroprotection against ischemic injury. In conclusion, we are the first to show that <span class="hlt">preconditioning</span> with poly-ICLC attenuates ischemia-induced BBB dysfunction. This mechanism is likely an important feature of poly-ICLC-mediated neuroprotection and highlights the therapeutic potential of targeting BBB signaling pathways to protect the brain against stroke. PMID:23050645</p> <div class="credits"> <p class="dwt_author">Gesuete, Raffaella; Packard, Amy E. B.; Vartanian, Keri B.; Conrad, Valerie K.; Stevens, Susan L.; Bahjat, Frances R.; Yang, Tao; Stenzel-Poore, Mary P.</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">325</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://ntrs.nasa.gov/search.jsp?R=20020041100&hterms=apriori+algorithm&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D20%26Ntt%3Dapriori%2Balgorithm"> <span id="translatedtitle">Some Experiences with Nonoverlapping Schur Complement Parallel <span class="hlt">Preconditioning</span> for CFD Calculations</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p class="result-summary">In this work we consider solving matrices which arise from the discretization of advection-diffusion field equations on arbitrary triangulated domains using stabilized numerical methods. The talk will discuss several candidate matrix <span class="hlt">preconditioning</span> algorithms based on the 2 x 2 block factorization induced by an apriori partitioning of the triangulated domain. Application of the 2 x 2 block preconditioner requires the formation and inversion of the Schur complement submatrix. We consider several strategies for simplifying this task: incomplete Schur complement factorizations, drop tolerance element filling, Schur complement probing, and localized Schur complement inversion. Numerical results will be shown comparing performance and efficiency of these approximations. The matrix preconditioner has also been embedded into a Newton algorithm for solving the nonlinear Euler and Navier-Stokes equations governing compressible flow. The remainder of the talk will show numerous examples in CFD to demonstrate the efficiency and robustness of the techniques.</p> <div class="credits"> <p class="dwt_author">Barth, Timothy J.; Chan, Tony F.; Tang, Wei-Pai; Kwak, Dochan (Technical Monitor)</p> <p class="dwt_publisher"></p> <p class="publishDate">1996-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">326</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3461466"> <span id="translatedtitle">Effects of diabetes on myocardial infarct size and cardioprotection by <span class="hlt">preconditioning</span> and postconditioning</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">In spite of the current optimal therapy, the mortality of patients with ischemic heart disease (IHD) remains high, particularly in cases with diabetes mellitus (DM) as a co-morbidity. Myocardial infarct size is a major determinant of prognosis in IHD patients, and development of a novel strategy to limit infarction is of great clinical importance. Ischemic <span class="hlt">preconditioning</span> (PC), postconditioning (PostC) and their mimetic agents have been shown to reduce infarct size in experiments using healthy animals. However, a variety of pharmacological agents have failed to demonstrate infarct size limitation in clinical trials. One of the possible reasons for the discrepancy between the results of animal experiments and clinical trials is that co-morbidities, including DM, modified myocardial responses to ischemia/reperfusion and to cardioprotective agents. Here we summarize observations of the effects of DM on myocardial infarct size and ischemic PC and PostC and discuss perspectives for protection of DM hearts. PMID:22694800</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">327</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/biblio/22230859"> <span id="translatedtitle">Fluid <span class="hlt">preconditioning</span> for Newton–Krylov-based, fully implicit, electrostatic particle-in-cell simulations</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">A recent proof-of-principle study proposes an energy- and charge-conserving, nonlinearly implicit electrostatic particle-in-cell (PIC) algorithm in one dimension [9]. The algorithm in the reference employs an unpreconditioned Jacobian-free Newton–Krylov method, which ensures nonlinear convergence at every timestep (resolving the dynamical timescale of interest). Kinetic enslavement, which is one key component of the algorithm, not only enables fully implicit PIC as a practical approach, but also allows <span class="hlt">preconditioning</span> the kinetic solver with a fluid approximation. This study proposes such a preconditioner, in which the linearized moment equations are closed with moments computed from particles. Effective acceleration of the linear GMRES solve is demonstrated, on both uniform and non-uniform meshes. The algorithm performance is largely insensitive to the electron–ion mass ratio. Numerical experiments are performed on a 1D multi-scale ion acoustic wave test problem.</p> <div class="credits"> <p class="dwt_author">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)</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-02-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">328</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/16454292"> <span id="translatedtitle">Transducer sensitivity compensation using diagonal <span class="hlt">preconditioning</span> for time reversal and Tikhonov inverse filtering in acoustic systems.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Filters are commonly used in sound reproduction and communication systems as a means of compensating for the response of the electro-acoustic plant. Two commonly used filter designs in the field of acoustics are the time reversal filter and the Tikhonov inverse filter. In this paper the influence of transducer sensitivities on the performance of these filters is examined. It is shown that the sensitivity of the transducers can negatively affect the performance of the resulting filter. To compensate for the decrease in performance, diagonal <span class="hlt">preconditioning</span> can be implemented in the system. It is shown that by using diagonal matrices, which minimize the condition number of the system, the loss in performance arising from unbalanced sensitivities is minimized. This paper proposes an algorithm to find such a set of diagonal matrices and results are presented showing the improvements in performance arising from the modified filter design. PMID:16454292</p> <div class="credits"> <p class="dwt_author">Dumuid, Pierre M; Cazzolato, Ben S; Zander, Anthony C</p> <p class="dwt_publisher"></p> <p class="publishDate">2006-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">329</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/15865305"> <span id="translatedtitle">Local fisheries management at the Swedish coast: biological and social <span class="hlt">preconditions</span>.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Most of the Swedish coastal fisheries are not sustainable from either a social, economic or ecological point of view. We propose the introduction of local fisheries management (LFM) as a tool for restructuring the present large-scale management system in order to achieve sustainability. To implement LFM two questions need to be answered: How to distribute the resource fish among different resource user groups? How to restructure present fisheries management to meet the criteria of sustainability? Starting from these questions we describe possible forms of LFM for Swedish coastal fishery supported by recent research. The biological and social <span class="hlt">preconditions</span> for restructuring fisheries management are derived from an analysis of the ecological and managerial situation in Swedish fishery. Three types of LFM--owner based, user based, and community based management--are analyzed with regard to the tasks to be carried outin LFM, the roles of management groups, and the definition and optimal size of management areas. PMID:15865305</p> <div class="credits"> <p class="dwt_author">Bruckmeier, Karl; Neuman, Erik</p> <p class="dwt_publisher"></p> <p class="publishDate">2005-03-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">330</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4040454"> <span id="translatedtitle">Epigenetics and the Environment: In Search of the “Toleroasome” Vital to Execution of Ischemic <span class="hlt">Preconditioning</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Activation and repression of gene expression are key features of ischemic tolerance. Converging lines of inquiry from several groups suggests that epigenetic proteins may transduce sublethal stresses, including bio-energetic or oxidative stress into durable (2–3 days) changes in gene expression that mediate ischemic tolerance. Here we discuss the potential mechanisms by which changes in cell state (e.g., ATP, NAD+, and oxygen) can modify specific targets including polycomb complexes, jumonji domain histone demethylases, and zinc and NAD-dependent histone decetylases and thus trigger an adaptive program. A major unanswered question is whether these proteins work in parallel or convergently as part of a “tolerosome” (tolero is the Latin word for tolerance), a multiprotein complex recruited to promoters or enhancers of specific genes, to mediate <span class="hlt">preconditioning</span>. Whatever the case may be, epigenetic proteins are fertile targets for the treatment of stroke. PMID:24323190</p> <div class="credits"> <p class="dwt_author">Brand, David</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">331</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2740718"> <span id="translatedtitle">Heme Oxygenase 1 Is Associated with Ischemic <span class="hlt">Preconditioning</span>-Induced Protection Against Brain Ischemia</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Ischemic <span class="hlt">preconditioning</span> (IPC) protects brain against ischemic injury by activating specific mechanisms. Our goal was to determine if the inducible heme oxygenase 1 (HO1) is required for such protection. IPC before transient or permanent ischemia reduced cortical infarct volumes by 57.4% and 33.9%, respectively at 48 h in wildtype adult mice. Interestingly, IPC failed to protect the HO1 gene deleted mice against permanent ischemic brain injury. IPC also resulted in a significant increase in HO1 protein levels in the brain and correlated with reduced neurological deficits after permanent and transient brain ischemia. Our study demonstrates that neuroprotective effects of IPC are at least partially mediated via HO1. Elucidating the physiological/cellular role by which HO1 is protective against brain ischemia may aid the development of selective drugs to treat stroke and its associated neurological disorders. PMID:19465127</p> <div class="credits"> <p class="dwt_author">Zeynalov, Emil; Shah, Zahoor A.; Li, Rung-chi; Doré, Sylvain</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">332</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3218381"> <span id="translatedtitle">Disruption of Caveolae Blocks Ischemic <span class="hlt">Preconditioning</span>-Mediated S-Nitrosylation of Mitochondrial Proteins</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Abstract Aims Nitric oxide (NO) and protein S-nitrosylation (SNO) play important roles in ischemic <span class="hlt">preconditioning</span> (IPC)-induced cardioprotection. Mitochondria are key regulators of <span class="hlt">preconditioning</span>, and most proteins showing an increase in SNO with IPC are mitochondrial. The aim of this study was to address how IPC transduces NO/SNO signaling to mitochondria in the heart. Results: In this study using Langendorff perfused mouse hearts, we found that IPC-induced cardioprotection was blocked by treatment with either N-nitro-L-arginine methyl ester (L-NAME, a constitutive NO synthase inhibitor), ascorbic acid (a reducing agent to decompose SNO), or methyl-?-cyclodextrin (M?CD, a cholesterol sequestering agent to disrupt caveolae). IPC not only activated AKT/eNOS signaling but also led to translocation of eNOS to mitochondria. M?CD treatment disrupted caveolar structure, leading to dissociation of eNOS from caveolin-3 and blockade of IPC-induced activation of the AKT/eNOS signaling pathway. A significant increase in mitochondrial SNO was found in IPC hearts compared to perfusion control, and the disruption of caveolae by M?CD treatment not only abolished IPC-induced cardioprotection, but also blocked the IPC-induced increase in SNO. Innovation: These results provide mechanistic insight into how caveolae/eNOS/NO/SNO signaling mediates cardioprotection induced by IPC. Conclusion: Altogether these results suggest that caveolae transduce eNOS/NO/SNO cardioprotective signaling in the heart. Antioxid. Redox Signal. 16, 45–56. PMID:21834687</p> <div class="credits"> <p class="dwt_author">Kohr, Mark J.; Nguyen, Tiffany; Aponte, Angel M.; Connelly, Patricia S.; Esfahani, Shervin G.; Gucek, Marjan; Daniels, Mathew P.; Steenbergen, Charles; Murphy, Elizabeth</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">333</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4120131"> <span id="translatedtitle">Cardiac <span class="hlt">preconditioning</span> with sphingosine-1-phosphate requires activation of signal transducer and activator of transcription-3</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Summary Aims Sphingosine-1-phosphate (S1P) is a cardioprotective agent. Signal transducer and activator of transcription 3 (STAT-3) is a key mediator of many cardioprotective agents. We aimed to explore whether STAT-3 is a key mediator in S1P-induced <span class="hlt">preconditioning</span>. Methods Langendorff-perfused hearts from Wistar rats and wild-type or cardiomyocyte-specific STAT-3 knockout mice were pre-treated with S1P (10 nmol/l), with or without the STAT-3 pathway inhibitor AG490, before an ischaemia–reperfusion insult. Triphenyltetrazolium chloride and Evans blue staining were used for the determination of infarct size. Western blot analysis was carried out on the S1P pre-treated hearts for detection of cytosolic, nuclear and mitochondrial phosphorylated and total STAT-3 proteins. Results Pre-treatment with S1P decreased the infarct size in isolated rat (5 ± 3% vs control 26 ± 8%, p < 0.01) and wild-type mouse hearts (13 ± 1% vs control 33 ± 3%, p < 0.05). This protective effect was abolished in the rat hearts pre-treated with AG490 (30 ± 10%, p = ns vs control) and in the hearts from STAT-3 knockout mice (35 ± 4% vs control 30 ± 3%, p = ns). Levels of phosphorylated STAT-3 were significantly increased in both the nuclear (p < 0.05 vs control) and mitochondrial (p < 0.05 vs control) fractions in the S1P pre-treated hearts, but remained unchanged in the cytosolic fraction (p = ns vs control). Conclusion These novel results demonstrate that pharmacological <span class="hlt">preconditioning</span> with S1P in the isolated heart is mediated by activation of mitochondrial and nuclear STAT-3, therefore suggesting that S1P may be a novel therapeutic target to modulate mitochondrial and nuclear function in cardiovascular disease in order to protect the heart against ischaemia–reperfusion. PMID:25000441</p> <div class="credits"> <p class="dwt_author">Kelly-Laubscher, Roisin F; King, Jonathan C; Hacking, Damian; Somers, Sarin; Hastie, Samantha; Stewart, Tessa; Imamdin, Aqeela; Maarman, Gerald; Pedretti, Sarah; Lecour, Sandrine</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">334</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2839162"> <span id="translatedtitle">Sca-1+ stem cell survival and engraftment in the infarcted heart: dual role for <span class="hlt">preconditioning</span> induced connexin-43</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background We report that elevated connexin-43 (Cx-43) in stem cells <span class="hlt">preconditioned</span> with insulin like growth factor-1 (IGF-1) is cytoprotective and reprograms the cells for cardiomyogenic differentiation. Methods and Results Sca-1+ cells were <span class="hlt">preconditioned</span> with 100nM IGF-1 for 30-minutes followed by 8-hours (h) of oxygen glucose deprivation (OGD) to assess the cytoprotective effects of <span class="hlt">preconditioning</span>. LDH release assay, cytochrome-c release and mitochondrial membrane potential assay showed improved survival of <span class="hlt">preconditioned</span> Sca-1+ cells (PCSca-1+) under OGD as compared to non-<span class="hlt">preconditioned</span> Sca-1+ cells (non-PCSca-1+) via PI3K/Akt dependent caspase-3 downregulation. We observed PI3K/Akt dependent upregulation of cardiac specific markers including MEF-2c (2.5-fold), GATA4 (3.1-fold) and Cx-43 (3.5-fold). Cx-43 inhibition with specific RNAi reduced the cell survival under OGD and post-transplantation. In vivo studies were performed in a female rat model of acute myocardial infarction (n=78). Animals were grouped to receive intramyocardially 70?l DMEM without cells (group-1), or containing male 1×106 non-PCSca-1+ (group-2) or PCSca-1+ (group-3) cells labeled with PKH26. Survival of the PCSca-1+ was 5.5-fold higher in group-3 compared to group-2 on 7-days post-transplantation. Confocal imaging after actinin and Cx-43 specific immunostaining showed extensive engraftment and myogenic differentiation of PCSca-1+. As compared to group-2, group-3 showed increased blood vessel density (22.3±1.7/microscopic field, p<0.0001) and attenuated infarction size (23.3±3.6%; p=0.002). Heart function indices including ejection fraction (56.2±3.5; p=0.029) and fractional shortening (24.3±2.1; p=0.03) were improved in group-3 compared to group-2. Conclusions <span class="hlt">Preconditioning</span> with IGF-1 reprograms Sca-1+ for pro-survival signaling and cardiomyogenic differentiation with an important role for Cx-43 in this process. PMID:19414636</p> <div class="credits"> <p class="dwt_author">Lu, Gang; Haider, Husnain Kh; Jiang, Shujia; Ashraf, Muhammad</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">335</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/29283591"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> Somatothermal Stimulation on Right Seventh Intercostal Nerve Territory Increases Hepatic Heat Shock Protein 70 and Protects the Liver from Ischemia–Reperfusion Injury in Rats</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Hyperthermic <span class="hlt">preconditioning</span> attenuates the heat-induced cellular response to a subsequent severe heat challenge. However, it is impractical to perform whole-body hyperthermia in humans. This study was designed to test the hypotheses that hepatic heat shock protein 70 (Hsp70) could be induced by local somatothermal stimulation (LSTS) on right seventh intercostal nerve territory and that <span class="hlt">preconditioning</span> the rats with LSTS protects</p> <div class="credits"> <p class="dwt_author">Yu-Hsien Lin; Jen-Hwey Chiu; Hwa-Hsung Tung; Meng-Ting Tsou; Wing-Yiu Lui; Chew-Wun Wu</p> <p class="dwt_publisher"></p> <p class="publishDate">2001-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">336</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.springerlink.com/index/xta52txqqdjb8g4g.pdf"> <span id="translatedtitle">Capsaicin-sensitive local sensory innervation is involved in pacing-induced <span class="hlt">preconditioning</span> in rat hearts: role of nitric oxide and CGRP?