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1

AICAR Preconditioning Prevents Postischemic Leukocyte Rolling and Adhesion: Role of KATP Channels and Heme Oxygenase  

PubMed Central

Objective We previously demonstrated that pharmacologic activation of AMP-activated protein kinase (AMPK) with 5-aminoimidazole-4-carboxamide 1-?-D-ribofuranoside (AICAR) 24 hours prior to (AICAR preconditioning; AICAR-PC) ischemia/reperfusion (I/R) prevents postischemic leukocyte-endothelial cell adhesive interactions (LEI) by a mechanism initiated by endothelial nitric oxide synthase (eNOS)-dependent NO production during the period of AICAR-PC. The major aim of this study was to examine the role of ATP-sensitive potassium (KATP) channels and heme oxygenase as mediators of the antiadhesive effects of AICAR-PC during I/R 24 hours later. Methods Intravital fluorescence microscopy was used to quantify LEI in the small intestine of AICAR-preconditioned C57BL/6J mice treated with KATP channel or heme oxygenase inhibitors during I/R 24 hours after AICAR-PC in separate experiments. Results I/R induced marked increases in LEI relative to sham control mice, proadhesive responses that were prevented by AICAR-PC 24 hours prior to I/R. The effects of AICAR-PC to prevent postischemic LEI were abolished by KATP channel or heme oxygenase inhibition during I/R. Discussion Our results indicate that the antiadhesive effects of AICAR-PC are mediated by KATP channel- and heme oxygenase-dependent mechanisms during I/R. PMID:19152177

GASKIN, F. SPENCER; KAMADA, KAZUHIRO; YUSOF, MOZOW; DURANTE, WILLIAM; GROSS, GARRETT; KORTHUIS, RONALD J.

2009-01-01

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

Rock preconditioning to prevent rock bursts  

SciTech Connect

A US Bureau of Mines method to precondition rocks to prevent rock bursts is presented. The approach uses deep drill holes from a mine opening in a radial pattern in the vein and load and blast to fracture the rock prior to production mining. The method was successfully tested on a sphalerite-galena vein in a hard gangue of quartz and quartzite at the 7700 level of the Hecla Mining Company's Star Mine in Burke, Idaho. (JMT)

Not Available

1981-05-01

4

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

5

Intermittent aortic crossclamping prevents cumulative adenosine triphosphate depletion, ventricular fibrillation, and dysfunction (stunning): Is it preconditioning?  

Microsoft Academic Search

This study was designed to determine whether intermittent warm aortic crossclamping induces cumulative myocardial stunning or if the myocardium becomes preconditioned after the first episode of ischemia in canine models in vivo. The role of adenosine triphosphate catabolism and subsequent release of purines on reperfusion-mediated postischemic ventricular dysfunction and arrhythmias was assessed with the use of selective inhibitors of nucleoside

Anwar S. Abd-Elfattah; Mai Ding; Andrew S. Wechsler

1995-01-01

6

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

7

Intermittent aortic crossclamping prevents cumulative adenosine triphosphate depletion, ventricular fibrillation, and dysfunction (stunning): is it preconditioning?  

PubMed

This study was designed to determine whether intermittent warm aortic crossclamping induces cumulative myocardial stunning or if the myocardium becomes preconditioned after the first episode of ischemia in canine models in vivo. The role of adenosine triphosphate catabolism and subsequent release of purines on reperfusion-mediated postischemic ventricular dysfunction and arrhythmias was assessed with the use of selective inhibitors of nucleoside transport, p-nitrobenzylthioinosine (NBMPR), and a specific adenosine deaminase inhibitor, erythro-9-[2-hydroxy-3-nonyl] adenine (EHNA). Thirty-two anesthetized dogs were instrumented to monitor left ventricular contractility, off bypass, by sonomicrometry. During cardiopulmonary bypass dogs were treated before ischemia with either saline solution (control group, n = 8) or EHNA (100 mumol/L) and NBMPR (25 mumol/L) (EHNA/NBMPR group, n = 8). Hearts were subjected to either 60 minutes of global ischemia and 120 minutes of reperfusion (n = 16) or 6 episodes of 10 minutes of global ischemia and 10 minutes of reperfusion, followed by 60 minutes of reperfusion (n = 16). Sixty minutes of sustained ischemia resulted in 80% loss of adenosine triphosphate and induced reperfusion-mediated ventricular fibrillation and severe left ventricular dysfunction in the control group. EHNA/NBMPR treatment augmented myocardial adenosine trapping during ischemia, attenuated ventricular fibrillation, and enhanced left ventricular functional recovery, despite similar depletion of adenosine triphosphate (80% loss). In the intermittent ischemia experiment, the first episode of 10 minutes of ischemia and reperfusion caused significant adenosine triphosphate depletion, ventricular fibrillation, and left ventricular stunning in both control and drug-treated groups. The prevalence of ventricular fibrillation was greater in the control group than in the drug-treated group after the first episode of ischemia (p < 0.05). Adenosine was the major nucleoside accumulated in the myocardium at the end of 10 minutes of ischemia in the EHNA/NBMPR-treated group (p < 0.05 versus control). Subsequent episodes of ischemia prevented ventricular fibrillation and did not cause cumulative left ventricular stunning in either group. Left ventricular function fully recovered in the EHNA/NBMPR-treated group after intermittent ischemia, but remained stunned in the control group. Unlike sustained ischemia, intermittent ischemia and reperfusion preserved myocardial adenosine triphosphate, limited purine release, and prevented ventricular fibrillation and cumulative stunning. These results suggest that intermittent ischemia and reperfusion augmented the endogenous protective mechanism or mechanisms of "preconditioning." Nucleoside trapping improved functional recovery after sustained or repetitive ischemia. It is concluded that adenosine triphosphate preservation or blockade of nucleoside transport may play an important role in the activation of endogenous myocardial protective mechanisms that "precondition" against subsequent ischemic stress. PMID:7637350

Abd-Elfattah, A S; Ding, M; Wechsler, A S

1995-08-01

8

The neuroprotective effect of the antioxidant flavonoid derivate di-tert-butylhydroxyphenyl is parallel to the preventive effect on post-ischemic Kir2.x impairment but not to post-ischemic endothelial dysfunction.  

PubMed

In the rat model of transient cerebral ischemia induced by intraluminal occlusion of the middle cerebral artery, we investigated the respective roles of ischemia and reperfusion in endothelium-dependent relaxation and smooth muscle relaxation related to the inward rectifier potassium current (Kir2.x), using the Halpern arteriography technique and/or patch-clamp technique. We first demonstrated that reperfusion is necessary to induce a significant impairment of smooth muscle Kir2.x, since ischemia alone has no effect on Kir2.x current density and function. In addition, we demonstrated that both ischemia and reperfusion are necessary for the occurrence of maximal post-ischemic endothelial dysfunction. The crucial role of reperfusion in post-ischemic vascular impairment prompted us to characterize the effect of a new antioxidant synthetic flavonoid derivate, 3'5'di- tert-butylhydroxyphenyl (dt-BC), on both neuronal and vascular injuries. Dt-BC (10 mg/kg) induced a neuroprotective effect as demonstrated by a significant decrease in infarct size, while there was no protective effect with the doses of 3 mg/kg and 30 mg/kg. Parallel to neuroprotection, dt-BC at a dose of 10 mg/kg, but not with doses of 3 mg/kg and 30 mg/kg, prevented post-ischemic impairment of smooth muscle Kir2.x current density and function, while dt-BC had no effect on the post-ischemic alteration of endothelial function whatever doses are used. These data demonstrate the potential of a new synthetic flavonoid derivate to induce neurovascular protection and support a possible relationship between vascular and neuronal protection via pharmacological modulation of oxidative stress. PMID:15502971

Pétrault, Olivier; Bastide, Michèle; Cotelle, Nicole; Gelé, Patrick; Gautier, Sophie; Laprais, Maud; Vamecq, Joseph; Duriez, Patrick; Bordet, Régis

2004-11-01

9

Glutamate preconditioning prevents neuronal death induced by combined oxygen-glucose deprivation in cultured cortical neurons.  

PubMed

The study of ischemic tolerance is critical in the development of strategies for the treatment of ischemic stroke. We used the oxygen and glucose deprivation (OGD) paradigm in cultured cortical neurons as an in vitro approach to elucidate the mechanism of protection conferred by glutamate preconditioning. Pretreatment of neurons with N-methyl-d-aspartate (NMDA) receptor antagonists prevented OGD-induced cell death whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor and voltage-dependent Ca(++) channel (VDCC) blockers were without effect. Neurons preconditioned with glutamate exhibited resistant to damage induced by OGD. The ischemic tolerance depended on the duration of preconditioning exposure and the interval between preconditioning exposure and test challenge. Protective efficacy was blocked by the NMDA or AMPA receptor antagonists but not by the VDCC blocker. Furthermore, neuroprotective effect was not seen if extracellular Ca(++) was omitted or removed with EGTA. Pretreatment with staurosporin and 2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methylbenzylamine (KN93) but not 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one (LY294002) or 1,4-diamino-2,3-dicyano-1, 4-bis[2-aminophenylthio] butadiene (U0126) significantly reduced ischemic tolerance. Preconditioning increased phosphorylated levels of cAMP responsive element binding protein (CREB) and pretreatment with CRE-decoy oligonucleotide completely blocked preconditioning-induced increase in cell viability. Importantly, glutamate preconditioning increased Bcl-2 expression that was blocked by KN93, staurosporin and CRE-decoy oligonucleotide. These results suggest that preconditioning with glutamate conferred neuroprotection against subsequent OGD by inducing p-CREB-mediated Bcl-2 expression. PMID:18589412

Lin, Chia-Ho; Chen, Po-See; Gean, Po-Wu

2008-07-28

10

Glutamate preconditioning prevents neuronal death induced by combined oxygen–glucose deprivation in cultured cortical neurons  

Microsoft Academic Search

The study of ischemic tolerance is critical in the development of strategies for the treatment of ischemic stroke. We used the oxygen and glucose deprivation (OGD) paradigm in cultured cortical neurons as an in vitro approach to elucidate the mechanism of protection conferred by glutamate preconditioning. Pretreatment of neurons with N-methyl-d-aspartate (NMDA) receptor antagonists prevented OGD-induced cell death whereas ?-amino-3-hydroxy-5-methyl-4-isoxazole

Chia-Ho Lin; Po-See Chen; Po-Wu Gean

2008-01-01

11

Remote Ischemic Preconditioning for Prevention of Contrast-induced Acute Kidney Injury in Diabetic Patients.  

PubMed

Introduction. There are some clinical trials showing that short-term ischemia in one organ can protect different organs against higher intensity and longer ischemic insult. We designed a study to assess whether remote ischemic preconditioning (RIPC) on one organ can decrease the rate of contrast-induced acute kidney injury (AKI) in diabetic patients who undergo coronary artery angiography (CAA). Materials and Methods. This randomized control trial included 96 diabetic patients who were candidates for CAA. Exclusion criteria were congestive heart failure and complications during CAA. All of the patients received 1000 mL of normal saline before CAA. The RIPC group underwent 3 cycles of 5-minute ischemia in their right arm. Serum creatinine was measured before and 24 hours after CAA. Results. Contrast-induced AKI was reported in 5 cases in the control group and 1 case in the RIPC group (P = .13, odds ratio, 5.4). The differences in serum creatinine level before and after the procedure was significantly lower in RIPC group than that in the control group (P = .04, odds ratio, 0.08). Serum creatinine rise significantly correlated with contrast dose (P = .02) and a history of hypertension (P = .02) in both groups. Conclusions. Ischemic preconditioning had a protective effect on contrast-induced AKI in our study. Since this method is harmless and cost effective, further studies on patients with chronic kidney disease is required to evaluate addition of ischemic preconditioning to our clinical practice for prevention of contrast-induced AKI. PMID:25362220

Savaj, Shokoufeh; Savoj, Javad; Jebraili, Ismail; Sezavar, Seyed Hashem

2014-11-01

12

Ischemic Preconditioning Prevents Free Radical Production and Mitochondrial Depolarization in Small-for-Size Rat Liver Grafts  

Microsoft Academic Search

Background. Ischemic preconditioning (IP) renders tissues more tolerant to subsequent longer episodes of ischemia. This study tested whether IP attenuates injury of small-for-size liver grafts by preventing free radical production and mitochondrial dysfunction. Methods. IP was induced by clamping the portal vein and hepatic artery for 9 min. Livers were harvested 5 min after releasing the clamp. Mitochondrial polarization and

Hasibur Rehman; Henry D. Connor; Venkat K. Ramshesh; Tom P. Theruvath; Ronald P. Mason; Gary L. Wright; John J. Lemasters; Zhi Zhong

2008-01-01

13

Dystrophin proteolysis: a potential target for MMP-2 and its prevention by ischemic preconditioning.  

PubMed

Dystrophin is responsible for the mechanical stabilization of the sarcolemma, and it has been shown that it is one of the most sensitive proteins to ischemic injury. However, the enzyme responsible for this proteolysis is still unknown. Isolated rabbit hearts were subjected to 30 min of global ischemia with and without reperfusion (180 min) to determine whether dystrophin is cleaved by matrix metalloproteinase (MMP)-2 during acute ischemia and whether ischemic preconditioning (PC) prevents dystrophin breakdown through MMP-2 inhibition. The activity of MMP-2 was evaluated by zymography and using doxycycline as an inhibitor. Also, to stimulate MMP-2 activity without ischemia, SIN-1 was administered in the absence and presence of doxycycline. Finally, we considered the PC effect on MMP-2 activity and dystrophin expression. The dystrophin level decreased during ischemia, reaching 21% of control values (P < 0.05), but the spectrin level remained unchanged. MMP-2 activity increased 71% during ischemia compared with control values (P < 0.05). Doxycycline administration before ischemia prevented dystrophin breakdown. In normoxic hearts, SIN-1 increased thiobarbituric acid-reactive substances by 33% (P < 0.05) and MMP-2 activity by 36% (P < 0.05) and significantly reduced the dystrophin level to 23% of control values (P < 0.05). PC significantly prevented dystrophin breakdown by inhibiting MMP-2 activity, and the dystrophin level reached 89% of control values (P < 0.05). In conclusion, MMP-2 could be responsible for the proteolysis of dystrophin. Thus, dystrophin emerges as a possible novel substrate for MMP-2 in the context of ischemic injury. Furthermore, our results demonstrate that ischemic PC prevents dystrophin breakdown most likely by inhibiting MMP-2 activity. PMID:24791785

Buchholz, Bruno; Perez, Virginia; Siachoque, Nadezda; Miksztowicz, Verónica; Berg, Gabriela; Rodríguez, Manuel; Donato, Martín; Gelpi, Ricardo J

2014-07-01

14

Neuroprotection by NMDA preconditioning against glutamate cytotoxicity is mediated through activation of ERK 1/2, inactivation of JNK, and by prevention of glutamate-induced CREB inactivation.  

PubMed

N-methyl-D-aspartate (NMDA) preconditioning is a major endogenous brain protective mechanism, activated by sub-lethal stimulation of the NMDA glutamate receptors. Selective drug activation of this mechanism is considered to be a promising neuroprotective treatment against stroke and other traumatic brain insults. We have established an experimental in vitro model of NMDA preconditioning in primary rat neuronal cultures composed of three consecutive periods: preconditioning (NMDA 50 9M for 18 h), insult (glutamic acid 200 9M for 1 h), and reperfusion (regular medium for 24 h). The insulted neuronal cultures exhibited a 2.8-fold increase in LDH release into the media during the post-insult reperfusion period, which was completely abolished in the preconditioned cultures. The alterations in the activity level of the pro-survival kinase extracellular signal-regulated kinase (ERK) 1/2, the death machine activator c-Jun N-terminal kinase (JNK), and the pro-survival transcription factor cAMP responsive element binding (CREB) were monitored in preconditioned neuronal cultures in comparison to non-preconditioned cells during the three periods of the experimental model. The preconditioned neurons exhibited increased activity levels of ERK 1/2 and decreased activity levels of JNK during all periods of the model. In addition, the non-preconditioned neurons exhibited a marked reduction in the activity level of CREB during the insult period, which was totally prevented in the preconditioned cultures. These results suggest that the neuroprotection conferred by NMDA preconditioning against glutamate cytotoxicity is mediated (at least in part) through activation of ERK 1/2, inactivation of JNK and by prevention of glutamate-induced CREB inactivation. PMID:21556733

Navon, Hila; Bromberg, Yael; Sperling, Oded; Shani, Esther

2012-01-01

15

Prevention of the ischemia-induced decrease in mitochondrial Tom20 content by ischemic preconditioning.  

PubMed

Preserved mitochondrial function (respiration, calcium handling) and integrity (cytochrome c release) is central for cell survival following ischemia/reperfusion. Mitochondrial function also requires import of proteins from the cytosol via the translocase of the outer and inner membrane (TOM and TIM complexes). Since mitochondrial function following ischemia/reperfusion is better preserved by ischemic preconditioning (IP), we now investigated whether expression of parts of the import machinery is affected by ischemia/reperfusion without or with IP in vivo. We analyzed the mitochondrial content of the presequence receptor Tom20, the pore forming unit Tom40 and Tim23. Goettinger minipigs were subjected to 90 min of low-flow ischemia without or with preconditioning by 10 min ischemia and 15 min reperfusion. Mitochondria were isolated from the ischemic or preconditioned anterior wall of the left ventricle and from the control posterior wall. Infarct size was significantly reduced by IP (20.1 +/- 1.6% of area at risk (non-preconditioned) vs. 6.5 +/- 2.5% of area at risk (IP)). Using Western blot analysis, the ratio of Tom20 (normalized to Ponceau S) between mitochondria isolated from the anterior ischemic and posterior control wall was reduced (0.72 +/- 0.11, a.u., n = 8), whereas the mitochondrial Tom20 content was preserved by IP (1.17 +/- 0.16 a.u., n = 7, P < 0.05). The mitochondrial Tom40, Tim23 and adenine nucleotide transporter (ANT) contents were not significantly different between non-preconditioned and preconditioned myocardium. The preservation of the mitochondrial Tom20 protein level may contribute to the improved mitochondrial function after IP. PMID:16828795

Boengler, Kerstin; Gres, Petra; Cabestrero, Alberto; Ruiz-Meana, Marisol; Garcia-Dorado, David; Heusch, Gerd; Schulz, Rainer

2006-09-01

16

Hyperthermic preconditioning prevents blood–brain barrier disruption produced by hypoxia–ischemia in newborn rat  

Microsoft Academic Search

Effect of hyperthermic preconditioning on disruption of blood–brain barrier induced by hypoxic–ischemic insult was examined. Seven-day-old Wistar rats were separated into (1) pre-heated (15 min of hyperthermia at 41.5–42.0°C) or (2) non-heated group (33°C). Twenty-four hours after conditioning, all rats were subjected to 2 h hypoxia–ischemia (8% oxygen\\/92% nitrogen, at 33°C), then 24 h later all brains were examined for

Tomoaki Ikeda; Xiao Y Xia; Yi X Xia; Tsuyomu Ikenoue

1999-01-01

17

Preconditioning Balloons  

NSDL National Science Digital Library

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

Integrated Teaching And Learning Program

18

Reduced expression of IA channels is associated with postischemic seizures in hyperglycemic rats.  

PubMed

Poststroke seizures are considered to be the major cause of epilepsy in the elderly. The mechanisms of poststroke seizures remain unclear. A history of diabetes mellitus has been identified as an independent predictor of acute poststroke seizures in stroke patients. The present study sought to reveal the mechanisms for the development of postischemic seizures under hyperglycemic conditions. Transient forebrain ischemia was produced in adult Wistar rats by using the four-vessel occlusion method. At the normal blood glucose level, seizures occurred in ?50% of rats after 25 min of ischemia. However, in rats with hyperglycemia, the incidence rate of postischemic seizures was significantly increased to 100%. The occurrence of postischemic seizures was not correlated with the severity of brain damage in hyperglycemic rats. Mannitol, an osmotic diuretic agent, could neither prevent postischemic seizures nor alleviate the exacerbated brain damage in the presence of hyperglycemia. K(+) channels play a critical role in controlling neuronal excitability. The expression of A-type K(+) channel subunit Kv4.2 in the hippocampus and the cortex was significantly reduced in hyperglycemic rats with seizures compared with those without seizures. These results suggest that the reduction of Kv4.2 expression could contribute to the development of postischemic seizures in hyperglycemia. © 2014 Wiley Periodicals, Inc. PMID:25043828

Lei, Zhigang; Zhang, Hui; Liang, Yanling; Cui, Qiliang; Xu, Zhiqiang; Xu, Zao C

2014-12-01

19

Ionizing radiation as preconditioning against transient cerebral ischemia in rats.  

PubMed

Induction of ischemic tolerance (IT), the ability of an organism to survive an otherwise lethal ischemia, is the most effective known approach to preventing postischemic damage. IT can be induced by exposing animals to a broad range of stimuli. In this study we tried to induce IT of brain neurons using ionizing radiation (IR). A preconditioning (pre-C) dose of 10, 20, 30 or 50 Gy of gamma rays was used 2 days before an 8 min ischemia in adult male rats. Ischemia alone caused the degeneration of almost one half of neurons in CA1 region of hippocampus. However, a significant decrease of the number of degenerating neurons was observed after higher doses of radiation (30 and 50 Gy). Moreover, ischemia significantly impaired the spatial memory of rats as tested in Morris's water maze. In rats with a 50 Gy pre-C dose, the latency times were reduced to values close to the control level. Our study is the first to reveal that IR applied in sufficient doses can induce IT and thus allow pyramidal CA1 neurons to survive ischemia. In addition, we show that the beneficial effect of IR pre-C is proportional to the radiation dose. PMID:25032511

Kokošová, Natália; Danielisová, Viera; Smajda, Be?adik; Burda, Jozef

2014-10-01

20

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

21

Ventilation Air Preconditioning Systems  

E-print Network

dedicated to preconditioning the outside air. This paper discusses two such systems for cooling and dehumidification applications: one with a separate preconditioning unit and one with separate ventilation and return air paths in a single unit. Both deep...

Khattar, M.; Brandemuehl, M. J.

1996-01-01

22

[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

23

Supplemental l-arginine during cardioplegic arrest and reperfusion avoids regional postischemic injury  

Microsoft Academic Search

Unenhanced hypothermic cardioplegia does not prevent postischemic endothelial and contractile dysfunction in hearts subjected to antecedent regional or global ischemia. This study tested the hypothesis that supplementing blood cardioplegic solution and reperfusion with the nitric oxide precursor l-arginine would preserve endothelial function, reduce infarct size, and reverse postcardioplegia regional contractile dysfunction by the L-arginine-nitric oxide pathway. In 23 anesthetized dogs,

Hiroki Sato; Zhi-Qing Zhao; D. Scott McGee; Mark W. Williams; John W. Hammon; J. Vinten-Johansen

1995-01-01

24

Fetal brain genomic reprogramming following asphyctic preconditioning  

PubMed Central

Background Fetal asphyctic (FA) preconditioning is effective in attenuating brain damage incurred by a subsequent perinatal asphyctic insult. Unraveling mechanisms of this endogenous neuroprotection, activated by FA preconditioning, is an important step towards new clinical strategies for asphyctic neonates. Genomic reprogramming is thought to be, at least in part, responsible for the protective effect of preconditioning. Therefore we investigated whole genome differential gene expression in the preconditioned rat brain. FA preconditioning was induced on embryonic day 17 by reversibly clamping uterine circulation. Male control and FA offspring were sacrificed 96 h after FA preconditioning. Whole genome transcription was investigated with Affymetrix Gene1.0ST chip. Results Data were analyzed with the Bioconductor Limma package, which showed 53 down-regulated and 35 up-regulated transcripts in the FA-group. We validated these findings with RT-qPCR for adh1, edn1, leptin, rdh2, and smad6. Moreover, we investigated differences in gene expression across different brain regions. In addition, we performed Gene Set Enrichment Analysis (GSEA) which revealed 19 significantly down-regulated gene sets, mainly involved in neurotransmission and ion transport. 10 Gene sets were significantly up-regulated, these are mainly involved in nucleosomal structure and transcription, including genes such as mecp2. Conclusions Here we identify for the first time differential gene expression after asphyctic preconditioning in fetal brain tissue, with the majority of differentially expressed transcripts being down-regulated. The observed down-regulation of cellular processes such as neurotransmission and ion transport could represent a restriction in energy turnover which could prevent energy failure and subsequent neuronal damage in an asphyctic event. Up-regulated transcripts seem to exert their function mainly within the cell nucleus, and subsequent Gene Set Enrichment Analysis suggests that epigenetic mechanisms play an important role in preconditioning induced neuroprotection. PMID:23800330

2013-01-01

25

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

PubMed Central

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

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

2010-01-01

26

Edinburgh Research Explorer MicroRNAs in Postischemic Vascular Repair  

E-print Network

version: Caporali, A & Emanueli, C 2012, 'MicroRNAs in Postischemic Vascular Repair' Cardiology research.1155/2012/486702 Link: Link to publication record in Edinburgh Research Explorer Published In: Cardiology research claim. Download date: 28. Jun. 2014 #12;Hindawi Publishing Corporation Cardiology Research and Practice

Millar, Andrew J.

27

Hyperbaric oxygen preconditioning attenuates postoperative cognitive impairment in aged rats.  

PubMed

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

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

2014-06-18

28

Preconditioning Methods for Multidimensional Aerodynamics  

E-print Network

Preconditioning Methods for Multidimensional Aerodynamics E. Turkel School of Mathematical Sciences of Design Aerodynamics Braunschweig, Germany 1 #12; Contents 1 Introduction 5 1.1 General requirements

Turkel, Eli

29

Cerebral Postischemic Hyperperfusion Assessed by Xenon133 SPECT  

Microsoft Academic Search

In this study, the functional and clinical evolution of the cerebral postischemic hyperperfusion (CPH)were evaluated. Methods: For ty-four noncomatose patients suffering from unilateral cerebral isch emia located in the internal carotid territories were studied. Twenty- five consecutive patients having CPH with 133Xe-SPECTcerebral blood flow (CBF) measurement and 19 patients without cerebral hyperperfusion matched for age. CBF, vasoreactivity to acetazol- amide

Yves R. Tran Dinh; Jean-Pierre Guichard; Jacques Seylaz; CNRS UÃ

30

Silymarin and its constituents in cardiac preconditioning.  

PubMed

Silymarin, a standardised extract of Silybum marianum (milk thistle), comprises mainly of silybin, with dehydrosilybin (DHSB), quercetin, taxifolin, silychristin and a number of other compounds which are known to possess a range of salutary effects. Indeed, there is evidence for their role in reducing tumour growth, preventing liver toxicity, and protecting a number of organs against ischemic damage. The hepatoprotective effects of silymarin, especially in preventing Amanita and alcohol intoxication induced damage to the liver, are a well established fact. Likewise, there is weighty evidence that silymarin possesses antimicrobial and anticancer activities. Additionally, it has emerged that in animal models, silymarin can protect the heart, brain, liver and kidneys against ischemia reperfusion injury, probably by preconditioning. The mechanisms of preconditioning are, in general, well studied, especially in the heart. On the other hand, the mechanism by which silymarin protects the heart from ischemia remains largely unexplored. This review, therefore, focuses on evaluating existing studies on silymarin induced cardioprotection in the context of the established mechanisms of preconditioning. PMID:24879900

Zholobenko, A; Modriansky, M

2014-09-01

31

Improved cardiac metabolism and activation of the RISK pathway contributes to improved post-ischemic recovery in calorie restricted mice.  

PubMed

Recent evidence has suggested that activation of AMP-activated protein kinase (AMPK) induced by short-term caloric restriction (CR) protects against myocardial ischemia-reperfusion (I/R) injury. Because AMPK plays a central role in regulating energy metabolism, we investigated whether alterations in cardiac energy metabolism contribute to the cardioprotective effects induced by CR. Hearts from control or short-term CR mice were subjected to ex vivo I/R and metabolism, as well as post-ischemic functional recovery was measured. Even in the presence of elevated levels of fatty acids, CR significantly improved recovery of cardiac function following ischemia. While rates of fatty acid oxidation or glycolysis from exogenous glucose were similar between groups, improved functional recovery post-ischemia in CR hearts was associated with high rates of glucose oxidation during reperfusion compared to controls. Consistent with CR improving energy supply, hearts from CR mice had increased ATP levels, as well as lower AMPK activity at the end of reperfusion compared to controls. Furthermore, in agreement with the emerging concept that CR is a non-conventional form of pre-conditioning, we observed a significant increase in phosphorylation of Akt and Erk1/2 at the end of reperfusion. These data also suggest that activation of the reperfusion salvage kinase (RISK) pathway also contributes to the beneficial effects of CR in reducing post-ischemia contractile dysfunction. These findings also suggest that short-term CR improves post-ischemic recovery by promoting glucose oxidation, and activating the RISK pathway. As such, pre-operative CR may be a clinically relevant strategy for increasing ischemic tolerance of the heart. PMID:21140129

Sung, Miranda M Y; Soltys, Carrie-Lynn M; Masson, Grant; Boisvenue, Jamie J; Dyck, Jason R B

2011-03-01

32

Reduction of postischemic brain damage and memory deficits following treatment with the selective adenosine A 1 receptor agonist  

Microsoft Academic Search

Agonists of adenosine A1 receptors have been frequently proposed as candidates for clinical development in treatment of cerebral ischemia and stroke. Numerous experimental studies have shown that pre- and postischemic administration of these drugs results in a very significant reduction of postischemic brain damage. However, only a few studies determined the impact of cerebral ischemia and drug treatment on postischemic

Mark Beenhakker; Rick C.-S. Lin; Margaret F. Carter; Ian A. Paul; Norbert Bischofberger; Kenneth A. Jacobson

1996-01-01

33

Mitochondrial ROS production and subsequent ERK phosphorylation are necessary for temperature preconditioning of isolated ventricular myocytes.  

PubMed

Hypothermia and hypothermic preconditioning are known to be profoundly cardioprotective, but the molecular mechanisms of this protection have not been fully explained. In this study, temperature preconditioning (16 °C) was found to be cardioprotective in isolated adult rat ventricular myocytes, enhancing contractile recovery and preventing calcium dysregulation after oxidative stress. Hypothermic preconditioning preserved mitochondrial function by delaying the pathological opening of the mitochondrial permeability transition pore (mPTP), whereas transient mPTP flickering remained unaltered. For the first time, reactive oxygen species (ROS) from the mitochondria are shown to be released exclusively during the hypothermic episodes of the temperature-preconditioning protocol. Using a mitochondrially targeted ROS biosensor, ROS release was shown during the brief bursts to 16 °C of temperature preconditioning. The ROS scavenger N-(2-mercaptopropionyl) glycine attenuated ROS accumulation during temperature preconditioning, abolishing the protective delay in mPTP opening. Temperature preconditioning induces ROS-dependant phosphorylation of the prosurvival kinase extracellular signal-regulated kinase (ERK)1/2. ERK1/2 activation was shown to be downstream of ROS release, as the presence of a ROS scavenger during temperature preconditioning completely blocked ERK1/2 activation. The cardioprotective effects of temperature preconditioning on mPTP opening were completely lost by inhibiting ERK1/2 activation. Thus, mitochondrial ROS release and ERK1/2 activation are both necessary to signal the cardioprotective effects of temperature preconditioning in cardiac myocytes. PMID:22764104

Bhagatte, Y; Lodwick, D; Storey, N

2012-01-01

34

Contribution of protons to post-ischemic Na(+) and Ca(2+) overload and left ventricular mechanical dysfunction.  

PubMed

The intracellular accumulation of Na(+) and Ca(2+) plays a key role in ischemia-induced myocardial injury that may be manifest as left ventricular (LV) mechanical dysfunction, dysrhythmias, or infarction. This review considers the potential contributions of protons (H(+)) produced during ischemia as well as reperfusion to intracellular Na(+) and Ca(2+) homeostasis. ATP hydrolysis produces H(+) and the resulting intracellular acidosis directly impairs LV contractility. However, it is the accumulation of intracellular H(+) and the activation of Na(+)-dependent pH regulatory mechanisms, including the Na(+)-H(+) exchanger (NHE-1) and the Na(+)-HCO(3) (-) cotransporter, which contribute to Na(+) accumulation. Intracellular Na(+) accumulation, coupled with the NHE-1, then causes Ca(2+) overload and further LV mechanical dysfunction. As glycolysis uncoupled from glucose oxidation is an important determinant of the rate of H(+) production, factors that affect glucose metabolism, including degree of ischemia, myocardial workload, and competition from other energy substrates, are expected to influence Na(+) and Ca(2+) accumulation, and hence the recovery of post-ischemic LV mechanical function. Whereas an increase in the uncoupling of glycolysis from glucose oxidation accelerates H(+) production and worsens the recovery of LV mechanical function, inhibition of H(+) production improves recovery of post-ischemic LV mechanical function. Thus, alteration of glucose metabolism, either by inhibition of an excessive rate of glycolysis or by stimulation of glucose oxidation, is an attractive drug target to reduce H(+) production and limit Na(+) and Ca(2+) accumulation and thereby prevent post-ischemic LV dysfunction. PMID:16686669

Clanachan, Alexander S

2006-05-01

35

Post-ischemic inflammation regulates neural damage and protection  

PubMed Central

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

Shichita, Takashi; Ito, Minako; Yoshimura, Akihiko

2014-01-01

36

40 CFR 86.1232-96 - Vehicle preconditioning.  

...Gas-Fueled, Liquefied Petroleum Gas-Fueled and Methanol-Fueled Heavy-Duty Vehicles § 86.1232-96 Vehicle preconditioning...canisters. During this time care must be taken to prevent entry of water or other contaminants into the fuel tank. During...

2014-07-01

37

Effects of Daflon 500mg on postischemic macromolecular leak syndrome in striated skin muscle of the hamster.  

PubMed

We have recently shown that the purified micronized flavonoid fraction (90% diosmin and 10% hesperidin) Daflon 500 mg attenuates reperfusion injury in the striated skin muscle of the hamster. Herein, we report on the action of Daflon 500 mg on postischemic macromolecular leakage of FITC-dextran 150 kD provoked by tourniquet ischemia. Intravital fluorescence microscopy was used for analysis of macromolecular leakage in the microcirculation model of the hamster. A tourniquet ischemia of 4 h duration was induced followed by reperfusion. Animals were treated by gavage of Daflon 500 mg (n = 6) for 8 days at a daily dose of 30 mg kg(-1) body weight. Control animals received equivalent volumes of the vehicle (5% Arabic gum solution, n = 6). Measurements of the microcirculatory parameters were made before induction of ischemia and at 0.5, 2 and 24 h of reperfusion. After induction of ischemia, macromolecular leakage from postcapillary venules was significantly enhanced in vehicle-treated animals. Treatment with Daflon 500 mg significantly attenuated macromolecular leakage of FITC-dextran 150 kD. Preliminary data from a histomorphometric analysis (n = 3/experimental group) indicated that the number of emigrated (extravascular) leukocytes after ischemia reperfusion was markedly reduced in Daflon 500 mg-treated animals as compared to controls. These data indicate that Daflon 500 mg prevents leakage of the macromolecular tracer FITC-dextran 150 kD from postcapillary venules after postischemic reperfusion, presumably through an inhibitory action on the emigration of activated leukocytes. PMID:9477038

Nolte, D; Pickelman, S; Schütze, E; Möllmann, M; Messmer, K

1997-01-01

38

Gene expression changes after seizure preconditioning in the three major hippocampal cell layers.  

PubMed

Rodents experience hippocampal damage after status epilepticus (SE) mainly in pyramidal cells while sparing the dentate granule cell layer (DGCL). Hippocampal damage was prevented in rats that had been preconditioned by brief seizures on 2 consecutive days before SE. To identify neuroprotective genes and biochemical pathways changed after preconditioning we compared the effect of preconditioning on gene expression in the CA1 and CA3 pyramidal and DGCLs, harvested by laser capture microscopy. In the DGCL the expression of 632 genes was altered, compared to only 151 and 58 genes in CA1 and CA3 pyramidal cell layers. Most of the differentially expressed genes regulate tissue structure and intra- and extracellular signaling, including neurotransmission. A selective upregulation of energy metabolism transcripts occurred in CA1 pyramidal cells relative to the DGCL. These results reveal a broad transcriptional response of the DGCL to preconditioning, and suggest several mechanisms underlying the neuroprotective effect of preconditioning seizures. PMID:17239605

Borges, Karin; Shaw, Renee; Dingledine, Raymond

2007-04-01

39

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

PubMed

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

Zarubina, I V; Shabanov, P D

2009-03-01

40

Ischemic preconditioning. Experimental facts and clinical perspective.  

PubMed

Brief periods of non-lethal ischemia and reperfusion render the myocardium more resistant to subsequent ischemia. This adaption occurs in a biphasic pattern: the first being active immediately and lasting for 2-3 hrs (early preconditioning), the second starting at 24 hrs until 72 hrs after the initial ischemia (delayed preconditioning) and requiring genomic activation with de novo protein synthesis. Early preconditioning is more potent than delayed preconditioning in reducing infarct size; delayed preconditioning also attenuates myocardial stunning. Early preconditioning depends on the ischemia-induced release of adenosine and opioids and, to a lesser degree, also bradykinin and prostaglandins. These molecules activate G-protein coupled receptors, initiate the activation of KATP channels and generation of oxygen radicals, and stimulate a series of protein kinases with essential roles for protein kinase C, tyrosine kinases and members of the MAP kinase family. Delayed preconditioning is triggered by a similar sequence of events, but in addition essentially depends on eNOS-derived NO. Both early and pharmacological preconditioning can be pharmacologically mimicked by exogenous adenosine, opioids, NO and activators of protein kinase C. Newly synthetized proteins associated with delayed preconditioning comprise iNOS, COX-2, manganese superoxide dismutase and possibly heat shock proteins. The final mechanism of protection by preconditioning is yet unknown; energy metabolism, KATP channels, the sodium-proton exchanger, stabilisation of the cytoskeleton and volume regulation will be discussed. For ethical reasons, evidence for ischemic preconditioning in humans is hard to provide. Clinical findings that parallel experimental ischemic preconditioning are reduced ST-segment elevation and pain during repetitive PTCA or exercise tests, a better prognosis of patients in whom myocardial infarction was preceded by angina, and reduced serum markers of myocardial necrosis after preconditioning protocols during cardiac surgery with cardiac arrest. The most promising approach to apply principles of ischemic preconditioning therapeutically appears to be the pharmacological recruitment of delayed protection, as recently demonstrated with intravenous nitroglycerine in patients undergoing PTCA 24 hrs later. PMID:12473980

Post, H; Heusch, G

2002-12-01

41

Cx40 Is Required for, and Cx37 Limits, Postischemic Hindlimb Perfusion, Survival and Recovery  

PubMed Central

Background/Aims Ischemia induced by large-vessel obstruction or vascular injury induces a complex cascade of vasodilatory, remodeling and inflammatory pathways; coordination of these processes by vascular endothelium is likely to involve endothelial gap junctions. Vascular endothelium predominantly expresses two connexin (Cx) isoforms: Cx37 and Cx40. The relevance of these Cxs to postischemic limb recovery remains unclear. Methods In this study, we use a well-established, severe femoral-saphenous artery-vein pair resection model of unilateral hindlimb ischemia to test the relevance of Cx37 and Cx40 to postischemic tissue survival and recovery of limb perfusion. Results Cx40-deficient animals (Cx40–/–) experienced a severe reduction in limb perfusion relative to wild-type (WT) animals and exhibited profound and rapid failure of ischemic limb survival. By contrast, the deficit in limb perfusion was less severe in Cx37-ablated (Cx37–/–) animals compared to WT, corresponding with more rapid recovery of limb appearance and use. These results demonstrate that Cx40 is necessary for postischemic limb survival and reperfusion, whereas Cx37 deletion reduces the extent of ischemia in the same model. Conclusion In summary, we present evidence demonstrating that Cx37 and Cx40 uniquely regulate postischemic limb perfusion, altering the severity of ischemic insult and consequent postischemic survival. PMID:21986401

Fang, Jennifer S.; Angelov, Stoyan N.; Simon, Alexander M.; Burt, Janis M.

2011-01-01

42

Amelioration of postischemic stunning by deferoxamine-blood cardioplegia.  

