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1

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

PubMed Central

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

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

2015-01-01

2

Limb ischemic preconditioning attenuates cerebral ischemic injury in rat model.  

PubMed

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

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

2014-05-01

3

Impact of hypoglycemic agents on myocardial ischemic preconditioning  

PubMed Central

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

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

2014-01-01

4

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

PubMed Central

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

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

2013-01-01

5

Ischemic preconditioning for cell-based therapy and tissue engineering.  

PubMed

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

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

2014-05-01

6

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

Microsoft Academic Search

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

Vasiliki Tsouka; Thomais Markou; Antigone Lazou

2002-01-01

7

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

PubMed

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

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

2005-01-01

8

Role of ischemic preconditioning in hepatic ischemia-reperfusion injury  

PubMed Central

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

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

2014-01-01

9

Ischemic preconditioning enhances integrity of coronary endothelial tight junctions  

SciTech Connect

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

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

2012-08-31

10

Can anaerobic performance be improved by remote ischemic preconditioning?  

PubMed

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

Lalonde, François; Curnier, Daniel Y

2015-01-01

11

Ischemic preconditioning reduces intestinal epithelial apoptosis in rats.  

PubMed

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

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

2003-06-01

12

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

PubMed

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

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

1997-08-01

13

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

Microsoft Academic Search

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

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

2003-01-01

14

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

PubMed Central

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

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

2014-01-01

15

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

PubMed

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

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

2007-06-01

16

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

Microsoft Academic Search

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

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

2000-01-01

17

Ischemic Preconditioning and the b-Adrenergic Signal Transduction Pathway  

Microsoft Academic Search

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

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

18

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

Microsoft Academic Search

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

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

2005-01-01

19

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

PubMed

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

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

2013-10-22

20

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

E-print Network

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

2013-01-01

21

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

22

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

Microsoft Academic Search

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

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

2007-01-01

23

Ischemic preconditioning during the use of the PercuSurge occlusion balloon for carotid angioplasty and stenting.  

PubMed

Ischemic preconditioning (IP) uses transient ischemia to render tissues tolerant to subsequent, prolonged ischemia. This study sought to evaluate factors that contributed to the development of cerebral ischemia during PercuSurge balloon (Medtronic, Santa Rosa, CA) occlusion in patients undergoing carotid angioplasty and stenting (CAS). The PercuSurge occlusion balloon was used in 43 of 165 patients treated with CAS for high-grade stenosis; 20% were symptomatic. Symptoms of cerebral hypoperfusion during temporary occlusion of the internal carotid artery occurred in 10 of 43 patients and included dysarthria, agitation, decreased level of consciousness, and focal hemispheric deficit. The development of neurologic symptoms after initial PercuSurge balloon inflation and occluded internal carotid artery flow was associated with a decrease in the mean Glasgow Coma Scale (GCS) from 15 to 10 (range 9-14); the GCS returned to normal after occlusion balloon deflation. The mean time to spontaneous recovery of full neurologic function was 8 minutes (range 4-15 minutes). The mean subsequent procedure duration was 11.9 minutes (range 6-21 minutes). No recurrence of neurologic symptoms occurred when the occlusion balloon was reinflated. All 10 patients underwent successful CAS without occlusion, dissection, cerebrovascular accident, or death. Ischemic preconditioning can be used to enable CAS with embolic protection in patients who cannot tolerate initial interruption of antegrade cerebral perfusion by PercuSurge occlusion. PMID:18258156

Faries, Peter L; DeRubertis, Brian; Trocciola, Susan; Karwowski, John; Kent, K Craig; Chaer, Rabih A

2008-01-01

24

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

PubMed Central

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

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

2015-01-01

25

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

PubMed

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

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

2012-03-01

26

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

PubMed

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

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

2015-01-01

27

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

PubMed Central

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

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

2012-01-01

28

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

PubMed

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

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

2000-02-01

29

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

Microsoft Academic Search

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

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

2003-01-01

30

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

Microsoft Academic Search

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

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

2000-01-01

31

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

PubMed

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

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

2015-01-01

32

Ischemic tolerance in an in vivo model of glutamate preconditioning.  

PubMed

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

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

2015-04-01

33

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

PubMed

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

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

2014-10-01

34

The COX-2/PGI2 Receptor Axis Plays an Obligatory Role in Mediating the Cardioprotection Conferred by the Late Phase of Ischemic Preconditioning  

PubMed Central

Background Pharmacologic studies with cyclooxygenase-2 (COX-2) inhibitors suggest that the late phase of ischemic preconditioning (PC) is mediated by COX-2. However, nonspecific effects of COX-2 inhibitors cannot be ruled out, and the selectivity of these inhibitors for COX-2 vs. COX-1 is only relative. Furthermore, the specific prostaglandin (PG) receptors responsible for the salubrious actions of COX-2-derived prostanoids remain unclear. Objective To determine the role of COX-2 and prostacyclin receptor (IP) in late PC by gene deletion. Methods COX-2 knockout (KO) mice (COX-2?/?), prostacyclin receptor KO (IP?/?) mice, and respective wildtype (WT, COX-2+/+ and IP+/+) mice underwent sham surgery or PC with six 4-min coronary occlusion (O)/4-min R cycles 24 h before a 30-min O/24 h R. Results There were no significant differences in infarct size (IS) between non-preconditioned (non-PC) COX-2+/+, COX-2?/?, IP+/+, and IP?/? mice, indicating that neither COX-2 nor IP modulates IS in the absence of PC. When COX-2?/? or IP?/? mice were preconditioned, IS was not reduced, indicating that the protection of late PC was completely abrogated by deletion of either the COX-2 or the IP gene. Administration of the IP selective antagonist, RO3244794 to C57BL6/J (B6) mice 30 min prior to the 30-min O had no effect on IS. When B6 mice were preconditioned 24 h prior to the 30-min O, IS was markedly reduced; however, the protection of late PC was completely abrogated by pretreatment of RO3244794. Conclusions This is the first study to demonstrate that targeted disruption of the COX-2 gene completely abrogates the infarct-sparing effect of late PC, and that the IP, downstream of the COX-2/prostanoid pathway, is a key mediator of the late PC. These results provide unequivocal molecular genetic evidence for an essential role of the COX-2/PGI2 receptor axis in the cardioprotection afforded by the late PC. PMID:22844439

Guo, Yiru; Tukaye, Deepali Nivas; Wu, Wen-Jian; Zhu, Xiaoping; Book, Michael; Tan, Wei; Jones, Steven P.; Rokosh, Gregg; Narumiya, Shuh; Li, Qianhong; Bolli, Roberto

2012-01-01

35

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

PubMed Central

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

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

2014-01-01

36

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

PubMed

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

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

2015-04-01

37

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

PubMed

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

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

2014-11-01

38

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

PubMed

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

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

2012-10-01

39

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

PubMed

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

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

2015-01-01

40

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

PubMed

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

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

2003-06-01

41

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

PubMed Central

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

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

2015-01-01

42

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

PubMed

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

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

2000-01-01

43

Effect of repetitive ischemic preconditioning on spinal cord ischemia in a rabbit model.  

PubMed

A completely randomized controlled study based on a rabbit model was designed to study the effect of repetitive ischemic preconditioning (IPC) on a spinal cord ischemic reperfusion injury. Twenty four white adult Japanese rabbits were randomly assigned to one of the 3 groups (n = 8 per group): Group I: sham-operation group, Group II: ischemic reperfusion group, and, Group III: IPC group. Spinal cord ischemia was induced by infra-renal aortic cross-clamp for 45 min in Group II. Before 45 min ischemia, the rabbits in Group III underwent four cycles of IPC (5 min of ischemia followed by 5 min of reperfusion). Post-operative neurological function, electromyography (EMG) of rear limbs, and spinal cord histopathological changes were measured. The concentrations of calcium, magnesium, copper, and zinc in spinal cord were measured in the 7th day. The neurological function and histopathological changes in Group II were significantly different from those in Group I or Group III (P < 0.05 or 0.01). There was a more significant change of EMG in Group II than that in Group III (P < 0.05). The concentrations of calcium and copper in Group II were significantly higher (P < 0.05 or 0.01), but magnesium and zinc were significantly lower (P < 0.05) than those in Group I. Calcium and copper in Group II were significantly higher (P < 0.05), but zinc was significantly lower (P < 0.01) than those in Group III. In conclusion, repetitive IPC can protect rabbit spinal cord from ischemic reperfusion injury in a timely manner, which is associated with corrections of imbalance of calcium, magnesium, copper, and zinc in the ischemic region. PMID:16707140

Yu, Qi Jing; Wang, Yan Ling; Zhou, Qing Shan; Huang, Hai Bo; Tian, Shu Fang; Duan, Dai Ming

2006-09-01

44

Using hormetic strategies to improve ischemic preconditioning and postconditioning against stroke.  