</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Among several mediators, nitric oxide (NO) and calcitonin gene-related peptide (CGRP) were suggested to be involved in the\\u000a mechanism of <span class="hlt">preconditioning</span>. We examined the possible role of the cardiac capsaicin-sensitive sensory innervation in pacing-induced\\u000a <span class="hlt">preconditioning</span>, as well as in the cardiac NO and CGRP content. Wistar rats were treated subcutaneously with capsaicin or\\u000a its solvent in the sequence of 10,</p> <div class="credits"> <p class="dwt_author">Peter Ferdinandy; Tamás Csont; Csaba Csonka; Marianna Török; Mária Dux; József Németh; László I. Horváth; László Dux; Zoltán Szilvássy; Gábor Jancsó</p> <p class="dwt_publisher"></p> <p class="publishDate">1997-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">337</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3045195"> <span id="translatedtitle">Isoflurane <span class="hlt">preconditioning</span> reduces oxygen-glucose deprivation-induced neuronal injury via B-cell lymphoma 2 protein</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">A brief exposure to isoflurane prior to brain ischemia reduces ischemic brain injury in rodents. Here we showed that exposure of rat cerebral cortical neuronal cultures to 2% isoflurane for 30 min at 24 h before a 2-h oxygen-glucose deprivation (OGD) reduced the OGD-induced cell injury. This effect was abolished by HA14-1, a selective inhibitor of B-cell lymphoma 2 (Bcl-2) protein. Bcl-2 is well-known for its anti-apoptotic property. HA14-1 alone did not change OGD-induced cell injury. OGD reduced the expression of Bcl-2 in these neurons. This reduction was attenuated by isoflurane <span class="hlt">preconditioning</span>. These results suggest that isoflurane <span class="hlt">preconditioning</span>-induced neuroprotection is mediated by Bcl-2. PMID:21359097</p> <div class="credits"> <p class="dwt_author">Gwak, Mi-Sook; Cao, Lin; Li, Liaoliao; Zuo, Zhiyi</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">338</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=294357"> <span id="translatedtitle">Localization of proliferating cell nuclear antigen, vimentin, c-Fos, and clusterin in the <span class="hlt">postischemic</span> kidney. Evidence for a heterogenous genetic response among nephron segments, and a large pool of mitotically active and dedifferentiated cells.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">The mechanisms leading to the recovery of the kidney after ischemic acute renal failure are poorly understood. To explore the role played by mitogenesis and dedifferentiation in this repair process and to identify whether the genetic response of the nephron segments reflects the level of susceptibility to injury, the temporal and nephron segment expressions of various proteins implicated in mitogenesis, differentiation, and injury were determined. Proliferating cell nuclear antigen (PCNA), a marker for the G1-S transition in the cell cycle and hence mitogenesis, was detected primarily in the S3 segment of the proximal tubule, with maximal expression at 2 d postischemia. Vimentin, normally present in mesenchymal cells but not epithelial cells, and hence a marker for the state of differentiation, was prominently expressed in the S3 segment 2-5 d postischemia. In the S3 segments in the outer stripe of the medulla cells that stained positively for PCNA also stained positively for vimentin. Clusterin, a marker for cell injury, was expressed primarily in the S3 segment and in the distal tubule with distinct staining patterns in each segment. None of the cells that stained with clusterin antibodies were positively stained with PCNA or vimentin antibodies. Likewise, none of the PCNA or vimentin-positive cells expressed clusterin at detectable levels. Thus, in the S3 segment, where there is significant ischemic injury, surviving cells express markers indicating that they undergo mitogenesis and dedifferentiate in the <span class="hlt">postischemic</span> period. While there is some expression of c-Fos in the S3 segment, c-Fos was expressed predominantly, at 1 and 3 h postischemia, in the nuclei of the distal nephron, particularly in the thick ascending limb. The data support the view that the mature renal S3 segment epithelial cell can be a progenitor cell. Images PMID:7910173</p> <div class="credits"> <p class="dwt_author">Witzgall, R; Brown, D; Schwarz, C; Bonventre, J V</p> <p class="dwt_publisher"></p> <p class="publishDate">1994-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">339</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25562631"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> effect of (S)-3,5-dihydroxyphenylglycine on ischemic injury in middle cerebral artery occluded Sprague-Dawley rats.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">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) <span class="hlt">preconditioning</span> elicits neuroprotection in the hippocampal slice cultures exposed to toxic level of N-methyl-d-aspartate (NMDA). We further investigated the <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> 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 <span class="hlt">preconditioning</span> induced protective effects against acute ischemic insult in vivo. PMID:25562631</p> <div class="credits"> <p class="dwt_author">Nik Ramli, Nik Nasihah; Omar, Nursyazwani; Husin, Andrean; Ismail, Zalina; Siran, Rosfaiizah</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-02-19</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">340</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/23416203"> <span id="translatedtitle">Application of coal gasification technology as a flue gas <span class="hlt">pre-conditioning</span> step for the catalytic reduction of acid gases</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Typical flue gas contains an excess amount of oxygen, which can deactivate the reduction catalyst for NOX and SO2, such as the lanthanum oxysulfide-based catalyst. The reductant available in a flue gas stream rich in oxygen is usually scarce and not sufficient for the reduction. Coal gasification was applied to <span class="hlt">pre-condition</span> the flue gas to remove the excessive oxygen and</p> <div class="credits"> <p class="dwt_author">Ming Fang; Jianxin Ma; Ngai T Lau; Lei Wang; Shaosong Qian; King L To</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-01-01</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_16");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" 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id="NextPageLink" onclick='return showDiv("page_19");' href="#" title="Next Page"> <img id="NextPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">341</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.springerlink.com/index/xut69h463523w612.pdf"> <span id="translatedtitle">Nitric Oxide Synthase (NOS) Does Not Contribute to Simulated Ischaemic <span class="hlt">Preconditioning</span> in an Isolated Rat Cardiomyocyte Model</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">It is widely accepted that nitric oxide (NO) is a trigger and mediator of late ischaemic <span class="hlt">preconditioning</span> (IP), however its\\u000a role in classic (protection observed within 2–4 hours after the IP stimulus) IP is less certain. In addition, the contribution\\u000a of cardiomyocyte nitric oxide synthase (NOS) activation to NO production in ischaemia is unknown. The aim of this study was</p> <div class="credits"> <p class="dwt_author">Hans Strijdom; Sonia Genade; Amanda Lochner</p> <p class="dwt_publisher"></p> <p class="publishDate">2004-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">342</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://circres.ahajournals.org/cgi/reprint/CIRCRESAHA.107.155879v1.pdf"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> Results in S-Nitrosylation of Proteins Involved in Regulation of Mitochondrial Energetics and Calcium Transport</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">Nitric oxide has been shown to be an important signaling messenger in ischemic <span class="hlt">preconditioning</span> (IPC). Accordingly, we investigated whether protein S-nitrosylation occurs in IPC hearts and whether S-nitrosoglutathione (GSNO) elicits similar effects on S-nitrosylation and cardioprotection. Preceding 20 minutes of no-flow ischemia and reperfusion, hearts from C57BL\\/6J mice were perfused in the Langendorff mode and subjected to the following conditions:</p> <div class="credits"> <p class="dwt_author">Junhui Sun; Meghan Morgan; Rong-Fong Shen; Charles Steenbergen; Elizabeth Murphy</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">343</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/47721831"> <span id="translatedtitle">Effects of fasting and hypoxic <span class="hlt">preconditioning</span> on the hypoxic-reoxygenated ventricular strips of the rat heart</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">The investigation aimed to assess the effects of hypoxic <span class="hlt">preconditioning</span> in right ventricle strips of fed and 24-h fasted\\u000a rats, which display a fast fatty acid catabolism, and to ascertain whether these effects are associated with changes in the\\u000a tissue levels of long-chain acylCoA and acyl carnitine and glycolytic activity. Strips were mounted isometrically in Krebs-bicarbonate\\u000a solution with 10 mM</p> <div class="credits"> <p class="dwt_author">S. Cerruti; G. Testoni; V. Dalamon; P. Karle; A. Varela; E. A. Savino</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">344</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/19715835"> <span id="translatedtitle">Effect of <span class="hlt">preconditioning</span> with triiodothyronine on renal ischemia/reperfusion injury and poly(ADP-ribose) polymerase expression in rats.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">The ischemia/reperfusion (I/R) model in rats allows pharmacological investigation of protective renal effects of certain agents to thereby diminish the incidence of delayed graft function (DGF). The aim of this study was to determine the effects of <span class="hlt">preconditioning</span> with triiodothyronine (T(3)) on renal function and oxidative status in renal I/R injury. Forty male Wistar rats were <span class="hlt">preconditioned</span> with T(3) (100 microg/kg) or control (normal saline) at 24 hours prior to 45 minutes of renal ischemia, followed by a 4-hour (groups C-4h and T(3)-4h) or 24-hour (groups C-24h and T(3)-24h) reperfusion period. We determined renal function parameters (urea, creatinine, and proteinuria), oxidative stress biomarkers in plasma (malondialdehyde [MDA], glutathione [GSH], and superoxide dismutase [SOD]), urine (hydrogen peroxide [H(2)O(2)]), and renal tissue (GSH and MDA), and poly(ADP-ribose) polymerase (PARP-1) expression. Proteinuria was significantly lower in the T(3)-treated group (4.63 +/- 1.9 vs 9.27 +/- 0.72 mg/mL/100 g body weight). Pretreated rats showed lower levels of plasma and tissue MDA and urine H(2)O(2) (50.57 +/- 1.17 vs 71.16 +/- 1.14 micromol/100 g body weight). The T(3) treatment was associated with lower postischemia GSH concentrations (3.82 +/- 1.16 vs 4.89 +/- 0.68 nmol/mg protein) and higher SOD levels at 24 hours (11.27 +/- 0.86 vs 9.92 +/- 1.77 nmol/mg protein). <span class="hlt">Preconditioning</span> with the hormone also reduced PARP-1 tissue expression by 18% (P <or= .05). These findings suggested that <span class="hlt">preconditioning</span> with T(3) reduced proteinuria, improved lipid peroxidation biomarkers, and increased antioxidant enzyme levels in renal I/R injury. PMID:19715835</p> <div class="credits"> <p class="dwt_author">Ferreyra, C; O'Valle, F; Osorio, J M; Moreno, J M; Rodríguez, I; Vargas, F; Osuna, A</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">345</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/15108368"> <span id="translatedtitle">[Pathogenicity basis in medical and social strategies in <span class="hlt">preventive</span> health services].</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Pathogenetic processes inherent in the social reform course <span class="hlt">pre-conditioning</span> an extra high and extra young mortality of population and the worsened physical development of children were analyzed. Four main factors, which confirm that the below processes are involved in the above phenomenon, are defined; they are: CNS (dynamic stereotype of the higher nervous activity) neuroendocrinal regulation (stress), free radical oxidation (phenoptosis) and population gene pool (heterozygosity). Social (deliberate labor motivation) and medical (individual <span class="hlt">prevention</span>) priorities are substantiated to improve the health state in Russia. PMID:15108368</p> <div class="credits"> <p class="dwt_author">Velichkovski?, B T</p> <p class="dwt_publisher"></p> <p class="publishDate">2004-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">346</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2014JCoPh.276..508S"> <span id="translatedtitle">Nonlinear <span class="hlt">preconditioning</span> for efficient and accurate interface capturing in simulation of multicomponent compressible flows</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">Single fluid schemes that rely on an interface function for phase identification in multicomponent compressible flows are widely used to study hydrodynamic flow phenomena in several diverse applications. Simulations based on standard numerical implementation of these schemes suffer from an artificial increase in the width of the interface function owing to the numerical dissipation introduced by an upwind discretization of the governing equations. In addition, monotonicity requirements which ensure that the sharp interface function remains bounded at all times necessitate use of low-order accurate discretization strategies. This results in a significant reduction in accuracy along with a loss of intricate flow features. In this paper we develop a nonlinear transformation based interface capturing method which achieves superior accuracy without compromising the simplicity, computational efficiency and robustness of the original flow solver. A nonlinear map from the signed distance function to the sigmoid type interface function is used to effectively couple a standard single fluid shock and interface capturing scheme with a high-order accurate constrained level set reinitialization method in a way that allows for oscillation-free transport of the sharp material interface. Imposition of a maximum principle, which ensures that the multidimensional <span class="hlt">preconditioned</span> interface capturing method does not produce new maxima or minima even in the extreme events of interface merger or breakup, allows for an explicit determination of the interface thickness in terms of the grid spacing. A narrow band method is formulated in order to localize computations pertinent to the <span class="hlt">preconditioned</span> interface capturing method. Numerical tests in one dimension reveal a significant improvement in accuracy and convergence; in stark contrast to the conventional scheme, the proposed method retains its accuracy and convergence characteristics in a shifted reference frame. Results from the test cases in two dimensions show that the nonlinear transformation based interface capturing method outperforms both the conventional method and an interface capturing method without nonlinear transformation in resolving intricate flow features such as sheet jetting in the shock-induced cavity collapse. The ability of the proposed method in accounting for the gravitational and surface tension forces besides compressibility is demonstrated through a model fully three-dimensional problem concerning droplet splash and formation of a crownlike feature.</p> <div class="credits"> <p class="dwt_author">Shukla, Ratnesh K.