PubMed

Limitation of oxygen free-radical injury was assessed in canine hearts by sonomicrometrically quantifying regional stroke work (RSW) in areas of myocardium perfused by the left anterior descending (LAD) and left circumflex (LCX) arteries. Volume loading of the left ventricle was performed on modified right-heart bypass before and 30 minutes after 20 minutes of LAD occlusion followed by 60 minutes of global cardioplegic arrest with either blood cardioplegia (group 1), blood cardioplegia with adjuvant deferoxamine (500 mg/l) plus 100 mg infused into the aortic root for 5 minutes after unclamping (group 2), or blood cardioplegia with adjuvant deferoxamine (600 mg/l) with unmodified reperfusion (group 3). Surgical revascularization was modeled by reopening the LAD with the first cardioplegia reinfusion. The slope of the RSW versus preload relation (a load-independent index of contractility) was decreased by a mean amount of 44% in the LAD region of group 1 hearts but was preserved in group 2 and 3 hearts. The slope of the LCX region was preserved in all groups. The use of adjuvant deferoxamine in this model of early surgical reperfusion eliminates measurable postischemic stunning. PMID:2805305

Illes, R W; Silverman, N A; Krukenkamp, I B; del Nido, P J; Levitsky, S

1989-11-01

43

Adhesion molecule expression in postischemic microvascular dysfunction: activity of a micronized purified flavonoid fraction.  

PubMed

Ischemia and reperfusion (I/R) induces neutrophil infiltration in skeletal muscle that is localized to the ischemic region. To transmigrate at ischemic regions, granulocytes must first arrest in the postcapillary venular segment of the microcirculation. Initially, leukocytes roll along the endothelium of these venules, a weak adhesive interaction that is mediated by the selectins (L-, E-, and P-selectin). Leukocyte rolling functions to slow the neutrophil during its transit through the microcirculation, thereby allowing it to monitor its local environment for the presence of activating factors arising from the ischemic tissues. When activated, the rolling granulocyte is rendered capable of forming the stronger adhesive interactions that allow the cell to become arrested in postcapillary venules in the ischemic region. These adhesive interactions are mediated by a leukocyte glycoprotein complex designated CD11/CD18 and intercellular adhesion molecule-1 (ICAM-1) expressed on endothelial cells. The stationary neutrophil uses the gradient in concentration of soluble chemoattractants liberated from ischemic tissues as a directional cue to move from the vascular to extravascular compartment, being guided in its transit across the endothelium by interactions with platelet endothelial cell adhesion molecule-1 (PECAM-1), an adhesive molecule localized to the interendothelial cleft. This paper reviews current understanding of the mechanisms underlying the establishment of leukocyte/endothelial cell interactions in postischemic skeletal muscle in terms of specific adhesion molecules that participate in neutrophil sequestration after I/R. Discovery of the molecular determinants of neutrophil/endothelial cell adhesion has uncovered potential mechanisms whereby agents exhibiting anti-adhesive properties may act. The micronized purified flavonoid fraction (450 mg diosmin, 50 mg hesperidin) prevents I/R-induced leukocyte adhesion in skeletal muscle. This anti-adhesive effect appears to be mediated at least in part by inhibition of induced expression of ICAM-1. PMID:10474047

Korthuis, R J; Gute, D C

1999-01-01

44

Myocardial preconditioning: a model or a phenomenon?  

PubMed

A brief ischemic episode (ischemic preconditioning) limits myocardial necrosis produced by a prolonged period of coronary artery occlusion and reperfusion. In absence of infarction, lack of cumulative ATP depletion, and ventricular arrhythmias and dysfunction "stunning" in models of intermittent ischemia and reperfusion also could be a component of an adaptive response to brief ischemia (preconditioning). Nonischemic stimuli also precondition the myocardium against ventricular arrhythmias and infarction by activating endogenous mechanism(s) of protection similar to that induced by ischemic preconditioning. Preservation of myocardial ATP, abolishing purine release, attenuation of free radical production, activation of adenosine receptors and KATP channels, and induction of heat shock proteins are common responses to ischemic and nonischemic stimuli of preconditioning. Although a significant reduction in myocardial infarction is critical to myocardial salvage and patient survival, it is equally important to have a functioning heart that can sustain systemic pressure without inotropic support or assist devices. It is scientifically challenging and clinically important to elucidate the mechanisms of myocardial preconditioning. However, it is necessary to expand the definition of myocardial preconditioning to include nonischemic stimuli of preconditioning and other important monitors of myocardial protection such as ventricular function and electrophysiological stability in addition to that of infarction. PMID:7579831

Abd-Elfattah, A S; Wechsler, A S

1995-07-01

45

Nonuniform Behavior of Intravenous Anesthetics on Postischemic Adhesion of Neutrophils in the Guinea Pig Heart  

Microsoft Academic Search

Adhesion of polymorphonuclear neutrophils (PMN) to the coronary endothelium is a crucial step in the develop- ment of ischemic myocardial injury. We tested the possi- ble effects of six widely used IV anesthetics on non- and postischemic coronary adhesion of PMN in isolated per- fused guinea pig hearts. Hearts (n 5 5-11\\/group) were perfused under conditions of constant coronary flow.

Andrea Szekely; Bernhard Heindl; Stefan Zahler; Peter F. Conzen; Bernhard F. Becker

2000-01-01

46

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

47

Neuronal Plasticity and Dendritic Spines: Effect of Environmental Enrichment on Intact and Postischemic Rat Brain  

Microsoft Academic Search

The authors compared the influence of environmental enrichment on intact and lesioned brain, and tested the hypothesis that postischemic exposure to an enriched environment can alter dendritic spine density in pyramidal neurons contralateral to a cortical infarct. The middle cerebral artery was occluded distal to the striatal branches in spontaneously hypertensive rats postoperatively housed either in a standard or in

Barbro B. Johansson; Pavel V. Belichenko

2002-01-01

48

Morphological characteristics of changes in limb skeletal muscle tissue during experimental postischemic recirculation  

Microsoft Academic Search

In a previous communication the writers gave data on changes in skeletal muscles in the ischemic period of acute arterial occlusion of the limbs, and the microscopic picture and functional morphology of the ischemic skeletal muscles 2 h after restoration of the blood flow to the limbs were stugied. Early postischemic recirculation is undoubtedly the most reliable test of viability

V. S. Savel'ev; G. A. Chekareva; O. D. Mishnev; O. A. Bogdanov

1985-01-01

49

Postischemic acute renal failure is reduced by short-term statin treatment in a rat model.  

PubMed

Postischemic acute renal failure (ARF) is common and often fatal. Cellular mechanisms include cell adhesion, cell infiltration and generation of oxygen free radicals, and inflammatory cytokine production. Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ("statins") directly influence inflammatory mechanisms. The hypothesis that ischemia-induced ARF could be ameliorated with statin treatment was investigated and possible molecular mechanisms were analyzed in a uninephrectomized rat model. Male Sprague-Dawley rats were pretreated with cerivastatin (0.5 mg/kg) or vehicle for 3 d. Ischemic ARF was induced by left renal artery clipping for 45 min, while the right kidney was being removed. After 24 h of ARF, serum creatinine levels were increased 7.5-fold in vehicle-treated control animals with ARF, compared with sham-operated animals (P < 0.005). Statin treatment reduced the creatinine level elevation by 40% (P < 0.005). Simultaneously, ischemia-induced severe decreases in GFR were significantly ameliorated by statin treatment (sham operation, 0.95 +/- 0.09 ml/min, n = 13; ischemia without treatment, 0.06 +/- 0.02 ml/min, n = 9; ischemia with statin pretreatment, 0.21 +/- 0.03 ml/min, n = 11; P < 0.001). Furthermore, statin pretreatment prevented the occurrence of tubular necrosis, with marked loss of the brush border, tubular epithelial cell detachment, and tubular obstruction in the S3 segment of the outer medullary stripe. In addition, monocyte and macrophage infiltration was almost completely prevented, intercellular adhesion molecule-1 upregulation was greatly decreased, and inducible nitric oxide synthase expression was reduced. Fibronectin and collagen IV expression was reduced, approaching levels observed in sham-operated animals. In vehicle-treated rats with ARF, mitogen-activated protein kinase extracellular activated kinase-1/2 activity was increased and the transcription factors nuclear factor-kappaB and activator protein-1 were activated. Statin treatment reduced this activation toward levels observed in sham-operated rats. The data suggest that hydroxy-3-methylglutaryl coenzyme A reductase inhibition protects renal tissue from the effects of ischemia-reperfusion injury and thus reduces the severity of ARF. The chain of events may involve anti-inflammatory effects, with inhibition of mitogen-activated protein kinase activation and the redox-sensitive transcription factors nuclear factor-kappaB and activator protein-1. PMID:12191973

Gueler, Faikah; Rong, Song; Park, Joon-Keun; Fiebeler, Anette; Menne, Jan; Elger, Marlies; Mueller, Dominik N; Hampich, Franziska; Dechend, Ralf; Kunter, Uta; Luft, Friedrich C; Haller, Hermann

2002-09-01

50

Roles of collateral arterial flow and ischemic preconditioning in protection of acutely ischemic myocardium.  

PubMed

The extent and rate at which necrosis develops in experimental acute myocardial infarction in the dog heart is presented together with an analysis of the role played by protective mechanisms in myocyte death. Preconditioning with ischemia delays but does not prevent myocyte death. Arterial collateral flows exceeding 30% of control flow essentially prevent myocyte death, while lesser amounts of collateral flow delay myocyte death to a variable extent. Flows of <0.09mlmin(-1)g(-1) wet exert no protective effect. Cell death occurs as quickly as it does with zero flow. Electrocardiography provides a means of detection of the preconditioned state in the dog heart in that the amount of ST elevation observed during the preconditioning episode is reduced during subsequent episodes of ischemia. Also, marked depression of arterial collateral flow can be detected by an increase in the duration of the QRS segment. PMID:24952922

Jennings, Robert B; Wagner, Galen S

2014-01-01

51

Ca3 neuronal activities of dorsal and ventral hippocampus are differentially altered in rats after prolonged post-ischemic survival.  

PubMed

The aim of the present study is to explore the potential hyper-excitability of hippocampal CA3 neurons in rats after prolonged post-ischemic survival. We conducted 15-min four-vessel-occlusion ischemic episodes in rats, allowed these animals to survive for approximately 8 months and then examined the basic morphological features and population synaptic activities of CA3 neurons. In fixed tissue sections obtained from dorsal hippocampi of post-ischemic rats, we observed a complete loss of the CA1 neurons together with a shrunken CA1 sector. Extracellular recordings in slices revealed that the overall synaptic activities of dorsal hippocampal CA3 neurons were decreased in post-ischemic rats compared with sham-operated controls. Both sham control and post-ischemic ventral hippocampal neurons were capable of exhibiting intermittent spontaneous field potentials in slices. These spontaneous field potentials spread from the CA3 to the CA1 area and their generation relied on the activity of glutamate alpha-amino-3-hydroxy-5-methyl-4 isoxazole proprionic acid (AMPA) receptors. The propensity for displaying these spontaneous field potentials appeared to be greater in post-ischemic slices than sham control slices. Our data suggest that the hyper-excitability of the post-ischemic hippocampus, if it occurs, may preferentially take place in the ventral CA3 circuitry. PMID:15664709

Wu, C P; Cheung, G; Rakhshani, N; Parvardeh, S; Asl, M Nassiri; Huang, H L; Zhang, L

2005-01-01

52

Preconditioning the Helmholtz Equation for Rigid Ducts.  

National Technical Information Service (NTIS)

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...

K. J. Baumeister, K. L. Kreider

1998-01-01

53

Preconditioning techniques for stochastic partial differential equations  

E-print Network

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

Spantini, Alessio

2013-01-01

54

Semidefinite Programming Based Preconditioning for More Robust ...  

E-print Network

Grant from the Natural Science and Engineering Research Council (Canada). 1 ... In practice, the input separable matrix is perturbed with some noise and it is ..... It is rather straightforward to analyze the influence of a preconditioning on SPA.

2013-10-08

55

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

56

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

Microsoft Academic Search

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

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

2001-01-01

57

Postischemic hyperthermia induces Alzheimer-like pathology in the rat brain  

Microsoft Academic Search

This study addresses the effects of induced hyperthermia on post-ischemic rat brain evaluated histologically and\\/or immunohistochemically after 7-day, 2-month or 6-month survival. Hyperthermia (38.5°-40°C) maintained (by heating the cage environment to 34-35°C) for two consecutive periods of 5 and 9 h timed, respectively, from 4- and 21-h recirculation following 10-min global ischemia (two-vessel occlusion + hypotension) induced chronic neuronal death

R. Sinigaglia-Coimbra; E. Cavalheiro; C. Coimbra

2002-01-01

58

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

Microsoft Academic Search

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.\\u000a It is not known whether CST contributes to ischemia\\/reperfusion injury or is a component of a cardioprotective response to\\u000a limit injury. Here, we tested whether CST by virtue of its negative inotropic activity improves post-ischemic cardiac function

Claudia Penna; Giuseppe Alloatti; Maria Pia Gallo; Maria Carmela Cerra; Renzo Levi; Francesca Tullio; Eleonora Bassino; Serena Dolgetta; Sushil K. Mahata; Bruno Tota; Pasquale Pagliaro

2010-01-01

59

Role of the cyclooxygenase pathway in the protection against postischemic stunning in conscious sheep  

Microsoft Academic Search

Objective: There are controversial reports in conscious animals regarding the role of cyclooxygenase-2 in late preconditioning (LP). This study analyzed the effect of COX-2 involvement in non-preconditioned hearts (NP) and in mediation of LP protection against stunning in conscious sheep submitted to a prolonged reversible ischemia. Methods: Six groups were considered: NP: 12 min ischemia and 120 min reperfusion; LP

Elena C. Lascano; Héctor F. del Valle; Jorge A. Negroni

2006-01-01

60

An electrocardiographic sign of ischemic preconditioning.  

PubMed

Ischemic preconditioning is a form of intrinsic cardioprotection where an episode of sublethal ischemia protects against subsequent episodes of ischemia. Identifying a clinical biomarker of preconditioning could have important clinical implications, and prior work has focused on the electrocardiographic ST segment. However, the electrophysiology biomarker of preconditioning is increased action potential duration (APD) shortening with subsequent ischemic episodes, and APD shortening should primarily alter the T wave, not the ST segment. We translated findings from simulations to canine to patient models of preconditioning to test the hypothesis that the combination of increased [delta (?)] T wave amplitude with decreased ST segment elevation characterizes preconditioning. In simulations, decreased APD caused increased T wave amplitude with minimal ST segment elevation. In contrast, decreased action potential amplitude increased ST segment elevation significantly. In a canine model of preconditioning (9 mongrel dogs undergoing 4 ischemia-reperfusion episodes), ST segment amplitude increased more than T wave amplitude during the first ischemic episode [?T/?ST slope = 0.81, 95% confidence interval (CI) 0.46-1.15]; however, during subsequent ischemic episodes the T wave increased significantly more than the ST segment (?T/?ST slope = 2.43, CI 2.07-2.80) (P < 0.001 for interaction of occlusions 2 vs. 1). A similar result was observed in patients (9 patients undergoing 2 consecutive prolonged occlusions during elective percutaneous coronary intervention), with an increase in slope of ?T/?ST of 0.13 (CI -0.15 to 0.42) in the first occlusion to 1.02 (CI 0.31-1.73) in the second occlusion (P = 0.02). This integrated analysis of the T wave and ST segment goes beyond the standard approach to only analyze ST elevation, and detects cellular electrophysiology changes of preconditioning. PMID:24778173

Meijs, Loek P B; Galeotti, Loriano; Pueyo, Esther P; Romero, Daniel; Jennings, Robert B; Ringborn, Michael; Warren, Stafford G; Wagner, Galen S; Strauss, David G

2014-07-01

61

Mitochondrial Preconditioning: A Potential Neuroprotective Strategy  

PubMed Central

Mitochondria have long been known as the powerhouse of the cell. However, these organelles are also pivotal players in neuronal cell death. Mitochondrial dysfunction is a prominent feature of chronic brain disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD), and cerebral ischemic stroke. Data derived from morphologic, biochemical, and molecular genetic studies indicate that mitochondria constitute a convergence point for neurodegeneration. Conversely, mitochondria have also been implicated in the neuroprotective signaling processes of preconditioning. Despite the precise molecular mechanisms underlying preconditioning-induced brain tolerance are still unclear, mitochondrial reactive oxygen species generation and mitochondrial ATP-sensitive potassium channels activation have been shown to be involved in the preconditioning phenomenon. This review intends to discuss how mitochondrial malfunction contributes to the onset and progression of cerebral ischemic stroke and AD and PD, two major neurodegenerative disorders. The role of mitochondrial mechanisms involved in the preconditioning-mediated neuroprotective events will be also discussed. Mitochondrial targeted preconditioning may represent a promising therapeutic weapon to fight neurodegeneration. PMID:20838473

Correia, Sónia C.; Carvalho, Cristina; Cardoso, Susana; Santos, Renato X.; Santos, Maria S.; Oliveira, Catarina R.; Perry, George; Zhu, Xiongwei; Smith, Mark A.; Moreira, Paula I.

2010-01-01

62

Xenon preconditioning: molecular mechanisms and biological effects  

PubMed Central

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

2013-01-01

63

Support graph preconditioning for elliptic finite element problems  

E-print Network

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

Wang, Meiqiu

2009-05-15

64

Postischemic leukocyte/endothelial cell interactions and microvascular barrier dysfunction in skeletal muscle: cellular mechanisms and effect of Daflon 500 mg.  

PubMed

A growing body of evidence indicates that neutrophils play a critical role in disrupting the microvascular barrier in skeletal muscle. Recent studies from our laboratory and by others indicate that administration of antibodies directed against P-selectin, ICAM-1, or the common subunit (CD18) of CD11/CD18 was as effective as neutrophil depletion in attenuating ischemia/reperfusion (I/R)-induced microvascular barrier disruption and edema formation in skeletal muscle. These studies have important implications with regard to the pathogenesis of leg ulceration in view of our more recent work indicating that the increase in tissue pressure induced by edema formation secondary to microvascular barrier disruption may lead to the development of capillary no-reflow. The resulting maldistribution of blood flow during reperfusion exacerbates muscle injury induced by ischemia. Daflon 500 mg is a purified, micronized flavonoid fraction that exhibits a number of anti-inflammatory properties and is used clinically to treat venous insufficiency. In view of these actions and the demonstrated role of neutrophil adhesion in the pathogenesis of I/R, we sought to determine whether this agent would prevent leukocyte adhesion and microvascular barrier disruption in postischemic rat cremaster muscles and small bowel. Rats were treated with Daflon 500 mg (80 mg/kg/day by gavage) or its vehicle for 2 (cremaster studies) or 10 (mesenteric studies) days prior to the experiments. Leukocyte/endothelial cell interactions and venular protein leakage were quantitated using intravital microscopic techniques in rat cremaster muscles and mesenteries subjected to ischemia (60 min for cremaster, 20 min for mesentery) and reperfusion (60 min). The results indicated that Daflon 500 mg was as effective as the anti-adhesive monoclonal antibodies in reducing postischemic leukocyte adhesion and emigration and venular protein leakage in these models. PMID:9477039

Korthuis, R J; Gute, D C

1997-01-01

65

A Mouse Model of Peripheral Postischemic Dysesthesia: Involvement of Reperfusion-Induced Oxidative Stress and TRPA1 Channel.  

PubMed

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

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

2014-12-01

66

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

67

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

68

Health and Nutrition: Preconditions for Educational Achievement.  

ERIC Educational Resources Information Center

This paper discusses the importance of maternal and infant health for children's educational achievement. Education, health, and nutrition are so closely related that changes in one causes changes in the others. Improvement of maternal and preschooler health and nutrition is a precondition for improved educational achievement. Although parental…

Negussie, Birgit

69

Postconditioning cardioprotection against infarct size and post-ischemic systolic dysfunction is influenced by gender  

Microsoft Academic Search

Whether cardioprotection by postconditioning (PostC) is gender dependent is not clear. We studied the effect of PostC in terms\\u000a of both infarct size (IS) and post-ischemic systolic dysfunction (PSD) reduction. Isolated male and female rat hearts were\\u000a subjected to 10- or 30-min of global ischemia and 120-min of reperfusion, with or without PostC (i.e., 5 cycles of 10-s reperfusion\\/ischemia\\u000a immediately

Claudia Penna; Francesca Tullio; Annalisa Merlino; Francesca Moro; Stefania Raimondo; Raffaella Rastaldo; Maria-Giulia Perrelli; Daniele Mancardi; Pasquale Pagliaro

2009-01-01

70

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

PubMed

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

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

2010-01-01

71

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

72

Tubulin ligands suggest a microtubule-NADPH oxidase relationship in postischemic cardiomyocytes.  

PubMed

Alterations of the microtubule network, which is involved in many vital processes, occur in several pathological conditions, such as cardiac ischemia. However, the connection between the microtubule assembly state and the factors affecting myocardial reperfusion injury, especially oxidative stress, is unknown. We aimed thus to study the effects of different tubulin ligands on the changes in the microtubule network and in several markers of cell injury and oxidative activity in cardiac muscle cells submitted to a reversible substrate-free, hypoxia-reoxygenation model of ischemia-reperfusion. The microtubule network was visualized by immunocytochemistry. Cell injury was evaluated via lactate dehydrogenase release and the mitochondrial function by the MTT test. Superoxide production was detected using dihydroethidium. The activity of NADPH oxidase and mRNA subunit expression were investigated. The microtubule disassembly induced by simulated ischemia was reversed by placing cardiomyocytes under normoxic conditions. This post-"ischemic" restoration of microtubule assembly was modulated by microtubule stabilizers (taxol: paclitaxel) and by microtubule disrupting drugs (nocodazole, colchicine). In addition, nocodazole decreased superoxide anion production as well as NADPH oxidase activity and mRNA expression of the NADPH oxidase subunit p22phox. These results demonstrated that the "ischemia"-induced microtubule network alteration is reversible and suggest a possible relationship between "reperfusion"-induced reassembly of microtubules and free radical generation in post-"ischemic" cardiomyocytes. PMID:16973157

Devillard, Lisa; Vandroux, David; Tissier, Cindy; Brochot, Amandine; Voisin, Sophie; Rochette, Luc; Athias, Pierre

2006-10-24

73

Effects of Cathepsin B and L Inhibition on Postischemic Protein Alterations in the Brain¶  

PubMed Central

The effects of selective inhibition of cathepsins B and L on postischemic protein alterations in the brain were investigated in a rat model of middle cerebral artery occlusion (MCAO). Cathepsin B activity increased predominantly in the subcortical region of the ischemic hemisphere where the levels of collapsing mediator response protein 2, heat shock cognate 70 kDa protein, 60 kDa heat shock protein, protein disulfide isomerase A3 and albumin, were found to be significantly elevated. Postischemic treatment with Cbz-Phe-Ser(OBzl)-CHN2, cysteine protease inhibitor 1 (CP-1), reduced infarct volume, neurological deficits and cathepsin B activity as well as the amount of heat shock proteins and albumin found in the brain. Our data strongly suggests that the decrease in heat shock protein levels and the significant reduction of serum albumin leakage into the brain following acute treatment with CP-1 is indicative of less secondary ischemic damage, which ultimately, is related to less cerebral tissue loss and improved neurological recovery of the animals. PMID:18060871

Anagli, John; Abounit, Kadija; Stemmer, Paul; Han, Yuxia; Allred, Lisa; Weinsheimer, Shantel; Movsisyan, Ashkhen; Seyfried, Donald

2009-01-01

74

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

75

Regeneration through autologous hypoxia preconditioned plasma  

PubMed Central

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

Hadjipanayi, Ektoras; Schilling, Arndt F

2014-01-01

76

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

77

A Recommendation System for Preconditioned Iterative Solvers  

E-print Network

December 2009 Major Subject: Computer Science A RECOMMENDATION SYSTEM FOR PRECONDITIONED ITERATIVE SOLVERS A Dissertation by THOMAS GEORGE Submitted to the Office of Graduate Studies of Texas A&M University in partial fulfillment of the requirements... for the degree of DOCTOR OF PHILOSOPHY Approved by: Chair of Committee, Vivek Sarin Committee Members, Patrick Lynett Valerie Taylor Yoonsuck Choe Head of Department, Valerie Taylor December 2009 Major Subject: Computer Science iii ABSTRACT A Recommendation...

George, Thomas

2011-02-22

78

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

79

Preconditioning the Human Brain: Practical Considerations for Proving Cerebral Protection  

Microsoft Academic Search

Ischemic preconditioning has evolved as one of the most powerful strategies for cerebral protection in laboratory models of\\u000a ischemia. Translating the success of laboratory studies to human cerebral protection will necessitate an approximation of\\u000a laboratory conditions. This would require a practical, easily implemented method of preconditioning and clinical settings\\u000a in which cerebral ischemia is anticipated, thereby allowing cerebral preconditioning prior

Sebastian Koch

2010-01-01

80

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

81

Toward the Optimal Preconditioned Eigensolver: Locally Optimal Block Preconditioned Conjugate Gradient Method  

Microsoft Academic Search

We describe new algorithms of the locally optimal block preconditioned conjugate gradient (LOBPCG) method for symmetric eigenvalue problems, based on a local optimization of a three-term recurrence, and suggest several other new methods. To be able to compare numerically different methods in the class, with different preconditioners, we propose a common system of model tests, using random preconditioners and initial

Andrew V. Knyazev

2001-01-01

82

Domain-decomposed preconditionings for transport operators  

NASA Technical Reports Server (NTRS)

The performance was tested of five different interface preconditionings for domain decomposed convection diffusion problems, including a novel one known as the spectral probe, while varying mesh parameters, Reynolds number, ratio of subdomain diffusion coefficients, and domain aspect ratio. The preconditioners are representative of the range of practically computable possibilities that have appeared in the domain decomposition literature for the treatment of nonoverlapping subdomains. It is shown that through a large number of numerical examples that no single preconditioner can be considered uniformly superior or uniformly inferior to the rest, but that knowledge of particulars, including the shape and strength of the convection, is important in selecting among them in a given problem.

Chan, Tony F.; Gropp, William D.; Keyes, David E.

1991-01-01

83

Clinical Applications of Remote Ischemic Preconditioning  

PubMed Central

Ischemia-reperfusion injury is a composite of damage accumulated during reduced perfusion of an organ or tissue and the additional insult sustained during reperfusion. Such injury occurs in a wide variety of clinically important syndromes, such as ischemic heart disease and stroke, which are responsible for a high degree of morbidity and mortality worldwide. Basic research has identified a number of interventions that stimulate innate resistance of tissues to ischemia-reperfusion injury. Here, we summarise the experimental and clinical trial data underpinning one of these “conditioning” strategies, the phenomenon of remote ischemic preconditioning. PMID:22400123

Veighey, Kristin; MacAllister, Raymond J.

2012-01-01

84

Fast Radial Basis Function Interpolation via Preconditioned Krylov Iteration  

Microsoft Academic Search

We consider a preconditioned Krylov subspace iterative algorithm presented by Faul et al. (IMA Journal of Numerical Analysis (2005) 25, 1—24) for computing the coefficients of a radial basis function interpolant over N data points. This preconditioned Krylov iteration has been demonstrated to be extremely robust and the iteration rapidly convergent. However, the iterative method has several steps whose computational

Nail A. Gumerov; Ramani Duraiswami

2007-01-01

85

Education for Social Responsibility: Preconditions in Retrospect and in Prospect.  

ERIC Educational Resources Information Center

One of the purposes of professional education is to educate professionals to honor their social responsibility. This paper presents three stories that identify important preconditions in education for social responsibility. The preconditions include socially responsive faculty and field integrity. Each story includes morals (i.e., lessons about…

Lawson, Hal A.

1999-01-01

86

Essential Role of Lipid Raft in Ischemic Preconditioning  

Microsoft Academic Search

Lipid rafts represent a subcompartment of the plasma membrane that coordinate and regulate varieties of signaling processes while caveolins are the integral membrane protein of the lipid raft. To study the role of lipid raft in ischemic preconditioning (PC) of the heart, rat hearts were perfused by working mode and then preconditioned in absence or presence of a lipid raft

Manika Das; Mihaela Gherghiceanu; Istvan Lekli; Subhendu Mukherjee; Lawrence M. Popescu; Dipak K. Das

2008-01-01

87

Effects of Cortical Ischemia and Postischemic Environmental Enrichment on Hippocampal Cell Genesis and Differentiation in the Adult Rat  

Microsoft Academic Search

The study aimed to elucidate the effects of cortical ischemia and postischemic environmental enrichment on hippocampal cell genesis. A cortical infarct was induced by a permanent ligation of the middle cerebral artery distal to the striatal branches in 6-month-old spontaneously hypertensive rats. Bromodeoxyuridine (BrdU) was administered as 7 consecutive daily injections starting 24 hours after surgery and animals were housed

Mila Komitova; Ekaterina Perfilieva; Bengt Mattsson; Peter S. Eriksson; Barbro B. Johansson

2002-01-01

88

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

Microsoft Academic Search

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

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

1998-01-01

89

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

90

Brain cortical tissue levels of noradrenaline and its glycol metabolites: effects of ischemia and postischemic administration of idazoxan.  

PubMed

The brain noradrenaline (NA) system is known to modulate ischemic neuronal damage, and the turnover of NA has been suggested to increase in the early recovery period following cerebral ischemia. Using HPLC and gas chromatography-mass spectrometry we analyzed the tissue levels of NA and its metabolites, 3,4-dihydroxyphenylethyleneglycol (DHPG) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), in rat brain cortex after 10 min of forebrain ischemia followed by 1 h of recirculation. The effect of idazoxan, given in cerebro-protective doses, as a bolus of 0.1 mg.kg-1 immediately after ischemia followed by 10 micrograms.kg-1.min-1 for 1 h, was also investigated. Ischemia decreased basal NA cortical levels from 384 ng/g tissue in control animals to 214 ng/g, while DHPG increased from 74 to 103 ng/g (+39%) and MHPG from 82 to 154 ng/g (+88%). Conjugated but not free DHPG increased, while both free and conjugated MHPG increased equally. The findings indicate an enhanced postischemic NA turnover with a major proportion of uptake and metabolism occurring extraneuronally, possibly secondary to a saturation of neuronal NA uptake in the postischemic phase. Idazoxan further increased NA turnover, as evidenced by higher postischemic levels of free MHPG and a higher MHPG/NA ratio. A correlation may exist between the protective action of idazoxan and its effect on NA turnover. PMID:1358670

Gustafson, I; Lidén, A; Wieloch, T

1992-01-01

91

Preconditioning reduces hypoxia-evoked alterations in glutamatergic Ca2+ signaling in rat cortex.  

PubMed

The aims of this study were (1) to characterize calcium signaling in rat cortex induced by repeated in vitro application of the glutamatergic agonists L-glutamate, NMDA, AMPA and DHPG, (2) to analyze the influence of transient severe hypobaric hypoxia (180 Torr) administered in vivo on calcium responses to stimulation of glutamate receptors by their agonists, and (3) to evaluate the effects of preconditioning with intermittent mild hypobaric hypoxia (360 Torr) 24 h before the severe hypoxia, on these Ca2+ responses. Intracellular Ca2+ dynamics was studied using the fluorescent probes fura-2 and chlortetracycline to monitor free and bound calcium (Cai and Cab) respectively. In control cortical slices, application of L-glutamate, NMDA and AMPA induced concomitant increases in Cai and Cab, reflecting Ca2+ influx and its intracellular accumulation in neurons. DHPG, an agonist of group I mGlu receptors induced a decrease in Cab accompanied by a rise in Cai levels, indicating Ca2+ mobilization. In cortical slices collected 24 h after severe hypoxia, the responses of Cab to glutamate administration were increased, DHPG-induced shifts were reversed, the increase in Cab after the first application of AMPA was reduced, while after the second, Cab rises were potentiated, and the increases in Cab evoked by NMDA application were slightly suppressed. The alterations of responses in Cab to the selective agonists were completely prevented by preconditioning with mild hypoxia. Our results suggest that protection of normal glutamatergic calcium signaling contributes to tolerance to hypoxia induced by preconditioning. PMID:18511953

Semenov, Dmitry G; Samoilov, Mikhail O; Lazarewicz, Jerzy W

2008-01-01

92

A fast, preconditioned conjugate gradient Toeplitz solver  

NASA Technical Reports Server (NTRS)

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

Pan, Victor; Schrieber, Robert

1989-01-01

93

Glutathione preconditioning ameliorates mitochondria dysfunction during warm pulmonary ischemia-reperfusion injury†, ‡  

PubMed Central

OBJECTIVES: Reduced glutathione (GSH) has been shown to improve pulmonary graft preservation. Mitochondrial dysfunction is regarded to be the motor of ischemia–reperfusion injury (IR) in solid organs. We have shown previously that IR induces pulmonary mitochondrial damage. This study elucidates the impact of GSH preconditioning on the integrity and function of pulmonary mitochondria in the setting of warm pulmonary IR. METHODS: Wistar rats were subjected to control, sham, and to two-study-group conditions (IR30/60 and GSH-IR30/60) receiving IR with or without GSH preconditioning. Rats were anesthetized and received mechanical ventilation. Pulmonary in situ clamping followed by reperfusion generated IR. Mitochondria were isolated from pulmonary tissue. Respiratory chain complexes activities (I–IV) were analyzed by polarography. Mitochondrial viability (Ca2+-induced swelling) and membrane integrity (citrate synthase assay) were determined. Subcellular-fractional cytochrome C-content (Cyt C) was quantified by enzyme-linked immunosorbent assay (ELISA). Mitochondrial membrane potential (??m) was analyzed by fluorescence-activated cell sorting (FACS) after energizing and uncoupling. Inflammatory activation was determined by myeloperoxidase activity (MPO), matrix-metalloproteinase 9 (MMP-9) activity by gel zymography. RESULTS: Pulmonary IR significantly reduced mitochondrial viability in combination with ??m hyper-polarization. GSH preconditioning improved mitochondrial viability and normalized ??m. Cyt C was reduced after IR; GSH protected from Cyt C liberation. Respiratory chain complex activities (I, II, III) declined during IR; GSH protected complex II function. GSH also protected from MMP-9 and neutrophil sequestration (P > .05). CONCLUSIONS: GSH preconditioning is effective to prevent mitochondrial death and improves complex II function during IR, but not mitochondrial membrane stability. GSH-mediated amelioration of ??m hyper-polarization appears to be the key factor of mitochondrial protection. PMID:21596579

Sommer, Sebastian-Patrick; Sommer, Stefanie; Sinha, Bhanu; Walter, Daniel; Aleksic, Ivan; Gohrbandt, Bernhard; Otto, Christoph; Leyh, Rainer G.

2012-01-01

94

The protective roles of autophagy in ischemic preconditioning  

PubMed Central

Autophagy, a process for the degradation of protein aggregates and dysfunctional organelles, is required for cellular homeostasis and cell survival in response to stress and is implicated in endogenous protection. Ischemic preconditioning is a brief and nonlethal episode of ischemia, confers protection against subsequent ischemia-reperfusion through the up-regulation of endogenous protective mechanisms. Emerging evidence shows that autophagy is associated with the protective effect of ischemic preconditioning. This review summarizes recent progress in research on the functions and regulations of the autophagy pathway in preconditioning-induced protection and cellular survival. PMID:23603984

Yan, Wen-jun; Dong, Hai-long; Xiong, Li-ze

2013-01-01

95

Signal pathway involved in the development of hypoxic preconditioning in rat hepatocytes  

Microsoft Academic Search

Ischemic preconditioning improves liver resistance to hypoxia and reduces reperfusion injury following transplantation. However, the intracellular signals that mediate the development of liver hypoxic preconditioning are largely unknown. We have investigated the signal pathway leading to preconditioning in freshly isolated rat hepatocytes. Hepatocytes were preconditioned by 10-minute incubation under hypoxic conditions followed by 10 minutes of reoxygenation and subsequently exposed

Rita Carini; Maria Grazia De Cesaris; Roberta Splendore; Daria Vay; Cinzia Domenicotti; Maria Paola Nitti; Dimitri Paola; Maria Adelaide Pronzato; Emanuele Albano

2001-01-01

96

GABA synapses mediate neuroprotection after ischemic and ?PKC preconditioning in rat hippocampal slice cultures  

Microsoft Academic Search

Delayed neuroprotection against ischemic challenges is conferred by both ischemic preconditioning (IPC) and preconditioning by activation of the ?-isoform of protein kinase C (?PKC-PC). In vivo, ischemic preconditioning enhances GABA release and ameliorates glutamate release during lethal cerebral ischemia. We tested the hypothesis that IPC and ?PKC-PC confer neuroprotection by GABA synapses in rat organotypic hippocampal slices. Ischemic preconditioning or

R Anthony DeFazio; Ami P Raval; Hung W Lin; Kunjan R Dave; David Della-Morte; Miguel A Perez-Pinzon

2009-01-01

97

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

PubMed Central

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

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

2013-01-01

98

Endothelialized and preconditioned natural umbilical arteries with long term patency open the route for future human uses.  

PubMed

The major challenge of vascular tissue engineering is to develop a small calibre vascular graft with a high patency rate. In native vessels, the thrombosis is prevented by the endothelium located at the luminal site of the vessel. The aim of this study was to develop a resistant endothelial lining on the inner surface of vascular graft using a polyelectrolyte multilayers (PEM) film. Umbilical arteries were de-endothelialized, coated with 3.5 bilayers of poly(styrene sulfonate) (PSS)/poly(allylamine hydrochloride) (PAH) and then cellularized with endothelial cells. The grafts were cultured for a week in static condition and preconditioned by exposure to a shear stress of at 1 Pa for three hours before implantation on the rabbit carotid site. Histological and confocal microscopy in vitro investigations showed that PEMs films improve cell adhesion and retention on the luminal surface after shear stress preconditioning. In vivo Doppler data showed that graft preconditioning is a crucial factor for graft patency. Indeed, preconditioned grafts remained over the whole experimental period, whereas unpreconditioned grafts were obstructed after only one week of implantation. These results open the route toward the development of a new generation of vascular substitutes having a long term patency. PMID:23609605

Paternotte, Estelle; Kerdjoudj, Halima; Kokten, Tunay; Stoltz, Jean-Francois; Kearney-Schwartz, Anna; Voegel, Jean-Claude; Menu, Patrick

2013-01-01

99

Autophagy Induced by Ischemic Preconditioning is Essential for Cardioprotection  

Microsoft Academic Search

Based on growing evidence linking autophagy to preconditioning, we tested the hypothesis that autophagy is necessary for cardioprotection\\u000a conferred by ischemic preconditioning (IPC). We induced IPC with three cycles of 5 min regional ischemia alternating with\\u000a 5 min reperfusion and assessed the induction of autophagy in mCherry-LC3 transgenic mice by imaging of fluorescent autophagosomes\\u000a in cryosections. We found a rapid and significant

Chengqun Huang; Smadar Yitzhaki; Cynthia N. Perry; Wayne Liu; Zoltan Giricz; Robert M. Mentzer Jr; Roberta A. Gottlieb

2010-01-01

100

Ischemic preconditioning in the rat brain enhances the repair of endogenous oxidative DNA damage by activating the base-excision repair pathway  

Microsoft Academic Search

The development of ischemic tolerance in the brain, whereby a brief period of sublethal ‘preconditioning’ ischemia attenuates injury from subsequent severe ischemia, may involve the activation of multiple intracellular signaling events that promote neuronal survival. In this study, the potential role of inducible DNA base-excision repair (BER), an endogenous adaptive response that prevents the detrimental effect of oxidative DNA damage,

Wenjin Li; Yumin Luo; Feng Zhang; Armando P Signore; Glenn T Gobbel; Roger P Simon; Jun Chen

2006-01-01

101

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

PubMed Central

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

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

2014-01-01

102

The Effects of Remote Ischemic Preconditioning and N-Acetylcysteine with Remote Ischemic Preconditioning in Rat Hepatic Ischemia Reperfusion Injury Model  

PubMed Central

Background. Remote ischemic preconditioning (RIP) and pharmacological preconditioning are the effective methods that can be used to prevent ischemia reperfusion (IR) injury. The aim of this study was to evaluate the effects of RIP and N-Acetylcysteine (NAC) with RIP in the rat hepatic IR injury model. Materials and Methods. 28 rats were divided into 4 groups. Group I (sham): only laparotomy was performed. Group II (IR): following 30 minutes of hepatic pedicle occlusion, 4 hours of reperfusion was performed. Group III (RIP + IR): following 3 cycles of RIP, hepatic IR was performed. Group IV (RIP + NAC + IR): following RIP and intraperitoneal administration of NAC (150?mg/kg), hepatic IR was performed. All the rats were sacrificed after blood samples were taken for the measurements of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and liver was processed for conventional histopathology. Results. The hepatic histopathological injury scores of RIP + IR and RIP + NAC + IR groups were significantly lower than IR group (P = 0.006, P = 0.003, resp.). There were no significant differences in AST and ALT values between the IR, RIP + IR, and RIP + NAC + IR groups. Conclusions. In the present study, it was demonstrated histopathologically that RIP and RIP + NAC decreased hepatic IR injury significantly. PMID:24511549

Uysal, Ali Ihsan; Ozkardesler, Sevda; Ergur, Bekir Ugur; Guneli, Ensari; Kume, Tuncay; Unal Togrul, Belgin

2014-01-01

103

Thallium 201 kinetics in stunned myocardium characterized by severe postischemic systolic dysfunction  

SciTech Connect

The hypothesis tested in this study was that despite the presence of severe postischemic myocardial dysfunction (stunning), the extraction and subsequent intracellular washout of thallium 201 should be preserved as long as irreversible sarcolemmal membrane injury was avoided. To produce myocardial stunning, 19 open-chested dogs with a critical left anterior descending coronary artery (LAD) stenosis underwent 10 5-minute periods of total LAD occlusion, each interspersed by 10 minutes of reperfusion by reflow through the critical stenosis. In another 12 control dogs observed for the same time period, no LAD occlusions were performed after placement of the critical stenosis. Hemodynamics, regional myocardial thickening by quantitative two-dimensional echocardiography, and microsphere-determined regional blood flows were serially measured. In 18 stunned dogs, systolic thickening in the LAD zone was markedly reduced to 0.4 +/- 2.4% at 40 minutes after the 10th reperfusion period compared with 32.5 +/- 2.2% thickening (p less than 0.001) in 12 control dogs at a matched time. The 201Tl first-pass extraction fraction determined by a double-isotope method using intracoronary 201Tl administration was comparable after the 10th reflow in a subgroup of 13 stunned (0.78) and six control (0.79) dogs. The T1/2 for the intracellular washout rate was also not significantly different in another group of six stunned (60 +/- 13 minutes) and six control (53 +/- 14 minutes) dogs, nor was the percentage of the 201Tl dose initially distributed in the interstitial compartment (11 +/- 3% vs. 7 +/- 2%). Systemic hemodynamics and regional flows were comparable in the two groups at 40 minutes after the 10th reflow. No dog had evidence of myocardial necrosis by triphenyl tetrazolium chloride staining.