PubMed

Both ischemic preconditioning (IPreC) and ischemic postconditioning (IPostC) trigger endogenous neuroprotective mechanisms in cerebral ischemia. IPreC is defined as a brief ischemia that protects against a subsequent severe ischemia, while IPostC refers to a series of brief cerebral blood vessel occlusions performed at reperfusion following an ischemic event. Hormesis describes a biphasic dose-response relationship in toxicology, where a low dose of toxicant stimulates and a high dose inhibits biological responses. In general, any minor stress will stimulate a biological system to generate an adaptive response; in most cases, if not all, such an adaptive response to a minor stress is beneficial to the biological system. Proponents of hormesis suggest that this effect is independent of any models, either in vivo or in vitro, from animal, plant, fungi, yeast, to bacteria, by any measurement of end points, survival ratio or time, growth, tissue repair, life span, cognition, learning and memory. In this review, we examine whether IPreC and IPostC are actually sub-forms of hormesis and whether quantitative hormetic strategies can be used to study IPreC and IPostC. By integrating the concepts of IPreC and IPostC with hormesis, we aim to broaden the avenues leading to clinical translation of IPreC and IPostC in stroke treatment. PMID:23750305

Zhao, Heng; Joo, Sungpil; Xie, Weiying; Ji, Xunming

2013-01-01

45

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

EPA Science Inventory

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

46

Ischemic Preconditioning and Brain Tolerance Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin1 Receptor Antagonist and Early Gene Expression  

Microsoft Academic Search

Background and Purpose—A short duration of ischemia (ie, ischemic preconditioning (PC)) can provide significant brain protection to subsequent ischemic events (ie, ischemic tolerance (IT)). The present series of studies was conducted to characterize the temporal pattern of a PC paradigm, to systematically evaluate the importance of protein synthesis in PC-induced IT, and to explore candidate gene expression changes associated with

Frank C. Barone; Raymond F. White; Patricia A. Spera; Julie Ellison; R. William Currie; Xinkang Wang; Giora Z. Feuerstein

47

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

PubMed Central

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

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

2001-01-01

48

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

PubMed

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

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

2013-11-01

49

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

PubMed Central

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

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

2014-01-01

50

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

51

Cardiac effect of ischemic preconditioning and heparin following intestinal ischemia and reperfusion in rats.  

PubMed

To study the role of heparin and ischemic preconditioning (IPC) in cardiac injury after intestinal ischemia (I) and reperfusion (R), 54 rats underwent 60 minutes of I, which was produced by occlusion of the superior mesenteric artery, and/or 120 minutes of R. The IPC group had the I procedure stimulation for 5 minutes and R for 10 minutes. The control group was subjected to sham surgery only, and the other groups were injected with saline solution (SS; 0.1 mL) or heparin (100 IU/kg) via the inferior cava vein 5 minutes before I and 5 minutes before R and 55 minutes after the R begins in I-R groups. In all animals, cardiac samples were stained with hematoxylin and eosin for optical microscopy analysis, and other sample was processed for lipid peroxidation determination. In I-R groups, both heparin and IPC showed significant protection compared to the SS group; conversely, in animals subjected only to I, no protection was observed. Moreover, when heparin was associated with IPC, I-R protection was compromised and the ischemic injury increased. Data showed that IPC and heparin attenuated cardiac dysfunction caused by intestinal I and I-R, but when used in association did not show beneficial effects. PMID:25131053

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

2014-01-01

52

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

PubMed

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

Vainer, Boris G; Markel, Arcady L

2015-04-01

53

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 Ertesvåg; Vaudel, Marc; Svendsen, Øyvind Sverre; Garberg, Hilde; Nordrehaug, Jan Erik; Berven, Frode Steingrimsen; Jonassen, Anne Kristine

2014-01-01

54

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

PubMed Central

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

2014-01-01

55

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

PubMed

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

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

2006-01-01

56

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

PubMed

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

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

2015-02-19

57

Late remote ischemic preconditioning provides benefit to patients undergoing elective percutaneous coronary intervention.  

PubMed

To assess whether late remote ischemic preconditioning (L-RIPC) is effective in myocardial protection in patients with ischemic heart disease undergoing elective percutaneous coronary intervention (PCI). L-RIPC is exerted by newly synthesized cardioprotective proteins. The cardioprotective effects of L-RIPC are more durable. 200 consecutive patients undergoing elective PCI were randomized to receive L-RIPC (induced by three 5-minute inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion) or control (an uninflated cuff around the arm) at 18 h before PCI. Creatine phosphokinase (CK), its cardiac isoenzyme (CK-MB), troponin I (TNI), and high-sensitivity C-reactive protein (hs-CRP) levels were measured at 24 h after PCI. Adverse events' rates at 6 months were assessed. Compared with the control group, patients in L-RIPC group were observed with significantly lower incidences in Chest pain score >1 and ECG ST deviation >1 mm (P < 0.05). The median TNI, CK, and CK-MB concentrations at 24 h were lower in the L-RIPC group (0.009 vs. 0.036 ng/mL, 123 vs. 186 IU/L, 15 vs. 27 IU/L; P < 0.05). There was no statistical difference in hs-CRP between two groups. At 6 months, the adverse events' rate was lower in the L-RIPC group (P = 0.036). L-RIPC is effective in myocardial protection in patients undergoing elective PCI and reduces adverse events' rate at 6 months. PMID:25015066

Liu, Zhi; Wang, Yan-Ling; Hua, Qi; Chu, Yan-Yan; Ji, Xun-Ming

2014-09-01

58

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

PubMed Central

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

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

2015-01-01

59

Impact of Ischemic Preconditioning on Outcome in Clinical Liver Surgery: A Systematic Review  

PubMed Central

Background. Ischemia-reperfusion injury is a major cause of post-liver-surgery complications. Ischemic preconditioning (IPC) has been demonstrated to protect against ischemia-reperfusion injury. Clinical studies have examined IPC in liver surgery but with conflicting results. This systematic review aimed to evaluate the effects of IPC on outcome in clinical liver surgery. Methods. An electronic search of OVID Medline and Embase databases was performed to identify studies that reported outcomes in patients undergoing liver surgery subjected to IPC. Basic descriptive statistics were used to summarise data from individual clinical studies. Results. 1093 articles were identified, of which 24 met the inclusion criteria. Seven topics were selected and analysed by subgroup. There were 10 studies in cadaveric liver transplantation, 2 in living-related liver transplantation, and 12 in liver resection. IPC decreases hepatocellular damage in liver surgery as determined by transaminases but does not translate to any significant clinical benefit in orthotopic liver transplant or liver resection. Conclusions. Available clinical evidence does not support routine use of IPC in liver surgery as it does not offer any apparent benefit in perioperative outcome. Further clinical studies will need to be carried out to determine the subset of patients that will benefit from IPC. PMID:25756045

Chu, Michael J. J.; Vather, Ryash; Hickey, Anthony J. R.; Phillips, Anthony R. J.; Bartlett, Adam S. J. R.

2015-01-01

60

Effect of ischemic preconditioning on repeated sprint ability in team sport athletes.  