</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-11-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">347</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2013AGUFM.S41D..07K"> <span id="translatedtitle">Strategies for visco-acoustic waveform inversion: Parameter resolution, <span class="hlt">preconditioning</span> and regularization</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">Visco-acoustic waveform inversion can potentially yield quantitative images of the distribution of both velocity and the attenuation parameters from seismic data. Simultaneous inversion of velocity and attenuation tend to cause significant ';cross-talk' between the resulting images, reflecting a lack of parameter resolution and indicating the need for <span class="hlt">pre-conditioning</span> and regularization of the inverse problem.We analyse the cross-talk issue by partitioning the inversion parameters into two classes; the velocity parameter class, and the attenuation parameter class. Both parameters are defined at a reference frequency, and a dispersion relation is assumed that describes these parameters at any other frequency. We formulate the model gradient of the objective function at a forward modelling frequency, and convert them to the reference frequency by employing the Jacobian of the coordinate change represented by the dispersion relation. At a given modelling frequency, the Frechet derivatives corresponding to these two parameter classes differ only by a 90 degree phase shift, meaning that the magnitudes of resulting model updates will be unscaled, and will not reflect the expected magnitudes in realistic (Q>>1) media. Due to the lack of scaling, cross-talk will be enhanced by poor subsurface illumination, by errors in kinematics, and by data noise. Initial results from a suite of synthetic cross-hole tests using a three-layer randomly heterogenous model with both intrinsic and extrinsic (scattering) attenuation demonstrate that cross-talk is a significant problem in attenuation inversion. Using the same model, we further show that cross-talk can be suppressed by varying the attenuation scaling term in our <span class="hlt">pre-conditioning</span> operator. This strategy is effective for simultaneous inversion of velocity and attenuation, and for sequential inversion (a two-stage approach in which only the velocity models are recovered in the first stage). Further regularization using a smoothing term applied to the attenuation parameters is also effective in reducing cross-talk, which is often highly oscillatory. The sequential inversion approach restricts the search space for attenuation parameters, and appears to be helpful in retrieving a reliable attenuation model.</p> <div class="credits"> <p class="dwt_author">Kamei, R.; Pratt, R. G.</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-12-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">348</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25419789"> <span id="translatedtitle">Voluntary exercise <span class="hlt">preconditioning</span> activates multiple anti-apoptotic mechanisms and improves neurological recovery after experimental traumatic brain injury.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Physical activity can attenuate neuronal loss, reduce neuroinflammation and facilitate recovery after brain injury. However, little is known about the mechanisms of exercise-induced neuroprotection after traumatic brain injury (TBI), or its modulation of posttraumatic neuronal cell death. Voluntary exercise using a running wheel was conducted for 4 weeks immediately preceding (<span class="hlt">preconditioning</span>) moderate level controlled cortical impact (CCI), a well-established experimental TBI model in mice. Compared to non-exercised controls, exercise <span class="hlt">preconditioning</span> (pre-exercise) improved recovery of sensorimotor performance in the beam walk task, and cognitive/affective functions in the Morris water maze, novel object recognition, and tail-suspension tests. Furthermore, pre-exercise reduced the lesion size; attenuated neuronal loss in the hippocampus, cortex and thalamus; and decreased microglial activation in the cortex. In addition, exercise <span class="hlt">preconditioning</span> activated the BDNF pathway before trauma and amplified the injury-dependent increased in HSP70 expression, thus attenuating key apoptotic pathways. The latter include reduction in CCI-induced up-regulation of pro-apoptotic BH3-only Bcl-2 family molecules (Bid, Puma); decreased mitochondria permeabilization with attenuated release of cytochrome c and AIF; reduced AIF translocation to the nucleus and attenuated caspase activation. Given these neuroprotective actions, voluntary physical exercise may serve to limit the consequences of TBI. PMID:25419789</p> <div class="credits"> <p class="dwt_author">Zhao, Zaorui; Sabirzhanov, Boris; Wu, Junfang; Faden, Alan I; Stoica, Bogdan A</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-11-24</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">349</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://prevention.cancer.gov/programs-resources/programs/prevent/awarded-tasks"> <span id="translatedtitle"><span class="hlt">PREVENT</span> Funded Projects</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.cancer.gov">Cancer.gov</a></p> <p class="result-summary"><span class="hlt">PREVENT</span> Cancer Preclinical Drug Development Program Funded Projects Breast Cancer (vaccines) Plac1 vaccine for breast cancer <span class="hlt">prevention</span> Efficacy of a multi-antigen vaccine in the <span class="hlt">prevention</span> of methynitrosourea-induced mammary cancers (ER+) in female</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">350</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.healthfinder.gov/HealthTopics/Category/everyday-healthy-living/safety/prevent-back-pain"> <span id="translatedtitle"><span class="hlt">Prevent</span> Back Pain</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... Everyday Healthy Living > Safety > <span class="hlt">Prevent</span> Back Pain <span class="hlt">Prevent</span> Back Pain The Basics Take Action! Ver en español Content ... Basics One of the best ways to <span class="hlt">prevent</span> back pain is to keep your back muscles strong. Follow ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">351</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.springerlink.com/index/v8913841757r4625.pdf"> <span id="translatedtitle"><span class="hlt">Preventive</span> Interventions: Overview</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">\\u000a <span class="hlt">Prevention</span> in old age is most appropriately defined by referring to <span class="hlt">prevention</span> of impairments, activity limitations, and inability\\u000a to participate in social activities. Thus, primary <span class="hlt">prevention</span> strives to <span class="hlt">prevent</span> activity limitation and nonparticipation (e.g., guidance on possibilities of refitting the home to <span class="hlt">prevent</span>\\u000a falls). Secondary <span class="hlt">prevention</span> focuses on discovering early signs of activity limitations and taking urgent and relevant steps</p> <div class="credits"> <p class="dwt_author">Kirsten Avlund; Mikkel Vass</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">352</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2006SPIE.6128..178M"> <span id="translatedtitle">Compact <span class="hlt">preconditioned</span> photonic crystal demultiplexers based on combined focusing and superprism effects</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">Wavelength demultiplexing is one of the major applications of unique dispersion properties of photonic crystals (PCs). Possibility of integration and compactness are two main advantages of PC based demultiplexers compared to other demultiplexing techniques for applications including compact spectrometers (for sensory applications) and WDM demultiplexers. Here, we show that resolution and size limitations of conventional superprism-based photonic crystal demultiplexers are caused by the choice of configuration. We suggest an alternative implementation (combining superprism effect and focusing) that improves the performance compared to the conventional implementation in terms of being more compact and relaxing the requirement for divergence angle of the incident beam. We use effective index model to describe the beam behavior inside the photonic crystal region. Using this model, effective indices (second order and third order) are calculated directly from the band structure and are used to find the optimal operation parameters for the demultiplexing device. Detailed calculations show that the required size of <span class="hlt">preconditioned</span> superprism photonic crystal demultiplexers scales up as N 5/2 (N being the number of channels which is proportional to the resolution of the device) which shows significant advantage over N 4 dependence in conventional superprism-based devices, especially for high resolutions required in practical DWDM systems or spectroscopic applications. Structures obtained through optimization have been fabricated in SOI wafers using e-beam writing and ICP etching, and spatial separation of channels (with good isolation) in focusing superprism devices is experimentally demonstrated.</p> <div class="credits"> <p class="dwt_author">Momeni, B.; Huang, J.; Soltani, M.; Askari, M.; Mohammadi, S.; Adibi, A.</p> <p class="dwt_publisher"></p> <p class="publishDate">2006-02-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">353</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://ntrs.nasa.gov/search.jsp?R=19940032140&hterms=american+memory+collection&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D20%26Ntt%3Damerican%2Bmemory%2Bcollection"> <span id="translatedtitle"><span class="hlt">Preconditioned</span> implicit solvers for the Navier-Stokes equations on distributed-memory machines</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p class="result-summary">The GMRES method is parallelized, and combined with local <span class="hlt">preconditioning</span> 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).</p> <div class="credits"> <p class="dwt_author">Ajmani, Kumud; Liou, Meng-Sing; Dyson, Rodger W.</p> <p class="dwt_publisher"></p> <p class="publishDate">1994-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">354</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2015MSSP...50..249W"> <span id="translatedtitle">A <span class="hlt">preconditioned</span> conjugate gradient method for computing eigenvector derivatives with distinct and repeated eigenvalues</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">A <span class="hlt">preconditioned</span> 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.</p> <div class="credits"> <p class="dwt_author">Wu, Baisheng; Yang, Shitong; Li, Zhengguang; Zheng, Shaopeng</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">355</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/11123240"> <span id="translatedtitle">Role of mitochondrial and sarcolemmal K(ATP) channels in ischemic <span class="hlt">preconditioning</span> of the canine heart.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">We tested whether mitochondrial or sarcolemmal ATP-sensitive K(+) (K(ATP)) channels play a key role in ischemic <span class="hlt">preconditioning</span> (IP) in canine hearts. In open-chest beagle dogs, the left anterior descending artery was occluded four times for 5 min each with 5-min intervals of reperfusion (IP), occluded for 90 min, and reperfused for 6 h. IP as well as cromakalim and nicorandil (nonspecific K(ATP) channel openers) markedly limited infarct size (6.3 +/- 1.2, 8.9 +/- 1.9, and 7.2 +/- 1.6%, respectively) compared with the control group (40.9 +/- 4.1%). A selective mitochondrial K(ATP) channel blocker, 5-hydroxydecanoate, partially blunted the limitation of infarct size in the animals subjected to IP and those treated with cromakalim and nicorandil (21.6 +/- 3.8, 25.1 +/- 4.6, and 19.8 +/- 5.2%, respectively). A nonspecific K(ATP) channel blocker, glibenclamide, completely abolished the effect of IP (38.5 +/- 6.2%). Intracoronary or intravenous administration of a mitochondria-selective K(ATP) channel opener, diazoxide, at >100 micromol/l could only partially decrease infarct size (19.5 +/- 4.3 and 20.1 +/- 4.4%, respectively). In conclusion, mitochondrial and sarcolemmal K(ATP) channels independently play an important role in the limitation of infarct size by IP in the canine heart. PMID:11123240</p> <div class="credits"> <p class="dwt_author">Sanada, S; Kitakaze, M; Asanuma, H; Harada, K; Ogita, H; Node, K; Takashima, S; Sakata, Y; Asakura, M; Shinozaki, Y; Mori, H; Kuzuya, T; Hori, M</p> <p class="dwt_publisher"></p> <p class="publishDate">2001-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">356</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3974524"> <span id="translatedtitle">Remote ischemic <span class="hlt">preconditioning</span> as treatment for non-ischemic gastrointestinal disorders: Beyond ischemia-reperfusion injury</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Common gastrointestinal diseases such as radiation enteritis (RE), acute pancreatitis, inflammatory bowel diseases (IBD) and drug-induced hepatotoxicity share pathophysiological mechanisms at the molecular level, mostly involving the activation of many pathways of the immune response, ultimately leading to tissue injury. Increased oxidative stress, inflammatory cytokine release, inflammatory cell infiltration and activation and the up-regulation of inflammatory transcription factors participate in the pathophysiology of these complex entities. Treatment varies in each specific disease, but at least in the cases of RE and IBD immunosuppressors are effective. However, full therapeutic responses are not always achieved. The pathophysiology of ischemia-reperfusion (IR) injury shares many of these mechanisms. Brief and repetitive periods of ischemia in an organ or limb have been shown to protect against subsequent major IR injury in distant organs, a phenomenon called remote ischemic <span class="hlt">preconditioning</span> (RIP). This procedure has been shown to protect the gut, pancreas and liver by modulating many of the same inflammatory mechanisms. Since RIP is safe and tolerable, and has shown to be effective in some recent clinical trials, I suggest that RIP could be used as a physiologically relevant adjunct treatment for non-ischemic gastrointestinal inflammatory conditions. PMID:24707140</p> <div class="credits"> <p class="dwt_author">Camara-Lemarroy, Carlos Rodrigo</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">357</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/22907469"> <span id="translatedtitle">Odour assessment: determining the optimum temperature and time for Tedlar sampling bag <span class="hlt">pre-conditioning</span>.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Odours present in new Tedlar bags can impact the assessment of emissions from sewer collection systems and wastewater treatment plants. Conditioning protocols are needed to minimise the impact of background materials emissions on the sampling and assessment of odourous emissions. Olfactometry analysis has shown that background odour concentrations for new Tedlar bags can be as high as 130 OU(E)/m(3). Experimental studies were undertaken to investigate the impact of different conditioning temperatures in order to determine the optimum temperature for cleaning new Tedlar bags to a level when no detectable odours were present in the sampling bags via dilution olfactometry. For the purpose of this study, new Tedlar bags were cleaned in a temperature-controlled oven that had a constant filtered air flow-rate. From the analysis of odour and volatile organic compounds (VOCs) concentrations found in new Tedlar bags during the cleaning process, it was observed that odour and VOCs concentrations decreased with time. It was also found that the temperature setting plays a significant role in the cleaning of the Tedlar bags as large concentrations of phenols and acetamide, N,N-dimethyl were found in new Tedlar bags and their concentrations decreased following the temperature <span class="hlt">pre-conditioning</span>. PMID:22907469</p> <div class="credits"> <p class="dwt_author">Bokowa, A H</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">358</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/15774507"> <span id="translatedtitle">Tissue <span class="hlt">preconditioning</span> may explain concentric lesions in Baló's type of multiple sclerosis.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Lesions of Baló's concentric sclerosis are characterized by alternating layers of myelinated and demyelinated tissue. The reason for concentric demyelination in this variant of multiple sclerosis is unclear. In the present study we investigated the immunopathology in autopsy tissue of 14 patients with acute multiple sclerosis or fulminant exacerbations of chronic multiple sclerosis with Baló-type lesions in the CNS, focusing on the patterns of tissue injury in actively demyelinating lesions. We found that all active concentric lesions followed a pattern of demyelination that bears resemblances to hypoxia-like tissue injury. This was associated with high expression of inducible nitric oxide synthase in macrophages and microglia. At the edge of active lesions and, less consistently, in the outermost layer of preserved myelin, proteins involved in tissue <span class="hlt">preconditioning</span>, such as hypoxia-inducible factor 1alpha and heat-shock protein 70, were expressed mainly in oligodendrocytes and to a lesser degree also in astrocytes and macrophages. Due to their neuroprotective effects, the rim of periplaque tissue, where these proteins are expressed, may be resistant to further damage in an expanding lesion and may therefore remain as a layer of preserved myelinated tissue. PMID:15774507</p> <div class="credits"> <p class="dwt_author">Stadelmann, Christine; Ludwin, Sam; Tabira, Takeshi; Guseo, Andras; Lucchinetti, Claudia F; Leel-Ossy, Lorant; Ordinario, Artemio T; Brück, Wolfgang; Lassmann, Hans</p> <p class="dwt_publisher"></p> <p class="publishDate">2005-05-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">359</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/8867278"> <span id="translatedtitle">Comparison of the responses to hypoxia, ischaemia and ischaemic <span class="hlt">preconditioning</span> in wild marmot and laboratory rabbit hearts.