Moore, C.A.; Cannon, J.; Watson, D.D.; Kaul, S.; Beller, G.A. (Univ. of Virginia Health Sciences Center, Charlottesville (USA))

1990-05-01

104

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; Mihailovic-Stanojevic, Nevena; Grujic Milanovic, Jelica; Jovovic, ?ur?ica; Markovic-Lipkovski, Jasmina; Cirovic, Sanja; Miloradovic, Zoran

2014-01-01

105

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

PubMed

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

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

2012-02-01

106

Postischemic administration of idazoxan, an alpha-2 adrenergic receptor antagonist, decreases neuronal damage in the rat brain.  

PubMed

The effect of an alpha-2 receptor antagonist, idazoxan, on ischemic neuronal damage in the hippocampus and neocortex was studied in rats following 10 min of forebrain ischemia. Idazoxan was given 0.1 mg/kg i.v. immediately after recirculation, followed by 48 h of continuous infusion at a rate of 10 micrograms/kg/min. A histopathological examination of the CA1 region of the dorsal hippocampus and neocortex from each hemisphere was made on paraffin-embedded sections following 7 days of survival. In ischemic animals receiving an infusion of saline, 71% of the neurons in the hippocampal CA1 region were degenerated. In contrast, in the idazoxan-treated animals only 31% of the neurons were irreversibly damaged (p less than 0.01). We conclude that postischemic administration of the alpha-2 antagonist idazoxan protects neurons against damage following cerebral ischemia. Rapid postischemic administration of alpha-2 adrenergic receptor antagonists could be an effective treatment after stroke and cardiac arrest. PMID:2564004

Gustafson, I; Miyauchi, Y; Wieloch, T W

1989-04-01

107

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

108

Preconditioning with Physiological Levels of Ethanol Protect Kidney against Ischemia/Reperfusion Injury by Modulating Oxidative Stress  

PubMed Central

Background Oxidative stress due to excessive production of reactive oxygen species (ROS) and subsequent lipid peroxidation plays a critical role in renal ischemia/reperfusion (IR) injury. The purpose of current study is to demonstrate the effect of antecedent ethanol exposure on IR-induced renal injury by modulation of oxidative stress. Materials and Methods Bilateral renal warm IR was induced in male C57BL/6 mice after ethanol or saline administration. Blood ethanol concentration, kidney function, histological damage, inflammatory infiltration, cytokine production, oxidative stress, antioxidant capacity and Aldehyde dehydrogenase (ALDH) enzymatic activity were assessed to evaluate the impact of antecedent ethanol exposure on IR-induced renal injury. Results After bilateral kidney ischemia, mice preconditioned with physiological levels of ethanol displayed significantly preserved renal function along with less histological tubular damage as manifested by the reduced inflammatory infiltration and cytokine production. Mechanistic studies revealed that precondition of mice with physiological levels of ethanol 3 h before IR induction enhanced antioxidant capacity characterized by significantly higher superoxidase dismutase (SOD) activities. Our studies further demonstrated that ethanol pretreatment specifically increased ALDH2 activity, which then suppressed lipid peroxidation by promoting the detoxification of Malondialdehyde (MDA) and 4-hydroxynonenal (HNE). Conclusions Our results provide first line of evidence indicating that antecedent ethanol exposure can provide protection for kidneys against IR-induced injury by enhancing antioxidant capacity and preventing lipid peroxidation. Therefore, ethanol precondition and ectopic ALDH2 activation could be potential therapeutic approaches to prevent renal IR injury relevant to various clinical conditions. PMID:22022451

Zeng, Li; Liu, Fang; Ding, Guoshan; Kang, Yindong; Mao, Jingyan; Cai, Ming; Zhu, Youhua; Wang, Quan-xing

2011-01-01

109

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

110

Immunizing Beef Calves: A Preconditioning Immunization Concept  

E-print Network

milk). Calves are protected until 2 to 3 months of age against nursing calf diseases. Passive immunity is expect- ed to minimize infection and shedding of disease agents and prevent development of sickness and death. Susceptible baby calves are those... diseases at the time of boosters within 3 to 6 weeks before breeding. The active immunity developed by the nursing calves is expected to minimize infection and shedding and prevent sickness and death from disease caused by exposures before and after...

Faries Jr., Floron C.

2000-12-20

111

Global gene expression profiling of ischemic preconditioning in the rat retina  

PubMed Central

Purpose To obtain and analyze the gene expression changes after ischemic preconditioning (IPC) in the rat retina. Methods Ischemic damage to the inner retina can be prevented by a short, non-deleterious, ischemic insult of 5 min applied 24 h preceding a full ischemic insult of 60 min; a phenomenon termed tolerance or IPC. The time course of changes in gene expression after induction of IPC was assessed by 22K oligonucleotide microarrays, followed by real-time quantitative polymerase chain reaction (qPCR) validation. Functional pathways of interest were identified by Gene Ontology-term analysis. Results Histology confirmed that IPC induction by 5 min of retinal ischemia results in a complete protection against the neurodegenerative effects of a 60 min ischemic period applied 24 or 48 h later. The microarray analysis revealed differential expression of 104 known genes at one or more time points between 1 h and 7 days after IPC. The group of altered genes contained a significant overrepresentation of genes involved in aminoacyl-tRNA synthetase activity (Iars, Lars, Cars, Yars, Gars, Tars), amino acid transport (Slc3a2, Slc6a6, Slc7a1, Slc38a2), regulation of transcription (including Egr1, Egr4, Nr4a1, Nr4a3, c-fos), and cell death (including Anxa1, Trib3). qPCR assays on cDNA of individual animals confirmed the microarray results. Conclusions Endogenous neuroprotection, provoked by ischemic preconditioning is associated with changes in transcript levels of several functionally-related groups of genes. During the time window of effective protection, transcript levels of genes encoding for aminoacyl-tRNA synthetases and for amino acid transport are reduced. These changes suggest that a reduction of translational activity may play a significant role in preconditioning-mediated neuroprotection. PMID:17653046

Dijk, F.; van Soest, S.; Bergen, A.A.B.

2007-01-01

112

Preconditioned Krylov subspace methods for solving nonsymmetric matrices from CFD applications  

E-print Network

Preconditioned Krylov subspace methods for solving nonsymmetric matrices from CFD applications Jun arising computational dynamics (CFD) applications. preconditioned iterative methods consist of KrylovCGSTAB, GMRES and TFQMR. Numerical experiments, using several matrices arising various relevant CFD applications

Zhang, Jun

113

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

114

Remote preconditioning in normal and hypertrophic rat hearts  

Microsoft Academic Search

Background  The aim of our study was to investigate whether remote preconditioning (RPC) improves myocardial function after ischemia\\/reperfusion\\u000a injury in both normal and hypertrophic isolated rat hearts. This is the first time in world literature that cardioprotection\\u000a by RPC in hypertrophic myocardium is investigated.\\u000a \\u000a \\u000a \\u000a \\u000a Methods  Four groups of 7 male Wistar rats each, were used: Normal control, normal preconditioned, hypertrophic control and

Christos Voucharas; Antigoni Lazou; Filippos Triposkiadis; Nikolaos Tsilimingas

2011-01-01

115

CBF changes associated with focal ischemic preconditioning in the spontaneously hypertensive rat  

Microsoft Academic Search

Experimental stroke models exhibit robust protection after prior preconditioning (PC) insults. This study comprehensively examined cerebral blood flow (CBF) responses to permanent middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats preconditioned by noninjurious transient focal ischemia, using [14C]iodoantipyrine autoradiography at varied occlusion intervals. Preconditioning was produced by 10-min occlusion of the MCA and ipsilateral common carotid artery under halothane

Liang Zhao; Thaddeus S Nowak

2006-01-01

116

PRIMME: PRECONDITIONED ITERATIVE MULTIMETHOD EIGENSOLVE R: METHODS AND SOFTWARE DESCRIPTION  

Microsoft Academic Search

This paper describes the PRIMME software package for the solving large, sparse Hermitian and real symmetric eigenvalue problems. The difficulty and importan ce of these problems have increased over the years, necessitating the use of preconditioning and near optimally converging iterative methods. On the other hand, the complexity of tuning or even using such methods has kept them outside the

ANDREAS STATHOPOULOS; JAMES R. MCCOMBS

117

Parallel Hybrid Sparse Solvers Through Flexible Incomplete Cholesky Preconditioning  

Microsoft Academic Search

Abstract. We consider parallel preconditioning schemes to accelerate the conver- gence of Conjugate Gradients (CG) for sparse linear system solution. We develop methods for constructing and applying preconditioners on multiprocessors using incomplete factorizations with selective inversion for improved,latency-tolerance. We provide empirical results on the efficiency, scalability and quality of our pre- conditioners for sparse matrices from model grids and some

Keita Teranishi; Padma Raghavan

2004-01-01

118

Preconditioned Iterative Solvers for the Generalized Stokes Problem  

E-print Network

and Vivek Sarin Department of Computer Science Texas A&M University College Station, TX 77843 Abstract [1] S. R. Sambavaram and V. Sarin. Preconditioned solenoidal basis method for incompressible fluid Applications, Apr. 2001. [2] V. Sarin. Parallel linear solvers for incompressible fluid problems

119

Ultra-compact preconditioned superprism-based photonic crystal demultiplexers  

Microsoft Academic Search

A preconditioned demultiplexing device is proposed. It based on modifying the behavior of beam during propagation inside the photonic crystal (PC) region. With proper design, the optical beams corresponding to different wavelength channels are spatially separated at their focal plane. Therefore, less area is occupied by each channel, and the total area of the device is considerably reduced. Also, the

B. Momeni; M. Soltani; M. Askari; D. K. Brown; A. Adibi

2005-01-01

120

40 CFR 86.132-00 - Vehicle preconditioning.  

Code of Federal Regulations, 2011 CFR

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

2011-07-01

121

Implementation of Preconditioned Dual-Time Procedures in OVERFLOW  

Microsoft Academic Search

Preconditioning methods have become the method of choice for the solution of flowfields involving the simultaneous presence of low Mach number flow and transonic flow regions. It is well known that these methods are important for insuring accurate numeri- cal discretization as well as convergence efficiency over various operating conditions such as low Mach num- ber,low Reynolds number and high

Shishir A. Pandya; Sankaran Venkateswaran; Thomas H. Pulliam

2003-01-01

122

A Parallel Implementation of the Block Preconditioned GCR Method  

E-print Network

with GCR. To precondition the GCR method a block Gauss-Jacobi method is used. Approximate solvers are used methods 1 Introduction This paper addresses the parallel implementation of a Krylov accelerated block Gauss-Jacobi method for the DeFT Navier-Stokes solver described in [15], and is the continuation of work

Vuik, Kees

123

40 CFR 86.132-96 - Vehicle preconditioning.  

...after completion of the preconditioning drive. (g) The vehicle shall be soaked...concentration provides at least a 4:1 safety factor against the lean flammability limit...concentration provides at least a 4:1 safety factor against the lean flammability...

2014-07-01

124

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

E-print Network

diffusion flames. We con­ sider a flame sheet problem with one­step chemical reaction. The governingPreconditioned Multigrid Simulation of an Axisymmetric Laminar Diffusion Flame \\Lambda Samir Karaa of an elliptic flame sheet problem. By selecting the generalized minimum residual method as the linear smoother

Zhang, Jun

125

Ischemic preconditioning and preinfarction angina in the clinical arena  

Microsoft Academic Search

In animals, brief episodes of ischemia before a total coronary occlusion protect the heart and result in a smaller myocardial infarct size. In humans, episodes of angina before acute myocardial infarction might also confer a preconditioning or protective effect; numerous studies show that preinfarction angina is associated with smaller infarcts. Preinfarction angina is also associated with reductions in ventricular dysfunction,

Robert A Kloner; Shereif H Rezkalla

2004-01-01

126

Mitigation of postischemic cardiac contractile dysfunction by CaMKII inhibition: effects on programmed necrotic and apoptotic cell death.  

PubMed

While Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been suggested to be an important protein regulating heart function upon ischemia/reperfusion (I/R), the mechanisms responsible are not fully known. Furthermore, it is not known whether CaMKII activation can modulate necroptosis, a recently described form of programmed cell death. In order to investigate these issues, Langendroff-perfused rat hearts were subjected to global ischemia and reperfusion, and CaMKII inhibition was achieved by adding the CaMKII inhibitor KN-93 (0.5 ?mol/dm(3)) to the perfusion solution before the induction of ischemia. Immunoblotting was used to detect changes in expression of proteins modulating both necroptotic and apoptotic cell death. CaMKII inhibition normalized I/R induced increases in expression of necroptotic RIP1 and caspase-8 along with proteins of the intrinsic apoptotic pathway, namely cytochrome c and caspase-9. In addition, it increased the Bcl-2/Bax ratio and reduced caspase-3 and cleaved PARP1 content suggesting reduction of cell death. These changes coexisted with improvement of postischemic contractile function. On the other hand, there was no correlation between levels of pT287-CaMKII? and LVDP recovery after I/R. These results demonstrate for the first time that CaMKII inhibition may mitigate cardiac contractile dysfunction, at least partially, by limiting the contents of not only apoptotic, but also necroptotic proteins. Phosphorylation of CaMKII seems unlikely to determine the degree of postischemic recovery of contractile function. PMID:24347176

Szobi, Adrian; Rajtik, Tomas; Carnicka, Slavka; Ravingerova, Tana; Adameova, Adriana

2014-03-01

127

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

PubMed Central

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

Panahpour, Hamdollah; Dehghani, Gholam Abbas

2012-01-01

128

Insulin inhibits myocardial ischemia-induced apoptosis and alleviates chronic adverse changes in post-ischemic cardiac structure and function.  

PubMed

Insulin has been shown to possess significant anti-apoptotic effect in myocardial ischemia/reperfusion (MI/R). However, the contribution by this protection of insulin to the prolonged cardiac function in rats subjected to ischemia remains unclear. The present study attempted to test whether early insulin treatment influences adverse prolonged post-ischemic cardiac structural and functional changes. Adult male rats were subjected to left anterior descending coronary artery occlusion and were randomized to receive one of the following treatments: saline (4 ml/kg/h i.v. injection beginning 10 min before the ischemia and continuing for 2 h), insulin (60 U/l, i.v. injection following the same routine, and hypodermic injection of insulin (0.5 U/ml, 1 ml/kg/d) for 3 days after the ischemia surgery) or insulin plus wortmannin (15 mug/kg i.v. injection 15 min before each insulin administration). Treatment with insulin significantly reduced infarct size, decreased plasma creatine kinase and lactate dehydrogenase activities, decreased apoptosis index and caspase-3 activity (all P < 0.01 vs. saline), and improved cardiac function 24 h after ischemia. Importantly, at the end of 4 weeks after the ischemia surgery, MI rats receiving insulin treatment showed smaller left ventricle (LV) cavity and thicker systolic interventricular septum, and increased cardiac ejection fraction and LV fractional shortening (all P < 0.05 vs. saline). Inhibition of insulin signaling with wortmannin not only blocked insulin's anti-apoptotic effect, but also almost completely abolished effects of insulin on cardiac structure and function. These data indicate that inhibition of apoptosis by early insulin treatment alleviates chronic adverse changes in post-ischemic cardiac structure and function. PMID:19590963

Xing, Wenjuan; Yan, Wenjun; Fu, Feng; Jin, Yulan; Ji, Lele; Liu, Wenchong; Wang, Li; Lv, Anlin; Duan, Yunyan; Zhang, Jun; Zhang, Haifeng; Gao, Feng

2009-09-01

129

Hypoxic preconditioning protects rat hearts against ischaemia-reperfusion injury: role of erythropoietin on progenitor cell mobilization  

PubMed Central

Preconditioning, such as by brief hypoxic exposure, has been shown to protect hearts against severe ischaemia. Here we hypothesized that hypoxic preconditioning (HPC) protects injured hearts by mobilizing the circulating progenitor cells. Ischaemia–reperfusion (IR) injury was induced by left coronary ligation and release in rats kept in room air or preconditioned with 10% oxygen for 6 weeks. To study the role of erythropoietin (EPO), another HPC + IR group was given an EPO receptor (EPOR) antibody via a subcutaneous mini-osmotic pump 3 weeks before IR induction. HPC alone gradually increased haematocrit, cardiac and plasma EPO, and cardiac vascular endothelial growth factor (VEGF) only in the first two weeks. HPC improved heart contractility, reduced ischaemic injury, and maintained EPO and EPOR levels in the infarct tissues of IR hearts, but had no significant effect on VEGF. Interestingly, the number of CD34+CXCR4+ cells in the peripheral blood and their expression in HPC-treated hearts was higher than in control. Preconditioning up-regulated cardiac expression of stromal derived factor-1 (SDF-1) and prevented its IR-induced reduction. The EPOR antibody abolished HPC-mediated functional recovery, and reduced SDF-1, CXCR4 and CD34 expression in IR hearts, as well as the number of CD34+CXCR4+ cells in blood. The specificity of neutralizing antibody was confirmed in an H9c2 culture system. In conclusion, exposure of rats to moderate hypoxia leads to an increase in progenitor cells in the heart and circulation. This effect is dependent on EPO, which induces cell homing by increased SDF-1/CXCR4 and reduces the heart susceptibly to IR injury. PMID:18845609

Lin, Jih-Shyong; Chen, Yih-Sharng; Chiang, Han-Sun; Ma, Ming-Chieh

2008-01-01

130

Intramyocardial injection of hypoxia-preconditioned adipose-derived stromal cells treats acute myocardial infarction: an in vivo study in swine.  

PubMed

Hypoxic preconditioning is a promising method for improving the anti-apoptotic and paracrine signaling capabilities of adipose-derived stromal cells (ADSCs). The purpose of this study was to analyze the influence of different hypoxic conditions on ADSCs and the therapeutic effects of hypoxia-preconditioned ADSCs (HPADSCs) on an animal model of myocardial infarction (MI). For the in vitro studies, ADSCs were divided into five groups and cultured in different oxygen concentrations (1, 3, 5, 10, and 21 %). After 24 h, RT-PCR and western blots showed that 3 % oxygen preconditioning could improve the viability and cytokine secretion of the ADSCs. A Matrigel assay indicated that the HPADSC-conditioned medium could stimulate endothelial cells to form capillary-like tubes. For the in vivo studies, MI was induced by coronary occlusion in 24 mature Chinese minipigs. The animals were divided into three groups and treated by intramyocardial injection with vehicle alone (saline group), with 1?×?10(8) ADSCs cultured in normoxic conditions (ADSCs group) or with 1?×?10(8) ADSCs precultured in 3 % oxygen (HPADSCs group). SPECT and echocardiography demonstrated that cardiac function was improved significantly in the HPADSC transplant group compared with the vehicle control group (P?preconditioning treatment for ADSCs. HPADSC transplantation can prevent ventricular remodeling and reduce the infarct size. PMID:25135062

Jiang, Yiyao; Chang, Pengyu; Pei, Yu; Li, Baojiang; Liu, Yongjun; Zhang, Zhang; Yu, Jing; Zhu, Delin; Liu, Xiaocheng

2014-11-01

131

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

132

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

133

Preconditioning the non-relativistic many-fermion problem  

E-print Network

Preconditioning is at the core of modern many-fermion Monte Carlo algorithms, such as Hybrid Monte Carlo, where the repeated solution of a linear problem involving an ill-conditioned matrix is needed. We report on a performance comparison of three preconditioning strategies, namely Chebyshev polynomials, strong-coupling approximation and weak-coupling expansion. We use conjugate gradient (CG) on the normal equations as well as stabilized biconjugate gradient (BiCGStab) as solvers and focus on the fermion matrix of the unitary Fermi gas. Our results indicate that BiCGStab is by far the most efficient strategy, both in terms of the number of iterations and matrix-vector operations.

Timour Ten; Joaquín E. Drut; Timo A. Lähde

2010-08-21

134

PRECONDITIONING A MIXED DISCONTINUOUS FINITE ELEMENT METHOD FOR RADIATION DIFFUSION  

SciTech Connect

We propose a multilevel preconditioning strategy for the iterative solution of large sparse linear systems arising from a finite element discretization of the radiation diffusion equations. In particular, these equations are solved using a mixed finite element scheme in order to make the discretization discontinuous, which is imposed by the application in which the diffusion equation will be embedded. The essence of the preconditioner is to use a continuous discretization of the original, elliptic diffusion equation for preconditioning the discontinuous equations. We have found that this preconditioner is very effective and makes the iterative solution of the discontinuous diffusion equations practical for large problems. This approach should be applicable to discontinuous discretizations of other elliptic equations. We show how our preconditioner is developed and applied to radiation diffusion problems on unstructured, tetrahedral meshes and show numerical results that illustrate its effectiveness.

JAMES S. WARSA; MICHELE BENZI; TODD A. WAREING; JIM E. MOREL

2002-06-18

135

Xenon preconditioning reduces brain damage from neonatal asphyxia in rats  

Microsoft Academic Search

Xenon attenuates on-going neuronal injury in both in vitro and in vivo models of hypoxic–ischaemic injury when administered during and after the insult. In the present study, we sought to investigate whether the neuroprotective efficacy of xenon can be observed when administered before an insult, referred to as ‘preconditioning’. In a neuronal–glial cell coculture, preexposure to xenon for 2 h

Daqing Ma; Mahmuda Hossain; Garry K J Pettet; Yan Luo; Ta Lim; Stanislav Akimov; Robert D Sanders; Nicholas P Franks; Mervyn Maze

2006-01-01

136

Naloxone Blockade of Myocardial Ischemic Preconditioning is Stereoselective  

Microsoft Academic Search

This study tested the hypothesis that endogenous opioids are involved in the infarct limitation of myocardial ischemic preconditioning (IP). Blockade of IP-induced infarct limitation by (?)naloxone hydrochloride (?NAL) or its receptor-inactive stereoisomer (+)naloxone (+NAL) was evaluated. Fifty-two pentobarbitone-anesthetized, open-chest rabbits underwent 30 min coronary artery occlusion and 180 min reperfusion. Treatment groups were: control (n=9), IP (n=8), ?NAL (n=9) and

Grace L. Chien; Donna M. Van Winkle

1996-01-01

137

Local pressure preconditioning method for steady incompressible flows  

Microsoft Academic Search

The convergence and accuracy characteristics of the preconditioned incompressible Euler and Navier–Stokes equations are studied. An object-oriented C++ numerical code has been developed for solving the inviscid and viscous, steady, incompressible flows problems. The code is based on the cell-centred finite volume method. In this scheme, two-dimensional incompressible Euler and Navier–Stokes equations are modified by a robust artificial compressibility (AC)

V. Esfahanian; P. Akbarzadeh

2010-01-01

138

Preconditions for successful guideline implementation: perceptions of oncology nurses  

PubMed Central

Background Although evidence-based guidelines are important for improving the quality of patient care, implementation in practice is below expectations. With the recent focus on team care, guidelines are intended to promote the integration of care across multiple disciplines. We conducted an exploratory study to understand oncology nurses' perceptions of guideline implementation and to learn their views on how their experiences affected the implementation. Methods A qualitative study was used with focus group interviews. We collected data from 11 nurses with more than 5 years of oncology nursing experience in Japan. The data were analyzed using grounded theory. Results Results of the analysis identified "preconditions for successful guideline implementation" as a core category. There were 4 categories (goal congruence, equal partnership, professional self-development and user-friendliness) and 11 subcategories related to organizational, multidisciplinary, individual, and guideline levels. Conclusions Although the guidelines were viewed as important, they were not fully implemented in practice. There are preconditions at the organizational, multidisciplinary, individual, and guideline levels that must be met if an organization is to successfully implement the guideline in clinical settings. Prioritizing strategies by focusing on these preconditions will help to facilitate successful guideline implementation. PMID:22067513

2011-01-01

139

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

140

Intracellular Free Calcium and Mitochondrial Membrane Potential in Ischemia\\/Reperfusion and Preconditioning  

Microsoft Academic Search

Moderation of calcium perturbations has been implicated in ischemic preconditioning. As mitochondria possess an effective Ca2+transporting system driven by the mitochondrial membrane potential, experiments were performed to study time-averaged intracellular free calcium and the mitochondrial membrane potential during preconditioning and ischemia–reperfusion. Isolated rat hearts were subjected to 5 min of preconditioning, a 9-min intervening reperfusion and 21 min of ischemia

Kari V Ylitalo; Antti Ala-Rämi; Erkki V Liimatta; Keijo J Peuhkurinen; Ilmo E Hassinen

2000-01-01

141

Preconditioning improves cardioplegia-related coronary microvascular smooth muscle hypercontractility: Role of KATP channels  

Microsoft Academic Search

Objectives: The effect of preconditioning before hyperkalemic cardioplegia on the coronary smooth muscle remains to be elucidated. We tested the hypothesis that hypoxic preconditioning could protect coronary smooth muscle against subsequent hyperkalemic cardioplegia-induced coronary vasospasm and that this preconditioning effect could be mediated by KATP channels. Methods: Rat coronary arterioles (endothelium-denuded) were studied in a pressurized, no-flow, normothermic state. Simultaneous

Naruto Matsuda; Kathleen G. Morgan; Frank W. Sellke

1999-01-01

142

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

143

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

SciTech Connect

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

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

1986-07-01

144

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

Miloradovic, Zoran; Ivanov, Milan; Mihailovic-Stanojevic, Nevena; Grujic Milanovic, Jelica; Jovovic, ?ur?ica; Vajic, Una-Jovana; Markovic-Lipkovski, Jasmina

2014-01-01

145

[Current decubitus prevention and treatment algorhytm].  

PubMed

Decubitus ulcer treatment options, as well as the etiology, classification and prevention guidelines are presented. The importance of a multidisciplinary approach along with prevention and education is emphasized. The National Pressure Ulcer Advisory Panel guidelines ensure contemporary decubitus ulcer treatment all over the world, while adoption of the basic algorithm is a precondition of good medical practice and nursing care. Upgrading the patient quality of life and complete healing of decubitus ulcer is definitely achievable by strict application of these recommendations. PMID:25327000

Gaji?, Aleksandar

2014-10-01

146

The neuroprotective effect of the antioxidant flavonoid derivate di- tert -butylhydroxyphenyl is parallel to the preventive effect on post-ischemic Kir2.x impairment but not to post-ischemic endothelial dysfunction  

Microsoft Academic Search

In the rat model of transient cerebral ischemia induced by intraluminal occlusion of the middle cerebral artery, we investigated the respective roles of ischemia and reperfusion in endothelium-dependent relaxation and smooth muscle relaxation related to the inward rectifier potassium current (Kir2.x), using the Halpern arteriography technique and\\/or patch-clamp technique. We first demonstrated that reperfusion is necessary to induce a significant

Olivier Pétrault; Michèle Bastide; Nicole Cotelle; Patrick Gelé; Sophie Gautier; Maud Laprais; Joseph Vamecq; Patrick Duriez; Régis Bordet

2004-01-01

147

Role of ischemic preconditioning in hepatic ischemia-reperfusion injury  

PubMed Central

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

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

2014-01-01

148

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

149

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

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

MSP: A Class of Parallel Multistep Successive Sparse Approximate Inverse Preconditioning Strategies  

Microsoft Academic Search

We develop a class of parallel multistep successive preconditioning strategies to en- hance efficiency and robustness of standard sparse approximate inverse preconditioning techniques. The key idea is to compute a series of simple sparse matrices to approximate the inverse of the original matrix. Studies are conducted to show the advantages of such an approach in terms of both im- proving

Kai Wang; Jun Zhang

2003-01-01

152

Preconditioned Krylov subspace methods for solving nonsymmetric matrices from CFD applications q  

E-print Network

Preconditioned Krylov subspace methods for solving nonsymmetric matrices from CFD applications q dynamics (CFD) applications. The preconditioned iterative methods consist of Krylov subspace accelerators matrices arising from various relevant CFD applications, are reported. Ã? 2000 Elsevier Science S.A. All

Zhang, Jun

153

Effect of heat preconditioning by microwave hyperthermia on human skeletal muscle after eccentric exercise  

Microsoft Academic Search

The purpose of this study was to clarify whether heat precondi- tioning results in less eccentric exercise-induced muscle damage and muscle soreness, and whether the repeated bout effect is enhanced by heat preconditioning prior to eccentric exercise. Nine untrained male volunteers aged 23 ± 3 years participated in this study. Heat preconditioning included treatment with a mi- crowave hyperthermia unit

Norio Saga; Shizuo Katamoto; Hisashi Naito

154

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

E-print Network

A Preconditioned Newton-Krylov Method for Computing Stationary Pulse Solutions of Mode-locked laser cavity using a preconditioned matrix-implicit Newton-Krylov solver. Solutions are obtained two solving the periodic boundary value problem for the nonlinear cavity using a Newton-Raphson method

Polz, Martin

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

Relationships between mixis in Brachionus plicatilis and preconditioning of culture medium by crowding  

Microsoft Academic Search

Several experiments with Brachionus plicatilis have been conducted to test the existence of chemical-mediated induction of mixis. In a first experimental set, bioassays were used to test relationships between preconditioning of culture medium to high population density and the occurrence of mixis in mass cultures with these media. The results show that a preconditioned medium has inducing properties that are

Maria José Carmona; Manuel Serra; Maria Rosa Miracle

1993-01-01

157

A Taxonomy of Buffer Overflow Preconditions Matt Bishop, Damien Howard, Sophie Engle, and Sean Whalen  

E-print Network

A Taxonomy of Buffer Overflow Preconditions Matt Bishop, Damien Howard, Sophie Engle, and Sean on vulnerabilities has focused on buffer overflows, in which data exceeding the bounds of an array is loaded of buffer overflow vulnerabilities based upon preconditions, or conditions that must hold for an exploitable

California at Davis, University of

158

Accelerated scaled memoryless BFGS preconditioned conjugate gradient algorithm for unconstrained optimization  

Microsoft Academic Search

An accelerated scaled memoryless BFGS preconditioned conjugate gradient algorithm for solving unconstrained optimization problems is presented. The basic idea is to combine the scaled memoryless BFGS method and the preconditioning technique in the frame of the conjugate gradient method. The preconditioner, which is also a scaled memoryless BFGS matrix, is reset when the Beale-Powell restart criterion holds. The parameter scaling

Neculai Andrei

2010-01-01

159

THE SOLUTION OF LARGE EFIE PROBLEMS VIA PRECONDITIONED MULTILEVEL FAST MULTIPOLE  

E-print Network

THE SOLUTION OF LARGE EFIE PROBLEMS VIA PRECONDITIONED MULTILEVEL FAST MULTIPOLE ALGORITHM T. Malas an effective preconditioning scheme for the iterative solution of the systems formulated by the electric- field the efficiency of the inner-outer solution scheme. We report the solution of large EFIE systems of several

Gürel, Levent

160

Inhalational anesthetics as neuroprotectants or chemical preconditioning agents in ischemic brain  

Microsoft Academic Search

This review will focus on inhalational anesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury. The limitations and challenges of past and current research in this area will be addressed before reviewing experimental and clinical studies evaluating the effects of inhalational anesthetics before and during cerebral ischemia. Mechanisms underlying volatile anesthetic neuroprotection and preconditioning will also

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

2007-01-01

161

Effects of Ischemic Preconditioning of Different Intraoperative Ischemic Times of Vascularized Bone Graft Rabbit Models  

PubMed Central

Background Ischemic preconditioning has been shown to improve the outcomes of hypoxic tolerance of the heart, brain, lung, liver, jejunum, skin, and muscle tissues. However, to date, no report of ischemic preconditioning on vascularized bone grafts has been published. Methods Sixteen rabbits were divided into four groups with ischemic times of 2, 6, 14, and 18 hours. Half of the rabbits in each group underwent ischemic preconditioning. The osteomyocutaneous flaps consisted of the tibia bone, from which the overlying muscle and skin were raised. The technique of ischemic preconditioning involved applying a vascular clamp to the pedicle for 3 cycles of 10 minutes each. The rabbits then underwent serial plain radiography and computed tomography imaging on the first, second, fourth, and sixth postoperative weeks. Following this, all of the rabbits were sacrificed and histological examinations were performed. Results The results showed that for clinical analysis of the skin flaps and bone grafts, the preconditioned groups showed better survivability. In the plain radiographs, except for two non-preconditioned rabbits with intraoperative ischemic times of 6 hours, all began to show early callus formation at the fourth week. The computed tomography findings showed more callus formation in the preconditioned groups for all of the ischemic times except for the 18-hour group. The histological findings correlated with the radiological findings. There was no statistical significance in the difference between the two groups. Conclusions In conclusion, ischemic preconditioning improved the survivability of skin flaps and increased callus formation during the healing process of vascularized bone grafts. PMID:24286040

Wan Ahmad Kamal, Wan Syazli Rodzaia; Noor, Norizal Mohd; Abdullah, Shafie

2013-01-01

162

Remote ischaemic preconditioning of the hind limb reduces experimental liver warm ischaemia–reperfusion injury  

Microsoft Academic Search

Background: Direct ischaemic preconditioning of the liver reduces ischaemia-reperfusion injury (IRI). Remote ischaemic preconditioning (RIPC) of a limb has been shown to reduce IRI to the heart. This study determined the effect of brief remote ischaemia to the limb in reducing early liver warm IRI. Methods: Twenty-eight male rabbits were allocated into four groups: sham operated, RIPC alone, IRI alone

S. Kanoria; R. Jalan; N. A. Davies; A. M. Seifalian; R. Williams; B. R. Davidson

2006-01-01

163

Robust Parallel Preconditioned Power Grid Simulation on GPU With Adaptive Runtime Performance Modeling and Optimization  

Microsoft Academic Search

Leveraging the power of nowadays graphics process- ing units for robust power grid simulation remains a challenging task. Existing preconditioned iterative methods that require incomplete matrix factorizations cannot be effectively accelerated on graphics processing unit (GPU) due to its limited hardware resource as well as data parallel computing. This paper presents an efficient GPU-based multigrid preconditioning algorithm for robust power

Zhuo Feng; Xueqian Zhao; Zhiyu Zeng

2011-01-01

164

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

Code of Federal Regulations, 2012 CFR

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

2012-07-01

165

Role of miRs in Cardiac Preconditioning  

PubMed Central

Preconditioning of the heart by sub-lethal ischemia, mild heat shock or hypoxia have evolved as powerful experimental tools to discover novel signaling mechanisms in cardioprotection. The ultimate goal is to determine novel therapeutic targets for potential application in humans in protecting the heart against ischemia-related injuries. In recent years, there has been a tremendous interest in understanding the role of small non-coding RNAs, microRNAs (miRs), in cardiovascular diseases. miRs have been recognized as regulators of gene expression by destabilization and translational inhibition of target mRNAs. Studies have shown that several miRs including miR-1, miR-133, miR-21, miR-126, miR-320, miR-92a and miR-199a are regulated after preconditioning and play an active role in protection of the heart against ischemia/reperfusion injury. These miRs also drive the synthesis of important cardioprotective proteins including HSP-70, eNOS, iNOS, HSP-20, Sirt-1 and HIF-1?. We believe that identification and targeted delivery of miR(s) in the heart could have an immense therapeutic potential in reducing myocardial infarction in patients suffering from heart disease. PMID:20980922

Salloum, Fadi N.; Yin, Chang; Kukreja, Rakesh C.

2014-01-01

166

Oxidant Preconditioning Protects Human Proximal Tubular Cells against Lethal Oxidant Injury via p38 MAPK and Heme Oxygenase1  

Microsoft Academic Search

Ischemic preconditioning protects the kidney from subsequent ischemic injury but the signal transduction pathways involved are unknown. Human proximal tubular (HK-2) cells were protected from injury with 2.5 mM H2O2 by preconditioning with a single 15-min exposure to 500 ?M H2O2 followed by 16 h of recovery (oxidant preconditioning). To identify the signaling pathways involved in oxidant preconditioning, we utilized

H. Thomas Lee; Hua Xu; Ayuko Ota-Setlik; Charles W. Emala

2003-01-01

167

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation  

Microsoft Academic Search

Postconditioning (PostC) modifies the early post-ischemic pH, redox environment, and activity of enzymes. We hypothesized\\u000a that early acidosis in PostC may affect superoxide dismutase (SOD) and catalase (CAT) activities, may reduce 3-nitrotyrosine\\u000a (3-NT) protein levels, and may increase S-nitrosylated (SNO) protein levels, thus deploying its protective effects. To verify\\u000a this hypothesis, we studied the early (7th min) and late (120th

Claudia Penna; Maria-Giulia Perrelli; Francesca Tullio; Francesca Moro; Maria Laura Parisella; Annalisa Merlino; Pasquale Pagliaro

168

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells  

PubMed Central

Ischemia causes kidney tubular cell damage and abnormal renal function. The kidney is capable of morphological restoration of tubules and recovery of function. Recently, it has been suggested that cells repopulating the ischemically injured tubule derive from bone marrow stem cells. We studied kidney repair in chimeric mice expressing GFP or bacterial ?-gal or harboring the male Y chromosome exclusively in bone marrow-derived cells. In GFP chimeras, some interstitial cells but not tubular cells expressed GFP after ischemic injury. More than 99% of those GFP interstitial cells were leukocytes. In female mice with male bone marrow, occasional tubular cells (0.06%) appeared to be positive for the Y chromosome, but deconvolution microscopy revealed these to be artifactual. In ?-gal chimeras, some tubular cells also appeared to express ?-gal as assessed by X-gal staining, but following suppression of endogenous (mammalian) ?-gal, no tubular cells could be found that stained with X-gal after ischemic injury. Whereas there was an absence of bone marrow–derived tubular cells, many tubular cells expressed proliferating cell nuclear antigen, which is reflective of a high proliferative rate of endogenous surviving tubular cells. Upon i.v. injection of bone marrow mesenchymal stromal cells, postischemic functional renal impairment was reduced, but there was no evidence of differentiation of these cells into tubular cells of the kidney. Thus, our data indicate that bone marrow–derived cells do not make a significant contribution to the restoration of epithelial integrity after an ischemic insult. It is likely that intrinsic tubular cell proliferation accounts for functionally significant replenishment of the tubular epithelium after ischemia. PMID:16007251

Duffield, Jeremy S.; Park, Kwon Moo; Hsiao, Li-Li; Kelley, Vicki R.; Scadden, David T.; Ichimura, Takaharu; Bonventre, Joseph V.