PubMed

This study investigated whether ischemic preconditioning (IPC) in a trained population affected repeated sprint performance. A secondary aim was to assess responses according to gender. Sixteen (nine females and seven males) well trained team sport athletes took part in a randomised crossover study design. Participants underwent an IPC and placebo treatment involving three periods of 5 min occlusion applied unilaterally (3 × 5 min occlusion to each leg) at either 220 mmHg or 50 mmHg. Each period of occlusion was followed by 5 min reperfusion. Following treatment 5 × 6 s maximal effort sprints were undertaken on a cycle ergometer against 7.5% body mass, each interspersed by 24 s recovery. Measured parameters included peak power, total power, percentage decrement, post-exercise blood lactate and ratings of perceived exertion. Nor within subject main effect for IPC was observed, neither was there an interaction effect with gender. Effect sizes were trivial (ES < 0.2) with the exception of a moderate (ES < 1.2) change in post-exercise blood lactate in the female cohort (1.6 ± 0.4 mmol(-1) lower following IPC). Results suggest no benefit to team sport players in utilising IPC as a means of enhancing repeated sprint performance. A lower blood lactate response in female participants following IPC may suggest improved blood flow through vasodilation. PMID:25517761

Gibson, Neil; Mahony, Ben; Tracey, Claire; Fawkner, Samantha; Murray, Andrew

2015-06-01

61

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

PubMed

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

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

2008-08-29

62

THE LATE PHASE OF ISCHEMIC PRECONDITIONING INDUCES A PROSURVIVAL GENETIC PROGRAM THAT RESULTS IN MARKED ATTENUATION OF APOPTOSIS  

PubMed Central

Although the cardioprotection afforded by the late phase of ischemic preconditioning (PC) in ischemia/reperfusion (I/R) injury has been well studied, it is unknown whether this beneficial effect can be attributed to inhibition of apoptosis. We hypothesized that ischemic PC affords protection by suppressing apoptosis and examined the underlying mechanisms. Myocardial infarction was produced in mice (30-min coronary occlusion). In animals preconditioned 24 h earlier with six 4-min coronary occlusion/4-min reperfusion (O/R) cycles, there was a marked decrease in apoptosis as assessed by three different parameters: hairpin-1 assay, caspase-3 activity, and immunohistochemical analysis of active caspase-3 and cleaved poly (ADP-ribose) polymerase-1 (PARP-1). This protective effect was accompanied by increased expression of multiple antiapoptotic proteins that regulate both the mitochondria-mediated (Bcl-xL and Mcl-1) and the death receptor-mediated (c-FLIPL and c-FLIPS) pathway of apoptosis and by decreased expression of the proapoptotic protein Bad. This is the first demonstration that the late phase of ischemic PC attenuates cardiac apoptosis after ischemia/reperfusion injury and that this salubrious effect is associated with a complex genetic prosurvival program that results in modulation of several key proteins involved in both the mitochondrial and the death receptor pathways of apoptosis. PMID:17490677

Stein, Adam B.; Bolli, Roberto; Guo, Yiru; Wang, Ou-Li; Tan, Wei; Wu, Wen-Jian; Zhu, Xiaoping; Zhu, Yanqing; Xuan, Yu-Ting

2007-01-01

63

Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans.  

PubMed

Repeated bouts of ischemia followed by reperfusion, known as ischemic preconditioning (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance, we examined the hypothesis that IPC improves functional sympatholysis in healthy, young humans. In a randomized study, 15 healthy young men performed a 10-min resting period, dynamic handgrip exercise at 10% maximal voluntary contraction (MVC), and 25% MVC. This protocol was preceded by IPC (IPC; 4 × 5-min 220-mmHg unilateral occlusion) or a sham intervention (CON; 4 × 5-min 20-mmHg unilateral occlusion). Near-infrared spectroscopy was used to assess changes in oxygenated hemoglobin and myoglobin in skeletal muscle (HbO2 + MbO2) in response to sympathetic activation (via cold pressor test (CPT)) at baseline and during handgrip exercise (at 10% and 25%). In resting conditions, HbO2 + MbO2 significantly decreased during CPT (-11.0 ± 1.0%), which was significantly larger during the IPC-trial (-13.8 ± 1.2%, P = 0.006). During handgrip exercise at 10% MVC, changes in HbO2 + MbO2 in response to the CPT were blunted after IPC (-8.8 ± 1.5%) and CON (-8.3 ± 0.4%, P = 0.593). During handgrip exercise at 25% MVC, HbO2 + MbO2 in response to the CPT increased (2.0 ± 0.4%), whereas this response was significantly larger when preceded by IPC (4.2 ± 0.6%, P = 0.027). Collectively, these results indicate that IPC-induced different vascular changes at rest and during moderate exercise in response to sympathetic activation. This suggests that, in healthy volunteers, exposure to IPC may alter tissue oxygenation during sympathetic stimulation at rest and during exercise. PMID:25713329

Horiuchi, Masahiro; Endo, Junko; Thijssen, Dick H J

2015-02-01

64

Remote ischemic preconditioning delays the onset of acute mountain sickness in normobaric hypoxia  

PubMed Central

Acute mountain sickness (AMS) is a neurological disorder occurring when ascending too fast, too high. Remote ischemic preconditioning (RIPC) is a noninvasive intervention protecting remote organs from subsequent hypoxic damage. We hypothesized that RIPC protects against AMS and that this effect is related to reduced oxidative stress. Fourteen subjects were exposed to 18 hours of normoxia (21% oxygen) and 18 h of normobaric hypoxia (12% oxygen, equivalent to 4500 m) on different days in a blinded, randomized order. RIPC consisted of four cycles of lower limb ischemia (5 min) and 5 min of reperfusion, and was performed immediately before the study room was entered. A control group was exposed to hypoxia (12% oxygen, n = 14) without RIPC. AMS was evaluated by the Lake Louise score (LLS) and the AMS-C score of the Environmental Symptom Questionnaire. Plasma concentrations of ascorbate radicals, oxidized sulfhydryl (SH) groups, and electron paramagnetic resonance (EPR) signal intensity were measured as biomarkers of oxidative stress. RIPC reduced AMS scores (LLS: 1.9 ± 0.4 vs. 3.2 ± 0.5; AMS-C score: 0.4 ± 0.1 vs. 0.8 ± 0.2), ascorbate radicals (27 ± 7 vs. 65 ± 18 nmol/L), oxidized SH groups (3.9 ± 1.4 vs. 14.3 ± 4.6 ?mol/L), and EPR signal intensity (0.6 ± 0.2 vs. 1.5 ± 0.4 × 106) after 5 h in hypoxia (all P < 0.05). After 18 hours in hypoxia there was no difference in AMS and oxidative stress between RIPC and control. AMS and plasma markers of oxidative stress did not correlate. This study demonstrates that RIPC transiently reduces symptoms of AMS and that this effect is not associated with reduced plasma levels of reactive oxygen species. PMID:25742960

Berger, Marc M; Köhne, Hannah; Hotz, Lorenz; Hammer, Moritz; Schommer, Kai; Bärtsch, Peter; Mairbäurl, Heimo

2015-01-01

65

Remote ischemic preconditioning delays the onset of acute mountain sickness in normobaric hypoxia.  