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">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 (<span class="hlt">preconditioning</span>), the rabbit hearts were protected by this brief ischaemic insult and recovered better than the hearts that had not been subjected to the <span class="hlt">preconditioning</span> ischaemia. This was not true in the marmot hearts, however, as the <span class="hlt">preconditioning</span> ischaemia did not promote a greater recovery over that in its absence. When <span class="hlt">preconditioned</span> marmots hearts were compared with <span class="hlt">preconditioned</span> 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</p> <div class="credits"> <p class="dwt_author">McKean, T; Mendenhall, W</p> <p class="dwt_publisher"></p> <p class="publishDate">1996-03-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">360</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.facingdisability.com/expert-topics/preventing-pressure-sores"> <span id="translatedtitle"><span class="hlt">Preventing</span> Pressure Sores</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.nlm.nih.gov/medlineplus/videosandcooltools.html">MedlinePLUS Videos and Cool Tools</a></p> <p class="result-summary">Experts \\ <span class="hlt">Preventing</span> Pressure Sores Topics Adult Injuries Spinal Cord Injury 101 The Basics of Spinal Cord Injury Rehabilitation <span class="hlt">Preventing</span> Pressure Sores Transition from Hospital to Home Spasticity, Physical ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_17");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' 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src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">361</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3539417"> <span id="translatedtitle">Essential role of nitric oxide in acute ischemic <span class="hlt">preconditioning</span>: S-Nitros(yl)ation versus sGC/cGMP/PKG signaling?</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Nitric oxide (NO) plays an important role in acute ischemic <span class="hlt">preconditioning</span> (IPC). In addition to activating soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathways, NO-mediated protein S-nitros(yl)ation (SNO) has been recently shown to play an essential role in cardioprotection against ischemia–reperfusion (I/R) injury. In our previous studies, we have shown that IPC-induced cardioprotection could be blocked by treatment with either N-nitro-L-arginine methyl ester (L-NAME, a constitutive NO synthase inhibitor) or ascorbate (a reducing agent to decompose SNO). To clarify NO-mediated sGC/cGMP/PKG-dependent or -independent (i.e., SNO) signaling involved in IPC-induced cardioprotection, mouse hearts were Langendorff-perfused in the dark to <span class="hlt">prevent</span> SNO decomposition by light exposure. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, a highly selective inhibitor of sGC) or KT5823 (a potent and selective inhibitor of PKG) did not abolish IPC-induced acute protection, suggesting that the sGC/cGMP/ PKG signaling pathway does not play an important role in NO-mediated cardioprotective signaling during acute IPC. In addition, treatment with ODQ in IPC hearts provided an additional protective effect on functional recovery, in parallel with a higher SNO level in these ODQ+IPC hearts. In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/ cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection. PMID:22989471</p> <div class="credits"> <p class="dwt_author">Sun, Junhui; Aponte, Angel M.; Kohr, Mark J.; Tong, Guang; Steenbergen, Charles; Murphy, Elizabeth</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">362</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25416193"> <span id="translatedtitle">Interval exercise, but not endurance exercise, <span class="hlt">prevents</span> endothelial ischemia-reperfusion injury in healthy subjects.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Endothelial ischemia-reperfusion (I/R) injury importantly contributes to the poor prognosis during ischemic (myocardial) events. <span class="hlt">Preconditioning</span>, i.e., repeated exposure to short periods of ischemia, effectively reduces endothelial I/R injury. In the present study, we examined the hypothesis that exercise has <span class="hlt">preconditioning</span> effects on endothelial I/R injury. Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. In 17 healthy young subjects, we examined changes in brachial artery endothelial function using flow-mediated dilation (FMD) before and after a bout of high-intensity interval exercise, moderate-intensity endurance exercise, or a control intervention. Subsequently, I/R injury was induced by inflation of a blood pressure cuff around the upper arm to 220 mmHg for 20 min and 20 min of reperfusion followed by another FMD measurement. Near-infrared spectrometry was used to examine local tissue oxygenation during exercise. No differences in brachial artery FMD were found at baseline for the three conditions. I/R induced a significant decline in FMD (7.1 ± 2.3 to 4.3 ± 2.3, P < 0.001). When preceded by the interval exercise bout, no change in FMD was present after I/R (7.7 ± 3.1 to 7.2 ± 3.1, P = 0.56), whereas the decrease in FMD after I/R could not be <span class="hlt">prevented</span> by the endurance exercise bout (7.8 ± 3.1 to 3.8 ± 1.7, P < 0.001). In conclusion, a single bout of lower limb interval exercise, but not moderate-intensity endurance exercise, effectively <span class="hlt">prevents</span> brachial artery endothelial I/R injury. This indicates the presence of a remote <span class="hlt">preconditioning</span> effect of exercise, which is selectively present after short-term interval but not continuous exercise in healthy young subjects. PMID:25416193</p> <div class="credits"> <p class="dwt_author">Seeger, Joost P H; Lenting, Charlotte J; Schreuder, Tim H A; Landman, Thijs R J; Timothy Cable, N; Hopman, Maria T E; Thijssen, Dick H J</p> <p class="dwt_publisher"></p> <p class="publishDate">2015-02-15</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">363</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.epa.gov/region5/waste/solidwaste/p2pages/toolbox.htm"> <span id="translatedtitle">Pollution <span class="hlt">Prevention</span> Toolbox</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://nsdl.org/nsdl_dds/services/ddsws1-1/service_explorer.jsp">NSDL National Science Digital Library</a></p> <p class="result-summary">The Pollution <span class="hlt">Prevention</span> Toolbox is a series of four-page fact sheets containing lesson plans and hands-on activities about various pollution <span class="hlt">prevention</span> concepts for schools. Topics include pollution <span class="hlt">prevention</span>, energy conservation, pesticides reduction, and household hazardous waste reduction. The Toolbox also contains sample academic standards and frameworks which the Toolbox meets, and other pollution <span class="hlt">prevention</span> education resources.</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">364</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/17291539"> <span id="translatedtitle"><span class="hlt">Preconditioning</span> with hyperbaric oxygen induces tolerance against oxidative injury via increased expression of heme oxygenase-1 in primary cultured spinal cord neurons.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Hyperbaric oxygen (HBO) <span class="hlt">preconditioning</span> can induce ischemic tolerance in the spinal cord. The effect can be attenuated by the administration of an oxygen free radical scavenger or by inhibition of antioxidant enzymes. However, the mechanism underlying HBO <span class="hlt">preconditioning</span> of neurons against ischemic injury remains enigmatic. Therefore, in the present study primary cultured spinal cord neurons were treated with HBO and then subjected to a hydrogen peroxide (H(2)O(2)) insult. The results show that H(2)O(2) stimulation of the cultured spinal neurons caused severe DNA damage and decreased cell viability, and that these neurons were well protected against damage after a single exposure to HBO <span class="hlt">preconditioning</span> (0.35 MPa, 98% O(2), 37 degrees C, 2 h). The protective effect started 4 h after pretreatment and lasted for at least 24 h. The cultured neurons after HBO treatment also exhibited increased heme oxygenase-1 (HO-1) expression at both the protein and mRNA levels, which paralleled the protective effect of HBO. Treatment with tin-mesoporphyrin IX (SnMP), a specific HO-1 inhibitor, before HBO pretreatment abolished the HBO-induced adaptive protection noted in the cultured spinal neurons. In conclusion, HBO <span class="hlt">preconditioning</span> can protect primary cultured spinal cord neurons against oxidative stress, and the upregulation of HO-1 expression plays an essential role in HBO induced <span class="hlt">preconditioning</span> effect. PMID:17291539</p> <div class="credits"> <p class="dwt_author">Li, Qingbo; Li, Jinsheng; Zhang, Lifan; Wang, Bairen; Xiong, Lize</p> <p class="dwt_publisher"></p> <p class="publishDate">2007-02-27</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">365</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4198105"> <span id="translatedtitle">Exploring the Human Plasma Proteome for Humoral Mediators of Remote Ischemic <span class="hlt">Preconditioning</span> - A Word of Caution</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Despite major advances in early revascularization techniques, cardiovascular diseases are still the leading cause of death worldwide, and myocardial infarctions contribute heavily to this. Over the past decades, it has become apparent that reperfusion of blood to a previously ischemic area of the heart causes damage in and of itself, and that this ischemia reperfusion induced injury can be reduced by up to 50% by mechanical manipulation of the blood flow to the heart. The recent discovery of remote ischemic <span class="hlt">preconditioning</span> (RIPC) provides a non-invasive approach of inducing this cardioprotection at a distance. Finding its endogenous mediators and their operative mode is an important step toward increasing the ischemic tolerance. The release of humoral factor(s) upon RIPC was recently demonstrated and several candidate proteins were published as possible mediators of the cardioprotection. Before clinical applicability, these potential biomarkers and their efficiency must be validated, a task made challenging by the large heterogeneity in reported data and results. Here, in an attempt to reproduce and provide more experimental data on these mediators, we conducted an unbiased in-depth analysis of the human plasma proteome before and after RIPC. From the 68 protein markers reported in the literature, only 28 could be mapped to manually reviewed (Swiss-Prot) protein sequences. 23 of them were monitored in our untargeted experiment. However, their significant regulation could not be reproducibly estimated. In fact, among the 394 plasma proteins we accurately quantified, no significant regulation could be confidently and reproducibly assessed. This indicates that it is difficult to both monitor and reproduce published data from experiments exploring for RIPC induced plasma proteomic regulations, and suggests that further work should be directed towards small humoral factors. To simplify this task, we made our proteomic dataset available via ProteomeXchange, where scientists can mine for novel potential targets. PMID:25333471</p> <div class="credits"> <p class="dwt_author">Helgeland, Erik; Breivik, Lars Ertesvåg; Vaudel, Marc; Svendsen, Øyvind Sverre; Garberg, Hilde; Nordrehaug, Jan Erik; Berven, Frode Steingrimsen; Jonassen, Anne Kristine</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">366</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3871481"> <span id="translatedtitle">Effects of hyperbaric oxygen <span class="hlt">preconditioning</span> on cardiac stress markers after simulated diving</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) can protect the heart from injury during subsequent ischemia. The presence of high loads of venous gas emboli (VGE) induced by a rapid ambient pressure reduction on ascent from diving may cause ischemia and acute heart failure. The aim of this study was to investigate the effect of diving-induced VGE formation on cardiac stress marker levels and the cardioprotective effect of HBO-PC. To induce high loads of VGE, 63 female Sprague–Dawley rats were subjected to a rapid ambient pressure reduction from a simulated saturation dive (50 min at 709 kPa) in a pressure chamber. VGE loads were measured for 60 min in anesthetized animals by the use of ultrasonography. The animals were divided into five groups. Three groups were exposed to either diving or to HBO-PC (100% oxygen, 38 min at 303 kPa) with a 45 or 180 min interval between HBO-PC and diving. Two additional groups were used as baseline controls for the measurements; one group was exposed to equal handling except for HBO-PC and diving, and the other group was completely unexposed. Diving caused high loads of VGE, as well as elevated levels of the cardiac stress markers, cardiac troponin T (cTnT), natriuretic peptide precursor B (Nppb), and ?B-crystallin, in blood and cardiac tissue. There were strong positive correlations between VGE loads and stress marker levels after diving, and HBO-PC appeared to have a cardioprotective effect, as indicated by the lower levels of stress marker expression after diving-induced VGE formation. PMID:24400168</p> <div class="credits"> <p class="dwt_author">Jørgensen, Arve; Foster, Philip P; Brubakk, Alf O; Eftedal, Ingrid</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">367</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23299244"> <span id="translatedtitle">SirT1 mediates hyperbaric oxygen <span class="hlt">preconditioning</span>-induced ischemic tolerance in rat brain.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Our previous studies have shown that hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) induces tolerance to cerebral ischemia/reperfusion (I/R). This study aimed to investigate whether SirT1, a class III histone deacetylase, is involved in neuroprotection elicited by HBO-PC in animal and cell culture models of ischemia. Rats were subjected to middle cerebral artery occlusion for 120?minutes after HBO-PC (once a day for 5 days). Primary cultured cortical neurons were exposed to 2?hours of HBO-PC after 2?hours of oxygen-glucose deprivation (OGD). We showed that HBO-PC increased SirT1 protein and mRNA expression, promoted neurobehavioral score, reduced infarct volume, and improved morphology at 24?hours and 7 days after cerebral I/R. Neuroprotection of HBO-PC was attenuated by SirT1 inhibitor EX527 and SirT1 knockdown by short interfering RNA (siRNA), whereas it was mimicked by SirT1 activator resveratrol. Furthermore, HBO-PC enhanced SirT1 expression and cell viability and reduced lactate dehydrogenase release 24?hours after OGD/re-oxygenation. The neuroprotective effect of HBO-PC was emulated through upregulating SirT1 and, reversely, attenuated through downregulating SirT1. The modulation of SirT1 was made by adenovirus infection carrying SirT1 or SirT1 siRNA. Besides, SirT1 increased B-cell lymphoma 2 (Bcl-2) expression and decrease cleaved caspase 3. These results indicate that SirT1 mediates HBO-PC-induced tolerance to cerebral I/R through inhibition of apoptosis. PMID:23299244</p> <div class="credits"> <p class="dwt_author">Yan, Wenjun; Fang, Zongping; Yang, Qianzi; Dong, Hailong; Lu, Yan; Lei, Chong; Xiong, Lize</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-03-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">368</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3587810"> <span id="translatedtitle">SirT1 mediates hyperbaric oxygen <span class="hlt">preconditioning</span>-induced ischemic tolerance in rat brain</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Our previous studies have shown that hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) induces tolerance to cerebral ischemia/reperfusion (I/R). This study aimed to investigate whether SirT1, a class III histone deacetylase, is involved in neuroprotection elicited by HBO-PC in animal and cell culture models of ischemia. Rats were subjected to middle cerebral artery occlusion for 120?minutes after HBO-PC (once a day for 5 days). Primary cultured cortical neurons were exposed to 2?hours of HBO-PC after 2?hours of oxygen–glucose deprivation (OGD). We showed that HBO-PC increased SirT1 protein and mRNA expression, promoted neurobehavioral score, reduced infarct volume, and improved morphology at 24?hours and 7 days after cerebral I/R. Neuroprotection of HBO-PC was attenuated by SirT1 inhibitor EX527 and SirT1 knockdown by short interfering RNA (siRNA), whereas it was mimicked by SirT1 activator resveratrol. Furthermore, HBO-PC enhanced SirT1 expression and cell viability and reduced lactate dehydrogenase release 24?hours after OGD/re-oxygenation. The neuroprotective effect of HBO-PC was emulated through upregulating SirT1 and, reversely, attenuated through downregulating SirT1. The modulation of SirT1 was made by adenovirus infection carrying SirT1 or SirT1 siRNA. Besides, SirT1 increased B-cell lymphoma 2 (Bcl-2) expression and decrease cleaved caspase 3. These results indicate that SirT1 mediates HBO-PC-induced tolerance to cerebral I/R through inhibition of apoptosis. PMID:23299244</p> <div class="credits"> <p class="dwt_author">Yan, Wenjun; Fang, Zongping; Yang, Qianzi; Dong, Hailong; Lu, Yan; Lei, Chong; Xiong, Lize</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">369</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3713468"> <span