2005-01-01

169

Tolerance to nitroglycerin-induced preconditioning of the endothelium: a human in vivo study.  

PubMed

Damage and dysfunction of the vascular endothelium critically influence clinical outcomes after ischemia and reperfusion (I/R). Brief exposure to organic nitrates can protect the vascular endothelium from I/R injury via a mechanism that is similar to ischemic preconditioning and is independent of hemodynamic changes. The clinical relevance of these protective effects clearly depends on whether they can be sustained over time. Twenty-four healthy (age 25-32) male volunteers were randomized to receive 1) transdermal nitroglycerin (GTN; 0.6 mg/h) administered for 2 h on 1 day only, 2) transdermal GTN for 2 h/day for 7 days, or 3) continuous therapy with transdermal GTN for 7 days. Eight volunteers underwent continuous GTN therapy followed by intra-arterial infusion of the antioxidant vitamin C. Finally, five additional subjects underwent no therapy and served as controls. Endothelial function measurements were performed before and after induction of I/R of the arm. I/R caused a significant blunting of the flow responses to acetylcholine in the control group (P < 0.01 vs. before I/R). A single 2-h GTN dosage, given 24 h before I/R, prevented I/R-induced endothelial dysfunction [P = not significant (NS) vs. before I/R], but this protective effect was completely lost after 1 wk of GTN administration 2 h/day (P < 0.05 vs. before I/R; P = NS vs. control). In subjects who received continuous GTN, endothelial responses were blunted before I/R, and I/R did not cause further endothelial dysfunction. Finally, vitamin C normalized acetylcholine responses and prevented the loss of preconditioning associated with prolonged GTN. In a separate experimental model using isolated human endothelial cells, short-term incubation with GTN caused upregulation of heme oxygenase, an effect that was lost after prolonged GTN administration. Although a single administration of GTN is able to protect the endothelium from I/R-induced endothelial dysfunction, this protection is lost upon prolonged exposure, likely via an oxidative mechanism. PMID:19933412

Gori, Tommaso; Dragoni, Saverio; Di Stolfo, Giuseppe; Sicuro, Silvia; Liuni, Andrew; Luca, Mary Clare; Thomas, George; Oelze, Matthias; Daiber, Andreas; Parker, John D

2010-02-01

170

A Preconditioned Newton-Krylov Method for Computing Steady-State Pulse Solutions of Mode-Locked Lasers  

E-print Network

A Preconditioned Newton-Krylov Method for Computing Steady-State Pulse Solutions of Mode and Optimization Program #12;2 #12;A Preconditioned Newton-Krylov Method for Computing Steady-State Pulse Solutions a specially preconditioned matrix-implicit Newton-Krylov solver. Solutions are obtained at least an order

Polz, Martin

171

Implementation of sparta, a highly parallel circuit simulator by the preconditioned Jacobi method, on a distributed memory machine  

Microsoft Academic Search

This paper investigates an efficient implementation of circuit simulator sparta based on the preconditionedJacobi method on a loosely coupled distributed memory machine Fujitsu AP1000. The preconditioned relaxationmethods are linear solvers effective in large scale circuit simulations. Because the preconditioned Jacobi methodhas a high parallelism, the only problem of parallelization of sparta is the application of the preconditioner to theresidual vector.

Reiji Suda; Yoshio Oyanagi

1995-01-01

172

Differential Effects of Delta and Epsilon Protein Kinase C in Modulation of Postischemic Cerebral Blood Flow  

PubMed Central

Cerebral ischemia causes cerebral blood flow (CBF) derangements resulting in neuronal damage by enhanced protein kinase C delta (?PKC) levels leading to hippocampal and cortical neuronal death after ischemia. Contrarily, activation of ?PKC mediates ischemic tolerance by decreasing vascular tone providing neuroprotection. However, whether part of this protection is due to the role of differential isozymes of PKCs on CBF following cerebral ischemia remains poorly understood. Rats pretreated with a ?PKC specific inhibitor (?V1-1, 0.5 mg/kg) exhibited attenuation of hyperemia and latent hypoperfusion characterized by vasoconstriction followed by vasodilation of microvessels after two-vessel occlusion plus hypotension. In an asphyxial cardiac arrest (ACA) model, rats treated with ? V1-1 (pre- and postischemia) exhibited improved perfusion after 24 h and less hippocampal CA1 and cortical neuronal death 7 days after ACA. On the contrary, ?PKC-selective peptide activator, conferred neuroprotection in the CA1 region of the rat hippocampus 30 min before induction of global cerebral ischemia and decreased regional CBF during the reperfusion phase. These opposing effects of ? v. ?PKC suggest a possible therapeutic potential by modulating CBF preventing neuronal damage after cerebral ischemia. PMID:22259083

Lin, Hung Wen; Della-Morte, David; Thompson, John W.; Gresia, Victoria L.; Narayanan, Srinivasan V.; DeFazio, R. Anthony; Raval, Ami P.; Saul, Isabel; Dave, Kunjan R.; Morris, Kahlilia C.; Si, Min-Liang

2014-01-01

173

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

PubMed Central

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

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

2013-01-01

174

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

175

A simple and efficient preconditioning scheme for heaviside enriched XFEM  

NASA Astrophysics Data System (ADS)

The eXtended Finite Element Method (XFEM) is an approach for solving problems with non-smooth solutions. In the XFEM, the approximate solution is locally enriched to capture discontinuities without requiring a mesh which conforms to the geometric features. One drawback of the XFEM is that an ill-conditioned system of equations results when the ratio of volumes on either side of the interface in an element is small. In this paper, to avoid this ill-conditioning, a simple and efficient scheme based on a geometric preconditioner and constraining degrees of freedom to zero for small intersections is proposed. This geometric preconditioner is computed from the nodal basis functions, and therefore may be constructed prior to building the system of equations. This feature and the low-cost of constructing the preconditioning matrix makes it well suited for nonlinear problems with fixed and moving interfaces.

Lang, Christapher; Makhija, David; Doostan, Alireza; Maute, Kurt

2014-11-01

176

Aerodynamic shape optimization using preconditioned conjugate gradient methods  

NASA Technical Reports Server (NTRS)

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

Burgreen, Greg W.; Baysal, Oktay

1993-01-01

177

Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia.  

PubMed

Changes in brain temperature are known to modulate the marked neuronal damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utilizing a dialysis electrode combined with ferrocene bovine serum albumin (BSA), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of postischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, although the intra-ischemic [Glu](e) elevation did not differ from that during intra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than directly modulating intra-ischemic [Glu](e) dynamics. PMID:10793187

Asai, S; Zhao, H; Kohno, T; Takahashi, Y; Nagata, T; Ishikawa, K

2000-05-01

178

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

PubMed Central

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.

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

2014-01-01

179

Preconditioned iterative methods for inhomogeneous acoustic scattering applications  

NASA Astrophysics Data System (ADS)

This thesis develops and analyzes efficient iterative methods for solving discretizations of the Lippmann--Schwinger integral equation for inhomogeneous acoustic scattering. Analysis and numerical illustrations of the spectral properties of the scattering problem demonstrate that a significant portion of the spectrum is approximated well on coarse grids. To exploit this, I develop a novel restarted GMRES method with adaptive deflation preconditioning based on spectral approximations on multiple grids. Much of the literature in this field is based on exact deflation, which is not feasible for most practical computations. This thesis provides an analytical framework for general approximate deflation methods and suggests a way to rigorously study a host of inexactly-applied preconditioners. Approximate deflation algorithms are implemented for scattering through thin inhomogeneities in photonic band gap problems. I also develop a short term recurrence for solving the one dimensional version of the problem that exploits the observation that the integral operator is a low rank perturbation of a self-adjoint operator. This method is based on strategies for solving Schur complement problems, and provides an alternative to a recent short term recurrence algorithm for matrices with such structure that we show to be numerically unstable for this application. The restarted GMRES method with adaptive deflation preconditioning over multiple grids, as well as the short term recurrence method for operators with low rank skew-adjoint parts, are very effective for reducing both the computational time and computer memory required to solve acoustic scattering problems. Furthermore, the methods are sufficiently general to be applicable to a wide class of problems.

Sifuentes, Josef

180

The effects of specific preconditioning activities on acute sprint performance.  

PubMed

Previous research suggests that specific preconditioning activities such as whole-body vibration (WBV) and resistance training may play an important role in ensuing dynamic activities. The purpose of this study was to examine the effects of 2 preconditioning activities, WBV and power cleans (PC), on acute sprint performance. Two studies were conducted in which 14 (WBV) and 9 (PC) male track and field athletes were subjects. The WBV treatment consisted of 4 bouts of 5 seconds of high-knee running on a vibrating platform at 0, 30, 40, or 50 Hz. The PC treatment consisted of 3 PC reps at 90% 1RM. In both cases, acute sprint performance was the dependent variable of interest. For WBV, split times were recorded at 10, 20, and 40 m. Reaction times (RXN) as well as 5-, 10-, and 40-m split times were recorded for the PC study. Results indicated no significant differences between treatment and nontreatment groups for both studies. However, significant correlations were present between RXN and 5-m splits (r = 0.65) and RXN and 10-m splits (r = 0.63), although they decreased as a function of sprint distance to r = 0.43 at 40 m. These results suggest little efficacy for the use of WBV and PC as a means of augmenting acute sprint performance. However, a trend within the 30-Hz protocol may suggest that WBV as part of a warm-up for sprinting activities greater than 40 m (i.e., 100 m) could potentially result in a decreased sprint time of nearly 1/10th of a second, which is worth future consideration. PMID:19528862

Guggenheimer, Joshua D; Dickin, D Clark; Reyes, Gabriel F; Dolny, Dennis G

2009-07-01

181

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

PubMed

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 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

182

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

183

Parvalbumin is overexpressed in the late phase of pharmacological preconditioning in skeletal muscle.  

PubMed

Pharmacological preconditioning (PPC) with mitochondrial ATP-sensitive K(+) channel openers such as diazoxide, provides protection against ischemia in cardiac muscle, skeletal muscle, and other tissues. Effects on Ca(2+) homeostasis during the late phase of PPC have been described in cardiomyocytes, but no information is available regarding intracellular Ca(2+) changes in skeletal muscle fibers during late PPC. Intracellular Ca(2+) signals were measured in single fibers of adult mouse skeletal muscle, with fluorescent probes, 48 h after the administration of diazoxide. Parvalbumin levels in the myofibers were quantitated by Western blot. Diazoxide induction of late PPC was confirmed by partial protection of muscles from peroxide-induced damage. Late PPC was associated with a significant decrease in the duration of Ca(2+) signals during single twitches and tetanus with no changes in peak values. This effect was prevented by the reactive oxygen species (ROS) scavenger tiron. Late PPC was accompanied by a 30% increase in parvalbumin levels, and this effect was also blocked by tiron. Our data show, for the first time, a role of parvalbumin in late PPC in skeletal muscle. PMID:24117265

Solis, Rosario; Carrillo, Elba D; Hernández, Ascención; García, María C; Sánchez, Jorge A

2013-11-01

184

Cardiac phosphoproteomics during remote ischemic preconditioning: a role for the sarcomeric Z-disk proteins.  

PubMed

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

185

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

186

Curative effect of an almitrine-raubasine combination in the postischemic syndrome following transient cerebral ischemia in dogs.  

PubMed

Cerebral hemodynamic and metabolic changes, occurring during delayed hypoperfusion following transient cerebral ischemia, and the influence of treatment with almitrine plus raubasine were studied in mongrel dogs. 10 min of transient cerebral ischemia was induced by bilateral clamping of both carotid and vertebral arteries. After declamping, the mean time necessary until cerebral venous PO2 (cvPO2) reached a value of 3.6 kPa, threshold for tissue hypoxia, was 80 min. At this time (T0), venous cerebral blood flow (vCBF) and cerebral perfusion pressure (Perf P) were below (60 and 20%, respectively) preischemic values, while cerebral vascular resistance (CVR) and oxygen and glucose extraction rates increased despite a normal cerebral oxygen consumption (CMRO2). At T0 ventilatory assistance without (control group) or with (treated group) intravenous infusion of almitrine plus raubasine was applied for 110 min. Between T0 and T110 min, 2 dogs died in the control group. During this period vCBF decreased by more than 60% in the control group while it slightly increased in the treated group. A strong decrease in Perf P (40%) and increase in CVR (140%) was observed in the control group while in the treated group Perf P and CVR slightly decreased (14 and 35%, respectively). CMRO2 decreased by 60% in the control group but remained within the normal range in the treated group. The fact that cvPO2 remained constantly below the initial value of 3.6 kPa in the control group and, on contrary, above this value in the group infused with raubasine plus almitrine indicates that the vCBF improvement leads to an increase in oxygen supply and is involved in the keeping of the adequacy between flow and metabolism. Our results support the hypothesis that the post-ischemic syndrome may play an important role in the acute prognosis of stroke. They clearly indicate that early cerebral resuscitation by infusion of almitrine plus raubasine, maintaining oxygen availability and CBF above initial thresholds, should improve the long-term neurological outcome. PMID:3368502

Cahn, R; Cahn, J

1988-01-01

187

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

188

Simulation of electrophoretic stretching of DNA in a microcontraction using an obstacle array for conformational preconditioning  

E-print Network

Recently our group has reported experiments using an obstacle array to precondition the conformations of DNA molecules to facilitate their stretch in a microcontraction. Based upon previous successes simulating electrophoretic ...

Doyle, Patrick S.

189

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

NASA Astrophysics Data System (ADS)

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

Cai, Yunfeng; Bai, Zhaojun; Pask, John E.; Sukumar, N.

2013-12-01

190

Block Locally Optimal Preconditioned Eigenvalue Xolvers (BLOPEX) in hypre and PETSc  

Microsoft Academic Search

We describe our software package Block Locally Optimal Preconditioned Eigenvalue Xolvers (BLOPEX) publicly released recently. BLOPEX is available as a stand-alone serial library, as an external package to PETSc (\\

A. V. Knyazev; M. E. Argentati; I. Lashuk; E. E. Ovtchinnikov

2007-01-01

191

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

192

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

SciTech Connect

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

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

2013-12-15

193

The Role of Erythropoetin in Ischemic Preconditioning, Postconditioning, and Regeneration of the Brain after Ischemia  

Microsoft Academic Search

Analysis of published data shows that erythropoietin plays an important role in controlling the tolerance of the brain to\\u000a the actions of ischemia and reperfusion. This cytokine has a role in ischemic preconditioning of the brain and can imitate\\u000a the phenomena of preconditioning and postconditioning. However, it is unclear whether endogenous erythropoietin is involved\\u000a in postconditioning of the brain. Erythropoetin

L. N. Maslov

2011-01-01

194

Translocation of PKC, protein phosphatase inhibition and preconditioning of rabbit cardiomyocytes.  

PubMed

This study was designed to test the hypothesis that induction of the preconditioned state results in a sustained translocation of protein kinase C (PKC) which accounts for the memory associated with preconditioning. Isolated rabbit cardiomyocytes were subjected to established preconditioning protocols using either adenosine or transient ischemia. At timed intervals during induction of preconditioning (PC), post-incubation or final sustained ischemia, cells were harvested, subjected to digitonin lysis and separated into cytosolic and particulate fractions. Samples were evaluated by Western blot analysis with monoclonal antibodies to alpha, epsilon, zeta and gamma PKC isozymes, and bands were qualified by densitometry. Internal controls for each experiment included oxygenated cardiomyocytes and cell with PKC translocation evoked by treatment with phorbol 12-myristate 13-acetate (PMA). For control oxygenated cells, the particulate fraction contained about 30% of PKC epsilon, 5-10% of PKC alpha and 60-70% of PKC zeta. Preconditioning with adenosine (100 microM) or 10 min ischemia had no significant effect on these percentages. Furthermore, the relative amounts of PKC isozymes associated with the particulate fraction of control and preconditioned cells did not differ after a postincubation in oxygenated buffer or during a final ischemic incubation. PMA and ingenol completely translocated the epsilon and alpha isoforms, while thymeleatoxin totally translocated PKC alpha but only partially (50%) translocated PKC epsilon. The distribution of PKC zeta between fractions was not affected by any drug. The protein phosphatase inhibitor calyculin A protected cells mimicking preconditioning. This protection was blocked by preincubation with the selective PKC inhibitor calphostin C but was largely retained if calphostin C was added only during the final ischemic period. It is concluded that PKC activity is required for preconditioning, but a sustained translocation of PKC above basal levels is not necessary for protection of rabbit cardiomyocytes in vitro. PMID:8841935

Armstrong, S C; Hoover, D B; Delacey, M H; Ganote, C E

1996-07-01

195

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

PubMed

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

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

2014-02-01

196

Short-term hypoxic preconditioning improved survival following cardiac arrest and resuscitation in rats.  

PubMed

Cardiac arrest and resuscitation produces delayed mortality and hippocampal neuronal death in rats. Hypoxic preconditioning has been to shown to protect the brain from ischemic insults. We have previously reported that with chronic hypobaric hypoxia, the accumulation of hypoxic-inducible factor-1 alpha (HIF-1?) and its target genes was increased for the first several days of hypoxic exposure, and returned to baseline level by 3 weeks when angiogenesis is completed. In this study, we investigated the effect of short-term (3 days) and long-term (21 days) hypoxic preconditioning on recovery from cardiac arrest and resuscitation in rats. Our data showed that the overall survival rate was considerably improved in the short-term hypoxic preconditioning group compared to the non-preconditioned controls (86 %, 6/7 vs. 54 %, 7/13); however, the survival rate in the long-term hypoxic preconditioning group was decreased. Our data suggest that hypoxic preconditioning provides protection after cardiac arrest and resuscitation more likely through increased accumulation of HIF-1? and its target genes rather than through successful vascular adaptation as a result of hypoxia-induced angiogenesis. PMID:24729248

Xu, Kui; Lamanna, Joseph C

2014-01-01

197

Remote Ischemic Preconditioning (RIPC) Modifies Plasma Proteome in Humans  

PubMed Central

Remote Ischemic Preconditioning (RIPC) induced by brief episodes of ischemia of the limb protects against multi-organ damage by ischemia-reperfusion (IR). Although it has been demonstrated that RIPC affects gene expression, the proteomic response to RIPC has not been determined. This study aimed to examine RIPC induced changes in the plasma proteome. Five healthy adult volunteers had 4 cycles of 5 min ischemia alternating with 5 min reperfusion of the forearm. Blood samples were taken from the ipsilateral arm prior to first ischaemia, immediately after each episode of ischemia as well as, at 15 min and 24 h after the last episode of ischemia. Plasma samples from five individuals were analysed using two complementary techniques. Individual samples were analysed using 2Dimensional Difference in gel electrophoresis (2D DIGE) and mass spectrometry (MS). Pooled samples for each of the time-points underwent trypsin digestion and peptides generated were analysed in triplicate using Liquid Chromatography and MS (LC-MS). Six proteins changed in response to RIPC using 2D DIGE analysis, while 48 proteins were found to be differentially regulated using LC-MS. The proteins of interest were involved in acute phase response signalling, and physiological molecular and cellular functions. The RIPC stimulus modifies the plasma protein content in blood taken from the ischemic arm in a cumulative fashion and evokes a proteomic response in peripheral blood. PMID:23139772

Hepponstall, Michele; Ignjatovic, Vera; Binos, Steve; Monagle, Paul; Jones, Bryn; Cheung, Michael H. H.; d'Udekem, Yves; Konstantinov, Igor E.

2012-01-01

198

Remote ischemic preconditioning in patients with intermittent claudication  

PubMed Central

OBJECTIVE: Remote ischemic preconditioning (RIPC) is a phenomenon in which a short period of sub-lethal ischemia in one organ protects against subsequent bouts of ischemia in another organ. We hypothesized that RIPC in patients with intermittent claudication would increase muscle tissue resistance to ischemia, thereby resulting in an increased ability to walk. METHODS: In a claudication clinic, 52 ambulatory patients who presented with complaints of intermittent claudication in the lower limbs associated with an absent or reduced arterial pulse in the symptomatic limb and/or an ankle-brachial index <0.90 were recruited for this study. The patients were randomly divided into three groups (A, B and C). All of the patients underwent two tests on a treadmill according to the Gardener protocol. Group A was tested first without RIPC. Group A was subjected to RIPC prior to the second treadmill test. Group B was subjected to RIPC prior to the first treadmill test and then was subjected to a treadmill test without RIPC. In Group C (control group), both treadmill tests were performed without RIPC. The first and second tests were conducted seven days apart. Brazilian Clinical Trials: RBR-7TF6TM. RESULTS: Group A showed a significant increase in the initial claudication distance in the second test compared to the first test. CONCLUSION: RIPC increased the initial claudication distance in patients with intermittent claudication; however, RIPC did not affect the total walking distance of the patients. PMID:23778346

Saes, Glauco Fernandes; Zerati, Antonio Eduardo; Wolosker, Nelson; Ragazzo, Luciana; Rosoky, Ruben Miguel Ayzin; Ritti-Dias, Raphael Mendes; Cucato, Gabriel Grizzo; Chehuen, Marcelo; Farah, Breno Quintella; Puech-Leao, Pedro

2013-01-01

199

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

200

Preconditioning Prevents the Inhibition of Na+,K+ATPase Activity after Brain Ischemia  

Microsoft Academic Search

Application of single transient forebrain ischemia (ISC) in adult Wistar rats, lasting 2 or 10 min, caused inhibition of Na+,K+-ATPase activity in cytoplasmic membrane fractions of hippocampus and cerebral cortex immediately after the event. In the 2-min ISC group followed by 60 min of reperfusion, the enzyme inhibition was maintained in the cortex, while there was an increase in hippocampal

AngelaTerezinha de Souza Wyse; EmílioLuiz Streck; Paulo Worm; André Wajner; Fabiana Ritter; CarlosAlexandre Netto

2000-01-01

201

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

PubMed Central

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

Huang, Lin

2013-01-01

202

Activation of ?1B-adrenoceptors contributes to intermittent hypobaric hypoxia-improved postischemic myocardial performance via inhibiting MMP-2 activation.  

PubMed

Inhibition of matrix metalloproteinases-2 (MMP-2) activation renders cardioprotection from ischemia/reperfusion (I/R) injury; however, the signaling pathways involved have not been fully understood. Intermittent hypobaric hypoxia (IHH) has been shown to enhance myocardial tolerance to I/R injury via triggering intrinsic adaptive responses. Here we investigated whether IHH protects the heart against I/R injury via the regulation of MMP-2 and how the MMP-2 is regulated. IHH (Po2 = 84 mmHg, 4-h/day, 4 wk) improved postischemic myocardial contractile performance, lactate dehydrogenase (LDH) release, and infarct size in isolated perfused rat hearts. Moreover, IHH reversed I/R-induced MMP-2 activation and release, disorders in the levels of MMP-2 regulators, peroxynitrite (ONOO(-)) and tissue inhibitor of metalloproteinase-4 (TIMP-4), and loss of the MMP-2 targets ?-actinin and troponin I. This protection was mimicked, but not augmented, by a MMP inhibitor doxycycline and lost by the ?1-adrenoceptor (AR) antagonist prazosin. Furthermore, IHH increased myocardial ?1A-AR and ?1B-AR density but not ?1D-AR after I/R. Concomitantly, IHH further enhanced the translocation of PKC epsilon (PKC?) and decreased the release of mitochondrial cytochrome c due to I/R via the activation of ?1B-AR but not ?1A-AR or ?1D-AR. IHH-conferred cardioprotection in the postischemic contractile function, LDH release, MMP-2 activation, and nitrotyrosine as well as TIMP-4 contents were mimicked but not additive by ?1-AR stimulation with phenylephrine and were abolished by an ?1B-AR antagonist chloroethylclonidine and a PKC? inhibitor PKC? V1-2. These findings demonstrate that IHH exerts cardioprotection through attenuating excess ONOO(-) biosynthesis and TIMP-4 loss and sequential MMP-2 activation via the activation of ?1B-AR/PKC? pathway. PMID:24705558

Gao, Ling; Chen, Le; Lu, Zhi-Zhen; Gao, Hong; Wu, Lan; Chen, Yi-Xiong; Zhang, Cai-Mei; Jiang, Yu-Kun; Jing, Qing; Zhang, You-Yi; Yang, Huang-Tian

2014-06-01

203

Effects of the phlebotropic drug Daflon 500 mg on postischemic microvascular disturbances in striated skin muscle: an intravital microscopic study in the hamster.  

PubMed

The objective of this study was to investigate the effects of the micronized purified flavonoid fraction Daflon 500 mg (90% diosmin and 10% hesperidin) on I/R-induced microvascular leukocyte-endothelium interaction and leakage of the high molecular weight plasma tracer FITC-dextran (relative molecular mass, 150 kd) as assessed in the striated skin muscle of the dorsal skin fold chamber model in the hamster. Intravital fluorescence microscopy was used for analysis of microvascular perfusion, leukocyte-endothelium interaction, and macromolecular leakage of FITC-dextran 150 kd in the striated skin muscle of the hamster. A tourniquet ischemia of 4 hours' duration was induced followed by reperfusion. Animals were treated with an oral administration of Daflon 500 mg (n = six) or its vehicle (5% Arabic gum solution, n = six) for 8 days at a daily dose of 30 mg/kg body weight. Measurements in the microcirculation were made before the 8-day feeding protocol before induction of ischemia and at 0.5, 2, and 24 hours of reperfusion. In the absence of I/R, no differences in microvascular perfusion, leukocyte-endothelium interaction, and macromolecular leakage were found in Daflon 500 mg and vehicle-treated control animals before and after administration of the drugs. Induction of ischemia and reperfusion, however, elicited a significant increase in venular leukocyte rolling and sticking in vehicle-treated animals, which was accompanied by enhancement of leakage of FITC-dextran 150 kd into the perivascular tissue. Treatment with Daflon 500 mg had no effect on postischemic leukocyte rolling and sticking, and macromolecular leakage of FITC-dextran 150 kd from arterioles and postcapillary venules was significantly reduced. These data indicate that Daflon 500 mg preserves the endothelial barrier function of striated skin muscle arterioles and venules after I/R, which appears to be independent of an action on postischemic intravascular leukocyte rolling and sticking. PMID:10560947

Nolte, D; Pickelmann, S; Möllmann, M; Schütze, E; Kübler, W; Leiderer, R; Messmer, K

1999-11-01

204

Slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after high-flow bypass for a carotid intracavernous aneurysm.  

PubMed

The authors report a rare case of slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after radial artery/external carotid artery-middle cerebral artery bypass graft surgery for an intracavernous carotid artery aneurysm. Under barbiturate protection, a 69-year-old man underwent high-flow bypass surgery combined with carotid artery sacrifice for a symptomatic intracavernous aneurysm. The patient became restless postoperatively, and this restlessness peaked on postoperative Day (POD) 7. Diffusion-weighted and FLAIR MR images obtained on PODs 1 and 7 revealed subtle cortical hyperintensity in the temporal cortex subjected to temporary occlusion. On POD 13, (123)I-iomazenil ((123)I-IMZ) SPECT clearly showed increased distribution on the early image and mildly decreased binding on the delayed image with count ratios of the affected-unaffected corresponding regions of interest of 1.23 and 0.84, respectively, suggesting postischemic hyperperfusion. This was consistent with the finding on (123)I-iodoamphetamine SPECT. Of note, neuronal density in the affected cortex on the delayed (123)I-IMZ image further decreased to the affected/unaffected ratio of 0.44 on POD 55 during the subacute stage when characteristic cortical hyperintensity on T1-weighted MR imaging, typical of cortical laminar necrosis, was emerging. The affected cortex showed marked atrophy 8 months after the operation despite complete neurological recovery. This report illustrates, for the first time, dynamic neuroradiological correlations between slowly progressive neuronal death shown by (123)I-IMZ SPECT and cortical laminar necrosis on MR imaging in human stroke. PMID:19877803

Iihara, Koji; Okawa, Masakazu; Hishikawa, Tomohito; Yamada, Naoaki; Fukushima, Kazuhito; Iida, Hidehiro; Miyamoto, Susumu

2010-06-01

205

Inhibition of Myocardial Apoptosis by Ischaemic and Beta-Adrenergic Preconditioning is Dependent on p38 MAPK  

Microsoft Academic Search

Summary  Introduction: Apoptosis occurring during ischaemia \\/reperfusion contributes independently to tissue damage, and involves activation of\\u000a the stress-kinase, p38 MAPK during reperfusion. Ischaemic preconditioning (IPC) protects against ischaemia\\/reperfusion mediated\\u000a necrosis and apoptosis. The role of p38 MAPK in the protective effect of preconditioning against apoptosis is unknown. Pharmacologic\\u000a preconditioning with isoproterenol (?-PC) also protects against necrosis, but it is not known

Johannes A. Moolman; Shahiem Hartley; Johanna Van Wyk; Erna Marais; Amanda Lochner

2006-01-01

206

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

207

Lipopolysaccharide preconditioning facilitates M2 activation of resident microglia after spinal cord injury.  

PubMed

The inflammatory response following spinal cord injury (SCI) has both harmful and beneficial effects; however, it can be modulated for therapeutic benefit. Endotoxin/lipopolysaccharide (LPS) preconditioning, a well-established method for modifying the immune reaction, has been shown to attenuate damage induced by stroke and brain trauma in rodent models. Although such effects likely are conveyed by tissue-repairing functions of the inflammatory response, the mechanisms that control the effects have not yet been elucidated. The present study preconditioned C57BL6/J mice with 0.05 mg/kg of LPS 48 hr before inducing contusion SCI to investigate the effect of LPS preconditioning on the activation of macrophages/microglia. We found that LPS preconditioning promotes the polarization of M1/M2 macrophages/microglia toward an M2 phenotype in the injured spinal cord on quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemical analyses. Flow cytometric analyses reveal that LPS preconditioning facilitates M2 activation in resident microglia but not in infiltrating macrophages. Augmented M2 activation was accompanied by vascularization around the injured lesion, resulting in improvement in both tissue reorganization and functional recovery. Furthermore, we found that M2 activation induced by LPS preconditioning is regulated by interleukin-10 gene expression, which was preceded by the transcriptional activation of interferon regulatory factor (IRF)-3, as demonstrated by Western blotting and an IRF-3 binding assay. Altogether, our findings demonstrate that LPS preconditioning has a therapeutic effect on SCI through the modulation of M1/M2 polarization of resident microglia. The present study suggests that controlling M1/M2 polarization through endotoxin signal transduction could become a promising therapeutic strategy for various central nervous system diseases. © 2014 Wiley Periodicals, Inc. PMID:25044014

Hayakawa, Kentaro; Okazaki, Rentaro; Morioka, Kazuhito; Nakamura, Kozo; Tanaka, Sakae; Ogata, Toru

2014-12-01

208

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

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

Ischemic preconditioning enhances integrity of coronary endothelial tight junctions.  

PubMed

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. PMID:22846574

Li, Zhao; Jin, Zhu-Qiu

2012-08-31

211

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

212

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

213

Houston's unusually large hourly ozone increases: Preconditions and geographical origins  

NASA Astrophysics Data System (ADS)

Many of Houston's highest measured 8-hr ozone (O3) peaks are characterized by sudden increases in concentrations of at least 40 ppb in one hour, or 60 ppb in two hours. Measurements show that these large hourly changes appear at only a few monitors and span a narrow geographic area suggesting a spatially heterogeneous field of O3 concentrations. Regulatory air quality modeling has been unable to reproduce the magnitude or location of some of the highest observed hourly O3 changes, and it also failed to capture the limited spatial extent. The cause(s) of these O3 events is an open question. Some observed large hourly changes in O3 concentrations have been linked to random releases of industrial volatile organic compounds (VOCs), and meteorological conditions are known to impact O3 formation in Houston. Days with rotating winds and low wind speeds often produce the greatest O3 concentrations, and the location of regional high-pressure zones also impact pollutant levels. It is unlikely, however, that meteorology alone can explain the rapid O3 increases. This work considers local and regional meteorological conditions and ambient VOC measurements in an attempt to determine the necessary preconditions for the large hourly O3 increases found in the observational record. Using over ten years of measurement data, we have identified candidate days with unusually large hourly O3 increases. We will combine wind field measurements, automated gas chromatograph data, and back trajectory modeling to determine the necessary conditions and likely geographical origins of the O3 events. Preliminary results show evidence for rapid photochemical production of O3 consistent with highly reactive plumes of oxidant precursors.

Couzo, E. A.; Jeffries, H. E.; Vizuete, W.

2012-12-01

214

Ischemic preconditioning, insulin, and morphine all cause hexokinase redistribution.  

PubMed

Association of hexokinase (HK) with mitochondria preserves mitochondrial integrity and is an important mechanism by which cancer cells are protected against hypoxic conditions. Maintenance of mitochondrial integrity also figures prominently as a major characteristic of many cardioprotective manipulations. In this study, we provide evidence that cardioprotective interventions may promote HK redistribution from the cytosol to the mitochondria in the heart. Isolated Langendorff-perfused rat hearts (n = 6/group) were subjected to normoxic perfusion (control, Con), three 5-min ischemia-reperfusion periods (ischemic preconditioning, IPC), 1 U/l insulin (Ins), or 1 microM morphine (Mor). Hearts were immediately homogenized and centrifuged to obtain whole cell, cytosolic, and mitochondrial fractions. HK, lactate dehydrogenase (LDH), and citrate synthase (CS) enzyme activities were determined. No change in LDH or CS present in the cytosol fraction relative to whole cell activity was observed with any of the cardioprotective interventions. By contrast, HK present in the cytosol fraction relative to whole cell activity decreased significantly (P < 0.05) with all cardioprotective interventions, from 0.58 +/- 0.03 (Con) to 0.46 +/- 0.04 (IPC), 0.41 +/- 0.01 (Ins), and 0.45 +/- 0.02 (Mor). In addition, HK relative to CS activity in the mitochondrial fraction increased significantly with cardioprotection, from 0.15 +/- 0.001 (Con) to 0.21 +/- 0.002 (IPC), 0.18 +/- 0.003 (Ins), and 0.21 +/- 0.005 (Mor). Our novel data suggest that well-known cardioprotective interventions share a common end-effector mechanism of cytosolic HK translocation. Association of HK with mitochondria may promote inhibition of the mitochondrial permeability transition pore and thereby reduce cell death and apoptosis. PMID:15764678

Zuurbier, Coert J; Eerbeek, Otto; Meijer, Alfred J

2005-07-01

215

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

PubMed

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

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

2014-06-15

216

Ischemia preconditioning protects rat submandibular glands from ischemia/reperfusion injuries.  

PubMed

To investigate the effects of ischemia/reperfusion on rat submandibular glands without denervation and the possible protective effects of ischemia preconditioning on the glands that experienced ischemia/reperfusion, in-situ ischemia/reperfusion and ischemia preconditioning experimental models of submandibular glands of healthy male Wistar rats were conducted. For ischemia/reperfusion groups, the glands were subjected to 90 min of ischemia without denervation, followed by 1, 12, 24, or 72 h of reperfusion. Ischemia preconditioning was achieved by 3 min of ischemia following 3 min of reperfusion, performed three times before ischemia/reperfusion. Salivary secretion, histological changes, alterations of tight junctions, myeloperoxidase activity, cellular apoptosis, and reactive oxygen species levels were detected. In ischemia/reperfusion glands, rising acute-inflammation responses, reduced tight-junction width, and increased myeloperoxidase activity, reactive oxygen species levels, and apoptotic cell numbers were observed, along with secretory dysfunction, especially at 1 and 12 h post-reperfusion, which seemed to gradually return to normal by 72 h post-reperfusion. In contrast, ischemia preconditioning showed the potential to ameliorate the injury-stress responses caused by ischemia/reperfusion. Our study revealed that ischemia/reperfusion could cause a series of injury-stress responses and ultimately lead to hyposecretion, independently of the parasympathetic nerve supply, which might play an important role in the early-phase dysfunction of the transplanted glands. Ischemia preconditioning could protect the involved glands and improve ischemia/reperfusion-induced hyposecretion. PMID:25216112

Shi, Liang; Xiao, Meng; Dai, Mei-Lu; Liu, Shao-Hua; Liu, Yun-Sheng; Wei, Feng-Cai

2014-10-01

217

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

PubMed Central

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

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

2014-01-01

218

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

219

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

220

Nitroglycerine and sodium trioxodinitrate: from the discovery to the preconditioning effect.  

PubMed

The history began in the 19th century with Ascanio Sobrero (1812-1888), the discoverer of glycerol trinitrate (nitroglycerine, NTG), and with Angelo Angeli (1864-1931), the discoverer of sodium trioxodinitrate (Angeli's salt). It is likely that Angeli and Sobrero never met, but their two histories will join each other more than a century later. In fact, it has been discovered that both NTG and Angeli's salt are able to induce a preconditioning effect. As NTG has a long history as an antianginal drug its newly discovered property as a preconditioning agent has also been tested in humans. Angeli's salt properties as a preconditioning and inotropic agent have only been tested in animals so far. PMID:23695182

Pagliaro, Pasquale; Gattullo, Donatella; Penna, Claudia

2013-10-01

221

Incomplete Gaussian elimination as a preconditioning for generalized conjugate gradient acceleration  

SciTech Connect

This paper discusses the application of preconditioned generalized conjugate gradient acceleration to fully implicit thermal simulation. The preconditioning step utilizes incomplete Gaussian elimination (IGE) to form an approximate factorization of the Jacobian matrix. IGE preconditioning and its implementation is discussed with respect to five, seven, nine or eleven-point finite difference approximations and optional well constraint equations. Numerical results were obtained using a thermal model allowing any number N/SUB c/ of components. The model's implicit formulation requires the solution of a linear system of equations in which each grid block has N /SUB c/ + 1 unknowns. Test problems involved combustion, steam drive and cyclic steam stimulation processes, some of which exhibited ill-conditioning, negative transmissabilities and high transmissability ratios. Numerical results indicate how different grid block orderings, different levels of incomplete factorization and different acceleration procedures affect convergence, storage and work requirements.

Wallis, J.R.

1983-11-01

222

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

223

Expression of signal transduction genes differs following hypoxic or isoflurane preconditioning of rat hippocampal slice cultures  

PubMed Central

Background Preconditioning neurons with non-injurious hypoxia (hypoxic preconditioning, HPC) or the anesthetic isoflurane (APC) induces tolerance of severe ischemic stress. The mechanisms of both types of preconditioning in the hippocampus require moderate increases in intracellular Ca2+ and activation of protein kinase signaling. We hypothesized that the expression of signal transduction genes would be similar following APC and HPC. Methods Hippocampal slice cultures prepared from 9 day-old rats were preconditioned with hypoxia (5 min 95% nitrogen/5% carbon dioxide) or 1% isoflurane in air/5% carbon dioxide for 1 hr. A day later cultures were subjected to 10 min oxygen and glucose deprivation (simulated ischemia). Intracellular Ca2+, measured in CA1 neurons at the completion of preconditioning, and cell death in CA1, CA3 and dentate regions was assessed 48 hr after simulated ischemia. Message RNA encoding 119 signal transduction genes was quantified with rat complimentary DNA micro arrays from pre oxygen-glucose deprivation samples. Results Both APC and HPC increased intracellular Ca2+ approximately 50 nM and decreased CA1, CA3 and dentate neuron death by about 50% following simulated ischemia. Many signaling genes were increased after preconditioning, with hypoxia increasing more apoptosis/survival genes (8 of 10) than isoflurane (0 of 10). In contrast, isoflurane increased more cell cycle/development/growth genes than did hypoxia (8 of 14 genes, versus 1 of 14). Conclusions Despite sharing similar upstream signaling and neuroprotective outcomes, the genomic response to APC and HPC is different. Increased expression of anti-apoptosis genes following HPC and cell development genes following APC has implications both for neuroprotection and long-term effects of anesthetics. PMID:19568165

Bickler, Philip E.; Fahlman, Christian S.

2012-01-01

224

Sensory Stimulation as a Precondition for the Learning of a Language Task by Fourth and Sixth Grade Children.  