PubMed

Acute mountain sickness (AMS) is a neurological disorder occurring when ascending too fast, too high. Remote ischemic preconditioning (RIPC) is a noninvasive intervention protecting remote organs from subsequent hypoxic damage. We hypothesized that RIPC protects against AMS and that this effect is related to reduced oxidative stress. Fourteen subjects were exposed to 18 hours of normoxia (21% oxygen) and 18 h of normobaric hypoxia (12% oxygen, equivalent to 4500 m) on different days in a blinded, randomized order. RIPC consisted of four cycles of lower limb ischemia (5 min) and 5 min of reperfusion, and was performed immediately before the study room was entered. A control group was exposed to hypoxia (12% oxygen, n = 14) without RIPC. AMS was evaluated by the Lake Louise score (LLS) and the AMS-C score of the Environmental Symptom Questionnaire. Plasma concentrations of ascorbate radicals, oxidized sulfhydryl (SH) groups, and electron paramagnetic resonance (EPR) signal intensity were measured as biomarkers of oxidative stress. RIPC reduced AMS scores (LLS: 1.9 ± 0.4 vs. 3.2 ± 0.5; AMS-C score: 0.4 ± 0.1 vs. 0.8 ± 0.2), ascorbate radicals (27 ± 7 vs. 65 ± 18 nmol/L), oxidized SH groups (3.9 ± 1.4 vs. 14.3 ± 4.6 ?mol/L), and EPR signal intensity (0.6 ± 0.2 vs. 1.5 ± 0.4 × 10(6)) after 5 h in hypoxia (all P < 0.05). After 18 hours in hypoxia there was no difference in AMS and oxidative stress between RIPC and control. AMS and plasma markers of oxidative stress did not correlate. This study demonstrates that RIPC transiently reduces symptoms of AMS and that this effect is not associated with reduced plasma levels of reactive oxygen species. PMID:25742960

Berger, Marc M; Köhne, Hannah; Hotz, Lorenz; Hammer, Moritz; Schommer, Kai; Bärtsch, Peter; Mairbäurl, Heimo

2015-03-01

66

Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans  

PubMed Central

Repeated bouts of ischemia followed by reperfusion, known as ischemic preconditioning (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance, we examined the hypothesis that IPC improves functional sympatholysis in healthy, young humans. In a randomized study, 15 healthy young men performed a 10-min resting period, dynamic handgrip exercise at 10% maximal voluntary contraction (MVC), and 25% MVC. This protocol was preceded by IPC (IPC; 4 × 5-min 220-mmHg unilateral occlusion) or a sham intervention (CON; 4 × 5-min 20-mmHg unilateral occlusion). Near-infrared spectroscopy was used to assess changes in oxygenated hemoglobin and myoglobin in skeletal muscle (HbO2 + MbO2) in response to sympathetic activation (via cold pressor test (CPT)) at baseline and during handgrip exercise (at 10% and 25%). In resting conditions, HbO2 + MbO2 significantly decreased during CPT (?11.0 ± 1.0%), which was significantly larger during the IPC-trial (?13.8 ± 1.2%, P = 0.006). During handgrip exercise at 10% MVC, changes in HbO2 + MbO2 in response to the CPT were blunted after IPC (?8.8 ± 1.5%) and CON (?8.3 ± 0.4%, P = 0.593). During handgrip exercise at 25% MVC, HbO2 + MbO2 in response to the CPT increased (2.0 ± 0.4%), whereas this response was significantly larger when preceded by IPC (4.2 ± 0.6%, P = 0.027). Collectively, these results indicate that IPC-induced different vascular changes at rest and during moderate exercise in response to sympathetic activation. This suggests that, in healthy volunteers, exposure to IPC may alter tissue oxygenation during sympathetic stimulation at rest and during exercise. PMID:25713329

Horiuchi, Masahiro; Endo, Junko; Thijssen, Dick H J

2015-01-01

67

Muscle microdialysis to confirm sublethal ischemia in the induction of remote ischemic preconditioning.  

PubMed

Exposure of one tissue to ischemia-reperfusion confers a systemic protective effect, referred to as remote ischemic preconditioning (RIPC). Confirmation that the desired effect of ischemia is occurring in tissues used to induce RIPC requires an objective demonstration before this technique can be used consistently in the clinical practice. Enrolled patients underwent three to four RIPC sessions on non-consecutive days. Sessions consisted of 4 cycles of 5 min of leg cuff inflation to 30 mmHg above the systolic blood pressure followed by reperfusion. Absence of leg pulse was confirmed by Doppler evaluation. To evaluate limb transient ischemia, patients were monitored with muscle microdialysis. Glucose, lactate, lactate/pyruvate ratio, and glycerol levels were measured. Fourteen microdialysis sessions were performed in seven patients undergoing RIPC (42.8 % male; mean age, 51.8; Fisher grade 4 in all seven patients, Hunt and Hess grade 5 in five patients, four in one patient and one in one patient). An average follow-up of 29 days demonstrated no complications associated with the procedure. Muscle microdialysis during RIPC sessions showed a significant increase in lactate/pyruvate ratio (21.2 to 26.8, p?=?0.001) and lactate (3.0 to 3.9 mmol/L, p?=?0.002), indicating muscle ischemia. There was no significant variation in glycerol (234 to 204 ?g/L, p?=?0.43), indicating no permanent cell damage. The RIPC protocol used in this study is safe, well tolerated, and induces transient metabolic changes consistent with sublethal ischemia. Muscle microdialysis can be used safely as a confirmatory tool in the induction of RIPC. PMID:24323782

Bilgin-Freiert, Arzu; Dusick, Joshua R; Stein, Nathan R; Etchepare, Maria; Vespa, Paul; Gonzalez, Nestor R

2012-06-01

68

Nrf2 activation in astrocytes contributes to spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning.  

PubMed

In this study, we investigated whether nuclear factor erythroid 2-related factor 2 (Nrf2) activation in astrocytes contributes to the neuroprotection induced by a single hyperbaric oxygen preconditioning (HBO-PC) against spinal cord ischemia/reperfusion (SCIR) injury. In vivo: At 24?h after a single HBO-PC at 2.5 atmospheres absolute for 90?min, the male ICR mice underwent SCIR injury by aortic cross-clamping surgery and observed for 48?h. HBO-PC significantly improved hindlimb motor function, reduced secondary spinal cord edema, ameliorated the reactivity of spinal motor-evoked potentials, and slowed down the process of apoptosis to exert neuroprotective effects against SCIR injury. At 12?h or 24?h after HBO-PC without aortic cross-clamping surgery, Western blot, enzyme-linked immunosorbent assay, realtime-polymerase chain reaction and double-immunofluorescence staining were used to detect the Nrf2 activity of spinal cord tissue, such as mRNA level, protein content, DNA binding activity, and the expression of downstream gene, such as glutamate-cysteine ligase, ?-glutamyltransferase, multidrug resistance protein 1, which are key proteins for intracellular glutathione synthesis and transit. The Nrf2 activity and downstream genes expression were all enhanced in normal spinal cord with HBO-PC. Glutathione content of spinal cord tissue with HBO-PC significantly increased at all time points after SCIR injury. Moreover, Nrf2 overexpression mainly occurs in astrocytes. In vitro: At 24?h after HBO-PC, the primary spinal astrocyte-neuron co-cultures from ICR mouse pups were subjected to oxygen-glucose deprivation (OGD) for 90?min to simulate the ischemia-reperfusion injury. HBO-PC significantly increased the survival rate of neurons and the glutathione content in culture medium, which was mainly released from asctrocytes. Moreover, the Nrf2 activity and downstream genes expression induced by HBO-PC were mainly enhanced in astrocytes, but not in neurons. In conclusion, our findings demonstrated that spinal cord ischemic tolerance induced by HBO-PC may be mainly related to Nrf2 activation in astrocytes. PMID:24716787

Xu, Jiajun; Huang, Guoyang; Zhang, Kun; Sun, Jinchuan; Xu, Tao; Li, Runping; Tao, Hengyi; Xu, Weigang

2014-08-01

69

New insights into mechanism for the effect of resveratrol preconditioning against cerebral ischemic stroke: Possible role of matrix metalloprotease-9.  