id="translatedtitle">Hypercholesterolemia blunts NO donor-induced late <span class="hlt">preconditioning</span> against myocardial infarction in conscious rabbits</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Although NO donors have been shown to confer late <span class="hlt">preconditioning</span> (PC) against myocardial ischemia/reperfusion injury in healthy rabbits, it is unknown whether concurrent systemic disorders affect NO donor-induced cardioprotection. Since many patients with coronary artery disease have hypercholesterolemia (HC), we examined the effect of this condition on late PC induced by the NO donor diethylenetriamine/nitric oxide (DETA/NO). Chronically instrumented rabbits were fed a normal diet (normocholesterolemia, NC) or a diet enriched with 1% cholesterol (HC) for 4 weeks. Plasma cholesterol levels were significantly elevated and the arterial pressure response to the endothelium-dependent vasodilator bradykinin was blunted in cholesterol diet-fed rabbits. Conscious rabbits underwent a 30-minute coronary occlusion followed by 3 days of reperfusion. When NC rabbits were pretreated with DETA/NO (0.1 mg/kg, i.v. × 4, group II, n = 7) 24 hours before the 30-minute occlusion, infarct size was reduced by 52% (29.7 ± 3.4% versus 62.4 ± 4.0% of the region at risk in NC controls [group I, n = 5], P < 0.05), indicating that DETA/NO induced a late PC effect against myocardial infarction. In contrast, when HC rabbits were pretreated with the same dose of DETA/NO (group IV, n = 6), infarct size was not significantly reduced (61.0 ± 5.7% versus 68.1 ± 4.5% of the region at risk in HC [group III, n = 5], P = NS), suggesting that DETA/NO failed to induce a delayed cardioprotective effect. These data demonstrate, for the first time, that HC blunts NO donor-induced late PC against myocardial infarction, implying that the inhibitory effects of HC on ischemia-induced and NO donor-induced late PC are caused by disruption of biochemical pathways distal to the generation of NO that triggers these adaptations. PMID:15372283</p> <div class="credits"> <p class="dwt_author">Tang, Xian-Liang; Stein, Adam B.; Shirk, Gregg</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">370</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3389686"> <span id="translatedtitle">Effects of a <span class="hlt">Preconditioning</span> Oral Nutritional Supplement on Pig Livers after Warm Ischemia</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background. Several approaches have been proposed to pharmacologically ameliorate hepatic ischemia/reperfusion injury (IRI). This study was designed to evaluate the effects of a <span class="hlt">preconditioning</span> oral nutritional supplement (pONS) containing glutamine, antioxidants, and green tea extract on hepatic warm IRI in pigs. Methods. pONS (70?g per serving, Fresenius Kabi, Germany) was dissolved in 250?mL tap water and given to pigs 24, 12, and 2?hrs before warm ischemia of the liver. A fourth dose was given 3?hrs after reperfusion. Controls were given the same amount of cellulose with the same volume of water. Two hours after the third dose of pONS, both the portal vein and the hepatic artery were clamped for 40?min. 0.5, 3, 6, and 8?hrs after reperfusion, heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), portal venous flow (PVF), hepatic arterial flow (HAF), bile flow, and transaminases were measured. Liver tissue was taken 8?hrs after reperfusion for histology and immunohistochemistry. Results. HR, MAP, CVP, HAF, and PVF were comparable between the two groups. pONS significantly increased bile flow 8?hrs after reperfusion. ALT and AST were significantly lower after pONS. Histology showed significantly more severe necrosis and neutrophil infiltration in controls. pONS significantly decreased the index of immunohistochemical expression for TNF-?, MPO, and cleaved caspase-3 (P < 0.001). Conclusion. Administration of pONS before and after tissue damage protects the liver from warm IRI via mechanisms including decreasing oxidative stress, lipid peroxidation, apoptosis, and necrosis. PMID:22791934</p> <div class="credits"> <p class="dwt_author">Nickkholgh, Arash; Li, Zhanqing; Yi, Xue; Mohr, Elvira; Liang, Rui; Mikalauskas, Saulius; Gross, Marie-Luise; Zorn, Markus; Benzing, Steffen; Schneider, Heinz; Büchler, Markus W.; Schemmer, Peter</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">371</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/19631642"> <span id="translatedtitle">Mitogen-activated protein kinase p38alpha and retinal ischemic <span class="hlt">preconditioning</span>.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">In previous studies, inhibition of mitogen-activated protein kinase (MAP) p38 significantly improved recovery and attenuated apoptosis after retinal ischemia in rats. Yet, ischemic <span class="hlt">preconditioning</span> (IPC) attenuated the ischemia-induced increase in p38 expression. We hypothesized that p38 was required for induction of ischemic tolerance by IPC. We examined the mechanisms of involvement of p38 in IPC neuroprotection. IPC or ischemia was induced in rat retina in vivo. Recovery after ischemia performed 24h after IPC was assessed functionally (electroretinography) and histologically at 7d after ischemia in the presence or absence of inhibition of p38. We examined the role of p38alpha in the mimicking of IPC produced by opening mitochondrial KATP channels using diazoxide, or stimulation of p38 activation by anisomycin. The importance of adenosine receptors in p38 activation after IPC was assessed using specific blockers of adenosine A1 and A2a receptors. Interfering RNA (siRNA) or SB203580 was used to block p38alpha. Phosphorylated p38 levels were measured. Phosphorylated p38 protein increased with IPC. Interfering RNA (siRNA) to p38alpha prior to IPC, or inhibiting p38 activation with SB203580, with ischemia following 24h later, significantly attenuated the neuroprotective effect of IPC. Anisomycin administered to increase p38 mimicked IPC, an effect blocked by SB203580. IPC-mimicking with diazoxide, an opener of mitochondrial KATP channels, was diminished with p38alpha siRNA. Adenosine receptor blockade did not decrease the elevated levels of phosphorylated p38 after IPC. Specific inhibition of p38alpha suggests that this MAPK is involved in the protective effects of IPC, and that p38 is downstream of mitochondrial KATP channels, but not adenosine receptors, in this neuroprotection. PMID:19631642</p> <div class="credits"> <p class="dwt_author">Dreixler, John C; Barone, Frank C; Shaikh, Afzhal R; Du, Eugenie; Roth, Steven</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-11-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">372</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3125073"> <span id="translatedtitle">Cardiac-specific overexpression of GTP cyclohydrolase 1 restores ischaemic <span class="hlt">preconditioning</span> during hyperglycaemia</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Aims Hyperglycaemia (HG) decreases intracellular tetrahydrobiopterin (BH4) concentrations, and this action may contribute to injury during myocardial ischaemia and reperfusion. We investigated whether increased BH4 by cardiomyocyte-specific overexpression of the GTP cyclohydrolase (GTPCH) 1 gene rescues myocardial and mitochondrial protection by ischaemic <span class="hlt">preconditioning</span> (IPC) during HG through a nitric oxide (NO)-dependent pathway. Methods and results Mice underwent 30 min of myocardial ischaemia followed by 2 h of reperfusion with or without IPC elicited with four cycles of 5 min ischaemia/5 min of reperfusion in the presence or absence of HG produced by d-glucose. In C57BL/6 wild-type mice, IPC increased myocardial BH4 and NO concentrations and decreased myocardial infarct size (30 ± 3% of risk area) compared with control (56 ± 5%) experiments. This protective effect was inhibited by HG (48 ± 3%) but not hyperosmolarity. GTPCH-1 overexpression increased myocardial BH4 and NO concentrations and restored cardioprotection by IPC during HG (32 ± 4%). In contrast, a non-selective NO synthase inhibitor NG-nitro-l-arginine methyl ester attenuated the favourable effects of GTPCH-1 overexpression (52 ± 3%) during HG. Mitochondria isolated from myocardium subjected to IPC required significantly higher in vitro Ca2+ concentrations (184 ± 14 µmol mg?1 protein) to open the mitochondrial permeability transition pore when compared with mitochondria isolated from control experiments (142 ± 10 µmol mg?1 protein). This beneficial effect of IPC was reversed by HG and rescued by GTPCH-1 overexpression. Conclusion Increased BH4 by cardiomyocyte-specific overexpression of GTPCH-1 preserves the ability of IPC to elicit myocardial and mitochondrial protection that is impaired by HG, and this action appears to be dependent on NO. PMID:21422102</p> <div class="credits"> <p class="dwt_author">Ge, Zhi-Dong; Ionova, Irina A.; Vladic, Nikolina; Pravdic, Danijel; Hirata, Naoyuki; Vásquez-Vivar, Jeannette; Pratt, Phillip F.; Warltier, David C.; Pieper, Galen M.; Kersten, Judy R.</p> <p class="dwt_publisher"></p> <p class="publishDate">2011-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">373</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3702658"> <span id="translatedtitle">Ischemic <span class="hlt">preconditioning</span> attenuates lipid peroxidation and apoptosis in the cecal ligation and puncture model of sepsis</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Sepsis and septic shock are are among the major causes of mortality in intensive care units. The lung and kidney are the organs most affected by sepsis. Evidence exists that lipid peroxidation and apoptosis may be responsible for the high mortality due to sepsis. Ischemic <span class="hlt">preconditioning</span> (IP) is a method for the protection of tissues and organs against ischemia/reperfusion injury by reducing reactive oxygen species levels, lipid peroxidation and apoptosis. In the present study, the effects of IP were investigated in cecal ligation and puncture (CLP)-induced sepsis in rats. The three groups of animals used in the present controlled study were the sham-operated group (sham, n=7), which only underwent a laparotomy; the sepsis group (sepsis, n=7), which underwent cecal ligation and perforation; and the IP + sepsis group (IP+sepsis, n=7), which underwent CLP immediately prior to the application of three cycles of IP to the hind limb. The study was terminated at 6 h after the induction of CLP. Blood, kidney and lung tissue samples were collected for the determination of serum creatinine, blood urea nitrogen (BUN), neutrophil gelatinase-associated lipocalin (NGAL) and lung tissue malondialdehyde (MDA) levels, as well as histological examination. The serum creatinine, plasma NGAL and lung tissue MDA levels in the sepsis group were significantly increased compared with those in the sham and the IP+sepsis groups (P<0.05). Alveolar macrophage counts, histological kidney and lung injury scores, kidney (caspase 3) and lung tissue immuonreactivity (M30) scores in the sepsis group were also significantly increased compared with those in the sham and IP+sepsis groups (P<0.05). The alveolar macrophage count in the IP+sepsis group was increased compared with that in the sham group (P<0.05). In conclusion, IP inhibits lipid peroxidation and attenuates histological injury and apoptosis in the lung and kidney during sepsis. PMID:23837035</p> <div class="credits"> <p class="dwt_author">OLGUNER, ÇIMEN GÜLBEN; KOCA, U?UR; ALTEKIN, EMEL; ERGÜR, BEKIR U?UR; DURU, SEDEN; GIRGIN, PELIN; TA?DÖ?EN, AYDIN; GÜNDÜZ, KERIM; GÜZELDA?, SEDA; AKKU?, MUHAMMED; MICILI, SERAP CILAKER</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">374</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3351373"> <span id="translatedtitle">Hyperbaric oxygen <span class="hlt">preconditioning</span> attenuates hyperglycemia enhanced hemorrhagic transformation after transient MCAO in rats</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background Hemorrhagic transformation (HT) can be a devastating complication of ischemic stroke. Hyperbaric oxygen <span class="hlt">preconditioning</span> (HBO-PC) has been shown to improve blood-brain barrier (BBB) permeability in stroke models. The purpose of this study is to examine whether HBO-PC attenuates HT after focal cerebral ischemia, and to investigate whether the mechanism of HBO-PC against HT includes up-regulation of antioxidants in hyperglycemic rats. Methods Male Sprague-Dawley rats (280-320 g) were divided into the following groups: sham, middle cerebral artery occlusion (MCAO) for 2 h, and MCAO treated with HBO-PC. HBO-PC was conducted giving 100% oxygen at 2.5 atm absolute (ATA), for 1 h at every 24 h interval for 5 days. At 24 h after the last session of HBO-PC, rats received an injection of 50% glucose (6 ml/kg intraperitoneally) and were subjected to MCAO 15 min later. At 24 h after MCAO, neurological behavior tests, infarct volume, blood-brain barrier permeability, and hemoglobin content were measured to evaluate the effect of HBO-PC. Western blot analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was evaluated at multiple time-points before and after MCAO. Results HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO. Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO. Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group. Conclusions HBO-PC improved neurological deficits, infarction volume, BBB disruption, and HT after focal cerebral ischemia. However, its mechanism against focal cerebral ischemia and HT may not include activation of Nrf2 and subsequent HO-1 expression. PMID:22494892</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">375</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2944496"> <span id="translatedtitle">Molecular mechanisms mediating <span class="hlt">preconditioning</span> following chronic ischemia differ from those in classical second window</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">A major difference between experimental ischemic <span class="hlt">preconditioning</span> (IPC), induced by brief ischemic episodes, and the clinical situation is that patients generally have repetitive episodes of ischemia. We used a swine model to examine differences in genes regulated by classical second-window IPC (SWOP) [two 10-min episodes of coronary artery occlusion (CAO) followed by 24 h reperfusion] compared with repetitive CAO/reperfusion (RCO), i.e., two 10-min CAO 12 h apart, and to repetitive coronary stenosis (RCS), six episodes of 90 min coronary stenosis 12 h apart (n = 5/group). All three models reduced infarct size by 60–85%, which was mediated by nitric oxide in SWOP but not in the other two models. We employed microarray analyses to discover additional molecular pathways intrinsic to models of repetitive ischemia and different from classical SWOP. There was an 85% homology in gene response between the RCO and RCS models, whereas SWOP was qualitatively different. Both RCO and RCS, but not SWOP, showed downregulation of genes encoding proteins involved in oxidative metabolism and upregulation of genes involved in protein synthesis, unfolded protein response, autophagy, heat shock response, protein secretion, and an activation of the NF-?B signaling pathway. Therefore, the regulated genes mediating IPC with repetitive ischemia differ radically from SWOP both quantitatively and qualitatively, showing that a repetitive pattern of ischemia, rather than the difference between no-flow vs. low-flow ischemia, dictates the genomic response of the heart. These findings illustrate new cardioprotective mechanisms developed by repetitive IPC, which are potentially more relevant to patients with chronic ischemic heart disease, who are subjected to repetitive episodes of ischemia. PMID:20581088</p> <div class="credits"> <p class="dwt_author">Park, Ji Yeon; Shen, You-Tang; Zhao, Xin; Qiu, Hongyu; Yan, Lin; Tian, Bin; Vatner, Stephen F.; Vatner, Dorothy E.</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">376</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2920351"> <span id="translatedtitle">Metabolic <span class="hlt">Preconditioning</span> of Cells with AICAR-Riboside: Improved Cryopreservation and Cell-Type Specific Impacts on Energetics and Proliferation</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">In species whose evolutionary history has provided natural tolerance to dehydration and freezing, metabolic depression is often a pre-requisite for survival. We tested the hypothesis that <span class="hlt">preconditioning</span> of mammalian cells with 5-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside (AICAR) to achieve metabolic depression will promote greater survivorship during cryopreservation. AICAR is used extensively to stimulate AMP-activated protein kinase (AMPK), which can result in downregulation of biosynthetic processes. We showed that the metabolic interconversion of AICAR was cell-type dependent. Accumulation of 5-aminoimidazole-4-carboxamide-1b-D-ribofuranosyl-5?-monophosphate (ZMP), as well as other metabolites that possess multiple phosphates (i.e., ZDP, ZTP), varied approximately 3.5-fold across the cell lines tested. AICAR treatment also significantly influenced the concentrations of cellular adenylates (ATP, ADP, AMP). Depression of cell metabolism and proliferation with AICAR treatment differed among cell lines. Proliferation for a given cell line was negatively correlated with the fold-increase achieved in the ‘effective adenylate ratio’ ([AMP]+[ZMP])/[ATP]) after AICAR treatment. Metabolic <span class="hlt">preconditioning</span> with AICAR promoted a significant increase in viability post-freezing in J774.A1 macrophages, HepG2/C3A cells and primary hepatocytes but not in NIH/3T3 fibroblasts or OMK cells. The effect of AICAR on viability after freezing was positively correlated (r2 = 0.94) with the fold-increase in the ‘effective adenylate ratio’. Thus for each cell line, the greater the depression of metabolism and proliferation due to <span class="hlt">preconditioning</span> with AICAR, the greater was the survivorship post-freezing. PMID:20510224</p> <div class="credits"> <p class="dwt_author">Menze, Michael A.; Chakraborty, Nilay; Clavenna, Matthew; Banerjee, Mitali; Liu, Xiang-Hong; Toner, Mehmet; Hand, Steven C.