ERIC Educational Resources Information Center

This study was designed to explore learning behavior of children following four specific preconditioning experiences: sensory deprivation, sensory bombardment, routine worksheet exercises, and a sensory awareness game. The study occurred in three parts: preconditioning of the subjects, teaching of a language skill, and performance of a task…

March, Lester William

225

PKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice  

Microsoft Academic Search

Glutamate receptors and calcium have been implicated as triggering factors in the induction of tolerance by ischemic preconditioning (IPC) in the brain. However, little is known about the signal transduction pathway that ensues after the IPC induction pathway. The main goals of the present study were to determine whether NMDA induces preconditioning via a calcium pathway and promotes translocation of

Ami P. Raval; Kunjan R. Dave; Daria Mochly-Rosen; Thomas J. Sick; Miguel A. Perez-Pinzon

226

Effects of condition number on preconditioning for low Mach number flows  

NASA Astrophysics Data System (ADS)

The effects of the condition number on convergence characteristics and solution quality for the preconditioned Navier-Stokes equations are studied. A general approach to the construction of preconditioning parameters is proposed to account for the effects of the condition number on these parameters. To verify this technique, laminar flows past a circular cylinder at Reynolds numbers of 20 and 40, and laminar flows past a NACA0012 airfoil at Reynolds numbers of 2500 and 5000 are solved. It is shown that the condition number has effects on the convergence characteristics and solution qualities, and also that a condition number exists that optimizes the convergence characteristics and solution quality.

Lee, Sang-Hyeon

2012-05-01

227

Preconditioning matrices for the pseudospectral approximation of first-order operators  

NASA Technical Reports Server (NTRS)

The behavior of the eigenvalues of preconditioning matrices for the pseudospectral approximation to the derivative operator has been analyzed in one and two dimensions. The one-dimensional analysis resulted in real and positive eigenvalues for the selected tridiagonal matrices. In the two-dimensional analysis, the eigenvalues of the selected block-diagonal matrices behaved well, but the preconditioner is full and therefore not suitable for applications. The Richardson scheme has been applied in the unpreconditioned as well as the preconditioned version to find the solution of the model problem.

Funaro, D.; Rothman, E.

1989-01-01

228

PRECONDITIONED BI-CONJUGATE GRADIENT METHOD FOR RADIATIVE TRANSFER IN SPHERICAL MEDIA  

SciTech Connect

A robust numerical method called the Preconditioned Bi-Conjugate Gradient (Pre-BiCG) method is proposed for the solution of the radiative transfer equation in spherical geometry. A variant of this method called Stabilized Preconditioned Bi-Conjugate Gradient (Pre-BiCG-STAB) is also presented. These are iterative methods based on the construction of a set of bi-orthogonal vectors. The application of the Pre-BiCG method in some benchmark tests shows that the method is quite versatile, and can handle difficult problems that may arise in astrophysical radiative transfer theory.

Anusha, L. S.; Nagendra, K. N. [Indian Institute of Astrophysics, Koramangala, Bangalore 560 034 (India); Paletou, F.; Leger, L. [Laboratoire d'Astrophysique de Toulouse-Tarbes, Universite de Toulouse, CNRS, 14 Ave. E. Belin, 31400 Toulouse (France)

2009-10-10

229

CX43 change in LPS preconditioning against apoptosis of mesenchymal stem cells induced by hypoxia and serum deprivation is associated with ERK signaling pathway.  

PubMed

This study was designed to investigate the effect and mechanism of lipopolysaccharide (LPS) preconditioning on survival and connexin 43 (CX43) expression in rat bone marrow mesenchymal stem cells (bMSCs) under hypoxia and serum deprivation (Hypoxia/SD) conditions. Whole marrow cells were obtained from the femora and tibiae of SD rats, and bMSCs were isolated by density gradient centrifugation and attachment culture. Surface antigens were determined by FACS before the experiment using antibodies conjugated directly against anti-rat CD34, anti-CD45, anti-CD29, and anti-CD44. Passage 3 bMSCs were used for all experiments. The effect of LPS preconditioning on bMSCs apoptosis in response to Hypoxia/SD was investigated by an Annexin V-FITC/PI binding assay and a mitochondrial membrane potential (??m) assay. Cyc-c released into the cytosol from mitochondria and CX43 in bMSCs was determined by Western blot before and after LPS preconditioning. Subsequently, extracellular signal-regulated kinase (ERK) was inhibited with PD98059 to analyze the role of ERK in modulating CX43 expression after LPS preconditioning. The bMSCs surface antigen profiles obtained by flow cytometry were positive for CD29 and CD44 and negative for CD34 and CD45. The Hypoxia/SD conditions induced significant apoptosis of bMSCs. Compared with the Hypoxia/SD group, cells treated with LPS prevented ??m from falling significantly. LPS inhibited Hypoxia/SD-induced Cyc-c release. These results were consistent with the total analysis of apoptosis of MSCs. Compared with the control group, the level of CX43 expression in the Hypoxia/SD group and LPS + Hypoxia/SD group decreased significantly at each time point. The level of CX43 expression in the Hypoxia/SD group was lower than that in the LPS + Hypoxia/SD group, while the difference was not significant between the PD98059 + LPS + Hypoxia/SD group and the PD98059 + Hypoxia/SD group (P > 0.05). Compared with the LPS + Hypoxia/SD group, CX43 level in the PD98059 + LPS + Hypoxia/SD group and PD98059 + Hypoxia/SD group decreased significantly (P < 0.05). These results demonstrated that Hypoxia/SD conditions could induce apoptosis of bMSCs markedly. Low-dose LPS preconditioning may preserve the mitochondrial function by maintaining the mitochondrial transmembrane potential and inhibiting Cyc-c release in Hypoxia/SD-induced bMSCs apoptosis. LPS preconditioning also had a stabilizing effect on the cell membrane by inhibiting the decrease of CX43, and this modulating mechanism may be related to the ERK signaling pathway. PMID:23712704

Wang, Jun; Li, Zhi; Zhang, Yangyang; Liu, Xiang; Chen, Liang; Chen, Yijiang

2013-08-01

230

The Nonsingularity of Sparse Approximate Inverse Preconditioning and Its Performance Based on Processor Virtualization  

Microsoft Academic Search

In this paper, we analyze the properties of the sparse approximate inverse precon- ditioner, and prove that for a strictly diagonally dominant M matrix, the computed preconditioning matrix can be guaranteed to be nonsingular if it is nonnegative. Then we investigate the use of the processor virtualization technique to parallelize the sparse approximate inverse solver. Numerical experiments on a distributed

Kai Wangy; Orion Lawlor; Laxmikant V. Kale

231

A Comparative Study on Dynamic and Static Sparsity Patterns in Parallel Sparse Approximate Inverse Preconditioning  

Microsoft Academic Search

Sparse approximate inverse (SAI) techniques have recently emerged as a new classof parallel preconditioning techniques for solving large sparse linear systems on highperformance computers. The choice of the sparsity pattern of the SAI matrix is probablythe most important step in constructing an SAI preconditioner. Both dynamicand static sparsity pattern selection approaches have been proposed by researchers.

Kai Wang; Sangbae Kim; Jun Zhang

2003-01-01

232

An efficient preconditioning scheme for real-fluid mixtures using primitive pressure-temperature variables  

Microsoft Academic Search

An improved preconditioning scheme incorporating a unified treatment of general fluid thermodynamics is developed for treating fluid flows over the entire regime of fluid thermodynamic states at all speeds. All of the thermodynamic and numerical properties (such as eigenvalues and Jacobian matrices) are derived directly from fundamental thermodynamics theories, rendering a self- consistent and robust algorithm. Further efficiency is obtained

Nan Zong; Vigor Yang

2007-01-01

233

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

234

Early Pliocene increase in thermohaline overturning: A precondition for the development of the modern equatorial Pacific  

E-print Network

], the modern Northern Hemisphere ice cap was absent, and sea level was 25 m higher than today [e.g., Raymo etClick Here for Full Article Early Pliocene increase in thermohaline overturning: A precondition Atlantic meridional overturning circulation between 4.8 and 4.0 million years ago, initiated

Gilli, Adrian

235

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

236

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

E-print Network

1 PURDUE EXTENSIONManagingYour Beef Herd: Highlighting Key Determinants of Success in Preconditioning ID-446-W PURDUE EXTENSION Managing Your Beef Herd: Highlighting Key Determinants of Success from a bunk and drink from a fountain/tank. Many PC programs encompass a beef quality assurance

237

Sarcolemmal Versus Mitochondrial ATP-Sensitive K1 Channels and Myocardial Preconditioning  

Microsoft Academic Search

Ischemic preconditioning (IPC) is a phenomenon in which single or multiple brief periods of ischemia have been shown to protect the heart against a more prolonged ischemic insult, the result of which is a marked reduction in myocardial infarct size, severity of stunning, or incidence of cardiac arrhythmias. Although a number of substances and signaling pathways have been proposed to

Garrett J. Gross; Ryan M. Fryer

2010-01-01

238

Preconditioned conjugate gradient based fast computation of indirect decision feedback equalizer  

Microsoft Academic Search

We use the preconditioned conjugate gradient (PCG) method to compute rapidly the tap weights of a minimum mean-square error (MMSE) decision feedback equalizer (DFE). The equalizer setting is computed indirectly after channel estimation. According to the Toeplitz block structure of the MMSE DFE equation, Rw=r (R is the system matrix), the preconditioner, P, is chosen to be a block diagonal

Peilu Ding; Michael D. Zoltowski; Mark Fimoff

2004-01-01

239

Towards a Sustainable FTAA: DOes Latin America Meet the Necessary Financial Preconditions?  

Microsoft Academic Search

This paper focuses on identifying preconditions that will ensure the sustainability of a Free Trade Area of the Americas (FTAA). It argues that the macro, micro, and political conditions advanced in the literature to measure a country's ability to compete internationally, while necessary, are not sufficient to ensure the success and permanence of a free trade agreement. Instead, two additional

Liliana Rojas-Suarez

2002-01-01

240

Toward a Sustainable FTAA: Does Latin America Meet the Necessary Financial Preconditions?  

Microsoft Academic Search

This paper focuses on identifying preconditions that will ensure the sustainability of a Free Trade Area of the Americas (FTAA). It argues that the macro, micro, and political conditions advanced in the literature to measure a country's ability to compete internationally, while necessary, are not sufficient to ensure the success and permanence of a free trade agreement. Instead, two additional

Liliana Rojas-Suarez

2002-01-01

241

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, Jurgen; Stoppe, Christian

2014-01-01

242

Protein Kinase C- ? is Responsible for the Protection of Preconditioning in Rabbit Cardiomyocytes  

Microsoft Academic Search

The role of protein kinase C (PKC) in the protection of ischemic preconditioning (PC) is still controversial, partly because of the multiple isozymes of PKC and the inability to directly measure PKC activity in vivo. In this study we have used novel peptide inhibitors which correspond to part of the amino acid sequence from the isozyme-specific RACK-binding site on the

Guang S. Liu; Michael V. Cohen; Daria Mochly-Rosen; James M. Downey

1999-01-01

243

A New Class of Parallel Two-level Nonlinear Schwarz Preconditioned Inexact Newton  

E-print Network

. Key words: Incompressible Navier-Stokes equations; multilevel nonlinear preconditioning; inexact is to solve large, sparse, nonlinear systems of equations arising from the discretization of incompressible. Let F(x ) = 0 (1.1) be a nonlinear system of equations and x(0) a given initial guess. Assume x

Cai, Xiao-Chuan

244

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

245

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

Microsoft Academic Search

BACKGROUND: Retinal degeneration is a main cause of blindness in humans. Neuroprotective therapies may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1? in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. To address the molecular mechanisms of the protection, we analyzed the transcriptome of the hypoxic

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

2008-01-01

246

Restoration of rocky slopes based on planted gabions and use of drought-preconditioned woody species  

Microsoft Academic Search

The restoration of steep rock faces with shrubs and trees is difficult due to extreme microclimatic and edaphic conditions. In this study, we tested the applicability of free-standing planted gabions to improve the landscape and achieve protection against rockfall, erosion and enhanced surface flow. Furthermore, we analyzed the effect of preconditioning on drought tolerance of several planted species (Ligustrum vulgare,

Barbara Beikircher; Florin Florineth; Stefan Mayr

2010-01-01

247

Delta opioid receptor stimulation mimics ischemic preconditioning in human heart muscle  

Microsoft Academic Search

OBJECTIVESThe objective of this study was to examine whether the delta (?) opioid receptor isoform is expressed in the human heart and whether this receptor improves contractile function after hypoxic\\/reoxygenation injury.BACKGROUNDDelta opioid receptor agonists mimic preconditioning (PC) in rat myocardium, corresponding to known cardiac ? opioid receptor expression in this species.METHODSThe messenger RNA transcript encoding the ? opioid receptor was

Sam P Bell; Michael N Sack; Asha Patel; Lionel H Opie; Derek M Yellon

2000-01-01

248

Coronary microembolization does not induce acute preconditioning against infarction in pigs—the role of adenosine  

Microsoft Academic Search

Objective: After coronary microembolization (ME) adenosine is released from ischemic areas of the microembolized myocardium. This adenosine dilates vessels in adjacent nonembolized myocardium and increases coronary blood flow. For ischemic preconditioning (IP) to protect the myocardium against infarction, an increase in the interstitial adenosine concentration (iADO) prior to the subsequent ischemia\\/reperfusion is necessary. We hypothesized that the adenosine release after

Andreas Skyschally; Rainer Schulz; Petra Gres; Ina Konietzka; Claus Martin; Michael Haude; Raimund Erbel; Gerd Heusch

249

Preconditioning to mild oxidative stress mediates astroglial neuroprotection in an IL-10-dependent manner.  

PubMed

Oxidative stress plays an important role in the pathogenesis of various brain insults, including stroke. Astroglia are the main glial cells that play a fundamental role in maintaining the homeostasis of the CNS. They are important for protection from injury and aid the brain in functional recovery after injuries. It has been shown that the brain can be prepared to withstand an oxidative stress insult by a process known as preconditioning. We used primary astroglial cell culture to investigate whether preconditioning to mild oxidative stress and glucose deprivation (OSGD) can increase both astroglia survival and neuroprotective features. We found that preconditioning astroglia to mild OSGD increases astroglial survival of a second insult through activation of the NF-E2-related factor-2 (Nrf-2) pathway. Moreover, we found that Nrf-2 is highly expressed in adult brain astroglia and that preconditioning to OSGD in vivo, such as in a murine model of ischemic stroke, leads to a significant increase in astroglial Nrf-2 expression. Furthermore, we discovered an increase in neuroprotection, as measured by increased neuronal cell survival, following OSGD in the presence of medium from astroglia exposed to a mild OSGD condition. Interestingly, we discovered a significant increase in astroglial secretion of the anti-inflammatory cytokine IL-10 vs. the pro-inflammatory cytokine IL-1? in mild vs. severe oxidative stress, respectively. We demonstrated that preconditioning astroglia to mild oxidative stress increases neuroprotection in an IL-10-dependent manner. By using tert-butylhydroquinone (tBHQ), a known specific activator of Nrf-2, we found that Nrf-2 can enhance IL-10 expression. Further studies of Nrf-2-mediated cellular pathways in astroglia through IL-10 may provide useful insights into the development of therapeutic interventions following oxidative stress insults such as ischemic stroke. PMID:23313057

Segev-Amzaleg, Niva; Trudler, Dorit; Frenkel, Dan

2013-05-01

250

Lipopolysaccharide preconditioning attenuates apoptotic processes and improves neuropathologic changes after spinal cord injury in rats.  

PubMed

We have shown earlier that administration of low-dose lipopolysaccharide (LPS) significantly contributed to recovery of motor function after traumatic spinal cord injury in the adult female rat. Using the same standardized animal model, we have now designed a set of experiments to test the hypothesis that LPS preconditioning attenuates stress-related apoptotic processes early after spinal cord trauma. The lower thoracic spinal cord injury in adult female Sprague-Dawley rats was caused by a 10 g weight rod drop from 25 mm on the dural surface of the exposed spinal cord at T10. The rats were randomly assigned to three groups: Sham injury, control (received normal saline alone), and LPS preconditioning (0.2 mg/kg, ip; 72 h prior to the injury). The animals were euthanized at 72 h postinjury. Neuropathologic changes were assessed using hematoxylin and eosin staining. SCI-induced apoptosis were observed by transmission electron microscopy. Caspase-3, cleaved caspase-3, Bax, and Bcl-2 were examined with immunohistochemistry or Western blotting. Compared with the control group, LPS preconditioning group showed significant improvement in the SCI-induced morphology changes. Furthermore, LPS preconditioning reduced the expressions of apoptotic markers caspase-3, cleaved caspase-3, and Bax, upregulated the expression of antiapoptotic marker Bcl-2 in the samples of spinal cord. Low-dose LPS attenuated the recruitment of inflammatory cells and the proliferation of glial cells in the site of injury. LPS preconditioning has neuroprotective effects against TSCI in rats due to its antiapoptosis properties as shown by the inhibition of caspase pathway and the upregulation of antiapoptotic protein. PMID:24205811

Li, Wei-Chao; Jiang, Rong; Jiang, Dian-Ming; Zhu, Feng-Chen; Su, Bao; Qiao, Bo; Qi, Xiao-Tong

2014-08-01

251

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

252

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

Code of Federal Regulations, 2012 CFR

...ancillary repair and alteration project? 102-72.68 Section...ancillary repair and alteration project? The preconditions that...estimates, and schedule for the project, and such other information...building, the building's structural, mechanical,...

2012-01-01

253

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

Code of Federal Regulations, 2013 CFR

...ancillary repair and alteration project? 102-72.68 Section...ancillary repair and alteration project? The preconditions that...estimates, and schedule for the project, and such other information...building, the building's structural, mechanical,...

2013-07-01

254

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

Code of Federal Regulations, 2011 CFR

...ancillary repair and alteration project? 102-72.68 Section...ancillary repair and alteration project? The preconditions that...estimates, and schedule for the project, and such other information...building, the building's structural, mechanical,...

2011-01-01

255

A preconditioned Newton-Krylov method for computing steady-state pulse solutions of mode-locked lasers  

E-print Network

We solve the periodic boundary value problem for a mode-locked laser cavity using a specially preconditioned matrix-implicit Newton-Krylov solver. Solutions are obtained at least an order of magnitude faster than with ...

Birge, Jonathan R. (Jonathan Richards)

2008-01-01

256

Dexmedetomidine preconditioning activates pro-survival kinases and attenuates regional ischemia/reperfusion injury in rat heart .  

E-print Network

??Pharmacological preconditioning limits myocardial infarct size after ischemia/reperfusion. Dexmedetomidine is an alpha(2)-adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia/reperfusion injury.… (more)

Ibacache Figueroa, Mauricio

2012-01-01

257

Effects of the phlebotropic drug Daflon 500 mg on postischemic reperfusion injury in striated skin muscle: a histomorphologic study in the hamster.  

PubMed

The objective of this study was to investigate the effects of the purified, micronized, flavonoid fraction Daflon 500 mg (S 5682, 90% diosmin and 10% hesperidin) on tissue damage and leukocyte emigration in striated skin muscle after ischemia-reperfusion, as assessed by histomorphometric analysis. The experimental model used was the transparent dorsal skin fold chamber in the awake Syrian golden hamster. Sixty-four animals were randomly allotted to two treatment groups and time points of investigation. Animals were fed with 30 mg kg(-1) body weight Daflon 500 mg (n = 32) or its vehicle, 5% Arabic gum solution (n = 32), as control 8 hours before ischemia. Before induction of a tourniquet ischemia of 4 hours' duration and at 0.5, 2, and 24 hours of reperfusion, tissue sections were preserved for light and electron microscopic analysis (n = seven or eight animals per time point). The number of intravascular and extravascular leukocytes was determined by light microscopic analysis of esterase-positive leukocytes. For quantitative analysis of ischemia-induced endothelial cell damage, the endothelial thickness of capillaries was calculated by a computer-assisted imaging system, whereas the ischemic tissue damage was assessed by means of a score system (grade 0-3) by an independent investigator. The number of emigrated leukocytes was significantly reduced in Daflon 500 mg-treated animals compared with numbers found in control animals. The histomorphologic muscle fiber damage increased after reperfusion in both groups but was significantly reduced in the Daflon 500 mg-treated animals 2 and 24 hours after reperfusion. These results suggest that the emigration of leukocytes plays an important role in the development of postischemic reperfusion injury of striated skin muscle. PMID:10560948

Pickelmann, S; Nolte, D; Leiderer, R; Möllmann, M; Schütze, E; Messmer, K

1999-11-01

258

Preconditioning on subspace quasi-Newton method for large scale unconstrained optimization  

NASA Astrophysics Data System (ADS)

Recently, subspace quasi-Newton (SQN) method has been widely used in solving large scale unconstrained optimization. Besides constructing sub-problems in low dimensions so that the storage requirement as well as computational cost can be reduced, it can also be implemented extremely fast when the objective function is a combination of computationally cheap non-linear functions. However, the main deficiency of SQN method is that it can be very slow on certain type of non-linear problem. Hence, a preconditioner which is computationally cheap and is a good approximation to the actual Hessian is constructed to speed up the convergence of the quasi-Newton methods since the evaluation of the actual Hessian is considered as impractical and costly. For this purpose, a diagonal updating matrix has been derived to replace the identity matrix in approximating the initial inverse Hessian. The numerical results show that the preconditioned SQN method performs better than the standard SQN method that without preconditioning.

Sim, Hong Seng; Leong, Wah June; Ismail, Fudziah

2014-09-01

259

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

260

Preconditioning for stratospheric sudden warmings - Sensitivity studies with a numerical model  

NASA Technical Reports Server (NTRS)

The phenomenon of preconditioning for sudden stratospheric warming events is investigated using a 3D primitive equation model adapted from the model used by Rose and Brasseur (1989). In order to identify the conditions that make the flow preconditioned, the model was initialized alternately with observed and with artificially constructed 'hybrid' stratospheric flow patterns. Two observed warmings were investigated, February 1979 and February 1989. The artificially constructed hybrid flow fields used upper-level winds (above 10 mb) from one period and lower-level winds (below 10 mb) from another. The results of model simulations indicate that the flow in the lower and middle stratosphere is capable of serving as a predictor of the potential for a major sudden warming, with the occurrence of a warming depending only on the lower-level winds.

Smith, Anne K.

1992-01-01

261

Microglial ablation and lipopolysaccharide preconditioning affects pilocarpine-induced seizures in mice  

SciTech Connect

Activated microglia have been associated with neurodegeneration in patients and in animal models of Temporal Lobe Epilepsy (TLE), however their precise functions as neurotoxic or neuroprotective is a topic of significant investigation. To explore this, we examined the effects of pilocarpine-induced seizures in transgenic mice where microglia/macrophages were conditionally ablated. We found that unilateral ablation of microglia from the dorsal hippocampus did not alter acute seizure sensitivity. However, when this procedure was coupled with lipopolysaccharide (LPS) preconditioning (1 mg/kg given 24 h prior to acute seizure), we observed a significant pro-convulsant phenomenon. This effect was associated with lower metabolic activation in the ipsilateral hippocampus during acute seizures, and could be attributed to activity in the mossy fiber pathway. These findings reveal that preconditioning with LPS 24 h prior to seizure induction may have a protective effect which is abolished by unilateral hippocampal microglia/macrophage ablation.

Mirrione, M.M.; Mirrione, M.M.; Konomosa, D.K.; Ioradanis, G.; Dewey, S.L.; Agzzid, A.; Heppnerd, F.L.; Tsirka, St.E.

2010-04-01

262

Intravenous Phenylephrine Preconditioning of Cardiac Grafts From Non–Heart-Beating Donors  

Microsoft Academic Search

Background. Hypoxia and warm ischemia produce severe injury to cardiac grafts harvested from non–heart-beating donors. To potentially improve recovery of such grafts, we studied the effects of intravenous phenylephrine preconditioning.Methods. Thirty-seven blood-perfused rabbit hearts were studied. Three groups of non–heart-beating donors underwent intravenous treatment with phenylephrine at 12.5 (n = 8), 25 (n = 7), or 50 ?g\\/kg (n =

1997-01-01

263

Evaluation of High-intensity and Low-intensity Preconditioning Systems  

E-print Network

OF SCIENCE Approved by: Chair of Committee, Jason E. Sawyer Committee Members, Andy D. Herring David P. Anderson Tryon A. Wickersham Head of Department, Gary Acuff December 2010 Major Subject: Animal Science iii ABSTRACT Evaluation... of High-intensity and Low-intensity Preconditioning Systems. (December 2010) Andrew Nathan Orsak, B.S., Texas A&M University Chair of Committee: Dr. Jason E. Sawyer Steer calves n = 345 (year 1 n = 183; 253 ? 35 kg, year 2 n = 162; 241 ? 36 kg...

Orsak, Andrew Nathan

2012-02-14

264

Sarcolemmal Blebs and Osmotic Fragility as Correlates of Irreversible Ischemic Injury in Preconditioned Isolated Rabbit Cardiomyocytes  

Microsoft Academic Search

The hypothesis that irreversible ischemic injury is related to sub-sarcolemmal blebbing and an inherent osmotic fragility of the blebs was tested by subjecting isolated control and ischemically preconditioned (IPC) or calyculin A (CalA)-pretreated (protected) rabbit cardiomyocytes to ischemic pelleting followed by resuspension in 340, 170 or 85 mosmol medium containing trypan blue. At time points from 0–240 min, osmotic fragility

Stephen C. Armstrong; Christine L. Shivell; Charles E. Ganote

2001-01-01

265

Delphi-research exploring essential components and preconditions for case management in people with dementia  

PubMed Central

Background Case management programmes for home-dwelling people with dementia and their informal carers exist in multiple forms and shapes. The aim of this research was to identify the essential components of case management for people with dementia as well as the preconditions for an effective delivery of case management services. Method The method used to carry out the research was a modified four-phase Delphi design. First, a list of potentially essential components and preconditions for the provision of case management was drawn up on the basis of a literature review and a subsequent focus group interview. The list was then validated by experts in a first Delphi survey round, following which the researchers translated the list items into 75 statements. In the second Delphi survey, the experts rated the statements; in the third Delphi round, they rated 18 statements on which no consensus had been reached in the second round. Results The experts were able to build consensus on 61 of the 75 statements. Essential components of case management for people with dementia are: information, support and counselling, coordination of the care provided and, to a lesser extent, practical help. A patient-centred approach was found to be one of the key aspects of providing case management services. Essential preconditions are: vision, care relationship, structured methodology, integration of case management into the health care chain, and the case manager's level of training and expertise. Conclusions We recommend that, based on the essential components and preconditions referred to above, quality criteria be developed for the provision of case management for people with dementia. Furthermore, we suggest the conduct of additional research to assess the effectiveness of case management in people with dementia. PMID:20696035

2010-01-01

266

Electroacupuncture preconditioning reduces cerebral ischemic injury via BDNF and SDF-1? in mice  

PubMed Central

Background This study was designed to determine if electroacupuncture (EA) preconditioning improves tissue outcome and functional outcome following experimentally induced cerebral ischemia in mice. In addition, we investigated whether the expression of brain-derived neurotrophic factor (BDNF) and stromal cell derived factor-1? (SDF-1?) and infarct volume were related with improvement in neurological and motor function by interventions in this study. Methods After treatment with EA at the acupoints ‘Baihui (GV20)’ and ‘Dazhui (GV14)’ for 20 min, BDNF was assessed in the cortical tissues based on Western blot and the SDF-1? and vascular endothelial growth factor (VEGF) levels in the plasma determined by ELISA. To assess the protective effects of EA against ischemic injury, the mice received once a day 20 min EA preconditioning for three days prior to the ischemic event. Focal cerebral ischemia was then induced by photothrombotic cortical ischemia. Infarct volumes, neurobehavioral deficit and motor deficit were evaluated 24 h after focal cerebral ischemia. Results The expression of BDNF protein increased significantly from 6 h, reaching a plateau at 12 h after the end of EA treatment in the cerebral cortex. Furthermore, SDF-1?, not VEGF, increased singnificantly from 12 h to 48 h after EA stimulation in the plasma. Moreover, EA preconditioning reduced the infarct volume by 43.5% when compared to control mice at 24 h after photothrombotic cortical ischemia. Consistent with a smaller infarct size, EA preconditioning showed prominent improvement of neurological function and motor function such as vestibule-motor function, sensori-motor function and asymmetric forelimb use. The expression of BDNF colocalized within neurons and SDF-1? colocalized within the cerebral vascular endothelium was observed throughout the ischemic cortex by EA. Conclusions Pretreatment with EA increased the production of BDNF and SDF-1?, which elicited protective effects against focal cerebral ischemia. These results suggest a novel mechanism of EA pretreatment-induced tolerance against cerebral ischemic injury. PMID:23356671

2013-01-01

267

A Principal Cognitive Precondition of Successful Child Computer Interactions in the Information Society  

Microsoft Academic Search

A hypothesis about what is the principal cognitive precondition of successful systematic acquainting children with computers is put forward. For this, the notion of the Thought-Producing Self of the child is introduced. It is stated that the System of Emotional -Imaginative Teaching (EIT-system) based on the Theory of Dynamic Conceptual Mappings allows for realizing the Thought-Producing Self of each normal

Olga S. Fomichova

2001-01-01

268

Preconditions for Product Re-innovation in Taiwan: Evidence from High-Technology Firms  

Microsoft Academic Search

The phenomenon of product re-innovation has often characterized Taiwanese high-technology firms over the last decade. However, the literature reflects surprisingly little effort to understand their preconditions. Based on extant knowledge and 68 field interviews with managers in diverse departments and firms of high-technology industries in Taiwan in mid-2006, the authors provide a foundation for future research by developing research propositions

Colin Chi-Jyun Cheng; Eric C. Shiu

2008-01-01

269

Heart-rate changes in asphyxic preconditioning in rats depend on light-dark cycle  

Microsoft Academic Search

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 preconditioning protective

Pavol Svorc; Ivana Bacova; Roman Benacka; Ruzena Galanova; Benjamin Lee Fulton

2011-01-01

270

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

NASA Astrophysics Data System (ADS)

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

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

2014-12-01

271

Improving fat graft survival through preconditioning of the recipient site with microneedling.  

PubMed

Although fat grafts are considered the ideal soft-tissue fillers, the main concern dealing with this technique is not being able to predict long-term graft survival due to high absorption rates. The purpose of this study was to investigate the angiogenic effects of preconditioning the recipient area with micro-needling and to determine its overall impact on fat graft survival. The study consisted of a sham, control and study group. The source of fat was the Wistar albino rat inguinal fat pad while the recipient area was a dorsal subcutaneous pouch. The dorsal area was preconditioned with standard technique micro-needling 1-week prior to fat graft transfer in the study group while the control group did not undergo micro-needling. At the end of 15 weeks, morphological, biochemical, histological and immunohistochemical evaluation was carried out. Fat grafts in the study group had better integrity and a higher level of vascularity compared to the control group. Volume analysis demonstrated higher graft survival in the study group in comparison to the control group. Histomorphometric and immunohistochemical evaluation showed better graft integrity and uniform adipocytes, less fibrosis, less vacuolisation and inflammation and better vascularisation in the study group. Although higher triglyceride concentrations were measured for the study group, the difference between the two groups was statistically insignificant. In conclusion, fat grafting performed in an area preconditioned with micro-needling results in higher graft volume, better integrity and vascularisation and an overall higher graft survival rate. PMID:24529693

Sezgin, Billur; Ozmen, Selahattin; Bulam, Hakan; Omeroglu, Suna; Yuksel, Seher; Cayci, Banu; Peker, Tuncay

2014-05-01

272

Hypoxic preconditioning involves system Xc- regulation in mouse neural stem cells.  

PubMed

In animals, hypoxic preconditioning has been used as a form of neuroprotection. The exact mechanism involved in neuroprotective hypoxic preconditioning has not been described, yet could be valuable for possible neuroprotective strategies. The overexpression of the cystine-glutamate exchanger, system Xc-, has been demonstrated as being neuroprotective (Shih, Erb et al. 2006). Here, using immunohistochemistry, we demonstrate that C57BL/6 mice exposed to hypoxia showed an increase in system Xc- expression, with the highest level of intensity in the hippocampus. Western Blot analysis also showed an almost 2-fold increase in system Xc- protein in hypoxia-exposed versus control mice. The mRNA for the regulatory subunit of system Xc-, xCT, and the xCT/actin ratio were also increased under hypoxic conditions. Experiments using hypoxia-inducible factor (HIF-1?) siRNA showed a statistically significant decrease in HIF-1? and system Xc- expression. Under hypoxic conditions, system Xc- activity, as determined by cystine uptake, increased 2-fold. Importantly, hypoxic preconditioning was attenuated in neural stem cells by pharmacological inhibition of system Xc- activity with S4-carboxyphenylglycine. These data provide the first evidence of hypoxic regulation of the cystine glutamate exchanger system Xc-. PMID:22056639

Sims, Brian; Clarke, Melinda; Francillion, Ludwig; Kindred, Elijah; Hopkins, Elana Shuford; Sontheimer, Harald

2012-03-01

273

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

NASA Astrophysics Data System (ADS)

Software evolution process model (EPM) is created in terms of a formal evolution process meta-model (EPMM) and semi-formal approach to modeling based on EPMM [1]. In order to better manage and control the software evolution process and make the best of existing software technology, the method to transform any EPM to its execution model based logic programming has been proposed. Completeness of conversion depends on completeness of the rules, that is, all the expressions of the original model are found the correspondence in the target model. Since transformation rules are proposed based on precondition or post-condition types of activities in anyone EPM, this need to prove that activity type set in anyone EPM is completeness set. To this end, the precondition and post-condition of activities in EPM are classified based on analyzing all expressions in EPMs and the semantics of the activity execution. Type completeness set of activity's precondition and its post-condition is presented. Lastly we prove that the activity type set in anyone EPM is completeness set by mathematical induction.

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

2013-12-01

274

Nucleus accumbens core neurons encode value-independent associations necessary for sensory preconditioning.  

PubMed

Reinforcement-based learning models predict that the strength of association between cues and outcomes is driven by aspects of outcome value. However, animals routinely make associations between contingent stimuli in the world, even if those associations hold no value to the organism. At the neural level, the nucleus accumbens (NAc) is known to encode associative information, but it is not known whether this encoding is specific for value-based information (consistent with reinforcement-based models) or if the NAc additionally plays a more general role in forming predictive associations, independent of outcome value. To test this, we employed a sensory preconditioning (SPC) task where rats initially (Preconditioning) received either contingent pairings of 2 neutral stimuli (e.g., tone [A] and light [X]; "Paired"), or random noncontingent presentations ("Unpaired"). After cue X was subsequently conditioned with food (First-Order Conditioning), the effect of preconditioning was assessed in Phase 3 (Test) by presentations of cue A alone. Electrophysiological recordings from the NAc core showed significant increases in phasic encoding for the stimuli in the Paired (but not Unpaired) condition as well as during test. Further, these effects were only seen in Paired rats that showed successful behavior during test (Good Learners), but not those who did not (Poor Learners) or Unpaired controls. These findings reveal a role for the NAc in the encoding of associative contingencies independent of value, and suggest that this structure also plays a more general role in forming associations necessary for predictive behavior. PMID:25244086

Cerri, Domenic H; Saddoris, Michael P; Carelli, Regina M

2014-10-01

275

[The effect of ischemic preconditioning on early death in acute Q-wave myocardial infarction].  

PubMed

Ischaemic preconditioning is still a laboratory-based phenomenon, not conclusively documented in patients. In this study it was of interest whether there is any beneficial influence of ischemic preconditioning on 30-day in-hospital mortality in patients undergoing acute Q-wave myocardial infarction. All men and women admitted to our ward between December 1994 and July 1996 with their first acute Q-wave myocardial infarction were divided into two groups. I group--29 patients with prodromal angina, defined as chest pain episodes in the 24-hour period before myocardial infarction. II group--25 patients who showed no chest pain before infarction onset. Both groups did not differ statistically in view of age, sex, smoking habits and adjunctive therapy. The use of streptokinase in the I and II group was also similar--in 58.6% and 56% of patients respectively in the first and second group. In the I group there was no fatal outcome, all 5 death cases occurred in the II group. The results are statistically significant and suggest lower in-hospital mortality in Q-wave myocardial infarction patients with previous ischaemic preconditioning. PMID:9557116

Stoch, K

1997-01-01

276

Acute bioenergetic intervention or pharmacological preconditioning protects neuron against ischemic injury  

PubMed Central

Although acute ischemic stroke has high mortality and morbidity rate but yet still has very limited treatment. In this study we have tested the concept of neuron protection by acute bioenergetic intervention or by pharmacological preconditioning with natural antioxidants. Adenosine triphosphate (ATP), pentobarbital, and suramin were encapsulated in pH-sensitive liposomes and used as bioenergy stabilizer. We induced ATP depletion model by incubating cells with media added with ATP-depleting agents for 2 hours. Treatment with bioenergy stabilizer started 10-min post inducing of ATP-depletion. The acute treatment with bioenergy stabilizer significantly increased cell viability in neuro-2a cells. In searching for a pharmacological preconditioning candidate for reducing ischemic injury, we tested cocoa-derived flavanols using bilateral common carotid artery occlusion (BCCAO). We pretreated mice with cocoa-derived flavanols (75 mg/kg) or water orally for 7 days and subjected mice for 12 minutes BCCAO. At 7 days post-ischemia, the number of surviving hippocampal CA1 neurons was significantly higher in the treated mice than in the water-treated controls. The protection from cocoa-derived flavanols was found associated with increased total antioxidant capacity in the brain. Our results indicate that for reducing acute ischemic injury bioenergetic intervention using advanced drug delivery tools is conceptually feasible, and for reducing reperfusion related secondary injury pharmacological preconditioning may provide significant protection. PMID:24285991

Liu, Shimin; Zhen, Gehua; Li, Rung-chi; Dore, Sylvain

2013-01-01

277

Preconditioned gradient methods for sparse linear systems for very `large structural` problems  

SciTech Connect

This paper deals with background and practical experience with preconditioned gradient methods for sparse linear systems for `very large` structural problems. The conjugate gradient method with diagonal preconditioning (CG/D) is demonstrated to substantially increase the size of structural problems that can be analyzed, significantly reduce computer storage requirements, and cut computing cost; thus allowing for much more detailed modeling and increased engineering efficiency. For one case for a structural system with 396,087 unknowns, the conjugate gradient method with diagonal preconditioning is demonstrated to be a factor of sixty faster than the direct method. For certain problems, however, the number of iterations required by the CG/D method is excessive and improved methods are needed. A stand-alone iterative solver research computer program was developed to evaluate the merits of various matrix preconditioners. A matrix preconditoner based on a shifted incomplete Cholesky factorization algorithm was demonstrated to be superior to other choices. The stand-alone program incorporates an effective data management strategy which utilizes disk and solid state auxiliary computer storage devices to make it possible to efficiently solve excessively large structural problems on state-of-the-art vector and parallel computers. The background of gradient methods, algorithms for their implementation, and practical experience in their applications to structural problems are presented.

Abu-Shumays, I.K.; Hutula, D.N.; Haan, J.J.; Myers, G.T.

1995-12-01

278

Preventing Pneumoconiosis  

MedlinePLUS

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

279

Sulforaphane preconditioning of the Nrf2/HO-1 defense pathway protects the cerebral vasculature against blood-brain barrier disruption and neurological deficits in stroke.  

PubMed

Disruption of the blood-brain barrier (BBB) and cerebral edema are the major pathogenic mechanisms leading to neurological dysfunction and death after ischemic stroke. The brain protects itself against infarction via activation of endogenous antioxidant defense mechanisms, and we here report the first evidence that sulforaphane-mediated preactivation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream target heme oxygenase-1 (HO-1) in the cerebral vasculature protects the brain against stroke. To induce ischemic stroke, Sprague-Dawley rats were subjected to 70 min middle cerebral artery occlusion (MCAo) followed by 4, 24, or 72 h reperfusion. Nrf2 and HO-1 protein expression was upregulated in cerebral microvessels of peri-infarct regions after 4-72 h, with HO-1 preferentially associated with perivascular astrocytes rather than the cerebrovascular endothelium. In naïve rats, treatment with sulforaphane increased Nrf2 expression in cerebral microvessels after 24h. Upregulation of Nrf2 by sulforaphane treatment prior to transient MCAo (1h) was associated with increased HO-1 expression in perivascular astrocytes in peri-infarct regions and cerebral endothelium in the infarct core. BBB disruption, lesion progression, as analyzed by MRI, and neurological deficits were reduced by sulforaphane pretreatment. As sulforaphane pretreatment led to a moderate increase in peroxynitrite generation, we suggest that hormetic preconditioning underlies sulforaphane-mediated protection against stroke. In conclusion, we propose that pharmacological or dietary interventions aimed to precondition the brain via activation of the Nrf2 defense pathway in the cerebral microvasculature provide a novel therapeutic approach for preventing BBB breakdown and neurological dysfunction in stroke. PMID:24017972

Alfieri, Alessio; Srivastava, Salil; Siow, Richard C M; Cash, Diana; Modo, Michel; Duchen, Michael R; Fraser, Paul A; Williams, Steven C R; Mann, Giovanni E

2013-12-01

280

Hexokinase cellular trafficking in ischemia-reperfusion and ischemic preconditioning is altered in type I diabetic heart.  