PubMed

Resveratrol, a natural polyphenolic compound, is found in a few edible materials and is well known for its phytoestrogenic and antioxidant properties. A growing body of in vivo and in vitro evidence indicates that resveratrol has protective effect on cerebral ischemic stroke. Here, we review the effect of resveratrol on cerebral ischemic stroke, and propose a possible mechanism. During acute phases after stroke, resveratrol preconditioning suppresses matrix metalloprotease-9 activity to ameliorate blood-brain barrier disruption, edema formation and neuronal cell death caused by ischemia and reperfusion. But during delayed phases after stroke, resveratrol preconditioning conduces to cerebral angiogenesis and brain regeneration through increasing matrix metalloprotease-9 activity and expression. Resveratrol's effect on matrix metalloprotease-9 is distinguishing in different phases because of temporal and spatial redistribution of matrix metalloprotease-9 within the cells of the neurovascular unit after cerebral ischemia. This paper also hypothesizes that resveratrol treatment after cerebral ischemia might be beneficial for cerebral angiogenesis and brain regeneration during delayed phases after stroke. PMID:17601679

Dong, Wenpeng; Gao, Dakuan; Lin, Hong; Zhang, Xiang; Li, Nanlin; Li, Fanfan

2008-01-01

70

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

71

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

PubMed

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

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

2014-12-01

72

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

PubMed

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

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

2015-02-01

73

HSP70.1 AND -70.3 ARE REQUIRED FOR LATE-PHASE PROTECTION INDUCED BY ISCHEMIC PRECONDITIONING OF MOUSE HEARTS  

EPA Science Inventory

Heat-Shock Proteins 70.1 and 70.3 Are Required for Late-phase Protection Induced by Ischemic Preconditioning of the Mouse Heart Craig R. Hampton 1 , Akira Shimamoto 1 , Christine L. Rothnie 1 , Jeaneatte Griscavage-Ennis 1 , Albert Chong 1 , David J. Dix 2 , Edward D. Ve...

74

In vitro hypoxic preconditioning of embryonic stem cells as a strategy of promoting cell survival and functional benefits after transplantation into the ischemic rat brain  

Microsoft Academic Search

Hypoxic preconditioning (HP) and stem cell transplantation have been extensively studied as individual therapies for ischemic stroke. The present investigation is an initial effort to combine these methods to achieve increased therapeutic effects after brain ischemia. Sublethal in vitro hypoxia pretreatment significantly enhanced the tolerance of neurally-differentiating embryonic stem (ES) cells and primary bone marrow mesenchymal stem cells (BMSC) to

Michelle Hedrick Theus; Ling Wei; Lin Cui; Kevin Francis; Xinyang Hu; Christine Keogh; Shan Ping Yu

2008-01-01

75

AMPK-Regulated and Akt-Dependent Enhancement of Glucose Uptake Is Essential in Ischemic Preconditioning-Alleviated Reperfusion Injury  

PubMed Central

Aims Ischemic preconditioning (IPC) is a potent form of endogenous protection. However, IPC-induced cardioprotective effect is significantly blunted in insulin resistance-related diseases and the underlying mechanism is unclear. This study aimed to determine the role of glucose metabolism in IPC-reduced reperfusion injury. Methods Normal or streptozotocin (STZ)-treated diabetic rats subjected to 2 cycles of 5 min ischemia/5 min reperfusion prior to myocardial ischemia (30 min)/reperfusion (3 h). Myocardial glucose uptake was determined by 18F-fluorodeoxyglucose-positron emission tomography (PET) scan and gamma-counter biodistribution assay. Results IPC exerted significant cardioprotection and markedly improved myocardial glucose uptake 1 h after reperfusion (P<0.01) as evidenced by PET images and gamma-counter biodistribution assay in ischemia/reperfused rats. Meanwhile, myocardial translocation of glucose transporter 4 (GLUT4) to plasma membrane together with myocardial Akt and AMPK phosphorylation were significantly enhanced in preconditioned hearts. Intramyocardial injection of GLUT4 siRNA markedly decreased GLUT4 expression and blocked the cardioprotection of IPC as evidence by increased myocardial infarct size. Moreover, the PI3K inhibitor wortmannin significantly inhibited activation of Akt and AMPK, reduced GLUT4 translocation, glucose uptake and ultimately, depressed IPC-induced cardioprotection. Furthermore, IPC-afforded antiapoptotic effect was markedly blunted in STZ-treated diabetic rats. Exogenous insulin supplementation significantly improved glucose uptake via co-activation of myocardial AMPK and Akt and alleviated ischemia/reperfusion injury as evidenced by reduced myocardial apoptosis and infarction size in STZ-treated rats (P<0.05). Conclusions The present study firstly examined the role of myocardial glucose metabolism during reperfusion in IPC using direct genetic modulation in vivo. Augmented glucose uptake via co-activation of myocardial AMPK and Akt in reperfused myocardium is essential to IPC-alleviated reperfusion injury. This intrinsic metabolic modulation and cardioprotective capacity are present in STZ-treated hearts and can be triggered by insulin. PMID:23922853

Liu, Wenchong; Huang, Qichao; Yang, Weidong; Fu, Feng; Ma, Heng; Su, Hui; Wang, Haichang; Wang, Jing; Zhang, Haifeng; Gao, Feng

2013-01-01

76

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

PubMed

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

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

2015-02-01

77

Ischemic but not mechanical preconditioning attenuates ischemia\\/reperfusion induced myocardial apoptosis in anaesthetized rabbits: The role of Bcl2 family proteins and ERK1\\/2  

Microsoft Academic Search

Objective: Recent studies suggest that ischemic preconditioning (IPC) inhibits myocardial apoptosis after ischemia and reperfusion.\\u000a This study aimed first, to examine whether short mechanical stretch with acute pressure overload (MPC), which has been shown\\u000a to reduce infarct size after ischemia\\/reperfusion, mimics IPC in attenuating myocardial apoptosis and second, to evaluate\\u000a whether induced cardioprotection involves modulation of the expression of the

Antigone Lazou; E. K. Iliodromitis; D. Cieslak; K. Voskarides; S. Mousikos; E. Bofilis; D. T. Kremastinos

2006-01-01

78

Postoperative Neurocognitive Dysfunction in Patients Undergoing Cardiac Surgery after Remote Ischemic Preconditioning: A Double-Blind Randomized Controlled Pilot Study  

PubMed Central

Background Remote ischemic preconditioning (RIPC) has been shown to enhance the tolerance of remote organs to cope with a subsequent ischemic event. We hypothesized that RIPC reduces postoperative neurocognitive dysfunction (POCD) in patients undergoing complex cardiac surgery. Methods We conducted a prospective, randomized, double-blind, controlled trial including 180 adult patients undergoing elective cardiac surgery with cardiopulmonary bypass. Patients were randomized either to RIPC or to control group. Primary endpoint was postoperative neurocognitive dysfunction 5–7 days after surgery assessed by a comprehensive test battery. Cognitive change was assumed if the preoperative to postoperative difference in 2 or more tasks assessing different cognitive domains exceeded more than one SD (1 SD criterion) or if the combined Z score was 1.96 or greater (Z score criterion). Results According to 1 SD criterion, 52% of control and 46% of RIPC patients had cognitive deterioration 5–7 days after surgery (p?=?0.753). The summarized Z score showed a trend to more cognitive decline in the control group (2.16±5.30) compared to the RIPC group (1.14±4.02; p?=?0.228). Three months after surgery, incidence and severity of neurocognitive dysfunction did not differ between control and RIPC. RIPC tended to decrease postoperative troponin T release at both 12 hours [0.60 (0.19–1.94) µg/L vs. 0.48 (0.07–1.84) µg/L] and 24 hours after surgery [0.36 (0.14–1.89) µg/L vs. 0.26 (0.07–0.90) µg/L]. Conclusions We failed to demonstrate efficacy of a RIPC protocol with respect to incidence and severity of POCD and secondary outcome variables in patients undergoing a wide range of cardiac surgery. Therefore, definitive large-scale multicenter trials are needed. Trial Registration ClinicalTrials.gov NCT00877305 PMID:23741380

Meybohm, Patrick; Renner, Jochen; Broch, Ole; Caliebe, Dorothee; Albrecht, Martin; Cremer, Jochen; Haake, Nils; Scholz, Jens; Zacharowski, Kai; Bein, Berthold

2013-01-01

79

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

PubMed

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

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

2014-08-23

80

Effects of ischemic preconditioning on VEGF and pFlk-1 immunoreactivities in the gerbil ischemic hippocampus after transient cerebral ischemia.  