</p> <p class="dwt_publisher"></p> <p class="publishDate">2010-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">377</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2568984"> <span id="translatedtitle">Reactive Oxygen Species and Mitochondrial KATP Channels Mediate Helium-Induced <span class="hlt">Preconditioning</span> Against Myocardial Infarction In Vivo</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Objectives Helium produces <span class="hlt">preconditioning</span> by activating prosurvival kinases, but the roles of reactive oxygen species (ROS) or mitochondrial KATP channels in this process are unknown. We tested the hypothesis that ROS and mitochondrial KATP channels mediate helium-induced <span class="hlt">preconditioning</span> in vivo. Design Randomized, prospective study. Setting University research laboratory. Participants Male New Zealand white rabbits. Interventions Rabbits (n=64) were instrumented for measurement of systemic hemodynamics and subjected to a 30 min left anterior descending coronary artery (LAD) occlusion and 3 h reperfusion. In separate experimental groups, rabbits (n=7 or 8 per group) were randomly assigned to receive 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before LAD occlusion with or without the ROS scavengers N-acetylcysteine (NAC; 150 mg/kg) or N-2-mercaptoproprionyl glycine (2-MPG; 75 mg/kg), or the mitochondrial KATP antagonist 5-hydroxydecanoate (5-HD; 5 mg/kg). Statistical analysis of data was performed with analysis of variance for repeated measures followed by Bonferroni's modification of Student's t test. Measurements and Main Results Myocardial infarct size was determined using triphenyltetrazolium chloride staining and presented as a percentage of the left ventricular area at risk. Helium significantly (P<0.05) reduced infarct size (23±4% of the area at risk; mean±SD) compared with control (46±3%). NAC, 2-MPG, and 5-HD did not affect irreversible ischemic injury when administered alone (49±5, 45±6, and 45±3%), but these drugs blocked reductions in infarct size produced by helium (45±4, 45±2, and 44±3%). Conclusions The results suggest that ROS and mitochondrial KATP channels mediate helium-induced <span class="hlt">preconditioning</span> in vivo. PMID:18662630</p> <div class="credits"> <p class="dwt_author">Pagel, Paul S.; Krolikowski, John G.; Pratt, Phillip F.; Shim, Yon Hee; Amour, Julien; Warltier, David C.; Weihrauch, Dorothee</p> <p class="dwt_publisher"></p> <p class="publishDate">2008-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">378</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://adsabs.harvard.edu/abs/2014GeoJI.197.1442K"> <span id="translatedtitle">Algebraic multigrid <span class="hlt">preconditioning</span> within parallel finite-element solvers for 3-D electromagnetic modelling problems in geophysics</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://adsabs.harvard.edu/abstract_service.html">NASA Astrophysics Data System (ADS)</a></p> <p class="result-summary">We present an elaborate <span class="hlt">preconditioning</span> scheme for Krylov subspace methods which has been developed to improve the performance and reduce the execution time of parallel node-based finite-element (FE) solvers for 3-D electromagnetic (EM) numerical modelling in exploration geophysics. This new preconditioner is based on algebraic multigrid (AMG) that uses different basic relaxation methods, such as Jacobi, symmetric successive over-relaxation (SSOR) and Gauss-Seidel, as smoothers and the wave front algorithm to create groups, which are used for a coarse-level generation. We have implemented and tested this new preconditioner within our parallel nodal FE solver for 3-D forward problems in EM induction geophysics. We have performed series of experiments for several models with different conductivity structures and characteristics to test the performance of our AMG <span class="hlt">preconditioning</span> technique when combined with biconjugate gradient stabilized method. The results have shown that, the more challenging the problem is in terms of conductivity contrasts, ratio between the sizes of grid elements and/or frequency, the more benefit is obtained by using this preconditioner. Compared to other <span class="hlt">preconditioning</span> schemes, such as diagonal, SSOR and truncated approximate inverse, the AMG preconditioner greatly improves the convergence of the iterative solver for all tested models. Also, when it comes to cases in which other preconditioners succeed to converge to a desired precision, AMG is able to considerably reduce the total execution time of the forward-problem code-up to an order of magnitude. Furthermore, the tests have confirmed that our AMG scheme ensures grid-independent rate of convergence, as well as improvement in convergence regardless of how big local mesh refinements are. In addition, AMG is designed to be a black-box preconditioner, which makes it easy to use and combine with different iterative methods. Finally, it has proved to be very practical and efficient in the parallel context.</p> <div class="credits"> <p class="dwt_author">Koldan, Jelena; Puzyrev, Vladimir; de la Puente, Josep; Houzeaux, Guillaume; Cela, José María</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-06-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">379</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3498359"> <span id="translatedtitle">Cardiac Protection by <span class="hlt">Preconditioning</span> Is Generated via an Iron-Signal Created by Proteasomal Degradation of Iron Proteins</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Ischemia associated injury of the myocardium is caused by oxidative damage during reperfusion. Myocardial protection by ischemic <span class="hlt">preconditioning</span> (IPC) was shown to be mediated by a transient ‘iron-signal’ that leads to the accumulation of apoferritin and sequestration of reactive iron released during the ischemia. Here we identified the source of this ‘iron signal’ and evaluated its role in the mechanisms of cardiac protection by hypoxic <span class="hlt">preconditioning</span>. Rat hearts were retrogradely perfused and the effect of proteasomal and lysosomal protease inhibitors on ferritin levels were measured. The iron-signal was abolished, ferritin levels were not increased and cardiac protection was diminished by inhibition of the proteasome prior to IPC. Similarly, double amounts of ferritin and better recovery after ex vivo ischemia-and-reperfusion (I/R) were found in hearts from in vivo hypoxia <span class="hlt">pre-conditioned</span> animals. IPC followed by normoxic perfusion for 30 min (‘delay’) prior to I/R caused a reduced ferritin accumulation at the end of the ischemia phase and reduced protection. Full restoration of the IPC-mediated cardiac protection was achieved by employing lysosomal inhibitors during the ‘delay’. In conclusion, proteasomal protein degradation of iron-proteins causes the generation of the ‘iron-signal’ by IPC, ensuing de-novo apoferritin synthesis and thus, sequestering reactive iron. Lysosomal proteases are involved in subsequent ferritin breakdown as revealed by the use of specific pathway inhibitors during the ‘delay’. We suggest that proteasomal iron-protein degradation is a stress response causing an expeditious cytosolic iron release thus, altering iron homeostasis to protect the myocardium during I/R, while lysosomal ferritin degradation is part of housekeeping iron homeostasis. PMID:23155431</p> <div class="credits"> <p class="dwt_author">Bulvik, Baruch E.; Berenshtein, Eduard; Meyron-Holtz, Esther G.</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">380</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://repository.tamu.edu/handle/1969.1/ETD-TAMU-1999-THESIS-C34"> <span id="translatedtitle">A robust locally <span class="hlt">preconditioned</span> semi-coarsening multigrid algorithm for the 2-D Navier-Stokes equations</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">'ourier error u&ode ivith grid iva&venumber (0, Fla) at it?i ation ii. I? tivo-diin&&n?i&mal Eouri?r?piic?. vvav&? wil, h 0 & 0? &epr&'??nt Iow frequency error mo?les in r and z & 0, & &r r?pre?&'nt 1&igb fn qnm&cv & rror &nodes ii& s? 6'aves in 0 can... convergence ralcs &vere scen ivlicn inatrix <span class="hlt">preconditioning</span> ivas coupled with . I-coarsening (co;irscning only in the . 1 direction). B. Thesis goals In this thesis, the performance of a multigrid algorithm for an upwind discretization of the two...</p> <div class="credits"> <p class="dwt_author">Cain, Michael D</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-06-07</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_18");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' 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showDiv("page_21");' href="#" title="Next Page"> <img id="NextPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">381</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3504536"> <span id="translatedtitle">Improved resistance to ischemia and reperfusion, but impaired protection by ischemic <span class="hlt">preconditioning</span> in patients with type 1 diabetes mellitus: a pilot study</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background In patients with type 1 diabetes mellitus (T1DM), cardiovascular events are more common, and the outcome following a myocardial infarction is worse than in nondiabetic subjects. Ischemic or pharmacological <span class="hlt">preconditioning</span> are powerful interventions to reduce ischemia reperfusion (IR)-injury. However, animal studies have shown that the presence of T1DM can limit these protective effects. Therefore, we aimed to study the protective effect of ischemic <span class="hlt">preconditioning</span> in patients with T1DM, and to explore the role of plasma insulin and glucose on this effect. Methods 99mTechnetium-annexin A5 scintigraphy was used to detect IR-injury. IR-injury was induced by unilateral forearm ischemic exercise. At reperfusion, Tc-annexin A5 was administered, and IR-injury was expressed as the percentage difference in radioactivity in the thenar muscle between the experimental and control arm 4 hours after reperfusion. 15 patients with T1DM were compared to 21 nondiabetic controls. The patients were studied twice, with or without ischemic <span class="hlt">preconditioning</span> (10 minutes of forearm ischemia and reperfusion). Patients were studied in either normoglycemic hyperinsulinemic conditions (n?=?8) or during hyperglycemic normoinsulinemia (n?=?7). The controls were studied once either with (n?=?8) or without (n?=?13) ischemic <span class="hlt">preconditioning</span>. Results Patients with diabetes were less vulnerable to IR-injury than nondiabetic healthy controls (12.8?±?2.4 and 11.0?±?5.1% versus 27.5?±?4.5% in controls; p?<?0.05). The efficacy of ischemic <span class="hlt">preconditioning</span> to reduce IR-injury, however, was lower in the patients and was even completely abolished during hyperglycemia. Conclusions Patients with T1DM are more tolerant to forearm IR than healthy controls in our experimental model. The efficacy of ischemic <span class="hlt">preconditioning</span> to limit IR-injury, however, is reduced by acute hyperglycemia. Trial Registration The study is registered at www.clinicaltrials.gov (NCT00184821) PMID:23051145</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">382</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/biblio/22215256"> <span id="translatedtitle">Involvement of SIRT1 in hypoxic down-regulation of c-Myc and ?-catenin and hypoxic <span class="hlt">preconditioning</span> effect of polyphenols</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">SIRT1 has been found to function as a Class III deacetylase that affects the acetylation status of histones and other important cellular nonhistone proteins involved in various cellular pathways including stress responses and apoptosis. In this study, we investigated the role of SIRT1 signaling in the hypoxic down-regulations of c-Myc and ?-catenin and hypoxic <span class="hlt">preconditioning</span> effect of the red wine polyphenols such as piceatannol, myricetin, quercetin and resveratrol. We found that the expression of SIRT1 was significantly increased in hypoxia-exposed or hypoxic <span class="hlt">preconditioned</span> HepG2 cells, which was closely associated with the up-regulation of HIF-1? and down-regulation of c-Myc and ?-catenin expression via deacetylation of these proteins. In addition, blockade of SIRT1 activation using siRNA or amurensin G, a new potent SIRT1 inhibitor, abolished hypoxia-induced HIF-1? expression but increased c-Myc and ?-catenin expression. SIRT1 was also found to stabilize HIF-1? protein and destabilize c-Myc, ?-catenin and PHD2 under hypoxia. We also found that myricetin, quercetin, piceatannol and resveratrol up-regulated HIF-1? and down-regulated c-Myc, PHD2 and ?-catenin expressions via SIRT1 activation, in a manner that mimics hypoxic <span class="hlt">preconditioning</span>. This study provides new insights of the molecular mechanisms of hypoxic <span class="hlt">preconditioning</span> and suggests that polyphenolic SIRT1 activators could be used to mimic hypoxic/ischemic <span class="hlt">preconditioning</span>. -- Graphical abstract: Polyphenols mimicked hypoxic <span class="hlt">preconditioning</span> by up-regulating HIF-1? and SIRT1 and down-regulating c-Myc, PHD2, and ?-catenin. HepG2 cells were pretreated with the indicated doses of myricetin (MYR; A), quercetin (QUR; B), or piceatannol (PIC; C) for 4 h and then exposed to hypoxia for 4 h. Levels of HIF-1?, SIRT1, c-Myc, ?-catenin, and PHD2 were determined by western blot analysis. The data are representative of three individual experiments. Highlights: ? SIRT1 expression is increased in hypoxia-exposed or hypoxic <span class="hlt">preconditioned</span> cells. ? SIRT1 deacetylates c-Myc and ?-catenin ? HIF-1? is up-regulated by down-regulation of c-Myc and ?-catenin expression. ? Polyphenolic SIRT1 activators mimics hypoxic <span class="hlt">preconditioning</span>.</p> <div class="credits"> <p class="dwt_author">Hong, Kyung-Soo [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Park, Jun-Ik [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of)] [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Mi-Ju; Kim, Hak-Bong; Lee, Jae-Won [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Dao, Trong Tuan; Oh, Won Keun [BK21 Project Team, College of Pharmacy, Chosun University, Gwangju (Korea, Republic of)] [BK21 Project Team, College of Pharmacy, Chosun University, Gwangju (Korea, Republic of); Kang, Chi-Dug, E-mail: kcdshbw@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of)] [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Sun-Hee, E-mail: ksh7738@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of)</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-03-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">383</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/1919586"> <span id="translatedtitle">Hypothermia <span class="hlt">prevents</span> the ischemia-induced translocation and inhibition of protein kinase C in the rat striatum.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">The effect of hypothermia on the ischemia-induced changes in the subcellular distribution of protein kinase C (PKC) (gamma), -(beta II), and -(alpha) and the activity of PKC was studied in striatal homogenates of rats subjected to 20 min of cerebral ischemia. The effect of <span class="hlt">postischemic</span> cooling was also studied. During normothermic ischemia, PKC(gamma) and -(beta II) increased 3.9- and 2.9-fold, respectively, in the particulate fraction, signifying a translocation of PKC to cell membranes. The levels of PKC(alpha) did not change significantly. PKC activity decreased during ischemia by 52% and 47% (p less than 0.05) in the particulate and cytosolic fractions, respectively, and remained inhibited for the 1 h recovery period. In hypothermic animals, there was no evidence of translocation, and the inhibition of PKC activity was completely abolished. Hypothermia induced in the recovery phase, however, did not affect PKC distribution or activity. The protective effect of intraischemic hypothermia may in part be due to the <span class="hlt">prevention</span> of the ischemia-induced translocation and subsequent downregulation of PKC, possibly through a temperature-dependent modification of the cell membranes. PMID:1919586</p> <div class="credits"> <p class="dwt_author">Cardell, M; Boris-Möller, F; Wieloch, T</p> <p class="dwt_publisher"></p> <p class="publishDate">1991-11-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">384</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www2.carleton.ca/ehs/ccms/wp-content/ccms-files/WorkplaceViolencePreventionProgram_March20111.pdf"> <span id="translatedtitle">Workplace Violence <span class="hlt">Prevention</span> Program</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">Workplace Violence <span class="hlt">Prevention</span> Program March 2011 Carleton University: committed to respect and safety in the workplace #12;Carleton University Workplace Violence <span class="hlt">Prevention</span> Program Page 2 of 26 rev............................................................................................................................. 4 V. Roles and Responsibilities: Workplace Violence</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">385</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www2.carleton.ca/ehs/ccms/wp-content/ccms-files/WorkplaceViolencePreventionProgram_Feb2011.pdf"> <span id="translatedtitle">Workplace Violence <span class="hlt">Prevention</span> Program</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">Workplace Violence <span class="hlt">Prevention</span> Program January 2011 Carleton University: committed to respect and safety in the workplace #12;Carleton University Workplace Violence <span class="hlt">Prevention</span> Program Page 2 of 27............................................................................................................................. 