PubMed

Diabetes mellitus (DM) has been reported to alter the cardiac response to ischemia-reperfusion (IR). In addition, cardioprotection induced by ischemic preconditioning (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 prevention 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 prevention of HK solubilisation at 35 min I. IPC improved cardiac function in CON but not in DM hearts. IPC in CON prevented 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

Gurel, Ebru; Ustunova, Savas; Kapucu, Aysegul; Yilmazer, Nadim; Eerbeek, Otto; Nederlof, Rianne; Hollmann, Markus W; Demirci-Tansel, Cihan; Zuurbier, Coert J

2013-07-01

281

Modulation of cardiac Na+,K+-ATPase cell surface abundance by simulated ischemia-reperfusion and ouabain preconditioning  

PubMed Central

Na+,K+-ATPase and cell survival were investigated in a cellular model of ischemia-reperfusion (I/R)-induced injury and protection by ouabain-induced preconditioning (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 prevented 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

Belliard, Aude; Sottejeau, Yoann; Duan, Qiming; Karabin, Jessa L.

2013-01-01

282

Estradiol modulates post-ischemic cerebral vascular remodeling and improves long-term functional outcome in a rat model of stroke  

PubMed Central

We previously observed that 17?-estradiol (E2) augments ischemic borderzone vascular density 10 days after focal cerebral ischemia-reperfusion in rats. We now evaluated the effect of E2 on vascular remodeling, lesional characteristics, and motor recovery up to 30 days after injury. Peri-lesional vascular density in tissue sections from rats treated with 0.72 mg E2 pellets was higher compared to 0.18 mg E2 pellets or placebo (P) pellets: vascular density index, 1.9 ± 0.2 (0.72 mg E2) vs. 1.4 ± 0.2 (0.18 mg E2) vs. 1.5 ± 0.4 (P), p=0.01. This was consistent with perfusion magnetic resonance imaging (MRI) measurements of lesional relative cerebral blood flow (rCBF): 1.89 ± 0.32 (0.72 mg E2) vs. 1.32 ± 0.19 (P), p=0.04. Post-ischemic angiogenesis occurred in P-treated as well as E2-treated rats. There was no treatment-related effect on lesional size, but lesional tissue was better preserved in E2-treated rats: cystic component as a % of total lesion, 30 ± 12 (0.72 mg E2) vs. 29 ± 17 (0.18 mg E2) vs. 61 ± 29 (P), p=0.008. Three weeks after right middle cerebral artery territory injury, rats treated with 0.72 mg E2 pellets used the left forelimb more than P-treated or 0.18 mg E2-treated rats: limb use asymmetry score, 0.09 ± 0.43 (0.72 mg E2) vs. 0.54 ± 0.12 (0.18 mg E2) vs. 0.54 ± 0.40 (P), p=0.05. We conclude that treatment with 0.72 mg E2 pellets beginning one week prior to ischemia/reperfusion and continuing through the one-month recovery period results in augmentation of lesional vascularity and perfusion, as well as improved motor recovery. PMID:22572084

Ardelt, Agnieszka A.; Carpenter, Randall S.; Lobo, Merryl R.; Zeng, Huadong; Solanki, Rajanikant B.; Zhang, An; Kulesza, Piotr; Pike, Martin M.

2012-01-01

283

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

284

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

PubMed Central

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

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

2014-01-01

285

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

PubMed Central

Ischemic preconditioning has been reported to protect against spinal cord ischemia-reperfusion (I-R) injury, but the underlying mechanisms are not fully understood. To investigate this, Japanese white rabbits underwent I-R (30 min aortic occlusion followed by reperfusion), ischemic preconditioning (three cycles of 5 min aortic occlusion plus 5 min reperfusion) followed by I-R, or sham surgery. At 4 and 24 h following reperfusion, neurological function was assessed using Tarlov scores, blood spinal cord barrier permeability was measured by Evan’s Blue extravasation, spinal cord edema was evaluated using the wet-dry method, and spinal cord expression of zonula occluden-1 (ZO-1), matrix metalloproteinase-9 (MMP-9), and tumor necrosis factor-? (TNF-?) were measured by Western blot and a real-time polymerase chain reaction. ZO-1 was also assessed using immunofluorescence. Spinal cord I-R injury reduced neurologic scores, and ischemic preconditioning treatment ameliorated this effect. Ischemic preconditioning inhibited I-R-induced increases in blood spinal cord barrier permeability and water content, increased ZO-1 mRNA and protein expression, and reduced MMP-9 and TNF-? mRNA and protein expression. These findings suggest that ischemic preconditioning attenuates the increase in blood spinal cord barrier permeability due to spinal cord I-R injury by preservation of tight junction protein ZO-1 and reducing MMP-9 and TNF-? expression. PMID:23685868

Fang, Bo; Li, Xiao-Man; Sun, Xi-Jia; Bao, Na-Ren; Ren, Xiao-Yan; Lv, Huang-Wei; Ma, Hong

2013-01-01

286

NMDA preconditioning protects against quinolinic acid-induced seizures via PKA, PI3K and MAPK/ERK signaling pathways.  

PubMed

Preconditioning by N-methyl-d-aspartate (NMDA) may be promoted in vivo by the administration of a sub-convulsing dose of NMDA, with a neuroprotective effect against seizures and neuronal death induced by the infusion of quinolinic acid (QA) in mice. This study aimed to evaluate the participation of protein kinase C (PKC), cyclic AMP-dependent protein kinase (PKA), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK), Ca(2+)/calmodulin dependent protein kinase II (CaMKII) and phosphatidilinositol-3 kinase (PI3K) signaling pathways in this neuroprotection model. Adult Swiss male mice were preconditioned with NMDA 24 h before the infusion of QA, and were treated with inhibitors of the aforementioned signaling pathways either 15 min before the preconditioning or infusion of QA. Inhibition of the PKA and PI3K pathways abolished the protection evoked by NMDA, and inhibition of the MEK pathway significantly diminished this protection. Treatment with PKC and CaMKII inhibitors did not alter the protection rate. Inhibition of the MEK and PKC pathways resulted in an increased mortality rate when followed by the infusion of QA, or NMDA preconditioning and QA infusion, respectively. These results suggest that the PKA, PI3K and MEK pathways have a crucial role in the achievement of a neuroprotective state following preconditioning. PMID:21185872

de Araújo Herculano, Bruno; Vandresen-Filho, Samuel; Martins, Wagner Carbolin; Boeck, Carina Rodrigues; Tasca, Carla Inês

2011-05-16

287

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

SciTech Connect

High altitude/hypoxia training is known to improve physical performance in athletes. Hypoxia induces hypoxia inducible factor-1 (HIF-1) and its downstream genes that facilitate hypoxia adaptation in muscle to increase physical performance. Cobalt chloride (CoCl{sub 2}), a hypoxia mimetic, stabilizes HIF-1, which otherwise is degraded in normoxic conditions. We studied the effects of hypoxia preconditioning by CoCl{sub 2} supplementation on physical performance, glucose metabolism, and mitochondrial biogenesis using rodent model. The results showed significant increase in physical performance in cobalt supplemented rats without (two times) or with training (3.3 times) as compared to control animals. CoCl{sub 2} supplementation in rats augmented the biological activities of enzymes of TCA cycle, glycolysis and cytochrome c oxidase (COX); and increased the expression of glucose transporter-1 (Glut-1) in muscle showing increased glucose metabolism by aerobic respiration. There was also an increase in mitochondrial biogenesis in skeletal muscle observed by increased mRNA expressions of mitochondrial biogenesis markers which was further confirmed by electron microscopy. Moreover, nitric oxide production increased in skeletal muscle in cobalt supplemented rats, which seems to be the major reason for peroxisome proliferator activated receptor-gamma coactivator-1? (PGC-1?) induction and mitochondrial biogenesis. Thus, in conclusion, we state that hypoxia preconditioning by CoCl{sub 2} supplementation in rats increases mitochondrial biogenesis, glucose uptake and metabolism by aerobic respiration in skeletal muscle, which leads to increased physical performance. The significance of this study lies in understanding the molecular mechanism of hypoxia adaptation and improvement of work performance in normal as well as extreme conditions like hypoxia via hypoxia preconditioning. -- Highlights: ? We supplemented rats with CoCl{sub 2} for 15 days along with training. ? CoCl{sub 2} supplementation augmented endurance performance and aerobic respiration. ? It increased glucose uptake and metabolism in muscle. ? It enhanced mitochondrial biogenesis in red gastrocnemius muscle.

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

2012-11-01

288

Hyperbaric oxygen preconditioning promotes neovascularization of transplanted skin flaps in rats  

PubMed Central

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

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

2014-01-01

289

Graph Embedding Techniques for Bounding Condition Numbers of Incomplete Factor Preconditioning  

NASA Technical Reports Server (NTRS)

We extend graph embedding techniques for bounding the spectral condition number of preconditioned systems involving symmetric, irreducibly diagonally dominant M-matrices to systems where the preconditioner is not diagonally dominant. In particular, this allows us to bound the spectral condition number when the preconditioner is based on an incomplete factorization. We provide a review of previous techniques, describe our extension, and give examples both of a bound for a model problem, and of ways in which our techniques give intuitive way of looking at incomplete factor preconditioners.

Guattery, Stephen

1997-01-01

290

[Myocardial ischemic preconditioning: pathophysiological mechanisms and prospects of clinical application (a literature review)].  

PubMed

Ischemic preconditioning (IPC, i.e. increase in the organ resistance to a prolonged ischemia which occurs after a brief ischemic challenge) seems to be one of the most powerful endogenous cardioprotective mechanisms known to date. Current data regarding molecular mechanisms of early (classic) IPC as well as the second window of protection are reviewed in the context of the concept of sequential three-staged development of protective effect. Based on original and published data, possible mechanisms of remote IPC are considered. The review comprises current ideas of existence of the IPC clinical correlates and its use in clinic. PMID:11452804

Petrishchev, N N; Shliakhto, E V; Vlasov, T D; Galagudza, M M

2001-05-01

291

Effect of electroacupuncture preconditioning on serum S100? and NSE in patients undergoing craniocerebral tumor resection  

Microsoft Academic Search

Objective  To investigate the effect of electroacupuncture preconditioning on the serum level of S100 calcium-binding protein beta (S100?)\\u000a and neuron-specific enolase (NSE) in patients undergoing craniocerebral tumor operation.\\u000a \\u000a \\u000a \\u000a \\u000a Methods  A total of 32 patients, who would go through craniocerebral tumor resection under general anesthesia, were randomly assigned\\u000a to two groups, 16 in each group. Patients in the electroacupuncture (EA) group received electroacupuncture

Zhi-hong Lu; Xiao-guang Bai; Li-ze Xiong; Yong-hui Wang; Yi Wang; Qiang Wang

2010-01-01

292

Effects of ischemic preconditioning on cyclinD1 expression during early ischemic reperfusion in rats  

PubMed Central

AIM: To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion. METHODS: Fifty-four SD rats were randomly divided into ischemic preconditioning group (IP), ischemia/reperfusion group (IR) and sham operation group (SO). The IP and IR groups were further divided into four sub-groups (n = 6). Sham operation group (SO) served as the control group (n = 6). A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. After 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinD1 mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS: Compared with IR group, IP group showed a significantly lower ALT level in 1 h to 4 h sub-groups (P < 0.05). Proliferation index(PI) indicated by the S-phase and G2/M-phase ratio [(S+G2/M)/(G0/G1+S+G2/M)] was significantly increased in IP group at 0 and 1 h (26.44± 7.60% vs 18.56 ± 6.40%,41.87 ± 7.27% vs 20.25 ± 6.70%, P < 0.05). Meanwhile, cyclinD1 protein expression could be detected in IP group. But in IR group, cyclinD1 protein expression occurred 2 h after reperfusion. The expression of cyclinD1 mRNA increased significantly in IP group at 0 and 1 h (0.568 ± 0.112 vs 0.274 ± 0.069, 0.762 ± 0.164 vs 0.348 ± 0.093, P < 0.05). CONCLUSION: Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion. PMID:16718823

Cai, Fang-Gang; Xiao, Jian-Sheng; Ye, Qi-Fa

2006-01-01

293

A preconditioned inexact spectral transform method for calculating resonance energies and widths, as applied to HCO  

NASA Astrophysics Data System (ADS)

We present a complex-symmetric version of the preconditioned inexact spectral transform (PIST) method, for calculating resonance energies and widths. The PIST method uses an iterative linear solver to compute inexact Lanczos vectors for (EI-H)-1, and then diagonalizes the Hamiltonian in the inexact Lanczos representation. Our new version requires complex-symmetric variants of: (1) the Lanczos algorithm, (2) the linear solver, (3) the preconditioner we introduced in a previous paper [J. Chem. Phys. 114, 9254 (2001)]. The new method works extremely well for HCO, enabling us to calculate the first 17 dissociative resonances in less then 90 second of CPU time.

Poirier, Bill; Carrington, Tucker

2002-01-01

294

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

SciTech Connect

This work presents a detailed implementation of a double precision, Non-Preconditioned, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{trademark} in conjunction with x86 Opteron{trademark} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.

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

2009-01-01

295

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

SciTech Connect

This work presents a detailed implementation of a double precision, non-preconditioned, Conjugate Gradient algorithm on a Roadrunner heterogeneous supercomputer node. These nodes utilize the Cell Broadband Engine Architecture{sup TM} in conjunction with x86 Opteron{sup TM} processors from AMD. We implement a common Conjugate Gradient algorithm, on a variety of systems, to compare and contrast performance. Implementation results are presented for the Roadrunner hybrid supercomputer, SRC Computers, Inc. MAPStation SRC-6 FPGA enhanced hybrid supercomputer, and AMD Opteron only. In all hybrid implementations wall clock time is measured, including all transfer overhead and compute timings.

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

2009-01-01

296

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 ...

297

Injury Prevention  

MedlinePLUS

... Injury Prevention Travel & Motor Vehicle Safety En Español ER 101 Where Should I Go? Check In Medical ... Admission to the Hospital Issues You Should Know ER Heroes Home > Health News > Injury Prevention About Emergencies ...

298

Comparison of ischaemic preconditioning with surgical delay technique to increase the viability of single pedicle island venous flaps: An experimental study.  

PubMed

Abstract The aim of the present study was to investigate the effect of ischaemic preconditioning compared with the surgical delay procedure in an effort to increase the survival rate of single pedicle island venous flaps. Eighteen male Wistar albino rats (250-350 g) were included. A 3 × 4 cm flap was planned at the right lower abdomen of the rat. Superficial epigastric vein constituted the pedicle of the flap. The rats were divided into three groups, each consisting of six rats. In the control group, a single pedicle venous island flap was elevated on each rat and no other surgical procedure was performed. In the ischaemic preconditioning group, ischaemic preconditioning was performed and, in the surgical delay procedure group, the surgical delay technique was performed before flap elevation. The mean necrosis areas were 56.85 ± 14.60%, 28.73 ± 15.60%, and 12.08 ± 3.65% in the control, ischaemic preconditioning, and surgical delay procedure groups, respectively. The necrosis areas were significantly smaller in the ischaemic preconditioning group and surgical delay procedure groups compared to the control group (p = 0.004 and p < 0.001, respectively). The necrosis areas were similar in the ischaemic preconditioning and surgical delay procedure groups. Histopathological parameters including necrosis, abscess formation, and skin ulceration scores were significantly lower in the ischaemic preconditioning group than in the control group, whereas the study groups were similar. In conclusion, ischaemic preconditioning may serve as an adjuvant technique in increasing venous island flap viability. PMID:24635552

Ceylan, Refika; Kaya, Burak; Caydere, Muzaffer; Terzio?lu, Ahmet; Aslan, Gürcan

2014-12-01

299

Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K\\/Akt pathways  

Microsoft Academic Search

We previously reported that hydrogen sulfide (H2S) preconditioning (SP) produces cardioprotective effects against ischemia in rat cardiac myocytes. The present study aims\\u000a to elucidate the signaling mechanisms involved in SP-induced cardioprotection by investigating the role of extracellular signal\\u000a regulated kinase (ERK1\\/2) and phosphatidylinositol 3-kinase (PI3K)\\/Akt. We found that preconditioning with NaHS (a H2S donor) for three cycles significantly decreased myocardial

Yeshi Hu; Xin Chen; Ting-Ting Pan; Kay Li Neo; Shiau Wei Lee; Ester Sandar Win Khin; Philip K. Moore; Jin-Song Bian

2008-01-01

300

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

PubMed Central

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

2014-01-01

301

Non-crossing large-margin probability estimation and its application to robust SVM via preconditioning  

PubMed Central

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 precondition our training data. The standard SVM is then applied to the preconditioned training data to achieve robustness. Simulations and real data are used to illustrate their finite sample performance. PMID:21151740

Wu, Yichao; Liu, Yufeng

2010-01-01

302

Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes  

PubMed Central

Aim: To investigate whether R-848 (resiquimod, toll-like receptor 7/8 agonist) can induce late preconditioning in neonatal cardiac myocytes. Methods: The protective effects of R-848 on neonatal myocytes against anoxia-reoxygenation-induced injury were tested, and intracellular reactive oxygen species (ROS) were determined. The protein synthesis inhibitor cyclohexamide (CH) and the ROS scavenger N-acetylcysteine (NAC) were used in this model to test if new protein synthesis and oxidative stress were necessary for their cardioprotective effects. The activation of nuclear factor kappa B (NF?B) and hypoxia inducible factor 1 (HIF1) was investigated by electrophoretic mobility shift assays (EMSA), and inducible nitric oxide synthase (iNOS) was assessed by immunoblotting. After iNOS was down-regulated by small interfering RNA (siRNA) transfection, the cardioprotective effect was reassessed. Results: ROS were triggered soon after R-848 (0.01–1.0 ?g/L) administration, however, the cardioprotective effect of which was induced 24 h later. This protection was abolished by CH or NAC pretreatment. NF?B and HIF1 activation and iNOS up-regulation were involved in this protective mechanism. The cardioprotective effect was also attenuated after iNOS was knocked down. Conclusion: R-848 provided a cardioprotective effect through a late preconditioning mechanism via a ROS/NF?B-HIF1/iNOS-dependent pathway. PMID:21516132

Wang, Yong-yi; Liu, Sha; Lian, Feng; Yang, Wen-gang; Xue, Song

2011-01-01

303

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

PubMed Central

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

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

2013-01-01

304

Metabolic Basis for Thyroid Hormone Liver Preconditioning: Upregulation of AMP-Activated Protein Kinase Signaling  

PubMed Central

The liver is a major organ responsible for most functions of cellular metabolism and a mediator between dietary and endogenous sources of energy for extrahepatic tissues. In this context, adenosine-monophosphate- (AMP-) activated protein kinase (AMPK) constitutes an intrahepatic energy sensor regulating physiological energy dynamics by limiting anabolism and stimulating catabolism, thus increasing ATP availability. This is achieved by mechanisms involving direct allosteric activation and reversible phosphorylation of AMPK, in response to signals such as energy status, serum insulin/glucagon ratio, nutritional stresses, pharmacological and natural compounds, and oxidative stress status. Reactive oxygen species (ROS) lead to cellular AMPK activation and downstream signaling under several experimental conditions. Thyroid hormone (L-3,3?,5-triiodothyronine, T3) administration, a condition that enhances liver ROS generation, triggers the redox upregulation of cytoprotective proteins affording preconditioning against ischemia-reperfusion (IR) liver injury. Data discussed in this work suggest that T3-induced liver activation of AMPK may be of importance in the promotion of metabolic processes favouring energy supply for the induction and operation of preconditioning mechanisms. These include antioxidant, antiapoptotic, and anti-inflammatory mechanisms, repair or resynthesis of altered biomolecules, induction of the homeostatic acute-phase response, and stimulation of liver cell proliferation, which are required to cope with the damaging processes set in by IR. PMID:22919323

Videla, Luis A.; Fernandez, Virginia; Cornejo, Pamela; Vargas, Romina

2012-01-01

305

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

PubMed Central

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

Haider, Husnain Kh; Ashraf, Muhammad

2008-01-01

306

Ischemic preconditioning affects hexokinase activity and HKII in different subcellular compartments throughout cardiac ischemia-reperfusion.  

PubMed

The glycolytic enzyme hexokinase (HK) is suggested to play a role in ischemic preconditioning (IPC). In the present study we determined how ischemic preconditioning affects HK activity and HKI and HKII protein content at five different time points and three different subcellular fractions throughout cardiac ischemia-reperfusion. Isolated Langendorff-perfused rat hearts (10 groups of 7 hearts each) were subjected to 35 min ischemia and 30 min reperfusion (control groups); the IPC groups were pretreated with 3 times 5-min ischemia. IPC was without effect on microsomal HK activity, and only decreased cytosolic HK activity at 35 min ischemia, which was mimicked by decreased cytosolic HKII, but not HKI, protein content. In contrast, mitochondrial HK activity at baseline and during reperfusion was elevated by IPC, without changes during ischemia. No effect of IPC on mitochondrial HK I protein content was observed. However, mitochondrial HK II protein content during reperfusion was augmented by IPC, albeit not following the IPC stimulus. It is concluded that IPC results in decreased cytosolic HK activity during ischemia that could be explained by decreased HKII protein content. IPC increased mitochondrial HK activity before ischemia and during reperfusion that was only mimicked by increased HK II protein content during reperfusion. IPC was without effect on the phosphorylation status of HK before ischemia. We conclude that IPC is associated with 1) a biphasic response of increased mitochondrial HK activity before and after ischemia, 2) decreased cytosolic HK activity during ischemia, and 3) cellular redistribution of HKII but not HKI. PMID:19228992

Gürel, Ebru; Smeele, Kirsten M; Eerbeek, Otto; Koeman, Anneke; Demirci, Cihan; Hollmann, Markus W; Zuurbier, Coert J

2009-06-01

307

Role of the parasympathetic nervous system in cardioprotection by remote hindlimb ischaemic preconditioning.  

PubMed

This investigation was designed to determine the participation of the vagus nerve and muscarinic receptors in the remote ischaemic preconditioning (rIPC) mechanism. New Zealand rabbits were anaesthetized, and the femoral artery was dissected. After 30 min of monitoring, the hearts were isolated and subjected to 30 min of global no-flow ischaemia and 180 min of reperfusion (non-rIPC group). The ventricular function was evaluated, considering the left ventricular developed pressure and the left ventricular end-diastolic pressure. In the rIPC group, the rabbits were subjected to three cycles of hindlimb ischaemia (5 min) and reperfusion (5 min), and the same protocol as that used in non-rIPC group was then repeated. In order to evaluate the afferent neural pathway during the rIPC protocol we used two groups, one in which the femoral and sciatic nerves were sectioned and the other in which the spinal cord was sectioned (T9-T10 level). To study the efferent neural pathway during the rIPC protocol, the vagus nerve was sectioned and, in another group, atropine was administered. The effect of vagal stimulation was also evaluated. An infarct size of 40.8 ± 3.1% was obtained in the non-rIPC group, whereas in rIPC group the infarct size decreased to 16.4 ± 3.5% (P < 0.05). During the preconditioning protocol, the vagus nerve section and the atropine administration each abolished the effect of rIPC on infarct size. Vagal stimulation mimicked the effect of rIPC, decreasing infarct size to 15.2 ± 4.7% (P < 0.05). Decreases in infarct size were accompanied by improved left ventricular function. We demonstrated the presence of a neural afferent pathway, because the spinal cord section completely abolished the effect of rIPC on infarct size. In conclusion, rIPC activates a neural afferent pathway, the cardioprotective signal reaches the heart through the vagus nerve (efferent pathway), and acetylcholine activates the ischaemic preconditioning phenomenon when acting on the muscarinic receptors. PMID:22872660

Donato, Martín; Buchholz, Bruno; Rodríguez, Manuel; Pérez, Virginia; Inserte, Javier; García-Dorado, David; Gelpi, Ricardo J

2013-02-01

308

Conventional, but not remote ischemic preconditioning, reduces iNOS transcription in liver ischemia/reperfusion  

PubMed Central

AIM: To study the effects of preconditioning on inducible nitric oxide synthase (iNOS) and interleukin 1 (IL-1) receptor transcription in rat liver ischemia/reperfusion injury (IRI). METHODS: Seventy-two male rats were randomized into 3 groups: the one-hour segmental ischemia (IRI, n = 24) group, the ischemic preconditioning (IPC, n = 24) group or the remote ischemic preconditioning (R-IPC, n = 24) group. The IPC and R-IPC were performed as 10 min of ischemia and 10 min of reperfusion. The iNOS and the IL-1 receptor mRNA in the liver tissue was analyzed with real time PCR. The total Nitrite and Nitrate (NOx) in continuously sampled microdialysate (MD) from the liver was analyzed. In addition, the NOx levels in the serum were analyzed. RESULTS: After 4 h of reperfusion, the iNOS mRNA was significantly higher in the R-IPC (?Ct: 3.44 ± 0.57) group than in the IPC (?Ct: 5.86 ± 0.82) group (P = 0.025). The IL-1 receptor transcription activity was reduced in the IPC group (?Ct: 1.88 ± 0.53 to 4.81 ± 0.21), but not in the R-IPC group, during reperfusion (P = 0.027). In the MD, a significant drop in the NOx levels was noted in the R-IPC group (12.3 ± 2.2 to 4.7 ± 1.2 ?mol/L) at the end of ischemia compared with the levels in early ischemia (P = 0.008). A similar trend was observed in the IPC group (11.8 ± 2.1 to 6.4 ± 1.5 ?mol/L), although this difference was not statistically significant. The levels of NOx rose quickly during reperfusion in both groups. CONCLUSION: IPC, but not R-IPC, reduces iNOS and IL-1 receptor transcription during early reperfusion, indicating a lower inflammatory reaction. NOx is consumed in the ischemic liver lobe. PMID:25071345

Bjornsson, Bergthor; Winbladh, Anders; Bojmar, Linda; Sundqvist, Tommy; Gullstrand, Per; Sandstrom, Per

2014-01-01

309

Modification of the Hepatic Mitochondrial Proteome in Response to Ischemic Preconditioning following Ischemia-Reperfusion Injury of the Rat Liver  

Microsoft Academic Search

Background\\/Aim: Ischemic preconditioning (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

R. Oshima; H. Nakano; M. Katayama; J. Sakurai; W. Wu; S. Koizumi; T. Asano; T. Watanabe; T. Asakura; T. Ohta; T. Otsubo

2008-01-01

310

Transcriptional signature of human adipose tissue-derived stem cells (hASCs) preconditioned for chondrogenesis in hypoxic conditions  

Microsoft Academic Search

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 preconditioning 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

L. Pilgaard; P. Lund; M. Duroux; H. Lockstone; J. Taylor; J. Emmersen; T. Fink; J. Ragoussis; V. Zachar

2009-01-01

311

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

E-print Network

. Transplantation of hypoxic preconditioned murine MSC (HypMSC) enhanced skeletal muscle regeneration at day 7 skeletal muscle fiber clearance. Moreover, HypMSC transplantation resulted in a large increase in Wnt4MSC, abrogated the hypoxia-induced vascular regenerative properties of these cells in the mouse hind limb

Paris-Sud XI, Université de

312

Heat-shock preconditioning reduces oxidative protein denaturation and ameliorates liver injury by carbon tetrachloride in rats  

Microsoft Academic Search

Membrane lipids and cytosolic proteins are major targets of oxidative injury. This study examined the effect of heat-shock preconditioning associated with the induction of heat-shock protein 72 on liver injury, from the aspect of lipid peroxidation and protein denaturation after carbon tetrachloride (CCl4) administration in rats - one of the representative oxidative injuries. Male Wistar rats were divided into two

Hidekazu Yamamoto; Yuzo Yamamoto; Kazuhiko Yamagami; Makoto Kume; Syuji Kimoto; Shinya Toyokuni; Koji Uchida; Manabu Fukumoto; Yoshio Yamaoka

2000-01-01

313

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

PubMed Central

The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise preconditioning promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise preconditioning is a promising strategy for facilitating functional recovery from SCI. PMID:25334068

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

2014-01-01

314

Jacobi and Gauss-Seidel preconditioned complex conjugate gradient method with GPU acceleration for finite element method  

Microsoft Academic Search

In this paper two implementations of iterative solvers for solving complex symmetric and sparse systems resulting from finite element method applied to wave equation are discussed. The problem under investigation is a dielectric resonator antenna (DRA) discretized by FEM with vector elements of the second order (LT\\/QN). The solvers use the preconditioned conjugate gradient (pcg) method implemented on Graphics Processing

Adam Dziekonski; Adam Lamecki; Michal Mrozowski

2010-01-01

315

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

PubMed Central

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

Kennedy, Donna; Mnich, Katarzyna; Samali, Afshin

2014-01-01

316

Lipopolysaccharide preconditioning attenuates neuroapoptosis and improves functional recovery through activation of Nrf2 in traumatic spinal cord injury rats.  

PubMed

The previous studies suggested that low-dose lipopolysaccharide (LPS) provides neuroprotection against subsequent challenge with ischemic/reperfusion injury in the brain. But there were few reports about the neuroprotective effects of low-dose LPS against spinal cord injury (SCI). In this study, we evaluated the effect of low-dose LPS preconditioning on neuroapoptosis status after traumatic SCI (TSCI), using a standardized contusion model (NYU, New York University, impactor). SCI-induced rats were randomly divided into three groups: sham operation, control (receiving only normal saline) and LPS preconditioning (0.2 mg/kg, ip; 72 hours before injury). Neurologic function was assessed by the Basso, Beattie and Bresnahan (BBB) score at 6, 12, 24, 48 and 72 hours after TSCI. Rats were sacrificed at 72 hours postinjury. Histological changes were studied using Nissl staining. Apoptotic neural cells were assessed using the TdT-mediated dUTP Nick End Labeling (TUNEL) assay. Nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3 were detected with immunohistochemistry and Western blot. LPS preconditioning reduced neuron apoptosis, improved neurologic outcome and actived Nrf2 expression. Moreover, Histological changes and the number of apoptotic cells were correlated with Nrf2 expression after the rats suffered the SCI. Our results suggest that LPS preconditioning exerted a neuroprotective effect against TSCI in rats, and activation of Nrf2 was believed to be one of the contributing mechanisms. PMID:23215850

Li, Wei-Chao; Jiang, Dian-Ming; Hu, Ning; Qi, Xiao-Tong; Qiao, Bo; Luo, Xiao-Ji

2013-04-01

317

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

PubMed

The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise preconditioning promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise preconditioning is a promising strategy for facilitating functional recovery from SCI. PMID:25334068

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

2014-01-01

318

A dual negative regulation model of Toll-like receptor 4 signaling for endotoxin preconditioning in human endotoxemia  

E-print Network

A dual negative regulation model of Toll-like receptor 4 signaling for endotoxin preconditioning Keywords: Mathematical modeling Lipopolysaccharide Endotoxin Potentiation Tolerance Humans a b s t r a c t We discuss a model illustrating how the outcome of repeated endotoxin administration experiments can

Androulakis, Ioannis (Yannis)

319

Microarray Analyses of Genes Regulated by Isoflurane Anesthesia In Vivo: A Novel Approach to Identifying Potential Preconditioning Mechanisms  

PubMed Central

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 preconditioning 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 preconditioning requires de novo protein synthesis, knowledge of anesthetic-regulated genes is incomplete. In this study we used the conserved nature of preconditioning 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 preconditioning. 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 preconditioning studies. PMID:23400992

Edmands, Scott D; Hall, Adam C.; LaDow, Eva

2012-01-01

320

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

PubMed

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

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

2010-11-15

321

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

PubMed Central

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

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

2010-01-01

322

Preconditioned conjugate gradient methods for the compressible Navier-Stokes equations  

NASA Technical Reports Server (NTRS)

The compressible Navier-Stokes equations are solved for a variety of two-dimensional inviscid and viscous problems by preconditioned conjugate gradient-like algorithms. Roe's flux difference splitting technique is used to discretize the inviscid fluxes. The viscous terms are discretized by using central differences. An algebraic turbulence model is also incorporated. The system of linear equations which arises out of the linearization of a fully implicit scheme is solved iteratively by the well known methods of GMRES (Generalized Minimum Residual technique) and Chebyschev iteration. Incomplete LU factorization and block diagonal factorization are used as preconditioners. The resulting algorithm is competitive with the best current schemes, but has wide applications in parallel computing and unstructured mesh computations.

Venkatakrishnan, V.

1990-01-01

323

Spatially distributed stochastic systems: Equation-free and equation-assisted preconditioned computations.  

PubMed

Spatially distributed problems are often approximately modeled in terms of partial differential equations (PDEs) for appropriate coarse-grained quantities (e.g., concentrations). The derivation of accurate such PDEs starting from finer scale, atomistic models, and using suitable averaging is often a challenging task; approximate PDEs are typically obtained through mathematical closure procedures (e.g., mean field approximations). In this paper, we show how such approximate macroscopic PDEs can be exploited in constructing preconditioners to accelerate stochastic computations for spatially distributed particle-based process models. We illustrate how such preconditioning can improve the convergence of equation-free coarse-grained methods based on coarse timesteppers. Our model problem is a stochastic reaction-diffusion model capable of exhibiting Turing instabilities. PMID:17144691

Qiao, Liang; Erban, Radek; Kelley, C T; Kevrekidis, Ioannis G

2006-11-28

324

Spatially distributed stochastic systems: Equation-free and equation-assisted preconditioned computations  

NASA Astrophysics Data System (ADS)

Spatially distributed problems are often approximately modeled in terms of partial differential equations (PDEs) for appropriate coarse-grained quantities (e.g., concentrations). The derivation of accurate such PDEs starting from finer scale, atomistic models, and using suitable averaging is often a challenging task; approximate PDEs are typically obtained through mathematical closure procedures (e.g., mean field approximations). In this paper, we show how such approximate macroscopic PDEs can be exploited in constructing preconditioners to accelerate stochastic computations for spatially distributed particle-based process models. We illustrate how such preconditioning can improve the convergence of equation-free coarse-grained methods based on coarse timesteppers. Our model problem is a stochastic reaction-diffusion model capable of exhibiting Turing instabilities.

Qiao, Liang; Erban, Radek; Kelley, C. T.; Kevrekidis, Ioannis G.

2006-11-01

325

Effects of diabetes on myocardial infarct size and cardioprotection by preconditioning and postconditioning  

PubMed Central

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 preconditioning (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

2012-01-01

326

Some Experiences with Nonoverlapping Schur Complement Parallel Preconditioning for CFD Calculations  

NASA Technical Reports Server (NTRS)

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 preconditioning 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.

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

1996-01-01

327

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

NASA Astrophysics Data System (ADS)

A recent proof-of-principle study proposes an energy- and charge-conserving, nonlinearly implicit electrostatic particle-in-cell (PIC) algorithm in one dimension [9]. The algorithm in the reference employs an unpreconditioned Jacobian-free Newton-Krylov method, which ensures nonlinear convergence at every timestep (resolving the dynamical timescale of interest). Kinetic enslavement, which is one key component of the algorithm, not only enables fully implicit PIC as a practical approach, but also allows preconditioning the kinetic solver with a fluid approximation. This study proposes such a preconditioner, in which the linearized moment equations are closed with moments computed from particles. Effective acceleration of the linear GMRES solve is demonstrated, on both uniform and non-uniform meshes. The algorithm performance is largely insensitive to the electron-ion mass ratio. Numerical experiments are performed on a 1D multi-scale ion acoustic wave test problem.

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

2014-02-01

328

Genomic analysis of ischemic preconditioning in adult rat hippocampal slice cultures.  

PubMed

Understanding endogenous mechanisms of neuroprotection may have important clinical applications. It is well established that brain tissue becomes more resistant to ischemic injury following a sublethal ischemic insult. This process, called ischemic preconditioning (IPC), can be induced in adult rat hippocampal slice cultures by a brief oxygen-glucose deprivation (OGD) [Hassen, G.W., Tian, D., Ding, D., Bergold, P.J., 2004. A new model of ischemic preconditioning using young adult hippocampal slice cultures. Brain Res. Brain Res. Protoc. 13, 135-143]. We have analyzed the changes in gene expression brought about by IPC in this model in order to understand the mechanisms involved. Total RNA was isolated at different time points following a brief OGD (3, 6 and 12 h) and used to probe genome-wide expression microarrays. Genes were identified that were significantly up- or down-regulated relative to controls. We placed genes that were differentially expressed into statistically significant groups based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and gene ontology (GO) terms. Genes involved in signal transduction, transcription, and oxidative phosphorylation are differentially expressed at each time point. The analysis demonstrates that alterations in signaling pathways (TGF-beta, Wnt, MAPK, ErbB, Toll-like receptor, JAK-STAT, VEGF) consistently accompany IPC. RT-PCR was used to confirm that members of these signaling pathways are regulated as predicted by the microarray analysis. We verified that protein translation following OGD is necessary for IPC. We also found that blocking the NMDA receptor during OGD does not significantly inhibit IPC in this model or produce large changes in gene expression. Our data thus suggests that changes in signaling pathways and their down-stream targets play an important role in triggering endogenous neuroprotection. PMID:19631194

Benardete, Ethan A; Bergold, Peter J

2009-10-01

329

Hypoxic preconditioning attenuates lipopolysaccharide-induced oxidative stress in rat kidneys  

PubMed Central

Chronic hypoxic (CH) preconditioning reduces superoxide-induced renal dysfunction via the upregulation of superoxide dismutase (SOD) activity and contents. Endotoxaemia reduces renal antioxidant status. We hypothesize that CH preconditioning might protect the kidney from subsequent endotoxaemia-induced oxidative injury. Endotoxaemia was induced by intraperitoneal injection of lipopolysaccharide (LPS; 4 mg kg?1) in rats kept at sea level (SL) and rats with CH in an altitude chamber (5500 m for 15 h day?1) for 4 weeks. LPS enhanced xanthine oxidase (XO) and gp91phox (catalytic subunit of NADPH oxidase) expression associated with burst amount of superoxide production from the SL kidney surface and renal venous blood detected by lucigenin-enhanced chemiluminescence. LPS induced a morphologic-independent renal dysfunction in baseline and acute saline loading stages and increased renal IL-1? protein and urinary protein concentration in the SL rats. After 4 weeks of induction, CH significantly increased Cu/ZnSOD, MnSOD and catalase expression (16 ± 17, 128 ± 35 and 48 ± 21, respectively) in renal cortex, and depressed renal cortex XO (44 ± 16%) and renal cortex (20 ± 9%) and medulla (28 ± 11%) gp91phox when compared with SL rats. The combined effect of enhanced antioxidant proteins and depressed oxidative proteins significantly reduced LPS-enhanced superoxide production, renal XO and gp91phox expression, renal IL-1? production, and urinary protein level. CH also ameliorated LPS-induced renal dysfunction in the baseline and acute saline loading periods. We conclude that CH treatment enhances the intrarenal antioxidant/oxidative protein ratio to overcome endotoxaemia-induced reactive oxygen species formation and inflammatory cytokine release. PMID:17317755

Yang, Chih-Ching; Ma, Ming-Chieh; Chien, Chiang-Ting; Wu, Ming-Shiou; Sun, Wan-Kuan; Chen, Chau-Fong

2007-01-01

330

Chronic Tempol treatment restores pharmacological preconditioning in the senescent rat heart.  