PubMed

Ischemia preconditioning (IPC) displays an important adaptation of the CNS to sub-lethal ischemia. In the present study, we examined the effect of IPC on immunoreactivities of VEGF-, and phospho-Flk-1 (pFlk-1) following transient cerebral ischemia in gerbils. The animals were randomly assigned to four groups (sham-operated-group, ischemia-operated-group, IPC plus (+) sham-operated-group, and IPC+ischemia-operated-group). IPC was induced by subjecting gerbils to 2 min of ischemia followed by 1 day of recovery. In the ischemia-operated-group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) alone 5 days after ischemia-reperfusion, however, in all the IPC+ischemia-operated-groups, pyramidal neurons in the SP were well protected. In immunohistochemical study, VEGF immunoreactivity in the ischemia-operated-group was increased in the SP at 1 day post-ischemia and decreased with time. Five days after ischemia-reperfusion, strong VEGF immunoreactivity was found in non-pyramidal cells, which were identified as pericytes, in the stratum oriens (SO) and radiatum (SR). In the IPC+sham-operated- and IPC+ischemia-operated-groups, VEGF immunoreactivity was significantly increased in the SP. pFlk-1 immunoreactivity in the sham-operated- and ischemia-operated-groups was hardly found in the SP, and, from 2 days post-ischemia, pFlk-1 immunoreactivity was strongly increased in non-pyramidal cells, which were identified as pericytes. In the IPC+sham-operated-group, pFlk-1 immunoreactivity was significantly increased in both pyramidal and non-pyramidal cells; in the IPC+ischemia-operated-groups, the similar pattern of VEGF immunoreactivity was found in the ischemic CA1, although the VEGF immunoreactivity was strong in non-pyramidal cells at 5 days post-ischemia. In brief, our findings show that IPC dramatically augmented the induction of VEGF and pFlk-1 immunoreactivity in the pyramidal cells of the CA1 after ischemia-reperfusion, and these findings suggest that the increases of VEGF and Flk-1 expressions may be necessary for neurons to survive from transient ischemic damage. PMID:25300771

Park, Yoo Seok; Cho, Jun Hwi; Kim, In Hye; Cho, Geum-Sil; Cho, Jeong-Hwi; Park, Joon Ha; Ahn, Ji Hyeon; Chen, Bai Hui; Shin, Bich-Na; Shin, Myoung Cheol; Tae, Hyun-Jin; Cho, Young Shin; Lee, Yun Lyul; Kim, Young-Myeong; Won, Moo-Ho; Lee, Jae-Chul

2014-12-15

81

SirT1 mediates hyperbaric oxygen preconditioning-induced ischemic tolerance in rat brain.  

PubMed

Our previous studies have shown that hyperbaric oxygen preconditioning (HBO-PC) induces tolerance to cerebral ischemia/reperfusion (I/R). This study aimed to investigate whether SirT1, a class III histone deacetylase, is involved in neuroprotection elicited by HBO-PC in animal and cell culture models of ischemia. Rats were subjected to middle cerebral artery occlusion for 120?minutes after HBO-PC (once a day for 5 days). Primary cultured cortical neurons were exposed to 2?hours of HBO-PC after 2?hours of oxygen-glucose deprivation (OGD). We showed that HBO-PC increased SirT1 protein and mRNA expression, promoted neurobehavioral score, reduced infarct volume, and improved morphology at 24?hours and 7 days after cerebral I/R. Neuroprotection of HBO-PC was attenuated by SirT1 inhibitor EX527 and SirT1 knockdown by short interfering RNA (siRNA), whereas it was mimicked by SirT1 activator resveratrol. Furthermore, HBO-PC enhanced SirT1 expression and cell viability and reduced lactate dehydrogenase release 24?hours after OGD/re-oxygenation. The neuroprotective effect of HBO-PC was emulated through upregulating SirT1 and, reversely, attenuated through downregulating SirT1. The modulation of SirT1 was made by adenovirus infection carrying SirT1 or SirT1 siRNA. Besides, SirT1 increased B-cell lymphoma 2 (Bcl-2) expression and decrease cleaved caspase 3. These results indicate that SirT1 mediates HBO-PC-induced tolerance to cerebral I/R through inhibition of apoptosis. PMID:23299244

Yan, Wenjun; Fang, Zongping; Yang, Qianzi; Dong, Hailong; Lu, Yan; Lei, Chong; Xiong, Lize

2013-03-01

82

Transcriptome Analysis of Renal Ischemia/Reperfusion Injury and Its Modulation by Ischemic Pre-Conditioning or Hemin Treatment  

PubMed Central

Ischemia/reperfusion injury (IRI) is a leading cause of acute renal failure. The definition of the molecular mechanisms involved in renal IRI and counter protection promoted by ischemic pre-conditioning (IPC) or Hemin treatment is an important milestone that needs to be accomplished in this research area. We examined, through an oligonucleotide microarray protocol, the renal differential transcriptome profiles of mice submitted to IRI, IPC and Hemin treatment. After identifying the profiles of differentially expressed genes observed for each comparison, we carried out functional enrichment analysis to reveal transcripts putatively involved in potential relevant biological processes and signaling pathways. The most relevant processes found in these comparisons were stress, apoptosis, cell differentiation, angiogenesis, focal adhesion, ECM-receptor interaction, ion transport, angiogenesis, mitosis and cell cycle, inflammatory response, olfactory transduction and regulation of actin cytoskeleton. In addition, the most important overrepresented pathways were MAPK, ErbB, JAK/STAT, Toll and Nod like receptors, Angiotensin II, Arachidonic acid metabolism, Wnt and coagulation cascade. Also, new insights were gained about the underlying protection mechanisms against renal IRI promoted by IPC and Hemin treatment. Venn diagram analysis allowed us to uncover common and exclusively differentially expressed genes between these two protective maneuvers, underscoring potential common and exclusive biological functions regulated in each case. In summary, IPC exclusively regulated the expression of genes belonging to stress, protein modification and apoptosis, highlighting the role of IPC in controlling exacerbated stress response. Treatment with the Hmox1 inducer Hemin, in turn, exclusively regulated the expression of genes associated with cell differentiation, metabolic pathways, cell cycle, mitosis, development, regulation of actin cytoskeleton and arachidonic acid metabolism, suggesting a pleiotropic effect for Hemin. These findings improve the biological understanding of how the kidney behaves after IRI. They also illustrate some possible underlying molecular mechanisms involved in kidney protection observed with IPC or Hemin treatment maneuvers. PMID:23166714

Amano, Mariane Tami; Gonçalves, Giselle Martins; Hyane, Meire Ioshie; Cenedeze, Marcos Antonio; Renesto, Paulo Guilherme; Pacheco-Silva, Alvaro; Moreira-Filho, Carlos Alberto; Câmara, Niels Olsen Saraiva

2012-01-01

83

Characterization of acute ischemia?related physiological responses associated with remote ischemic preconditioning: a randomized controlled, crossover human study  

PubMed Central

Abstract Remote Ischemic Preconditioning (RIPC) is emerging as a new noninvasive intervention that has the potential to protect a number of organs against ischemia–reperfusion (IR) injury. The standard protocols normally used to deliver RIPC involve a number of cycles of inflation of a blood pressure (BP) cuff on the arm and/or leg to an inflation pressure of 200 mmHg followed by cuff deflation for a short period of time. There is little evidence to support what limb (upper or lower) or cuff inflation pressures are most effective to deliver this intervention without causing undue discomfort/pain in nonanesthetized humans. In this preliminary study, a dose–response assessment was performed using a range of cuff inflation pressures (140, 160, and 180 mmHg) to induce limb ischemia in upper and lower limbs. Physiological changes in the occluded limb and any pain/discomfort associated with RIPC with each cuff inflation pressure were determined. Results showed that ischemia can be induced in the upper limb at much lower cuff inflation pressures compared with the standard 200 mmHg pressure generally used for RIPC, provided the cuff inflation pressure is ~30 mmHg higher than the resting systolic BP. In the lower limb, a higher inflation pressure, (~55 mmHg > resting systolic BP), is required to induce ischemia. Cyclical changes in capillary blood O2, CO2, and lactate levels during the RIPC stimulus were observed. RIPC at higher cuff inflation pressures of 160 and 180 mmHg was better tolerated in the upper limb. In summary, limb ischemia for RIPC can be more easily induced at lower pressures and is much better tolerated in the upper limb in young healthy individuals. However, whether benefits of RIPC can also be derived with protocols delivered to the upper limb using lower cuff inflation pressures and with lesser discomfort compared to the lower limb, remains to be investigated. PMID:25413320