4 V. Roles and Responsibilities: Workplace Violence</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">386</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.cdc.gov/nceh/lead/tips.htm"> <span id="translatedtitle">Lead Poisoning <span class="hlt">Prevention</span> Tips</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... can become contaminated from household dust or exterior soil. Both are known lead sources. Regularly wet-mop ... entering the house to <span class="hlt">prevent</span> bringing lead-contaminated soil in from outside. <span class="hlt">Prevent</span> children from playing in ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">387</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://womenshealth.gov/hiv-aids/preventing-hiv-infection/preventing-hiv-with-medicine.html"> <span id="translatedtitle"><span class="hlt">Preventing</span> HIV with Medicine</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... information in Spanish ( en español ) <span class="hlt">Preventing</span> HIV with medicine Get medicine right after you are exposed to ... to top More information on <span class="hlt">Preventing</span> HIV with medicine Explore other publications and websites National HIV and ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">388</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.cdc.gov/bloodpressure/healthy_living.htm"> <span id="translatedtitle"><span class="hlt">Preventing</span> High Blood Pressure</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ... this? Submit What's this? Submit Button Related CDC Web Sites Division for Heart Disease and Stroke <span class="hlt">Prevention</span> ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">389</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.cdc.gov/violenceprevention/childmaltreatment/"> <span id="translatedtitle">Child Maltreatment <span class="hlt">Prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://medlineplus.gov/">MedlinePLUS</a></p> <p class="result-summary">... Sources <span class="hlt">Prevention</span> Strategies Publications Risk and Protective Factors Translation Additional Resources References Fang X, Brown DS, Florence ... Links Publications Health Outcome Year Consequences <span class="hlt">Prevention</span> ... Resources CDC Special Supplement: Interrupting Child Maltreatment ...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">390</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3926678"> <span id="translatedtitle">Repetitive hypoxic <span class="hlt">preconditioning</span> induces an immunosuppressed B cell phenotype during endogenous protection from stroke</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">Background Repetitive hypoxic <span class="hlt">preconditioning</span> (RHP) creates an anti-inflammatory phenotype that protects from stroke-induced injury for months after a 2-week treatment. The mechanisms underlying long-term tolerance are unknown, though one exposure to hypoxia significantly increased peripheral B cell representation. For this study, we sought to determine if RHP specifically recruited B cells into the protected ischemic hemisphere, and whether RHP could phenotypically alter B cells prior to stroke onset. Methods Adult, male SW/ND4 mice received RHP (nine exposures over 2 weeks; 8 to 11 % O2; 2 to 4 hours) or identical exposures to 21 % O2 as control. Two weeks following RHP, a 60-minute transient middle cerebral artery occlusion was induced. Standard techniques quantified CXCL13 mRNA and protein expression. Two days after stroke, leukocytes were isolated from brain tissue (70:30 discontinuous Percoll gradient) and profiled on a BD-FACS Aria flow cytometer. In a separate cohort without stroke, sorted splenic CD19+ B cells were isolated 2 weeks after RHP and analyzed on an Illumina MouseWG-6 V2 Bead Chip. Final gene pathways were determined using Ingenuity Pathway Analysis. Student’s t-test or one-way analysis of variance determined significance (P?<?0.05). Results CXCL13, a B cell-specific chemokine, was upregulated in post-stroke cortical vessels of both groups. In the ischemic hemisphere, RHP increased B cell representation by attenuating the diapedesis of monocyte, macrophage, neutrophil and T cells, to quantities indistinguishable from the uninjured, contralateral hemisphere. Pre-stroke splenic B cells isolated from RHP-treated mice had >1,900 genes differentially expressed by microarray analysis. Genes related to B-T cell interactions, including antigen presentation, B cell differentiation and antibody production, were profoundly downregulated. Maturation and activation were arrested in a cohort of B cells from pre-stroke RHP-treated mice while regulatory B cells, a subset implicated in neurovascular protection from stroke, were upregulated. Conclusions Collectively, our data characterize an endogenous neuroprotective phenotype that utilizes adaptive immune mechanisms pre-stroke to protect the brain from injury post-stroke. Future studies to validate the role of B cells in minimizing injury and promoting central nervous system recovery, and to determine whether B cells mediate an adaptive immunity to systemic hypoxia that protects from subsequent stroke, are needed. PMID:24485041</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate">2014-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">391</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3682823"> <span id="translatedtitle">Autophagy is required for <span class="hlt">preconditioning</span> by the adenosine A1 receptor-selective agonist CCPA</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pmc">PubMed Central</a></p> <p class="result-summary">We have shown that the cellular process of macroautophagy plays a protective role in HL-1 cardiomyocytes subjected to simulated ischemia/reperfusion (sI/R) (Hamacher-Brady et al. in J Biol Chem 281(40):29776–29787). Since the nucleoside adenosine has been shown to mimic both early and late phase ischemic <span class="hlt">preconditioning</span>, a potent cardioprotective phenomenon, the purpose of this study was to determine the effect of adenosine on autophagosome formation. Autophagy is a highly regulated intracellular degradation process by which cells remove cytosolic long-lived proteins and damaged organelles, and can be monitored by imaging the incorporation of microtubule-associated light chain 3 (LC3) fused to a fluorescent protein (GFP or mCherry) into nascent autophagosomes. We investigated the effect of adenosine receptor agonists on autophagy and cell survival following sI/R in GFP-LC3 infected HL-1 cells and neonatal rat cardiomyocytes. The A1 adenosine receptor agonist 2-chloro-N(6)-cyclopentyl-adenosine (CCPA) (100 nM) caused an increase in the number of autophagosomes within 10 min of treatment; the effect persisted for at least 300 min. A significant inhibition of autophagy and loss of protection against sI/R measured by release of lactate dehydrogenase (LDH), was demonstrated in CCPA-pretreated cells treated with an A1 receptor antagonist, a phospholipase C inhibitor, or an intracellular Ca(+2) chelator. To determine whether autophagy was required for the protective effect of CCPA, autophagy was blocked with a dominant negative inhibitor (Atg5K130R) delivered by transient transfection (in HL-1 cells) or protein transduction (in adult rat cardiomyocytes). CCPA attenuated LDH release after sI/R, but protection was lost when autophagy was blocked. To assess autophagy in vivo, transgenic mice expressing the red fluorescent autophagy marker mCherry-LC3 under the control of the alpha myosin heavy chain promoter were treated with CCPA 1 mg/kg i.p. Fluorescence microscopy of cryosections taken from the left ventricle 30 min after CCPA injection revealed a large increase in the number of mCherry-LC3-labeled structures, indicating the induction of autophagy by CCPA in vivo. Taken together, these results indicate that autophagy plays an important role in mediating the cardioprotective effects conferred by adenosine pretreatment. PMID:19242639</p> <div class="credits"> <p class="dwt_author">Yitzhaki, Smadar; Huang, Chengqun; Liu, Wayne; Lee, Youngil; Gustafsson, Åsa B.; Mentzer, Robert M.</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">392</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://ntrs.nasa.gov/search.jsp?R=20120010416&hterms=Height&qs=Ntx%3Dmode%2Bmatchall%26Ntk%3DAll%26N%3D0%26No%3D10%26Ntt%3DHeight"> <span id="translatedtitle">Method for <span class="hlt">Pre-Conditioning</span> a Measured Surface Height Map for Model Validation</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://ntrs.nasa.gov/search.jsp">NASA Technical Reports Server (NTRS)</a></p> <p class="result-summary">This software allows one to up-sample or down-sample a measured surface map for model validation, not only without introducing any re-sampling errors, but also eliminating the existing measurement noise and measurement errors. Because the re-sampling of a surface map is accomplished based on the analytical expressions of Zernike-polynomials and a power spectral density model, such re-sampling does not introduce any aliasing and interpolation errors as is done by the conventional interpolation and FFT-based (fast-Fourier-transform-based) spatial-filtering method. Also, this new method automatically eliminates the measurement noise and other measurement errors such as artificial discontinuity. The developmental cycle of an optical system, such as a space telescope, includes, but is not limited to, the following two steps: (1) deriving requirements or specs on the optical quality of individual optics before they are fabricated through optical modeling and simulations, and (2) validating the optical model using the measured surface height maps after all optics are fabricated. There are a number of computational issues related to model validation, one of which is the "<span class="hlt">pre-conditioning</span>" or pre-processing of the measured surface maps before using them in a model validation software tool. This software addresses the following issues: (1) up- or down-sampling a measured surface map to match it with the gridded data format of a model validation tool, and (2) eliminating the surface measurement noise or measurement errors such that the resulted surface height map is continuous or smoothly-varying. So far, the preferred method used for re-sampling a surface map is two-dimensional interpolation. The main problem of this method is that the same pixel can take different values when the method of interpolation is changed among the different methods such as the "nearest," "linear," "cubic," and "spline" fitting in Matlab. The conventional, FFT-based spatial filtering method used to eliminate the surface measurement noise or measurement errors can also suffer from aliasing effects. During re-sampling of a surface map, this software preserves the low spatial-frequency characteristic of a given surface map through the use of Zernike-polynomial fit coefficients, and maintains mid- and high-spatial-frequency characteristics of the given surface map by the use of a PSD model derived from the two-dimensional PSD data of the mid- and high-spatial-frequency components of the original surface map. Because this new method creates the new surface map in the desired sampling format from analytical expressions only, it does not encounter any aliasing effects and does not cause any discontinuity in the resultant surface map.</p> <div class="credits"> <p class="dwt_author">Sidick, Erkin</p> <p class="dwt_publisher"></p> <p class="publishDate">2012-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">393</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.osti.gov/scitech/biblio/22209779"> <span id="translatedtitle">Transcriptional signature of human adipose tissue-derived stem cells (hASCs) <span class="hlt">preconditioned</span> for chondrogenesis in hypoxic conditions</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/scitech">SciTech Connect</a></p> <p class="result-summary">Hypoxia is an important factor involved in the control of stem cells. To obtain a better insight into the phenotypical changes brought about by hypoxic <span class="hlt">preconditioning</span> prior to chondrogenic differentiation; we have investigated growth, colony-forming and chondrogenic capacity, and global transcriptional responses of six adipose tissue-derived stem cell lines expanded at oxygen concentrations ranging from ambient to 1%. The assessment of cell proliferation and colony-forming potential revealed that the hypoxic conditions corresponding to 1% oxygen played a major role. The chondrogenic inducibility, examined by high-density pellet model, however, did not improve on hypoxic <span class="hlt">preconditioning</span>. While the microarray analysis revealed a distinctive inter-donor variability, the exposure to 1% hypoxia superseded the biological variability and produced a specific expression profile with 2581 significantly regulated genes and substantial functional enrichment in the pathways of cell proliferation and apoptosis. Additionally, exposure to 1% oxygen resulted in upregulation of factors related to angiogenesis and cell growth. In particular, leptin (LEP), the key regulator of body weight and food intake was found to be highly upregulated. In conclusion, the results of this investigation demonstrate the significance of donor demographics and the importance of further studies into the use of regulated oxygen tension as a tool for preparation of ASCs in order to exploit their full potential.</p> <div class="credits"> <p class="dwt_author">Pilgaard, L.; Lund, P.; Duroux, M. [Laboratory for Stem Cell Research, Aalborg University, Fredrik Bajers Vej 3B, 9220 Aalborg (Denmark)] [Laboratory for Stem Cell Research, Aalborg University, Fredrik Bajers Vej 3B, 9220 Aalborg (Denmark); Lockstone, H.; Taylor, J. [Bioinformatics and Statistical Genetics, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN (United Kingdom)] [Bioinformatics and Statistical Genetics, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN (United Kingdom); Emmersen, J.; Fink, T. [Laboratory for Stem Cell Research, Aalborg University, Fredrik Bajers Vej 3B, 9220 Aalborg (Denmark)] [Laboratory for Stem Cell Research, Aalborg University, Fredrik Bajers Vej 3B, 9220 Aalborg (Denmark); Ragoussis, J. [Genomics, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN (United Kingdom)] [Genomics, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN (United Kingdom); Zachar, V., E-mail: vlaz@hst.aau.dk [Laboratory for Stem Cell Research, Aalborg University, Fredrik Bajers Vej 3B, 9220 Aalborg (Denmark)</p> <p class="dwt_publisher"></p> <p class="publishDate">2009-07-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">394</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/24270688"> <span id="translatedtitle"><span class="hlt">Pre-conditioning</span> the epigenetic response to high vapor pressure deficit increases the drought tolerance of Arabidopsis thaliana.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Epigenetic modification of the genome via cytosine methylation is a dynamic process that responds to changes in the growing environment. This modification can also be heritable. The combination of both properties means that there is the potential for the life experiences of the parental generation to modify the methylation profiles of their offspring and so potentially to "<span class="hlt">pre-condition</span>" them to better accommodate abiotic conditions encountered by their parents. We recently identified high vapor pressure deficit (vpd)-induced DNA methylation at 2 gene loci in the stomatal development pathway and an associated reduction in leaf stomatal frequency. (1) Here, we test whether this epigenetic modification <span class="hlt">pre-conditioned</span> parents and their offspring to the more severe water stress of periodic drought. We found that 3 generations of high vpd-grown plants were better able to withstand periodic drought stress over 2 generations. This resistance was not directly associated with de novo methylation of the target stomata genes, but was associated with the cmt3 mutant's inability to maintain asymmetric sequence context methylation. If our finding applies widely, it could have significant implications for evolutionary biology and breeding for stressful environments. PMID:24270688</p> <div class="credits"> <p class="dwt_author">Tricker, Penny; Rodríguez López, Carlos; Hadley, Paul; Wagstaff, Carol; Wilkinson, Mike</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-10-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">395</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/24440653"> <span id="translatedtitle">Biodegradation of 3,4 dichloroaniline by fungal isolated from the <span class="hlt">preconditioning</span> phase of winery wastes subjected to vermicomposting.