PubMed

Cardioprotective effects of anesthetic preconditioning and cyclosporine A (CsA) are lost with aging. To extend our previous work and address a possible mechanism underlying age-related differences, we investigated the role of oxidative stress in the aging heart by treating senescent animals with the oxygen free radical scavenger Tempol. Old male Fischer 344 rats (22-24 mo) were randomly assigned to control or Tempol treatment groups for 2 or 4 wk (T×2wk and T×4wk, respectively). Rats received isoflurane 30 min before ischemia-reperfusion injury or CsA just before reperfusion. Myocardial infarction sizes were significantly reduced by isoflurane or CsA in the aged rats treated with Tempol (T×4wk) compared with old control rats. In other experiments, young (4-6 mo) and old rats underwent either chronic Tempol or vehicle treatment, and the levels of myocardial protein oxidative damage, antioxidant enzymes, mitochondrial Ca(2+) uptake, cyclophilin D protein, and mitochondrial permeability transition pore opening times were measured. T×4wk significantly increased MnSOD enzyme activity, GSH-to-GSSH ratios, MnSOD protein level, mitochondrial Ca(2+) uptake capacity, reduced protein nitrotyrosine levels, and normalized cyclophilin D protein expression in the aged rat heart. T×4wk also significantly prolonged mitochondrial permeability transition pore opening times induced by reactive oxygen species in old cardiomyocytes. Our studies demonstrate that 4 wk of Tempol pretreatment restores anesthetic preconditioning and cardioprotection by CsA in the old rat and that this is associated with decreased oxidative stress and improved mitochondrial function. Our results point to a new protective strategy for the ischemic myocardium in the high-risk older population. PMID:23275621

Zhu, Jiang; Rebecchi, Mario J; Wang, Qiang; Glass, Peter S A; Brink, Peter R; Liu, Lixin

2013-03-01

331

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

PubMed Central

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

2014-01-01

332

Subcutaneous preconditioning increases invasion and metastatic dissemination in mouse colorectal cancer models  

PubMed Central

Mouse colorectal cancer (CRC) models generated by orthotopic microinjection of human CRC cell lines reproduce the pattern of lymphatic, haematological and transcoelomic spread but generate low metastatic efficiency. Our aim was to develop a new strategy that could increase the metastatic efficiency of these models. We used subcutaneous implantation of the human CRC cell lines HCT116 or SW48 prior to their orthotopic microinjection in the cecum of nude mice (SC+ORT). This subcutaneous preconditioning significantly enhanced metastatic dissemination. In the HCT116 model it increased the number and size of metastatic foci in lymph nodes, lung, liver and peritoneum, whereas, in the SW48 model, it induced a shift from non-metastatic to metastatic. In both models the number of apoptotic bodies in the primary tumour in the SC+ORT group was significantly reduced compared with that in the direct orthotopic injection (ORT) group. Moreover, in HCT116 tumours the number of keratin-positive tumour buddings and single epithelial cells increased at the invasion front in SC+ORT mice. In the SW48 tumour model, we observed a trend towards a higher number of tumour buds and single cells in the SC+ORT group but this did not reach statistical significance. At a molecular level, the enhanced metastatic efficiency observed in the HCT116 SC+ORT model was associated with an increase in AKT activation, VEGF-A overexpression and downregulation of ?1 integrin in primary tumour tissue, whereas, in SW48 SC+ORT mice, the level of expression of these proteins remained unchanged. In summary, subcutaneous preconditioning increased the metastatic dissemination of both orthotopic CRC models by increasing tumour cell survival and invasion at the tumour invasion front. This approach could be useful to simultaneously study the mechanisms of metastases and to evaluate anti-metastatic drugs against CRC. PMID:24487410

Alamo, Patricia; Gallardo, Alberto; Pavón, Miguel A.; Casanova, Isolda; Trias, Manuel; Mangues, Maria A.; Vázquez, Esther; Villaverde, Antonio; Mangues, Ramon; Céspedes, Maria V.

2014-01-01

333

Left and right preconditioning for electrical impedance tomography with structural information  

NASA Astrophysics Data System (ADS)

A common problem in computational inverse problems is to find an efficient way of solving linear or nonlinear least-squares problems. For large-scale problems, iterative solvers are the method of choice for solving the associated linear systems, and for nonlinear problems, an additional effective local linearization method is required. In this paper, we discuss an efficient preconditioning scheme for Krylov subspace methods, based on the Bayesian analysis of the inverse problem. The model problem to which we apply this methodology is electrical impedance tomography (EIT) augmented with prior information coming from a complementary modality, such as x-ray imaging. The particular geometry considered here models the x-ray-guided EIT for breast imaging. The interest in applying EIT concurrently with x-ray breast imaging arises from the experimental observation that the impedivity spectra of certain types of malignant and benign tissues differ significantly from each other, thus offering a possibility of diagnosis without more invasive tissue sampling. After setting up the EIT inverse problem within a Bayesian framework, we present an inner and outer iteration scheme for computing a maximum a posteriori estimate. The prior covariance provides a right preconditioner and the modeling error covariance provides a left preconditioner for the iterative method used to solve the linear least-squares problem at each outer iteration of the optimization problem. Moreover, the stopping criterion for the inner iterations is coupled with the progress of the solution of the outer iteration. Besides the preconditioning scheme, the computational efficiency relies on a very efficient method to compute the Jacobian, obtained by carefully organizing the forward computation. Computed examples illustrate the robustness and computational efficiency of the proposed algorithm.

Calvetti, Daniela; McGivney, Debra; Somersalo, Erkki

2012-05-01

334

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

PubMed Central

Background Emulsified isoflurane (EIso) is a novel intravenous general anesthetic, which can provide rapid anesthetic induction and recovery. EIso preconditioning could attenuate heart, lung and liver ischemia/reperfusion (I/R) injury. We tested the hypothesis that intravenous pretreatment with EIso would protect kidneys against I/R injury by inhibiting systemic inflammatory responses and improving renal antioxidative ability. Methods Rats were randomly divided into these six groups: sham, I/R, intralipid, 1, 2 or 4 ml/kg EIso. Rats were subjected to 45 min left renal pedicle occlusion followed by 3 h reperfusion after right nephrectomy. Rat were treated with intravenous 8% EIso with 1, 2 or 4 ml/kg, or 30% intralipid with 2 ml/kg for 30 min before ischemia, respectively. After reperfusion, renal functional parameters, serum mediator concentrations and markers of oxidative stress in kidney tissues were determined, and renal histopathological analysis were performed. Results Serum creatinine, blood urea nitrogen, cystatin c, tumor necrosis factor-?, interleukin-6, and interleukin-10 concentrations were significantly increased after renal I/R as compared to the sham group. So was renal tissue MDA content and histological scores, but renal tissue SOD activity was decreased. Additionally, severe morphological damages were observed in these study groups. In contrast, 2 or 4 ml/kg EIso reduced serum creatinine, blood urea nitrogen, cystatin c, tumor necrosis factor-?, and interleukin-6 levels, decreased renal tissue MDA content and histological scores, increased serum interleukin-10 level and tissue SOD activity as compared to the I/R, intralipid and 1 ml/kg EIso groups. Renal morphological damages were alleviated after pretreatment of 2 or 4 ml/kg EIso. Conclusions Intravenous EIso produces preconditioning against renal I/R injury in rats, which might be mediated by attenuating inflammation and increasing antioxidation ability. PMID:24739487

2014-01-01

335

Preventative Maintenance.  

ERIC Educational Resources Information Center

Boards of education must be convinced that spending money up front for preventive maintenance will, in the long run, save districts' tax dollars. A good program of preventive maintenance can minimize disruption of service; reduce repair costs, energy consumption, and overtime; improve labor productivity and system equipment reliability; handle…

Migliorino, James

336

Violence Prevention  

MedlinePLUS

... Social Services During the 2 years preceding the study: • 93.9% of states provided funding for staff development or offered staff development on violence prevention services to school mental health or social services staff. • The percentage ...

337

Prevent Shingles  

MedlinePLUS

... 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 prevention tips. Find "Shingles" ...

338

Stroke prevention  

Microsoft Academic Search

Stroke prevention 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 prevention consists\\u000a of the combination of 3 strategies: an optimal management of vascular risk factors, associated when appropriate with antithrombotic\\u000a therapies, carotid

Didier Leys; Dominique Deplanque; Claire Mounier-Vehier; Marie-Anne Mackowiak-Cordoliani; Christian Lucas; Régis Bordet

2002-01-01

339

Mesenchymal stem cells facilitate mixed hematopoietic chimerism induction and prevent onset of diabetes in NOD mice  

PubMed Central

Objectives Allogeneic mesenchymal stem cells (MSCs) and bone marrow cells (BMCs) were co-transplanted in NOD mice following none myeloablative preconditioning and the development of chimerism, insulitis, diabetes, and graft versus host disease (GVHD) were monitored. Methods Eight-weeks-old female NOD mice were injected intravenously with 2×107 BMCs and 5×105 MSCs from C57BL/6 mice following treatment with 2 intraperitoneal injections of anti-CD3 antibody (days ?7 and ?4), and 3Gy total body irradiation (day ?1). Thereafter, blood glucose and chimerism were monitored on peripheral blood samples. Results Stable mixed chimerism (3->90% of donor phenotype) was induced in 63.2% of BMCs-MSCs-(n=19) and 45.0% of BMCs alone recipients (n=20, p=0.256). Insulitis was prevented and euglycemia persisted for >18 weeks in 89.5% of BMCs-MSCs recipients including those with <3% chimerism and 55% of BM alone recipients (p<0.05). In controls, 9.1% of mice receiving preconditioning treatment alone (n=11) and 16.7% of preconditioned mice receiving only MSCs (n=12) were non-diabetic. GVHD was not detected in all mice. Conclusion Co-injection of MSCs and BMCs increased the success rate in inducing chimerism and preventing insulitis and overt diabetes with no incidence of GVHD. Results also indicated that even micro-chimerism with <3% donor cells is sufficient for blocking autoimmunity. PMID:21562444

Asari, Sadaki; Itakura, Shin; Rawson, Jeffrey; Ito, Taihei; Todorov, Ivan; Nair, Indu; Shintaku, Jonathan; Liu, Chih-Pin; Kandeel, Fouad; Mullen, Yoko

2011-01-01

340

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

PubMed Central

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

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

2010-01-01

341

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

NASA Astrophysics Data System (ADS)

Single fluid schemes that rely on an interface function for phase identification in multicomponent compressible flows are widely used to study hydrodynamic flow phenomena in several diverse applications. Simulations based on standard numerical implementation of these schemes suffer from an artificial increase in the width of the interface function owing to the numerical dissipation introduced by an upwind discretization of the governing equations. In addition, monotonicity requirements which ensure that the sharp interface function remains bounded at all times necessitate use of low-order accurate discretization strategies. This results in a significant reduction in accuracy along with a loss of intricate flow features. In this paper we develop a nonlinear transformation based interface capturing method which achieves superior accuracy without compromising the simplicity, computational efficiency and robustness of the original flow solver. A nonlinear map from the signed distance function to the sigmoid type interface function is used to effectively couple a standard single fluid shock and interface capturing scheme with a high-order accurate constrained level set reinitialization method in a way that allows for oscillation-free transport of the sharp material interface. Imposition of a maximum principle, which ensures that the multidimensional preconditioned interface capturing method does not produce new maxima or minima even in the extreme events of interface merger or breakup, allows for an explicit determination of the interface thickness in terms of the grid spacing. A narrow band method is formulated in order to localize computations pertinent to the preconditioned interface capturing method. Numerical tests in one dimension reveal a significant improvement in accuracy and convergence; in stark contrast to the conventional scheme, the proposed method retains its accuracy and convergence characteristics in a shifted reference frame. Results from the test cases in two dimensions show that the nonlinear transformation based interface capturing method outperforms both the conventional method and an interface capturing method without nonlinear transformation in resolving intricate flow features such as sheet jetting in the shock-induced cavity collapse. The ability of the proposed method in accounting for the gravitational and surface tension forces besides compressibility is demonstrated through a model fully three-dimensional problem concerning droplet splash and formation of a crownlike feature.

Shukla, Ratnesh K.

2014-11-01

342

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

PubMed Central

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

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

2014-01-01

343

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

PubMed

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

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

2014-06-01

344

Acetylcholine, Bradykinin, Opioids, and Phenylephrine, but not Adenosine, Trigger Preconditioning by Generating Free Radicals and Opening Mitochondrial KATP Channels  

Microsoft Academic Search

Abstract—It has been assumed,that all G i-coupled receptors trigger the protective action of preconditioning by means,of an identical intracellular signaling pathway. To test this assumption, rabbit hearts were isolated and perfused with Krebs buffer. All hearts were subjected to a 30-minute coronary artery occlusion followed by 120 minutes of reperfusion. Risk area was measured,with fluorescent particles and infarct size with

Michael V. Cohen; Xi-Ming Yang; Guang S. Liu; Gerd Heusch; James M. Downey

345

The role of microRNAs in seizure Preconditioning and Temporal Lobe Epilepsy: Experimental and Clinical Investigations  

Microsoft Academic Search

The central nervous system (CNS) is a rich source of microRNAs (miRs). Within the CNS, miRs are implicated in a myriad of cellular processes and disease states. The present work is comprised of experimental and clinical investigations. We sought to characterise the role of miRs and their biogenesis machinery in seizure preconditioning (PC) and PC-induced epileptic tolerance. In parallel, we

Ross C McKiernan

2011-01-01

346

Effects of substitution of Cx43 by Cx32 on myocardial energy metabolism, tolerance to ischaemia and preconditioning protection.  

PubMed

Connexin 43 (Cx43) plays an important role in cardioprotective signalling by mechanisms at least in part independent of gap junctional communication. To investigate whether this role is related to specific properties of this connexin isoform, we used a knock-in mouse model in which the coding region of Cx43 is replaced by that of Cx32. Homozygous Cx43KI32 mice showed reduced cell-to-cell Lucifer Yellow transfer (P < 0.01), but QRS duration and left ventricular fractional shortening (echocardiography) were similar to those in wild-type animals. NMR spectroscopy detected reduced ATP and increased lactate content in myocardium from homozygous Cx43KI32 animals (P < 0.05). Despite this, isolated homozygous Cx43KI32 hearts showed smaller infarcts after ischaemia-reperfusion (40 min/60 min) as compared to hearts from heterozygous and wild-type animals (13 and 31% reduction, respectively, P < 0.05). Cardiac myocytes isolated from Cx43KI32 mouse hearts also showed a reduced rate of cell death after simulated ischaemia-reperfusion. In a separate series of experiments, both ischaemic (4 cycles of 3.5 min of ischaemia and 5 min of reperfusion) and pharmacological (50 micromol l(-1) diazoxide, 10 min) preconditioning reduced infarct size in hearts from wild-type mice (by 24.84 and 26.63%, respectively, P < 0.05), but only ischaemic preconditioning was effective in hearts from heterozygous animals and both preconditioning strategies failed to protect Cx43KI32 homozygous hearts. These results demonstrate that Cx43 has an important and previously unknown modulatory effect in myocardial energy metabolism and tolerance to ischaemia, and plays a critical role in preconditioning protection, by mechanisms that are specific for this connexin isoform. PMID:20156849

Rodríguez-Sinovas, Antonio; Sánchez, Jose A; González-Loyola, Alejandra; Barba, Ignasi; Morente, Miriam; Aguilar, Rio; Agulló, Esperanza; Miró-Casas, Elisatet; Esquerda, Neus; Ruiz-Meana, Marisol; García-Dorado, David

2010-04-01

347

Effects of continuous nitrogen application and nitrogen preconditioning on nodulation and growth of Ceanothus griseus var horizontalis  

Microsoft Academic Search

Rooted cuttings ofCeanothus griseus varhorizontalis were irrigated with 0, 10, 20, 50, 75 or 100ppm nitrogen as NH4NO3 for eight weeks prior to inoculation with infectiveFrankia. After inoculation, half of the plants for each treatment nitrogen level continued to be irrigated with the preconditioning nitrogen level and half were given no more supplemental nitrogen. For plants continuously receiving nitrogen, nodule

Kathryn A. Thomas; Alison M. Berry

1989-01-01

348

ATP-sensitive potassium channel openers may mimic the effects of hypoxic preconditioning on the coronary artery  

Microsoft Academic Search

Background. This study was designed to investigate the effects of the potassium channel opener KRN4884 in mimicking hypoxic preconditioning on coronary arteries and to explore the possible mechanisms.Methods. In the organ chamber, porcine coronary artery rings (n = 96) were studied in 6 groups (n = 16 in each group): I. Control: normoxia (pO2 > 200 mmHg); II. Hypoxia-reoxygenation: 60-minute

Zhen Ren; Qin Yang; H. Storm Floten; Anthony P Furnary; Anthony P. C Yim; Guo-Wei He

2001-01-01

349

Reactive oxygen species are not a required trigger for exercise-induced late preconditioning in the rat heart.  

PubMed

Reactive oxygen species (ROS) have been reported to play a primary role in triggering the cardioprotective adaptations by some preconditioning procedures, but whether they are required for exercise-induced preconditioning is unclear. Thus in this study we used the free radical scavenger N-(2-mercaptopropionyl)glycine (MPG) to test the hypothesis that ROS is the trigger for exercise-induced preconditioning of the heart against ischemia-reperfusion injury. Male F344 rats were assigned to four groups: sedentary (SED, n = 7), SED/MPG (100 mg/kg ip daily for 2 days, n = 12), exercised on a treadmill for 2 days at 20 m/min, 6° grade, for 60 min (RUN, n = 7), and RUN/MPG with 100 mg/kg MPG injected 15 min before exercise (n = 10). Preliminary experiments verified that MPG administration maintained myocardial redox status during the exercise bout. Twenty-four hours postexercise or MPG treatment isolated perfused working hearts were subjected to global ischemia for 22.5 min followed by reperfusion for 30 min. Recovery of myocardial external work (percentage of preischemic systolic pressure times cardiac output) for SED (50.4 ± 4.5) and SED/RUN (54.7 ± 6.6) was similar and improved in both exercise groups (P < 0.05) to 77.9 ± 3.0 in RUN and 76.7 ± 4.5 in RUN/MPG. A 2 × 2 ANOVA also revealed that exercise decreased lactate dehydrogenase release from the heart during reperfusion (marker of cell damage) without MPG effects or interactions. Expression of the cytoprotective protein inducible heat shock protein 70 increased by similar amounts in the left ventricles of RUN and RUN/MPG compared with sedentary groups (P < 0.05). We conclude that ROS are not a necessary trigger for exercise-induced preconditioning in rats. PMID:22955056

Taylor, Ryan P; Starnes, Joseph W

2012-11-01

350

Mitochondrial K ATP channel-dependent and -independent phases of ischemic preconditioning against myocardial infarction in the rat  

Microsoft Academic Search

To obtain insight into the role of the mitochondrial ATP-sensitive K+ (mitoKATP) channel in ischemic preconditioning (PC), we aimed to clarify the mitoKATP channel-dependent phase of PC in two PC protocols with different intervals between PC ischemia and an index ischemia. The\\u000a possible contribution of mitoKATP channel opening to protein kinase C activation in PC was also examined by Western

Yukinaga Nozawa; Tetsuji Miura; Takayuki Miki; Yoshito Ohnuma; Toshiyuki Yano; Kazuaki Shimamoto

2003-01-01

351

Hippocampal transcriptome after status epilepticus in mice rendered seizure damage-tolerant by epileptic preconditioning features suppressed calcium and neuronal excitability pathways.  

PubMed

Preconditioning brain with a sub-lethal stressor can temporarily generate a damage-refractory state. Microarray analyses have defined the changes in hippocampal gene expression that follow brief preconditioning seizures, but not the transcriptome after a prolonged and otherwise injurious seizure in previously preconditioned brain. Presently, microarray analysis was performed 24 h after status epilepticus in mice that had received previously either seizure preconditioning (tolerance) or sham-preconditioning (injury). Transcriptional changes in the hippocampal CA3 subfield of >or=2 fold were detected for 1357 genes in the tolerance group compared to a non-seizure control group, with 54% up-regulated. Of these regulated genes, 792 were also regulated in the injury group. Among the remaining 565 genes regulated only in tolerance, 73% were down-regulated. Analysis of the genes differentially suppressed in tolerance identified calcium signaling, ion channels and excitatory neurotransmitter receptors, and the synapse as over-represented among pathways, functions and compartments. Finally, 12 days continuous EEG recordings determined mice with induced tolerance had fewer spontaneous electrographic seizures compared to the injury group. Our data suggest the transcriptional phenotype of neuroprotection in tolerance may be dictated by the biology of the preconditioning stressor, functions by transcriptional reduction of vulnerability to excitotoxicity, and has anti-epileptogenic effects. PMID:18804535

Jimenez-Mateos, Eva M; Hatazaki, Seiji; Johnson, Martha B; Bellver-Estelles, Carmen; Mouri, Genshin; Bonner, Caroline; Prehn, Jochen H M; Meller, Robert; Simon, Roger P; Henshall, David C

2008-12-01

352

Intermittent hypoxia preconditioning-induced epileptic tolerance by upregulation of monocarboxylate transporter 4 expression in rat hippocampal astrocytes.  

PubMed

Noxious stimuli applied at doses close to but below the threshold of cell injury induce adaptive responses that provide a defense against additional stress. Epileptic preconditioning protects neurons against status epilepticus and ischemia; however, it is not known if the converse is true. During hypoxia/ischemia (H/I), lactate released from astrocytes is taken up by neurons and is stored for energy, a process mediated by monocarboxylate transporter 4 (MCT4) in astroglia. The present study investigated whether H/I preconditioning can provide protection to neurons against epilepsy through upregulation of MCT4 expression in astrocytes in vitro and in vivo. An oxygen/glucose deprivation protocol was used in primary astrocyte cultures, while rats were subjected to an intermittent hypoxia preconditioning (IHP) paradigm followed by lithium-pilocarpine-induced epilepsy as well as lactate transportation inhibitor injection, with a subsequent evaluation of protein expression as well as behavior. H/I induced an upregulation of MCT4 expression, while an IHP time course of 5 days provided the greatest protection against epileptic seizures, which was most apparent by 3 days after IHP. However, lactate transport function disturbances can block the protective effect induced by IHP. These findings provide a potential basis for the clinical treatment of epilepsy. PMID:25146899

Gao, Chen; Wang, Chao; Liu, Bei; Wu, Hao; Yang, Qianli; Jin, Jungong; Li, Huanfa; Dong, Shan; Gao, Guodong; Zhang, Hua

2014-11-01

353

Some mechanisms of the protective effect of ischemic preconditioning on rat liver ischemia-reperfusion injury  

PubMed Central

Ischemia-reperfusion (I/R) injury is a multifactorial process that affects graft function after liver transplantation. An understanding of the mechanisms involved in I/R injury is essential for the design of therapeutic strategies to improve the outcome of liver transplantation. The generation of reactive oxygen species subsequent to reoxygenation inflicts tissue damage and initiates a cascade of deleterious cellular responses, leading to inflammation, cell death, and ultimate organ failure. Increasing experimental evidence has suggested that Kupffer cells and T-cells mediate activation of neutrophil inflammatory responses. Activated neutrophils infiltrate the injured liver in parallel with increased expression of adhesion molecules on endothelial cells. The heme oxygenase system is among the most critical of the cytoprotective mechanisms activated during cellular stress, exerting antioxidant and anti-inflammatory functions, modulating the cell cycle, and maintaining the microcirculation. Finally, the activation of toll-like receptors on Kupffer cells may play a fundamental role in exploring new therapeutic strategies based on the concept that hepatic I/R injury represents a case for host “innate” immunity. In the present study, there was a significant decrease in hepatic activity of glycogen in the I/R group as compared with corresponding values in the control group. On the other hand, there was a significant increase in the hepatic activity of glycogen in the I/R-IP (ischemic preconditioning) group as compared with corresponding values in the I/R group. PMID:25382983

Adam, Abdel Nasser Ismail

2014-01-01

354

Fishermen's interests and cooperation: preconditions for joint management of Swedish coastal fisheries.  

PubMed

The participation of fishermen in fisheries management is discussed with varying ideas under the notions of "co-management", "participatory management" or "local management". Empirical studies within Swedish fishery have thrown new light on the preconditions for fishermen's participation in fisheries management. Among the important factors influencing failure or success are the two which we discuss here: the question of articulation, organization and representation of interests of fishermen and the question of trust between the groups that are usually cooperating in resource management, fishermen, governmental administrators and researchers. The research summarized has addressed the interests of fishermen with regard to resource management, local fisheries management, and participation of fishermen. The overarching question connecting the three themes is: How can the interests of fishermen be represented better within fisheries management? Interests and trust, "soft facts", can be as important for the success or failure of fisheries management and participation as can "hard facts" such as ownership rights, quantity and quality of resources or monetary value of resources. PMID:15865306

Bruckmeier, Karl; Ellegård, Anders; Píriz, Laura

2005-03-01

355

Discretization and Preconditioning Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes  

NASA Technical Reports Server (NTRS)

Several stabilized discretization procedures for conservation law equations on triangulated domains will be considered. Specifically, numerical schemes based on upwind finite volume, fluctuation splitting, Galerkin least-squares, and space discontinuous Galerkin discretization will be considered in detail. A standard energy analysis for several of these methods will be given via entropy symmetrization. Next, we will present some relatively new theoretical results concerning congruence relationships for left or right symmetrized equations. These results suggest new variants of existing FV, DG, GLS and FS methods which are computationally more efficient while retaining the pleasant theoretical properties achieved by entropy symmetrization. In addition, the task of Jacobian linearization of these schemes for use in Newton's method is greatly simplified owing to exploitation of exact symmetries which exist in the system. These variants have been implemented in the "ELF" library for which example calculations will be shown. The FV, FS and DG schemes also permit discrete maximum principle analysis and enforcement which greatly adds to the robustness of the methods. Some prevalent limiting strategies will be reviewed. Next, we consider embedding these nonlinear space discretizations into exact and inexact Newton solvers which are preconditioned using a nonoverlapping (Schur complement) domain decomposition technique. Elements of nonoverlapping domain decomposition for elliptic problems will be reviewed followed by the present extension to hyperbolic and elliptic-hyperbolic problems. Other issues of practical relevance such the meshing of geometries, code implementation, turbulence modeling, global convergence, etc. will be addressed as needed.

Barth, Timothy; Chancellor, Marisa K. (Technical Monitor)

1997-01-01

356

Discretization and Preconditioning Algorithms for the Euler and Navier-Stokes Equations on Unstructured Meshes  

NASA Technical Reports Server (NTRS)

Several stabilized demoralization procedures for conservation law equations on triangulated domains will be considered. Specifically, numerical schemes based on upwind finite volume, fluctuation splitting, Galerkin least-squares, and space discontinuous Galerkin demoralization will be considered in detail. A standard energy analysis for several of these methods will be given via entropy symmetrization. Next, we will present some relatively new theoretical results concerning congruence relationships for left or right symmetrized equations. These results suggest new variants of existing FV, DG, GLS, and FS methods which are computationally more efficient while retaining the pleasant theoretical properties achieved by entropy symmetrization. In addition, the task of Jacobean linearization of these schemes for use in Newton's method is greatly simplified owing to exploitation of exact symmetries which exist in the system. The FV, FS and DG schemes also permit discrete maximum principle analysis and enforcement which greatly adds to the robustness of the methods. Discrete maximum principle theory will be presented for general finite volume approximations on unstructured meshes. Next, we consider embedding these nonlinear space discretizations into exact and inexact Newton solvers which are preconditioned using a nonoverlapping (Schur complement) domain decomposition technique. Elements of nonoverlapping domain decomposition for elliptic problems will be reviewed followed by the present extension to hyperbolic and elliptic-hyperbolic problems. Other issues of practical relevance such the meshing of geometries, code implementation, turbulence modeling, global convergence, etc, will. be addressed as needed.

Barth, Timothy J.; Kutler, Paul (Technical Monitor)

1998-01-01

357

Human placental metabolic adaptation to chronic hypoxia, high altitude: hypoxic preconditioning  

PubMed Central

We have previously demonstrated placentas from laboring deliveries at high altitude have lower binding of hypoxia-inducible transcription factor (HIF) to DNA than those from low altitude. It has recently been reported that labor causes oxidative stress in placentas, likely due to ischemic hypoxic insult. We hypothesized that placentas of high-altitude residents acquired resistance, in the course of their development, to oxidative stress during labor. Full-thickness placental tissue biopsies were collected from laboring vaginal and nonlaboring cesarean-section term (37–41 wk) deliveries from healthy pregnancies at sea level and at 3,100 m. After freezing in liquid nitrogen within 5 min of delivery, we quantified hydrophilic and lipid metabolites using 31P and 1H NMR metabolomics. Metabolic markers of oxidative stress, increased glycolysis, and free amino acids were present in placentas following labor at sea level, but not at 3,100 m. In contrast, at 3,100 m, the placentas were characterized by the presence of concentrations of stored energy potential (phosphocreatine), antioxidants, and low free amino acid concentrations. Placentas from pregnancies at sea level subjected to labor display evidence of oxidative stress. However, laboring placentas at 3,100 m have little or no oxidative stress at the time of delivery, suggesting greater resistance to ischemia-reperfusion. We postulate that hypoxic preconditioning might occur in placentas that develop at high altitude. PMID:19864339

Murray, Andrew J.; Beckey, Virginia; Cindrova-Davies, Tereza; Johns, Jemma; Zwerdlinger, Lisa; Jauniaux, Eric; Burton, Graham J.; Serkova, Natalie J.

2010-01-01

358

Leptin signaling is required for augmented therapeutic properties of mesenchymal stem cells conferred by hypoxia preconditioning.  

PubMed

Hypoxia preconditioning enhances the therapeutic effect of mesenchymal stem cells (MSCs). However, the mechanism underlying hypoxia-induced augmentation of the protective effect of MSCs on myocardial infarction (MI) is poorly understood. We show that hypoxia-enhanced survival, mobility, and protection of cocultured cardiomyocytes were paralleled by increased expression of leptin and cell surface receptor CXCR4. The enhanced activities were abolished by either knockdown of leptin with a selective shRNA or by genetic deficiency of leptin or its receptor in MSCs derived, respectively, from ob/ob or db/db mice. To characterize the role of leptin in the regulation of MSC functions by hypoxia and its possible contribution to enhanced therapeutic efficacy, cell therapy using MSCs derived from wild-type, ob/ob, or db/db mice was implemented in mouse models of acute MI. Augmented protection by hypoxia pretreatment was only seen with MSCs from wild-type mice. Parameters that were differentially affected by hypoxia pretreatment included MSC engraftment, c-Kit(+) cell recruitment to the infarct, vascular density, infarct size, and long-term contractile function. These data show that leptin signaling is an early and essential step for the enhanced survival, chemotaxis, and therapeutic properties of MSCs conferred by preculture under hypoxia. Leptin may play a physiological role in priming MSCs resident in the bone marrow endosteum for optimal response to systemic signaling molecules and subsequent tissue repair. Stem Cells 2014;32:2702-2713. PMID:24989835

Hu, Xinyang; Wu, Rongrong; Jiang, Zhi; Wang, Lihan; Chen, Panpan; Zhang, Ling; Yang, Lu; Wu, Yan; Chen, Han; Chen, Huiqiang; Xu, Yinchuan; Zhou, Yu; Huang, Xin; Webster, Keith A; Yu, Hong; Wang, Jian'an

2014-10-01

359

Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning  

PubMed Central

Background Notch signaling is known to be activated following myocardial ischemia, but its role in cardioprotection provided by ischemic preconditioning (IPC) and ischemic postconditioning (IPost) remains unclear. Methods Lentiviral vectors were constructed to overexpress or knockdown N1ICD in H9c2 cardiomyocyte and rat heart exposed to ischemia reperfusion injury (IRI), IPC or IPost. Results Notch1 signaling was activated during myocardial IPC and IPost, and could enhance cell viability and inhibit apoptosis. Furthermore, activated Notch1 signaling stabilized mitochondrial membrane potential and reduced reactive oxygen species induced by IRI. The cardioprotection provided by activated Notch1 signaling resembled that of IPC and IPost, which was related to Stat3 activation and regulation of apoptosis related proteins. Furthermore, in langendorff heart perfusion model, activated Notch1 signaling restored cardiac function, decreased lactate dehydrogenase release and limited infarct size after myocardial ischemia. Conclusions: Notch1 signaling is activated and mediates cardioprotection provided by IPC and Ipost. Notch1 signaling may represent a potential new pharmacologic mimic for cardioprotection of ischemic heart disease. PMID:24098939

2013-01-01

360

Ischemic preconditioning and atenolol on lung injury after intestinal ischemia and reperfusion in rats.  

PubMed

The aim of this study was evaluate the beta blocker atenolol (AT) and ischemic preconditioning (IPC) strategies for tissue protection against systemic effects of intestinal ischemia (I) and reperfusion (R) injury. Forty-two rats were pretreated with AT (1.5 mg · kg(-1)), 0.9% saline solution (SS; 0.1 mL), or IPC and then subjected to prolonged occlusion of the superior mesenteric artery for 60 minutes leading to I followed or not by 120 minutes of R, according to the group. For IPC, 5 minutes of I prior to 10 minutes of R were established. After this process of I or I-R, the right lung of each animal was adequately prepared for staining with hematoxylin and eosin and subsequent histologic analysis for quantification of inflammatory infiltrate was done. The left lung was frozen and prepared for assessment of oxidative stress by the quantification of thiobarbituric acid-reactivity substances (TBARS). Histologic analysis showed an important inflammatory infiltrate in the I-R + SS (I-R + SS = 4.5), which was significantly (P < .05) reduced by IPC (I-R + IPC = 3.0) or AT (I-R + AT = 3.0). Likewise, the TBARS levels were decreased by both strategies (I-R + SS = 0.63; I-R + IPC = 0.23; I-R + AT = 0.38; P < .05). Our results showed that AT and IPC attenuate pulmonary lesions caused by intestinal I and R process. PMID:25131055

Bonservizi, W G S; Koike, M K; Saurim, R; Felix, G A A; da Silva, S M; Montero, E F S; Taha, M O

2014-01-01

361

Hippocampal hypertrophy and sleep apnea: a role for the ischemic preconditioning?  

PubMed

The full impact of multisystem disease such as obstructive sleep apnoea (OSA) on regions of the central nervous system is debated, as the subsequent neurocognitive sequelae are unclear. Several preclinical studies suggest that its purported major culprits, intermittent hypoxia and sleep fragmentation, can differentially affect adult hippocampal neurogenesis. Although the prospective biphasic nature of chronic intermittent hypoxia in animal models of OSA has been acknowledged, so far the evidence for increased 'compensatory' neurogenesis in humans is uncertain. In a cross-sectional study of 32 patients with mixed severity OSA and 32 non-apnoeic matched controls inferential analysis showed bilateral enlargement of hippocampi in the OSA group. Conversely, a trend for smaller thalami in the OSA group was noted. Furthermore, aberrant connectivity between the hippocampus and the cerebellum in the OSA group was also suggested by the correlation analysis. The role for the ischemia/hypoxia preconditioning in the neuropathology of OSA is herein indicated, with possible further reaching clinical implications. PMID:24349453

Rosenzweig, Ivana; Kempton, Matthew J; Crum, William R; Glasser, Martin; Milosevic, Milan; Beniczky, Sandor; Corfield, Douglas R; Williams, Steven C; Morrell, Mary J

2013-01-01

362

Hippocampal Hypertrophy and Sleep Apnea: A Role for the Ischemic Preconditioning?  

PubMed Central

The full impact of multisystem disease such as obstructive sleep apnoea (OSA) on regions of the central nervous system is debated, as the subsequent neurocognitive sequelae are unclear. Several preclinical studies suggest that its purported major culprits, intermittent hypoxia and sleep fragmentation, can differentially affect adult hippocampal neurogenesis. Although the prospective biphasic nature of chronic intermittent hypoxia in animal models of OSA has been acknowledged, so far the evidence for increased ‘compensatory’ neurogenesis in humans is uncertain. In a cross-sectional study of 32 patients with mixed severity OSA and 32 non-apnoeic matched controls inferential analysis showed bilateral enlargement of hippocampi in the OSA group. Conversely, a trend for smaller thalami in the OSA group was noted. Furthermore, aberrant connectivity between the hippocampus and the cerebellum in the OSA group was also suggested by the correlation analysis. The role for the ischemia/hypoxia preconditioning in the neuropathology of OSA is herein indicated, with possible further reaching clinical implications. PMID:24349453

Rosenzweig, Ivana; Kempton, Matthew J.; Crum, William R.; Glasser, Martin; Milosevic, Milan; Beniczky, Sandor; Corfield, Douglas R.; Williams, Steven C.; Morrell, Mary J.

2013-01-01

363

Remote ischemic preconditioning as treatment for non-ischemic gastrointestinal disorders: Beyond ischemia-reperfusion injury  

PubMed Central

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 preconditioning (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

Camara-Lemarroy, Carlos Rodrigo

2014-01-01

364

Ischemic preconditioning and tacrolimus pretreatment as strategies to attenuate intestinal ischemia-reperfusion injury in mice.  

PubMed

The intestine is highly sensitive to ischemia-reperfusion injury (IRI), a phenomenon occurring in different intestinal diseases. Several strategies to mitigate IRI are in experimental stages; unfortunately, no consensus has been reached about the most appropriate one. We report a protocol to study ischemic preconditioning (IPC) evaluation in mice and to combine IPC and tacrolimus (TAC) pretreatment in a warm ischemia model. Mice were divided into treated (IPC, TAC, and IPC + TAC) and untreated groups before intestinal ischemia. IPC, TAC, and IPC + TAC groups were able to decrease postreperfusion nitrites levels (P < .05). IPC-containing groups had a major beneficial effect by preserving the integrity of the intestinal histology (P < .05) and improving animal survival (P < .002) compared with TAC alone or the untreated group. The IPC + TAC group was the only one that showed significant improvement in lung histological analysis (P < .05). The TAC and IPC + TAC groups down-regulated intestinal expression of interleukin (II)-6 and IL1b more than 10-fold compared with the control group. Although IPC and TAC alone reduced intestinal IRI, the used of a combined therapy produced the most significant results in all the local and distant evaluated parameters. PMID:23953566

Stringa, P; Romanin, D; Lausada, N; Machuca, M; Raimondi, J C; Cabanne, A; Rumbo, M; Gondolesi, G

2013-01-01

365

How to heat up from the cold: examining the preconditions for (unconscious) mood effects.  

PubMed

What are the necessary preconditions to make people feel good or bad? In this research, the authors aimed to uncover the bare essentials of mood induction. Several induction techniques exist, and most of these techniques demand a relatively high amount of cognitive capacity. Moreover, to be effective, most techniques require conscious awareness. The authors proposed that the common and defining element in all effective mood induction techniques is the dominating salience of evaluative tone over descriptive meaning. This evaluative-tone hypothesis was tested in two paradigms in which the evaluative meaning of the "primed" concept was more salient than its descriptive meaning (i.e., when subliminal stimulus exposure was so short that mainly the evaluative meaning was activated [see D. A. Stapel, W. Koomen, & K. I. Ruys, 2002] and when the primed concepts were sufficiently extreme such that evaluative meaning always dominated descriptive meaning). Explicit and implicit mood measures showed that the activation of a dominating evaluative tone affected people's mood states. Implications of these findings for theories on unconscious mood induction are discussed. PMID:18444738

Ruys, Kirsten I; Stapel, Diederik A

2008-05-01

366

Plagiarism Prevention  

ERIC Educational Resources Information Center

Plagiarism does exist at universities today. In some cases, students are naive with respect to understanding what plagiarism is and how to avoid it. In other cases, students blatantly disregard and disrespect the written work of others, claiming it as their own. Regardless, educators must be vigilant in their efforts to discourage and prevent

Probett, Christine

2011-01-01

367

Preventing Tragedy.  

ERIC Educational Resources Information Center

The Navajo supervisor in the Office of Environmental Health in New Mexico identifies diseases and their risk factors, administers an injury prevention program, and ensures compliance with various health-related codes. She assists in the planning and direction of environmental health programs and public health education for local Navajo…

One Feather, Sandra

2003-01-01

368

Comparison of the responses to hypoxia, ischaemia and ischaemic preconditioning in wild marmot and laboratory rabbit hearts.  