Sharma, Vikram; Cunniffe, Brian; Verma, Amit P.; Cardinale, Marco; Yellon, Derek

2014-01-01

84

Effect of Remote Ischemic Preconditioning on Phosphorylated Protein Signaling in Children Undergoing Tetralogy of Fallot Repair: A Randomized Controlled Trial  

PubMed Central

Background Our previous randomized controlled trial demonstrated cardiorespiratory protection by remote ischemic preconditioning (RIPC) in children before cardiac surgery. However, the impact of RIPC on myocardial prosurvival intracellular signaling remains unknown in cyanosis. RIPC may augment phosphorylated protein signaling in myocardium and circulating leukocytes during tetralogy of Fallot (ToF) repair. Methods and Results Children (n=40) undergoing ToF repair were double?blind randomized to RIPC (n=11 boys, 9 girls) or control (sham RIPC: n=9 boys, 11 girls). Blood samples were taken before, immediately after, and 24 hours after cardiopulmonary bypass. Resected right ventricular outflow tract muscle and leukocytes were processed for protein expression and mitochondrial respiration. There was no difference in age (7.1±3.4 versus 7.1±3.4 months), weight (7.7±1.8 versus 7.5±1.9 kg), or bypass or aortic cross?clamp times between the groups (control versus RIPC, mean±SD). No differences were seen between the groups for an increase in the ratio of phosphorylated to total protein for protein kinase B, p38 mitogen activated protein kinase, signal transducer and activator of transcription 3, glycogen synthase kinase 3?, heat shock protein 27, Connexin43, or markers associated with promotion of necrosis (serum cardiac troponin I), apoptosis (Bax, Bcl?2), and autophagy (Parkin, Beclin?1, LC3B). A high proportion of total proteins were in phosphorylated form in control and RIPC myocardium. In leukocytes, mitochondrial respiration and assessed protein levels did not differ between groups. Conclusions In patients with cyanotic heart disease, a high proportion of proteins are in phosphorylated form. RIPC does not further enhance phosphorylated protein signaling in myocardium or circulating leukocytes in children undergoing ToF repair. Clinical Trial Registration URL: (http://www.anzctr.org.au/trial_view.aspx?id=335613. Unique identifier: Australian New Zealand Clinical Trials Registry number ACTRN12610000496011. PMID:23666460

Pepe, Salvatore; Liaw, Norman Y.; Hepponstall, Michele; Sheeran, Freya L.; Yong, Matthew S.; d'Udekem, Yves; Cheung, Michael M.; Konstantinov, Igor E.

2013-01-01

85

Remote Ischemic Preconditioning in Children Undergoing Cardiac Surgery With Cardiopulmonary Bypass: A Single?Center Double?Blinded Randomized Trial  

PubMed Central

Background Remote ischemic preconditioning (RIPC) harnesses an innate defensive mechanism that protects against inflammatory activation and ischemia?reperfusion injury, known sequelae of cardiac surgery with cardiopulmonary bypass. We sought to determine the impact of RIPC on clinical outcomes and physiological markers related to ischemia?reperfusion injury and inflammatory activation after cardiac surgery in children. Methods and Results Overall, 299 children (aged neonate to 17 years) were randomized to receive an RIPC stimulus (inflation of a blood pressure cuff on the left thigh to 15 mm Hg above systolic for four 5?minute intervals) versus a blinded sham stimulus during induction with a standardized anesthesia protocol. Primary outcome was duration of postoperative hospital stay, with serial clinical and laboratory measurements for the first 48 postoperative hours and clinical follow?up to discharge. There were no significant baseline differences between RIPC (n=148) and sham (n=151). There were no in?hospital deaths. No significant difference in length of postoperative hospital stay was noted (sham 5.4 versus RIPC 5.6 days; difference +0.2; adjusted P=0.91), with the 95% confidence interval (?0.7 to +0.9) excluding a prespecified minimal clinically significant differences of 1 or 1.5 days. There were few significant differences in other clinical outcomes or values at time points or trends in physiological markers. Benefit was not observed in specific subgroups when explored through interactions with categories of age, sex, surgery type, Aristotle score, or first versus second half of recruitment. Adverse events were similar (sham 5%, RIPC 6%; P=0.68). Conclusions RIPC is not associated with important improvements in clinical outcomes and physiological markers after cardiac surgery in children. Clinical Trial Registration URL: clinicaltrials.gov. Unique identifier: NCT00650507. PMID:25074698

McCrindle, Brian W.; Clarizia, Nadia A.; Khaikin, Svetlana; Holtby, Helen M.; Manlhiot, Cedric; Schwartz, Steven M.; Caldarone, Christopher A.; Coles, John G.; Van Arsdell, Glen S.; Scherer, Stephen W.; Redington, Andrew N.

2014-01-01

86

Remote Ischemic Preconditioning (RIPC) Modifies the Plasma Proteome in Children Undergoing Repair of Tetralogy of Fallot: A Randomized Controlled Trial  

PubMed Central

Background Remote ischemic preconditioning (RIPC) has been applied in paediatric cardiac surgery. We have demonstrated that RIPC induces a proteomic response in plasma of healthy volunteers. We tested the hypothesis that RIPC modifies the proteomic response in children undergoing Tetralogy of Fallot (TOF) repair. Methods and Results Children (n=40) were randomized to RIPC and control groups. Blood was sampled at baseline, after cardiopulmonary bypass (CPB) and 6, 12 and 24h post-CPB. Plasma was analysed by liquid chromatography mass spectrometry (LC-MS) in an untargeted approach. Peptides demonstrating differential expression (p<0.01) were subjected to tandem LC-MS/MS and protein identification. Corresponding proteins were identified using the NCBI protein database. There was no difference in age (7.3±3.5vs6.8±3.6 months)(p=0.89), weight (7.7±1.8vs7.5±1.9 kg)(p=0.71), CPB time (104±7vs94±7 min)(p=0.98) or aortic cross-clamp time (83±22vs75±20 min)(p=0.36). No peptides were differentially expressed at baseline or immediately after CPB. There were 48 peptides with higher expression in the RIPC group 6h post-CPB. This was no longer evident at 12 or 24h, with one peptide down-regulated in the RIPC group. The proteins identified were: inter-alpha globulin inhibitor (42.0±11.8 vs 820.8±181.1, p=0.006), fibrinogen preproprotein (59.3±11.2 vs 1192.6±278.3, p=0.007), complement-C3 precursor (391.2±160.9 vs 5385.1±689.4, p=0.0005), complement C4B (151.5±17.8 vs 4587.8±799.2, p=0.003), apolipoprotein B100 (53.4±8.3 vs 1364.5±278.2, p=0.005) and urinary proteinase inhibitor (358.6±74.9 vs 5758.1±1343.1, p=0.009). These proteins are involved in metabolism, haemostasis, immunity and inflammation. Conclusions We provided the first comprehensive analysis of RIPC-induced proteomic changes in children undergoing surgery. The proteomic changes peak 6h post-CPB and return to baseline within 24h of surgery. Trial Registration ACTR.org.au ACTRN12610000496011 PMID:25826479

Hepponstall, Michele; Ignjatovic, Vera; Binos, Steve; Attard, Chantal; Karlaftis, Vasiliki; d’Udekem, Yves; Monagle, Paul; Konstantinov, Igor E.

2015-01-01

87

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

PubMed

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

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

2015-04-01

88

Plasma from human volunteers subjected to remote ischemic preconditioning protects human endothelial cells from hypoxia-induced cell damage.  