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">A hazardous contaminant, 3,4-dichloroaniline (DCA) is widespread in the environment due to its extensive use in the manufacture of chemicals and its application in different sectors. The ability of fungi grow on in winery wastes in the <span class="hlt">preconditioning</span> period of vermicomposting to degrade DCA was investigated. Three filamentous fungi (F1, F2, and F3) were isolated and one identified as Aspergillus niger and two as Fusarium sp. strains. The culture media with the fungus alone or in consortium (Fmix) with DCA as the nitrogen source were analyzed by solid-phase microextraction and gas chromatography-mass spectrometry (SPME-GC/MS). The fastest degradation rate was measured in Fmix with a DT50 of 0.85day(-1). Fusarium sp. and A. niger differed in the metabolism of DCA. Five metabolites were identified as a result of oxidation, co-denitrification, N-acetylation, and polymerization reactions. The major metabolites were 3,4-dichloroacetanilide and dichloroquinolines. The azo-metabolites tetrachloroazobenzene and tetracloroazoxybenzene and 3,4-dichloronitrobenzene were found in minor amounts but appeared to be the most persistent in the Fusarium cultures (half-lives ranging from 8.3 to 30.9 days). This study highlights the metabolic potential of microorganisms in the <span class="hlt">preconditioning</span> period of the vermicomposting process and its possible application for in situ bioremediation strategies. PMID:24440653</p> <div class="credits"> <p class="dwt_author">Castillo, Jean Manuel; Nogales, Rogelio; Romero, Esperanza</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-02-28</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">396</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=wildfire&pg=3&id=ED472789"> <span id="translatedtitle">Wildfire <span class="hlt">Prevention</span> Strategies.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">This document provides information and guidance on wildfire <span class="hlt">prevention</span> strategies. Chapters include: (1) "Introduction"; (2) "How to Use this Guide"; (3) "Fire Cause Classification"; (4) "Relative Effectiveness"; (5) "Degree of Difficulty"; (6) "Intervention Techniques"; (7) "<span class="hlt">Prevention</span> Activities"; (8) "Sample <span class="hlt">Prevention</span> Strategies"; and (9)…</p> <div class="credits"> <p class="dwt_author">National Wildlife Coordinating Group, Boise, ID.</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">397</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=forensic+AND+materials&pg=6&id=ED251747"> <span id="translatedtitle">Suicide <span class="hlt">Prevention</span> Triangle.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">This manual provides resource tools and strategies to enhance the suicide <span class="hlt">prevention</span> capabilities of health professionals and the health care setting in which care is provided. In the first section, terms are defined and the suicide <span class="hlt">prevention</span> triangle model is described. Applications of the model and good practices for suicide <span class="hlt">prevention</span> in any…</p> <div class="credits"> <p class="dwt_author">Cutter, Fred</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">398</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://prevention.cancer.gov/prevent-governance-structure"> <span id="translatedtitle"><span class="hlt">PREVENT</span> Governance Structure</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.cancer.gov">Cancer.gov</a></p> <p class="result-summary">With the governance structure and unified <span class="hlt">PREVENT</span> program mission, NCI will make data-driven decisions to maximize potential for success at each consecutive stage. As such, the <span class="hlt">PREVENT</span> Program is envisioned to streamline the development and testing of promising new cancer <span class="hlt">preventative</span> agents and expedite their delivery to bedside.</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">399</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=bacterial+AND+growth&pg=3&id=ED121956"> <span id="translatedtitle"><span class="hlt">Prevention</span> of Food Poisoning.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">The programed text provides a single lesson, four-hour, correspondence subcourse on the <span class="hlt">prevention</span> of food poisoning. It covers the following areas: a definition of food poisoning; chemical food poisoning; biological food poisoning; causes and <span class="hlt">prevention</span> of trichinosis; six factors controlling bacteria growth; bacterial infection; <span class="hlt">prevention</span> of…</p> <div class="credits"> <p class="dwt_author">Army Quartermaster School, Ft. Lee, VA.</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">400</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://eric.ed.gov/?q=%22Preventive+Medicine%22&pg=2&id=EJ244146"> <span id="translatedtitle"><span class="hlt">Preventive</span> Medicine Redefined.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.eric.ed.gov/ERICWebPortal/search/extended.jsp?_pageLabel=advanced">ERIC Educational Resources Information Center</a></p> <p class="result-summary">Departments of <span class="hlt">preventive</span> medicine can survive through unity, which can be achieved through majority agreement on a new and specific definition of <span class="hlt">preventive</span> medicine. A definition is proposed that is based on a review and analysis of recent progress in the <span class="hlt">prevention</span> of the major causes of mortality. (MLW)</p> <div class="credits"> <p class="dwt_author">Moore, George</p> <p class="dwt_publisher"></p> <p class="publishDate">1981-01-01</p> </div> </div> </div> </div> <div id="filter_results_form" class="filter_results_form floatContainer" style="visibility: visible;"> <div style="width:100%" id="PaginatedNavigation" class="paginatedNavigationElement"> <a id="FirstPageLink" onclick='return showDiv("page_1");' href="#" title="First Page"> <img id="FirstPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.first.18x20.png" alt="First Page" /></a> <a id="PreviousPageLink" onclick='return showDiv("page_19");' href="#" title="Previous Page"> <img id="PreviousPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.previous.18x20.png" alt="Previous Page" /></a> <span id="PageLinks" class="pageLinks"> <span> <a onClick='return showDiv("page_1");' href="#">1</a> <a onClick='return showDiv("page_2");' href="#">2</a> <a onClick='return showDiv("page_3");' 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src="http://www.science.gov/scigov/images/icon.next.18x20.png" alt="Next Page" /></a> <a id="LastPageLink" onclick='return showDiv("page_25.0");' href="#" title="Last Page"> <img id="LastPageLinkImage" class="Icon" src="http://www.science.gov/scigov/images/icon.last.18x20.png" alt="Last Page" /></a> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">401</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/35866076"> <span id="translatedtitle">Diffusion of <span class="hlt">preventive</span> innovations</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">The present paper draws on the diffusion of innovations model to derive a series of strategies for speeding up the spread and implementation of new ideas in <span class="hlt">preventing</span> addiction. <span class="hlt">Preventive</span> innovations usually require an action at one point in time in order to avoid an unwanted future condition. Hence, <span class="hlt">preventive</span> innovations diffuse rather slowly, in part due to delayed rewards</p> <div class="credits"> <p class="dwt_author">Everett M Rogers</p> <p class="dwt_publisher"></p> <p class="publishDate">2002-01-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">402</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://fcsagents.tamu.edu/food_and_nutrition/general_nutrition/eat-smart/lesson-6-bone-health/6-lesson-contents.pdf"> <span id="translatedtitle">National Osteoporosis <span class="hlt">Prevention</span> Month</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">Service Texas A&M University System Eat Smart for Bone Health Exercise & Fall <span class="hlt">Prevention</span>- Lesson 6 Contents: Lesson - Exercise & Fall <span class="hlt">Prevention</span> Power Point # P6-1 Eat Smart for Bone Health # P6-2 Weight-Bearing Exercises # P6-3 Weight-Bearing Exercises (continued) # P6-4 Exercise Tips # P6-5 Fall <span class="hlt">Prevention</span> # P6</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">403</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://academic.research.microsoft.com/Publication/47823390"> <span id="translatedtitle">Obesity <span class="hlt">Prevention</span> During Adulthood</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">The weight distribution of the U.S. population has been shifting upwards, and overweight and obesity have increased steadily across all ages. As discussed in Chapters 18 through 20, it is important that obesity <span class="hlt">prevention</span> efforts begin during childhood. However, the importance of obesity <span class="hlt">prevention</span> in children should not overshadow the need and potential for <span class="hlt">prevention</span> of excess weight gain in</p> <div class="credits"> <p class="dwt_author">Suzanne Phelan; Meghan Butryn; Rena R. Wing</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">404</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://oaspub.epa.gov/eims/eimsapi.dispdetail?deid=42462"> <span id="translatedtitle">FACILITY POLLUTION <span class="hlt">PREVENTION</span> GUIDE</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://oaspub.epa.gov/eims/query.page">EPA Science Inventory</a></p> <p class="result-summary">The U.S. Environmental Protection Agency (U.S. EPA) has developed the Facility Pollution <span class="hlt">Prevention</span> Guide for those who are interested in and responsible for pollution <span class="hlt">prevention</span> in industrial or service facilities. t summarizes the benefits of a company-wide pollution <span class="hlt">prevention</span>...</p> <div class="credits"> <p class="dwt_author"></p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">405</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www-ehs.ucsd.edu/ih/hazaware_contractors.pdf"> <span id="translatedtitle">awareness and pollution <span class="hlt">prevention</span></span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.osti.gov/epsearch/">E-print Network</a></p> <p class="result-summary">..............................................5 Storm Water Pollution <span class="hlt">Prevention</span>.....................5 Sanitary Sewer System ManagementHazard awareness and pollution <span class="hlt">prevention</span> for contractors and visitors at UCSD #12;Hazard Awareness and Pollution <span class="hlt">Prevention</span> For Contractors and Visitors at UC San Diego This booklet was developed by UC San Diego</p> <div class="credits"> <p class="dwt_author">Tsien, Roger Y.</p> <p class="dwt_publisher"></p> <p class="publishDate"></p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">406</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/23097345"> <span id="translatedtitle">L-theanine administration results in neuroprotection and <span class="hlt">prevents</span> glutamate receptor agonist-mediated injury in the rat model of cerebral ischemia-reperfusion.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">While the neuroprotective effect of green tea (Camellia sinensis) might be explained by the presence of amino acid L-theanine in the tea leaves, it is not known whether <span class="hlt">postischemic</span> administration of L-theanine could also provide neuroprotection. In the present study, we investigated the neuroprotective effect of L-theanine (1 and 4?mg/kg) administered at 3, 12, and 24?h after reperfusion in the rat model of stroke. We also studied the effect of L-theanine on brain injury caused by exogenous administration of N-methyl-D-aspartate and ?-amino-3-hydroxy-5-methyl-isoxazole-4-propionate/kainate receptor agonists during reperfusion. Rats were subjected to 30-min middle cerebral artery occlusion followed by 48-h reperfusion. Neurological deficit and infarct size were determined at the end of reperfusion. At 3 and 12?h, but not at 24?h of reperfusion, L-theanine substantially reduced the size of brain infarct. Neurological status was improved when L-theanine was administered 3, 12, and 24?h after reperfusion. Repeated intrastriatal injections of L-theanine at a total dose of 800?µg/kg during reperfusion <span class="hlt">prevented</span> brain injury caused by glutamate receptor agonists. In conclusion, L-theanine at reperfusion exerts neuroprotective effect in the in vivo rat model of stroke. Local treatment with L-theanine at reperfusion <span class="hlt">prevents</span> glutamate receptor agonist-mediated brain injury. PMID:23097345</p> <div class="credits"> <p class="dwt_author">Zukhurova, Mavdzhuda; Prosvirnina, Maria; Daineko, Anastasia; Simanenkova, Anna; Petrishchev, Nikolay; Sonin, Dmitry; Galagudza, Michael; Shamtsyan, Mark; Juneja, Lekh R; Vlasov, Timur</p> <p class="dwt_publisher"></p> <p class="publishDate">2013-09-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">407</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25159328"> <span id="translatedtitle">High-fat diet-induced impairment of skeletal muscle insulin sensitivity is not <span class="hlt">prevented</span> by SIRT1 overexpression.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Skeletal muscle sirtuin 1 (SIRT1) expression is reduced under insulin-resistant conditions, such as those resulting from high-fat diet (HFD) feeding and obesity. Herein, we investigated whether constitutive activation of SIRT1 in skeletal muscle <span class="hlt">prevents</span> HFD-induced muscle insulin resistance. To address this, mice with muscle-specific overexpression of SIRT1 (mOX) and wild-type (WT) littermates were fed a control diet (10% calories from fat) or HFD (60% of calories from fat) for 12 wk. Magnetic resonance imaging and indirect calorimetry were used to measure body composition and energy expenditure, respectively. Whole body glucose metabolism was assessed by oral glucose tolerance test, and insulin-stimulated glucose uptake was measured at a physiological insulin concentration in isolated soleus and extensor digitorum longus muscles. Although SIRT1 was significantly overexpressed in muscle of mOX vs. WT mice, body weight and percent body fat were similarly increased by HFD for both genotypes, and energy expenditure was unaffected by diet or genotype. Importantly, impairments in glucose tolerance and insulin-mediated activation of glucose uptake in skeletal muscle that occurred with HFD feeding were not <span class="hlt">prevented</span> in mOX mice. In contrast, mOX mice showed enhanced <span class="hlt">postischemic</span> cardiac functional recovery compared with WT mice, confirming the physiological functionality of the SIRT1 transgene in this mouse model. Together, these results demonstrate that activation of SIRT1 in skeletal muscle alone does not <span class="hlt">prevent</span> HFD-induced glucose intolerance, weight gain, or insulin resistance. PMID:25159328</p> <div class="credits"> <p class="dwt_author">White, Amanda T; Philp, Andrew; Fridolfsson, Heidi N; Schilling, Jan M; Murphy, Anne N; Hamilton, D Lee; McCurdy, Carrie E; Patel, Hemal H; Schenk, Simon</p> <p class="dwt_publisher"></p> <p class="publishDate">2014-11-01</p> </div> </div> </div> </div> <div class="floatContainer result " lang="en"> <div class="resultNumber element">408</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.springerlink.com/index/t623076885k26010.pdf"> <span id="translatedtitle">Exploring the Genesis of Economic Innovations: The Religious Gestalt-Switch and the Duty to Invent as <span class="hlt">Preconditions</span> for Economic Growth</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://academic.research.microsoft.com/">Microsoft Academic Search </a></p> <p class="result-summary">This paper discusses changes in the level of knowledge, i.e. learning, as a key source of economic growth, and argues that historically a radical change in attitude towards new knowledge has been a necessary <span class="hlt">precondition</span> for economic growth. The Renaissance created this radically new attitude in Europe, and this paper discusses contributions to economic theory and economic policy of some</p> <div class="credits"> <p class="dwt_author">ERIK S. REINERT; Arno Mong Daastøl</p> <p class="dwt_publisher"></p> <p class="publishDate">1997-01-01</p> </div> </div> </div> </div> <div class="floatContainer result odd" lang="en"> <div class="resultNumber element">409</div> <div class="resultBody element"> <p class="result-title"><a target="resultTitleLink" href="http://science.gov/scigov/link.html?type=RESULT&redirectUrl=http://www.ncbi.nlm.nih.gov/pubmed/25443289"> <span id="translatedtitle">"<span class="hlt">Preconditioning</span>" with latrepirdine, an adenosine 5'-monophosphate-activated protein kinase activator, delays amyotrophic lateral sclerosis progression in SOD1(G93A) mice.</span></a>  </p> <div class="result-meta"> <p class="source"><a target="_blank" id="logoLink" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed">PubMed</a></p> <p class="result-summary">Adenosine 5'-monophosphate-activated protein kinase (AMPK) is a master regulator of energy balance. As energy imbalance is documented as a key pathologic feature of amyotrophic lateral sclerosis (ALS), we investigated AMPK as a pharmacologic target in SOD1(G93A) mice. We noted a strong activation of AMPK in lumbar spinal cords of SOD1(G93A) mice. Pharmacologic activation of AMPK has shown protective effects in neuronal "<span class="hlt">preconditioning</span>" models. We tested the hypothesis that "<span class="hlt">preconditioning</span>" with a small molecule activator of AMPK, latrepirdine, exerts beneficial effects on disease progression. SOD1(G93A) mice (n = 24 animals per group; sex and litter matched) were treated with latrepirdine (1 ?g/kg, intraperitoneal) or vehicle from postnatal day 70 to 120. Treatment with latrepirdine increased AMPK activity in primary mouse motor neuron cultures and