PubMed

Marmots (Marmota flaviventris) are burrowing mammals that may be subjected to low levels of oxygen and high levels of carbon dioxide in their underground environment. Since marmots successfully deal with this physiological challenge, we hypothesized that the isolated perfused marmot heart would be damaged less and recover better from a bout of induced hypoxia or ischaemia than would the heart of a comparison animal, the New Zealand laboratory rabbit (Oryctolagus cuniculus). Isolated marmot and rabbit hearts were made hypoxic by a 30 min perfusion with an oxygen-deficient buffer. The hearts were then perfused with an oxygen-replete buffer and measurements of heart rate, left ventricular pressure and lactate dehydrogenase (LDH) release (an indicator of cell damage) were made over 5 or 10 min intervals for 30 min of hypoxia and 30 min of recovery. There were no species differences in the responses, except that the heart rate in marmots was about 50% of the rate in rabbits during the hypoxia part of the experiment. There was no evidence that the marmot hearts were damaged less or recovered better from hypoxia and reoxgenation than the rabbit hearts. Marmot and rabbit hearts were also subjected to 30 min of total ischaemia; measurements of heart rate, left ventricular pressure and LDH release were obtained during 30 min of reperfusion and compared with the pre-ischaemia values for these variables. There were no significant species differences. When the 30 min ischaemic period was preceded by a 5 min period of ischaemia and a 10 min reperfusion period (preconditioning), the rabbit hearts were protected by this brief ischaemic insult and recovered better than the hearts that had not been subjected to the preconditioning ischaemia. This was not true in the marmot hearts, however, as the preconditioning ischaemia did not promote a greater recovery over that in its absence. When preconditioned marmots hearts were compared with preconditioned rabbit hearts, there were no statistical differences in the responses. The hypothesis that marmot hearts would be damaged less and recover better from hypoxia and ischaemia was not supported by the experimental data. PMID:8867278

McKean, T; Mendenhall, W

1996-03-01

369

PREEMPTIVE PREVENTION 223 PREEMPTIVE PREVENTION*  

E-print Network

prevented the window from being broken. Or did it? Had you not made the catch, I would have caught the ball instead. My leaping to catch the ball made your catch redun- dant. Given my presence, the ball was never, because it wouldn't have hit the window irre- spective of whether you had acted or not.' To this I say

Fitelson, Branden

370

Neuroprotective effects of preconditioning ischaemia on ischaemic brain injury through inhibition of mixed-lineage kinase 3 via NMDA receptor-mediated Akt1 activation.  

PubMed

A number of works show that the mitogen-activated protein kinase (MAPK) signalling pathway responds actively in cerebral ischaemia and reperfusion. We undertook our present studies to clarify the role of mixed-lineage kinase 3 (MLK3), a MAPK kinase kinase (MAPKKK) in MAPK cascades, in global ischaemia and ischaemic tolerance. The mechanism concerning NMDA receptor-mediated Akt1 activation underlying ischaemic tolerance, was also investigated. Sprague-Dawley rats were subjected to 6 min of ischaemia and differing times of reperfusion. Our results showed MLK3 was activated in the hippocampal CA1 region with two peaks occurring at 30 min and 6 h, respectively. This activation returned to base level 3 days later. Both preconditioning with 3 min of sublethal ischaemia and NMDA pretreatment inhibited the 6-h peak of activation. However, pretreatment of ketamine before preconditioning reversed the inhibiting effect of preconditioning on MLK3 activation at 6 h of reperfusion. In the case of Akt1, however, preconditioning and NMDA pretreatment enhanced Akt1 activation at 10 min of reperfusion. Furthermore, ketamine pretreatment reversed preconditioning-induced increase of Akt1 activation. We also noted that pretreatment of LY294002 before preconditioning reversed both the inhibition of MLK3 activation at 6 h of reperfusion and the increase in Akt1 activation at 10 min of reperfusion. The above-mentioned results lead us to conclude that, in the hippocampal CA1 region, preconditioning inhibits MLK3 activation after lethal ischaemia and reperfusion and, furthermore, this effect is mediated by Akt1 activation through NMDA receptor stimulation. PMID:15857405

Yin, Xiao-Hui; Zhang, Quan-Guang; Miao, Bei; Zhang, Guang-Yi

2005-05-01

371

Obesity Prevention  

Microsoft Academic Search

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

Shiriki K. Kumanyika; Stephen R. Daniels

372

[Early ischemic preconditioning against focal transient and permanent brain ischemia in rats: role of collateral circulation].  

PubMed

We hypothesize that early ischemic preconditioning (IPC) can afford protection against focal brief and prolonged cerebral ischemia with subsequent reperfusion as well as permanent brain ischemia in rats by amelioration of regional cerebral blood flow. Adult male Wistar rats (n=97) were subjected to transient (30 and 60 minutes) and permanent middle cerebral artery (MCA) occlusion. IPC protocol consisted of two episodes of 5-min common carotid artery occlusion + 5-min reperfusion prior to test ischemia either followed by 48 hours of reperfusion or not. Triphenyltetrazolium chloride and Evans blue were used for delineation of infarct size and anatomical area at risk (comprises ischemic penumbra and ischemic core), respectively. Blood flow in the MCA vascular bed was measured with use of Doppler ultrasound. The IPC resulted in significant infarct size limitation in both transient and permanent MCA occlusion. Importantly, IPC caused significant reduction of area at risk after 30 min of focal ischemia as compared to controls [med(min-max) 11.4% (3.59-2 0.35%) vs. 2.47% (0.8-9.31%), p = 0.018] but it failed to influence area at risk after 5 min of ischemia [med(min-max) 7.61% (6.32-10.87%) vs. 8.2% (4.87-9.65%), p > 0.05]. No differences in blood flow were found between IPC and control groups using Doppler ultrasound. This is suggestive of the fact that IPC does not really influence blood flow in the large cerebral arteries such as MCA but it might have some effect on smaller arteries. It seems that, along with well established cytoprotective effects of IPC, IPC-mediated reduction of area at risk by means of improvement in local cerebral blood flow may contribute to infarct size limitation after focal transient and permanent brain ischemia in rats. PMID:21598680

Shmonin, A A; Ba?sa, A E; Mel'nikova, E V; Vavilov, V N; Vlasov, T D

2011-02-01

373

Exploring the Human Plasma Proteome for Humoral Mediators of Remote Ischemic Preconditioning - A Word of Caution  

PubMed Central

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 preconditioning (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

Helgeland, Erik; Breivik, Lars Ertesvag; Vaudel, Marc; Svendsen, ?yvind Sverre; Garberg, Hilde; Nordrehaug, Jan Erik; Berven, Frode Steingrimsen; Jonassen, Anne Kristine

2014-01-01

374

Apolipoprotein A-I Is a Potential Mediator of Remote Ischemic Preconditioning  

PubMed Central

Background Remote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach. Methods and Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5?) or 10-min (RIPC 10?) reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10?. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI). Conclusions RIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism. PMID:24155931

Hibert, Pierre; Prunier-Mirebeau, Delphine; Beseme, Olivia; Chwastyniak, Maggy; Tamareille, Sophie; Lamon, Delphine; Furber, Alain; Pinet, Florence; Prunier, Fabrice

2013-01-01

375

Role of hypoxia inducible factor-1? in remote limb ischemic preconditioning.  

PubMed

Remote ischemic preconditioning (RIPC) has emerged as a feasible and attractive therapeutic procedure for heart protection against ischemia/reperfusion (I/R) injury. However, its molecular mechanisms remain poorly understood. Hypoxia inducible factor-1? (HIF-1?) is a transcription factor that plays a key role in the cellular adaptation to hypoxia and ischemia. This study's aim was to test whether RIPC-induced cardioprotection requires HIF-1? upregulation to be effective. In the first study, wild-type mice and mice heterozygous for HIF1a (gene encoding the HIF-1? protein) were subjected to RIPC immediately before myocardial infarction (MI). RIPC resulted in a robust HIF-1? activation in the limb and acute cardioprotection in wild-type mice. RIPC-induced cardioprotection was preserved in heterozygous mice, despite the low HIF-1? expression in their limbs. In the second study, the role of HIF-1? in RIPC was evaluated using cadmium (Cd), a pharmacological HIF-1? inhibitor. Rats were subjected to MI (MI group) or to RIPC immediately prior to MI (R-MI group). Cd was injected 18 0min before RIPC (Cd-R-MI group). RIPC induced robust HIF-1? activation in rat limbs and significantly reduced infarct size (IS). Despite Cd's inhibition of HIF-1? activation, RIPC-induced cardioprotection was preserved in the Cd-R-MI group. RIPC applied immediately prior to MI increased HIF-1? expression and attenuated IS in rats and wild-type mice. However, RIPC-induced cardioprotection was preserved in partially HIF1a-deficient mice and in rats pretreated with Cd. When considered together, these results suggest that HIF-1? upregulation is unnecessary in acute RIPC. PMID:24140799

Kalakech, Hussein; Tamareille, Sophie; Pons, Sandrine; Godin-Ribuot, Diane; Carmeliet, Peter; Furber, Alain; Martin, Valérie; Berdeaux, Alain; Ghaleh, Bijan; Prunier, Fabrice

2013-12-01

376

Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion  

PubMed Central

High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-?, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R. PMID:24944626

HU, XIAORONG; ZHANG, KAI; XU, CHANGWU; CHEN, ZHIQAING; JIANG, HONG

2014-01-01

377

Differential role of mGlu1 and mGlu5 receptors in rat hippocampal slice models of ischemic tolerance.  

PubMed

Activation of glutamate receptors has been proposed as a key factor in the induction of ischemic tolerance. We used organotypic rat hippocampal slices exposed to 30 min oxygen-glucose deprivation (OGD) to evaluate postischemic pyramidal cell death in the CA1 subregion. In this model, 10 min exposure to OGD 24 h before the exposure to toxic OGD was not lethal and reduced the subsequent OGD neurotoxicity by approximately 53% (ischemic preconditioning). Similarly, a 30 min exposure to the group I mGlu receptor agonist DHPG (10 microM) significantly reduced OGD neurotoxicity 24 h later (pharmacological preconditioning). Ischemic tolerance did not develop when either the selective mGlu1 antagonists LY367385 and 3-MATIDA or the AMPA/KA antagonist CNQX were present in the incubation medium during exposure to sublethal OGD. Neither the NMDA antagonist MK801 nor the mGlu5 antagonist MPEP affected the preconditioning process. On the other hand, pharmacological preconditioning was prevented not only by LY367385 or CNQX, but also by MPEP. In preconditioned slices, the toxic responses to AMPA or NMDA were reduced. The neurotoxicty of 100 microM DHPG in slices simultaneously exposed to a mild (20 min) OGD was differentially altered in the two preconditioning paradigms. After ischemic preconditioning, DHPG neurotoxicity was reduced in a manner that was sensitive to LY367385 but not to MPEP, whereas after pharmacological preconditioning it was enhanced in a manner that was sensitive to MPEP but not to LY367385. Our results show that mGlu1 and mGlu5 receptors are differentially involved in the induction and expression of ischemic tolerance following two diverse preconditioning stimuli. PMID:17610579

Werner, Claudia G; Scartabelli, Tania; Pancani, Tristano; Landucci, Elisa; Moroni, Flavio; Pellegrini-Giampietro, Domenico E

2007-06-01

378

The Mechanism of Sevoflurane Preconditioning-Induced Protections against Small Intestinal Ischemia Reperfusion Injury Is Independent of Mast Cell in Rats  

PubMed Central

The study aimed to investigate whether sevoflurane preconditioning can protect against small intestinal ischemia reperfusion (IIR) injury and to explore whether mast cell (MC) is involved in the protections provided by sevoflurane preconditioning. Sprague-Dawley rats exposed to sevoflurane or treated with MC stabilizer cromolyn sodium (CS) were subjected to 75-minute superior mesenteric artery occlusion followed by 2-hour reperfusion in the presence or absence of MC degranulator compound 48/80 (CP). Small intestinal ischemia reperfusion resulted in severe intestinal injury as demonstrated by significant elevations in intestinal injury scores and p47phox and gp91phox, ICAM-1 protein expressions and malondialdehyde and IL-6 contents, and MPO activities as well as significant reductions in SOD activities, accompanied with concomitant increases in mast cell degranulation evidenced by significant increases in MC counts, tryptase expression, and ?-hexosaminidase concentrations, and those alterations were further upregulated in the presence of CP. Sevoflurane preconditioning dramatically attenuated the previous IIR-induced alterations except MC counts, tryptase, and ?-hexosaminidase which were significantly reduced by CS treatment. Furthermore, CP exacerbated IIR injury was abrogated by CS but not by sevoflurane preconditioning. The data collectively indicate that sevoflurane preconditioning confers protections against IIR injury, and MC is not involved in the protective process. PMID:24369442

Su, Guangjie; Zhao, Weicheng; Huang, Pinjie; Luo, Gangjian; Hei, Ziqing

2013-01-01

379

Algebraic multigrid preconditioning within parallel finite-element solvers for 3-D electromagnetic modelling problems in geophysics  

NASA Astrophysics Data System (ADS)

We present an elaborate preconditioning 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 preconditioning 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 preconditioning 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.

Koldan, Jelena; Puzyrev, Vladimir; de la Puente, Josep; Houzeaux, Guillaume; Cela, José María

2014-06-01

380

Preconditioning of the Singular Domain Integral Equation Method for Transverse Electric Scattering on High-Contrast Inhomogeneous Cylinders  

NASA Astrophysics Data System (ADS)

Preconditioning of the domain integral equation (DIE) method for electromagnetic scattering is considered. The present study is focused on the transverse electric (TE) scattering from inhomogeneous objects having high permittivity value. We explicity derive the symbol and the essential spectrum of the two-dimensional singular integral operator, its left regularizer, and obtain a manifestly Fredholm operator of the form `identity plus compact'. This regularized system shows an improved performance in terms of convergence, and an even better performance is achieved by further applying deflation on a finite set of largest-magnitude eigenvalues.

Zouros, Grigorios P.; Budko, Neil V.

2011-09-01

381

Remote preconditioning lessens the deterioration of pulmonary function after repeated coronary artery occlusion and reperfusion in sheep  

Microsoft Academic Search

Purpose  We investigated whether remote organ preconditioning (RPC) can preserve pulmonary function following repeated myocardial ischemia\\/reperfusion\\u000a in a model mimicking multi-vessel off-pump coronary artery bypass (OPCAB) revascularization.\\u000a \\u000a \\u000a \\u000a Methods  Nine sheep (Group-RPC) underwent RPC by three episodes of five-minute occlusion and five-minute reperfusion of the iliac artery.\\u000a Five sheep (Group-C) were time-matched controls. Afterwards, ten-minute occlusion and reperfusion of the left anterior descending,

Zhengyuan Xia; Paul Herijgers; Takahiro Nishida; Shigeyuki Ozaki; Patrick Wouters; Willem Flameng

2003-01-01

382

Did a classic preconditioning study provide a clue to the identity of the mitochondrial permeability transition pore?  

PubMed Central

Summary A classic paper by Murry, Richard, Reimer and Jennings published in 1990 in Circulation Research showed that preconditioning showed the rate of ATP breakdown during a subsequent sustained period of ischemia. The mechanism responsible for reduced ATP breakdown is still unknown, but perhaps it is related to inhibition of the F1-F0 ATPase. This is an attractive hypothesis given a number of recent studies suggesting that the F1-F0 ATPase can form the mitochondrial permeability transition pore. PMID:24030020

Murphy, Elizabeth; Steenbergen, Charles

2014-01-01

383

Repetitive hypoxic preconditioning induces an immunosuppressed B cell phenotype during endogenous protection from stroke  

PubMed Central

Background Repetitive hypoxic preconditioning (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?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

2014-01-01

384

Triiodothyronine Prevents Cardiac Ischemia/Reperfusion Mitochondrial Impairment and Cell Loss by Regulating miR30a/p53 Axis.  

PubMed

Mitochondrial dysfunctions critically affect cardiomyocyte survival during ischemia/reperfusion (I/R) injury. In this scenario p53 activates multiple signaling pathways that impair cardiac mitochondria and promote cell death. p53 is a validated target of miR-30 whose levels fall under ischemic conditions. Although triiodothyronine (T3) rescues post-ischemic mitochondrial activity and cell viability, no data are available on its role in the modulation of p53 signaling in I/R. Here we test the hypothesis that early T3 supplementation in rats inhibits the post I/R activation of p53 pro-death cascade through the maintenance of miRNA 30a expression. In our model, T3 infusion improves the recovery of post-ischemic cardiac performance. At the molecular level, the beneficial effect of T3 is associated with restored levels of miR-30a expression in the area at risk (AAR) that correspond to p53 mRNA downregulation. The concomitant decrease in p53 protein content reduces Bax expression and limits mitochondrial membrane depolarization resulting in preserved mitochondrial function and decreased apoptosis and necrosis extent in the AAR. Also in primary cardiomyocyte culture of neonatal rats, T3 prevents both miR-30a downregulation and p53 raise induced by hypoxia. The regulatory effect of T3 is greatly suppressed by miR-30a knockdown. Overall these data suggest a new mechanism of T3-mediated cardioprotection that is targeted to mitochondria and acts, at least in part, through the regulation of miR-30a/p53 axis. PMID:25137026

Forini, Francesca; Kusmic, Claudia; Nicolini, Giuseppina; Mariani, Laura; Zucchi, Riccardo; Matteucci, Marco; Iervasi, Giorgio; Pitto, Letizia

2014-11-01

385

REACTIVE TRANSPORT MODELING USING A PARALLEL FULLY-COUPLED SIMULATOR BASED ON PRECONDITIONED JACOBIAN-FREE NEWTON-KRYLOV  

SciTech Connect

Systems of multicomponent reactive transport in porous media that are large, highly nonlinear, and tightly coupled due to complex nonlinear reactions and strong solution-media interactions are often described by a system of coupled nonlinear partial differential algebraic equations (PDAEs). A preconditioned Jacobian-Free Newton-Krylov (JFNK) solution approach is applied to solve the PDAEs in a fully coupled, fully implicit manner. The advantage of the JFNK method is that it avoids explicitly computing and storing the Jacobian matrix during Newton nonlinear iterations for computational efficiency considerations. This solution approach is also enhanced by physics-based blocking preconditioning and multigrid algorithm for efficient inversion of preconditioners. Based on the solution approach, we have developed a reactive transport simulator named RAT. Numerical results are presented to demonstrate the efficiency and massive scalability of the simulator for reactive transport problems involving strong solution-mineral interactions and fast kinetics. It has been applied to study the highly nonlinearly coupled reactive transport system of a promising in situ environmental remediation that involves urea hydrolysis and calcium carbonate precipitation.

Luanjing Guo; Chuan Lu; Hai Huang; Derek R. Gaston

2012-06-01

386

Heme oxygenase-1 mediates the anti-inflammatory effect of isoflurane preconditioning in LPS-stimulated macrophages  

PubMed Central

Aim: The aim of this study was to investigate the anti-inflammatory action of isoflurane preconditioning in a model of lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 macrophages and examine the role of heme oxygenase (HO)-1 in this process. Methods: Murine 264.7 macrophages were pretreated with or without 1%–3% isoflurane for 1 h. Thirty minutes later, the cells were incubated with or without LPS for 24 h. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and cell injury was assessed by measuring the release of lactate dehydrogenase (LDH). HO-1 and inducible nitric oxide synthase (iNOS) protein expression was analyzed by Western blotting. Tumor necrosis factor (TNF)-? levels, nitrite production and HO activity were also determined. Results: Pretreatment with the nontoxic and clinically approved anesthetic isoflurane potently attenuated the cell injury and the decrease in cell viability that was induced by LPS. Treatment or pretreatment with 2% isoflurane induced HO-1 protein expression and caused an induction of HO activity. This result correlated with a decrease in iNOS expression, a decrease in the production of nitric oxide (NO) and impaired release of TNF-? in LPS-stimulated macrophages. Blockade of HO activity with tin protoporphyrin (SnPP) reversed these effects. Conclusion: Isoflurane preconditioning exerts its anti-inflammatory activity through the HO-1 pathway in an in vitro inflammation model. PMID:19122672

Li, Qi-fang; Zhu, Ye-sen; Jiang, Hong; Xu, Hui; Sun, Yu

2009-01-01

387

Release of a humoral circulating cardioprotective factor by remote ischemic preconditioning is dependent on preserved neural pathways in diabetic patients.  

PubMed

Efficacy of ischemic preconditioning is decreased in animal models of type 2 diabetes mellitus while the responses in humans with diabetes are contradictory. It is unknown whether attenuation is related to decreased release of a mediating humoral cardioprotective factor or reduced ability to respond in the target tissue. The aim of the present study was to investigate the release and effect of a circulating cardioprotective factor in type 2 diabetes mellitus patients. Blood samples were drawn from nine non-diabetic subjects, eight diabetic patients without peripheral neuropathy, and eight diabetic patients with peripheral neuropathy before (control) and after a remote ischemic preconditioning (rIPC) stimulus. Blood samples were dialyzed against Krebs-Henseleit buffer and the cardioprotective effects of the dialysates were tested in rabbit hearts mounted on a Langendorff model and subjected to 30-min global ischemia and 120-min reperfusion. rIPC dialysate from non-diabetic and diabetic subjects without peripheral neuropathy reduced infarct size and improved hemodynamic recovery compared to control dialysate from non-diabetic and diabetic subjects. However, in the subgroup of diabetic patients with neuropathy the cardioprotective effect was attenuated. These findings indicate that the release mechanism involves neural pathways. PMID:22821347

Jensen, Rebekka Vibjerg; Støttrup, Nicolaj Brejnholt; Kristiansen, Steen Buus; Bøtker, Hans Erik

2012-09-01

388

Transcriptional signature of human adipose tissue-derived stem cells (hASCs) preconditioned for chondrogenesis in hypoxic conditions.  

PubMed

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 preconditioning 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 preconditioning. While the microarray analysis revealed a distinctive inter-donor variability, the exposure to 1% hypoxia superseded the biological variability and produced a specific expression profile with 2581 significantly regulated genes and substantial functional enrichment in the pathways of cell proliferation and apoptosis. Additionally, exposure to 1% oxygen resulted in upregulation of factors related to angiogenesis and cell growth. In particular, leptin (LEP), the key regulator of body weight and food intake was found to be highly upregulated. In conclusion, the results of this investigation demonstrate the significance of donor demographics and the importance of further studies into the use of regulated oxygen tension as a tool for preparation of ASCs in order to exploit their full potential. PMID:19331821

Pilgaard, L; Lund, P; Duroux, M; Lockstone, H; Taylor, J; Emmersen, J; Fink, T; Ragoussis, J; Zachar, V

2009-07-01

389

Acceleration of TDP43 and FUS/TLS protein expressions in the preconditioned hippocampus following repeated transient ischemia.  

PubMed

The 43-kDa transactivation response DNA binding protein (TDP43), fused in sarcoma/translocated in liposarcoma (FUS/TLS), heat shock protein 70 (HSP70), and ?-amyloid (A?) are induced and involved in cerebral ischemia, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD), but their relationships in ischemic tolerance have never been examined, although they could be involved in endogenous neuroprotection under ischemic preconditioning. In the present study, Mongolian gerbils were subjected to one or three incidents of basically nonlethal 2-min transient common carotid arteries occlusion (tCCAO). Hippocampal CA1 neurons were lost only in the 2-min three times group at 3 and 7 days, which then gradually recovered from 1 to 6 months. Inductions of TDP43 and FUS/TLS were accelerated from 3 months to 7 days or from 7 days to 1 day, respectively, after 2-min three times ischemia compared with once. The cytoplasmic stainings of TDP43 and FUS/TLS showed a further acceleration of the peaks from 1 months to 3 days or from 1 months to 7 days, respectively, after 2-min three times ischemia compared with once. In contrast, HSP70 was induced only at 7 days after 2-min tCCAO for three times, with no expression for A?. These data show that ischemic preconditioning offers a way to induce endogenous neuroprotection and neurogenesis in gerbils, with TDP43, FUS/TLS, and HSP70 involved in this function. PMID:24265138

Sun, Miao; Yamashita, Toru; Shang, Jingwei; Liu, Ning; Deguchi, Kentaro; Liu, Wentao; Ikeda, Yoshio; Feng, Juan; Abe, Koji

2014-01-01

390

Biodegradation of 3,4 dichloroaniline by fungal isolated from the preconditioning phase of winery wastes subjected to vermicomposting.  

PubMed

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 preconditioning 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 preconditioning period of the vermicomposting process and its possible application for in situ bioremediation strategies. PMID:24440653

Castillo, Jean Manuel; Nogales, Rogelio; Romero, Esperanza

2014-02-28

391

Giving rheumatology patients online home access to their electronic medical record (EMR): advantages, drawbacks and preconditions according to care providers.  

PubMed

Technology enables patients home access to their electronic medical record (EMR), via a patient portal. This study aims to analyse (dis)advantages, preconditions and suitable content for this service, according to rheumatology health professionals. A two-phase policy Delphi study was conducted. First, interviews were performed with nurses/nurse practitioners (n = 9) and rheumatologists (n = 13). Subsequently, collected responses were quantified, using a questionnaire among the interviewees. The following advantages of patient home access to the EMR were reported: (1) enhancement of patient participation in treatment, (2) increased knowledge and self-management, (3) improved patient-provider interaction, (4) increased patient safety, and (5) better communication with others. Foreseen disadvantages of the service included: (1) problems with interpretation of data, (2) extra workload, (3) a change in consultation content, and (4) disturbing the patient-provider interaction. Also, the following preconditions emerged from the data: (1) optimal security, (2) no extra record, but a patient-accessible section, (3) no access to clinical notes, and (4) a lag time on the release of lab data. Most respondents reported that data on diagnosis, medication, treatment plan and consultations could be released to patients. On releasing more complex data, such as bodily examinations, lab results and radiological images the opinions differed considerably. Providing patients home access to their medical record might be a valuable next step into patient empowerment and in service towards the patient, provided that security is optimal and content and presentation of data are carefully considered. PMID:22453527

van der Vaart, Rosalie; Drossaert, Constance H C; Taal, Erik; van de Laar, Mart A F J

2013-09-01

392

The Chronic Protective Effects of Limb Remote Preconditioning and the Underlying Mechanisms Involved in Inflammatory Factors in Rat Stroke  

PubMed Central

We recently demonstrated that limb remote preconditioning (LRP) protects against focal ischemia measured 2 days post-stroke. Here, we studied whether LRP provides long-term protection and improves neurological function. We also investigated whether LRP transmits its protective signaling via the afferent nerve pathways from the preconditioned limb to the ischemic brain and whether inflammatory factors are involved in LRP, including the novel galectin-9/Tim-3 inflammatory cell signaling pathway, which induces cell death in lymphocytes. LRP in the left hind femoral artery was performed immediately before stroke. LRP reduced brain injury size both at 2 days and 60 days post-stroke and improved behavioral outcomes for up to 2 months. The sensory nerve inhibitors capsaicin and hexamethonium, a ganglion blocker, abolished the protective effects of LRP. In addition, LRP inhibited edema formation and blood-brain barrier (BBB) permeability measured 2 days post-stroke. Western blot and immunostaining analysis showed that LRP inhibited protein expression of both galectin-9 and T-cell immunoglobulin domain and mucin domain 3 (Tim-3), which were increased after stroke. In addition, LRP decreased iNOS and nitrotyrosine protein expression after stroke. In conclusion, LRP executes long-term protective effects against stroke and may block brain injury by inhibiting activities of the galectin-9/Tim-3 pathway, iNOS, and nitrotyrosine. PMID:22347410

Chen, Xiaoyuan; Zhao, Heng

2012-01-01

393

Influence of genotype, growth regulators, sucrose level and preconditioning of donor plants on flax (Linum usitatissimum L.) anther culture.  

PubMed

The effect of genotype, growth regulators and preconditioning of donor plants on callus induction in anther culture of flax was investigated. Anthers were cultured on modified MS medium supplemented with five different combinations of plant growth regulators. The results suggested that specific combinations of growth regulators must be designed for each genotype. Major differences between the present results and previous reports are discussed. The influence of sucrose concentration was also investigated. For flax cultivar, 'Mikael', callus induction was higher in medium supplemented with 1 mg l(-1) BAP and 2 mg l(-1) 2,4D containing 6% sucrose, while this combination of growth regulators significantly increased callogenesis in cultivars 'Lirina', 'Barbara' and 'Szaphir' when supplemented with 9% or 12% sucrose. The preconditioning of donor plants influenced callogenesis in subsequently isolated anthers. Anthers from donor plants grown at a lower temperature (18/14 degrees C) significantly increased callus induction over those from plants grown at a higher temperature (22/18 degrees C), although each genotype still required optimization of growth regulator combinations in the induction medium. Only 'Mikael' regenerated shoots when the callus was from induction medium supplemented with 2 mg I(-1) BAP and 1 mg l(-1) NAA. PMID:16196207

Burbulis, Natalija; Blinstrubiene, Ausra; Sliesaravicius, A; Venskutoniene, Egidija

2005-01-01

394

Preventing pressure ulcers  

MedlinePLUS

Decubitus ulcer prevention; Bedsore prevention; Pressure sores prevention ... care protocol: Skin safety protocol: Risk assessment and prevention of pressure ulcers . Institute for Clinical Systems Improvement. 2nd ed. 2007 ...

395

Extracellular SOD-Derived H2O2 Promotes VEGF Signaling in Caveolae/Lipid Rafts and Post-Ischemic Angiogenesis in Mice  

PubMed Central

Reactive oxygen species (ROS), in particular, H2O2, is essential for full activation of VEGF receptor2 (VEGFR2) signaling involved in endothelial cell (EC) proliferation and migration. Extracellular superoxide dismutase (ecSOD) is a major secreted extracellular enzyme that catalyzes the dismutation of superoxide to H2O2, and anchors to EC surface through heparin-binding domain (HBD). Mice lacking ecSOD show impaired postnatal angiogenesis. However, it is unknown whether ecSOD-derived H2O2 regulates VEGF signaling. Here we show that gene transfer of ecSOD, but not ecSOD lacking HBD (ecSOD-?HBD), increases H2O2 levels in adductor muscle of mice, and promotes angiogenesis after hindlimb ischemia. Mice lacking ecSOD show reduction of H2O2 in non-ischemic and ischemic limbs. In vitro, overexpression of ecSOD, but not ecSOD-?HBD, in cultured medium in ECs enhances VEGF-induced tyrosine phosphorylation of VEGFR2 (VEGFR2-pY), which is prevented by short-term pretreatment with catalase that scavenges extracellular H2O2. Either exogenous H2O2 (<500 µM), which is diffusible, or nitric oxide donor has no effect on VEGF-induced VEGFR2-pY. These suggest that ecSOD binding to ECs via HBD is required for localized generation of extracellular H2O2 to regulate VEGFR2-pY. Mechanistically, VEGF-induced VEGFR2-pY in caveolae/lipid rafts, but non-lipid rafts, is enhanced by ecSOD, which localizes at lipid rafts via HBD. One of the targets of ROS is protein tyrosine phosphatases (PTPs). ecSOD induces oxidation and inactivation of both PTP1B and DEP1, which negatively regulates VEGFR2-pY, in caveolae/lipid rafts, but not non-lipid rafts. Disruption of caveolae/lipid rafts, or PTPs inhibitor orthovanadate, or siRNAs for PTP1B and DEP1 enhances VEGF-induced VEGFR2-pY, which prevents ecSOD-induced effect. Functionally, ecSOD promotes VEGF-stimulated EC migration and proliferation. In summary, extracellular H2O2 generated by ecSOD localized at caveolae/lipid rafts via HBD promotes VEGFR2 signaling via oxidative inactivation of PTPs in these microdomains. Thus, ecSOD is a potential therapeutic target for angiogenesis-dependent cardiovascular diseases. PMID:20422004

Oshikawa, Jin; Urao, Norifumi; Kim, Ha Won; Kaplan, Nihal; Razvi, Masooma; McKinney, Ronald; Poole, Leslie B.; Fukai, Tohru; Ushio-Fukai, Masuko

2010-01-01

396

Pentostatin-augmented interstitial adenosine prevents postcardioplegia injury in damaged hearts.  

PubMed

This study tests the hypothesis that the adenosine deaminase inhibitor pentostatin (2-deoxycoformycin), when given before ischemia or during infusions of blood cardioplegia, augments interstitial adenosine levels and prevents postcardioplegia dysfunction in hearts with antecedent ischemia. Twenty-one anesthetized dogs were placed on cardiopulmonary bypass, and the hearts were made globally ischemic for 30 minutes. Dogs received blood cardioplegia with no pentostatin (BCP group, n = 6), pretreatment pentostatin (0.2 mg/kg) infused 5 minutes before global ischemia (PS-PTx group, n = 7), or pentostatin included only in the blood cardioplegia without pretreatment (PS-BCP group, n = 8). Microdialysate myocardial adenosine levels (an index of interstitial fluid levels) increased only modestly in the BCP group (from 0.55 +/- 0.13 microM to 2.64 +/- 0.50 microM) and the PS-BCP group (from 0.55 +/- 0.18 microM to 1.08 +/- 0.48 microM) during normothermic ischemia, but interstitial adenosine levels were not augmented further during cardioplegic arrest in either group. In contrast, the adenosine level in the PS-PTx group was significantly (p < 0.05) augmented during global ischemia (from 0.50 +/- 0.13 microM to 63.16 +/- 28.08 microM) and cardioplegia infusion (to 15.26 microM +/- 5.61 microM). Relative to baseline, postischemic left ventricular performance (end-systolic pressure-volume relation) was depressed in both the BCP (from 5.5 +/- 1.2 mm Hg/mL to 3.8 +/- 0.4 mm Hg/mL) and PS-BCP groups (from 7.1 +/- 0.9 mm Hg/mL to 3.8 +/- 0.7 mm Hg/mL). In contrast, PS-PTx restored postischemic performance (from 6.2 +/- 0.5 mm Hg/mL to 7.5 +/- 0.9 mm Hg/mL).(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7944694

Hudspeth, D A; Williams, M W; Zhao, Z Q; Sato, H; Nakanishi, K; McGee, D S; Hammon, J W; Vinten-Johansen, J; Van Wylen, D G

1994-09-01

397

Slit2 Prevents Neutrophil Recruitment and Renal Ischemia-Reperfusion Injury  

PubMed Central

Neutrophils recruited to the postischemic kidney contribute to the pathogenesis of ischemia-reperfusion injury (IRI), which is the most common cause of renal failure among hospitalized patients. The Slit family of secreted proteins inhibits chemotaxis of leukocytes by preventing activation of Rho-family GTPases, suggesting that members of this family might modulate the recruitment of neutrophils and the resulting IRI. Here, in static and microfluidic shear assays, Slit2 inhibited multiple steps required for the infiltration of neutrophils into tissue. Specifically, Slit2 blocked the capture and firm adhesion of human neutrophils to inflamed vascular endothelial barriers as well as their subsequent transmigration. To examine whether these observations were relevant to renal IRI, we administered Slit2 to mice before bilateral clamping of the renal pedicles. Assessed at 18 hours after reperfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration, and rise in plasma creatinine. In vitro, Slit2 did not impair the protective functions of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils from killing the extracellular pathogen Staphylococcus aureus. In vivo, administration of Slit2 did not attenuate neutrophil recruitment or bacterial clearance in mice with ascending Escherichia coli urinary tract infections and did not increase the bacterial load in the livers of mice infected with the intracellular pathogen Listeria monocytogenes. Collectively, these results suggest that Slit2 may hold promise as a strategy to combat renal IRI without compromising the protective innate immune response. PMID:23766538

Chaturvedi, Swasti; Yuen, Darren A.; Bajwa, Amandeep; Huang, Yi-Wei; Sokollik, Christiane; Huang, Liping; Lam, Grace Y.; Tole, Soumitra; Liu, Guang-Ying; Pan, Jerry; Chan, Lauren; Sokolskyy, Yaro; Puthia, Manoj; Godaly, Gabriela; John, Rohan; Wang, Changsen; Lee, Warren L.; Brumell, John H.; Okusa, Mark D.

2013-01-01

398

Slit2 prevents neutrophil recruitment and renal ischemia-reperfusion injury.  

PubMed

Neutrophils recruited to the postischemic kidney contribute to the pathogenesis of ischemia-reperfusion injury (IRI), which is the most common cause of renal failure among hospitalized patients. The Slit family of secreted proteins inhibits chemotaxis of leukocytes by preventing activation of Rho-family GTPases, suggesting that members of this family might modulate the recruitment of neutrophils and the resulting IRI. Here, in static and microfluidic shear assays, Slit2 inhibited multiple steps required for the infiltration of neutrophils into tissue. Specifically, Slit2 blocked the capture and firm adhesion of human neutrophils to inflamed vascular endothelial barriers as well as their subsequent transmigration. To examine whether these observations were relevant to renal IRI, we administered Slit2 to mice before bilateral clamping of the renal pedicles. Assessed at 18 hours after reperfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration, and rise in plasma creatinine. In vitro, Slit2 did not impair the protective functions of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils from killing the extracellular pathogen Staphylococcus aureus. In vivo, administration of Slit2 did not attenuate neutrophil recruitment or bacterial clearance in mice with ascending Escherichia coli urinary tract infections and did not increase the bacterial load in the livers of mice infected with the intracellular pathogen Listeria monocytogenes. Collectively, these results suggest that Slit2 may hold promise as a strategy to combat renal IRI without compromising the protective innate immune response. PMID:23766538

Chaturvedi, Swasti; Yuen, Darren A; Bajwa, Amandeep; Huang, Yi-Wei; Sokollik, Christiane; Huang, Liping; Lam, Grace Y; Tole, Soumitra; Liu, Guang-Ying; Pan, Jerry; Chan, Lauren; Sokolskyy, Yaro; Puthia, Manoj; Godaly, Gabriela; John, Rohan; Wang, Changsen; Lee, Warren L; Brumell, John H; Okusa, Mark D; Robinson, Lisa A

2013-07-01

399

Preventive Health Services for Women  

MedlinePLUS

... Search Preventive care benefits Preventive health services for women Preventive health services for adults Preventive health services for women Preventive health services for children All Marketplace health ...

400

The Mitochondria-Targeted Antioxidants and Remote Kidney Preconditioning Ameliorate Brain Damage through Kidney-to-Brain Cross-Talk  

PubMed Central

Background Many ischemia-induced neurological pathologies including stroke are associated with high oxidative stress. Mitochondria-targeted antioxidants could rescue the ischemic organ by providing specific delivery of antioxidant molecules to the mitochondrion, which potentially suffers from oxidative stress more than non-mitochondrial cellular compartments. Besides direct antioxidative activity, these compounds are believed to activate numerous protective pathways. Endogenous anti-ischemic defense may involve the very powerful neuroprotective agent erythropoietin, which is mainly produced by the kidney in a redox-dependent manner, indicating an important role of the kidney in regulation of brain ischemic damage. The goal of this study is to track the relations between the kidney and the brain in terms of the amplification of defense mechanisms during SkQR1 treatment and remote renal preconditioning and provide evidence that the kidney can generate signals inducing a tolerance to oxidative stress-associated brain pathologies. Methodology/Principal Findings We used the cationic plastoquinone derivative, SkQR1, as a mitochondria-targeted antioxidant to alleviate the deleterious consequences of stroke. A single injection of SkQR1 before cerebral ischemia in a dose-dependent manner reduces infarction and improves functional recovery. Concomitantly, an increase in the levels of erythropoietin in urine and phosphorylated glycogen synthase kinase-3? (GSK-3?) in the brain was detected 24 h after SkQR1 injection. However, protective effects of SkQR1 were not observed in rats with bilateral nephrectomy and in those treated with the nephrotoxic antibiotic gentamicin, indicating the protective role of humoral factor(s) which are released from functional kidneys. Renal preconditioning also induced brain protection in rats accompanied by an increased erythropoietin level in urine and kidney tissue and P-GSK-3? in brain. Co-cultivation of SkQR1-treated kidney cells with cortical neurons resulted in enchanced phosphorylation of GSK-3? in neuronal cells. Conclusion The results indicate that renal preconditioning and SkQR1-induced brain protection may be mediated through the release of EPO from the kidney. PMID:23272118

Silachev, Denis N.; Isaev, Nikolay K.; Pevzner, Irina B.; Zorova, Ljubava D.; Stelmashook, Elena V.; Novikova, Svetlana V.; Plotnikov, Egor Y.; Skulachev, Vladimir P.; Zorov, Dmitry B.

2012-01-01

401

iNOS is a mediator of the heat stress-induced preconditioning against myocardial infarction in vivo in the rat  

E-print Network

1 iNOS is a mediator of the heat stress-induced preconditioning against myocardial infarction against myocardial infarction in vivo in the rat 1 Claire Arnaud, 1 Diane Godin-Ribuot, 1 Serge Bottari, 2 artery occlusion followed by a 120-min reperfusion, in vivo. The infarct size (tetrazolium staining

Paris-Sud XI, Université de