PubMed

Short repeated cycles of peripheral ischemia/reperfusion (I/R) can protect distant organs from subsequent prolonged I/R injury; a phenomenon known as remote ischemic preconditioning (RIPC). A RIPC-mediated release of humoral factors might play a key role in this protection and vascular endothelial cells are potential targets for these secreted factors. In the present study, RIPC-plasma obtained from healthy male volunteers was tested for its ability to protect human umbilical endothelial cells (HUVEC) from hypoxia-induced cell damage. 10 healthy male volunteers were subjected to a RIPC-protocol consisting of 4 × 5 min inflation/deflation of a blood pressure cuff located at the upper arm. Plasma was collected before (T0; control), directly after (T1) and 1 h after (T2) the RIPC procedure. HUVEC were subjected to 24 h hypoxia damage and simultaneously incubated with 5% of the respective RIPC-plasma. Cell damage was evaluated by lactate dehydrogenase (LDH)-measurements. Western blot experiments of hypoxia inducible factor 1 alpha (HIF1alpha), phosphorylated signal transducer and activator of transcription 5 (STAT5), protein kinase B (AKT) and extracellular signal-related kinase 1/2 (ERK-1/2) were performed. Furthermore, the concentrations of hVEGF were evaluated in the RIPC-plasma by sandwich ELISA. Hypoxia-induced cell damage was significantly reduced by plasma T1 (p = 0.02 vs T0). The protective effect of plasma T1 was accompanied by an augmentation of the intracellular HIF1alpha (p = 0.01 vs T0) and increased phosphorylation of ERK-1/2 (p = 0.03 vs T0). Phosphorylation of AKT and STAT5 remained unchanged. Analysis of the protective RIPC-plasma T1 showed significantly reduced levels of hVEGF (p = 0.01 vs T0). RIPC plasma protects endothelial cells from hypoxia-induced cell damage and humoral mediators as well as intracellular HIF1alpha may be involved. PMID:25716080

Weber, Nina C; Riedemann, Isabelle; Smit, Kirsten F; Zitta, Karina; van de Vondervoort, Djai; Zuurbier, Coert J; Hollmann, Markus W; Preckel, Benedikt; Albrecht, Martin

2015-03-01

89

Hypoxic Preconditioning with Cobalt of Bone Marrow Mesenchymal Stem Cells Improves Cell Migration and Enhances Therapy for Treatment of Ischemic Acute Kidney Injury  

PubMed Central

Mesenchymal stem cell (MSC) administration is known to enhance the recovery of the kidney following injury. Here we tested the potential of hypoxic-preconditioned-MSC transplantation to enhance the efficacy of cell therapy on acute kidney injury (AKI) by improving MSC migration to the injured kidney. Cobalt was used as hypoxia mimetic preconditioning (HMP). MSC were subjected to HMP through 24 h culture in 200 µmol/L cobalt. Compared to normoxia cultured MSC (NP-MSC), HMP significantly increased the expression of HIF-1? and CXCR4 in MSC and enhanced the migration of MSC in vitro. This effect was lost when MSC were treated with siRNA targeting HIF-1? or CXCR4 antagonist. SPIO labeled MSC were administered to rats with I/R injury followed immediately by magnetic resonance imaging. Imaging clearly showed that HMP-MSC exhibited greater migration and a longer retention time in the ischemic kidney than NP-MSC. Histological evaluation showed more HMP-MSC in the glomerular capillaries of ischemic kidneys than in the kidneys receiving NP-MSC. Occasional tubules showed iron labeling in the HMP group, while no tubules had iron labeling in NP group, indicating the possibility of tubular transdifferentiation after HMP. These results were also confirmed by fluorescence microscopy study using CM-DiI labeling. The increased recruitment of HMP-MSC was associated with reduced kidney injury and enhanced functional recovery. This effect was also related to the increased paracrine action by HMP-MSC. Thus we suggest that by enhancing MSC migration and prolonging kidney retention, hypoxic preconditioning of MSC may be a useful approach for developing AKI cell therapy. PMID:23671625

Liu, Hong; Rao, Shengxiang; Cai, Jieru; Liu, Shaopeng; Kriegel, Alison J.; Greene, Andrew S.; Liang, Minyu; Ding, Xiaoqiang

2013-01-01

90

Signaling pathways leading to ischemic mitochondrial neuroprotection.  

PubMed

There is extensive evidence that ischemic/reperfusion mediated mitochondrial dysfunction is a major contributor to ischemic damage. However data also indicates that mild ischemic stress induces mitochondrial dependent activation of ischemic preconditioning. Ischemic preconditioning is a neuroprotective mechanism which is activated upon a brief sub-injurious ischemic exposure and is sufficient to provide protection against a subsequent lethal ischemic insult. Current research demonstrates that mitochondria are not only the inducers of but are also an important target of ischemic preconditioning mediated protection. Numerous proteins and signaling pathways are activated by ischemic preconditioning which protect the mitochondria against ischemic damage. In this review we examine some of the proteins activated by ischemic precondition which counteracts the deleterious effects of ischemia/reperfusion thereby maintaining normal mitochondrial activity and lead to ischemic tolerance. PMID:25262285

Thompson, John W; Narayanan, Srinivasan V; Koronowski, Kevin B; Morris-Blanco, Kahlilia; Dave, Kunjan R; Perez-Pinzon, Miguel A

2015-04-01

91

Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium?loading or sarcKATP channel activation  

PubMed Central

Abstract Ischemic preconditioning (IPC) inhibits Ca2+?loading during ischemia which contributes to cardioprotection by inhibiting mechanical injury due to hypercontracture and biochemical injury through mitochondrial permeability transition (MPT) pores during reperfusion. However, whether remote?IPC reduced Ca2+?loading during ischemia and its subsequent involvement in inhibiting MPT pore formation during reperfusion has not been directly shown. We have developed a cellular model of remote IPC to look at the impact of remote conditioning on Ca2+?regulation and MPT pore opening during simulated ischemia and reperfusion, using fluorescence microscopy. Ventricular cardiomyocytes were isolated from control rat hearts, hearts preconditioned with three cycles of ischemia/reperfusion or naïve myocytes remotely conditioned with effluent collected from preconditioned hearts. Both conventional?IPC and remote?IPC reduced the loss of Ca2+?homeostasis and contractile function following reenergization of metabolically inhibited cells and protected myocytes against ischemia/reperfusion injury. However, only conventional?IPC reduced the Ca2+?loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na+?loading, reflecting a decrease in Na/H exchanger activity. Remote?IPC delayed opening of the MPT pores in response to ROS, which was dependent on PKC? and NOS?signaling. These data show that remote?IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca2+?loading in remote IPC. We suggest that inhibition of the MPT pore and not Ca2+?loading is the common link in cardioprotection between conventional and remote IPC. PMID:25428953

Turrell, Helen E.; Thaitirarot, Chokanan; Crumbie, Hayley; Rodrigo, Glenn

2014-01-01

92

Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.  

PubMed

Ischemic preconditioning (IPC) inhibits Ca(2+)-loading during ischemia which contributes to cardioprotection by inhibiting mechanical injury due to hypercontracture and biochemical injury through mitochondrial permeability transition (MPT) pores during reperfusion. However, whether remote-IPC reduced Ca(2+)-loading during ischemia and its subsequent involvement in inhibiting MPT pore formation during reperfusion has not been directly shown. We have developed a cellular model of remote IPC to look at the impact of remote conditioning on Ca(2+)-regulation and MPT pore opening during simulated ischemia and reperfusion, using fluorescence microscopy. Ventricular cardiomyocytes were isolated from control rat hearts, hearts preconditioned with three cycles of ischemia/reperfusion or naïve myocytes remotely conditioned with effluent collected from preconditioned hearts. Both conventional-IPC and remote-IPC reduced the loss of Ca(2+)-homeostasis and contractile function following reenergization of metabolically inhibited cells and protected myocytes against ischemia/reperfusion injury. However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity. Remote-IPC delayed opening of the MPT pores in response to ROS, which was dependent on PKC? and NOS-signaling. These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC. We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC. PMID:25428953

Turrell, Helen E; Thaitirarot, Chokanan; Crumbie, Hayley; Rodrigo, Glenn

2014-11-01

93

Repetitive Ischemic Preconditioning Attenuates Inflammatory Reaction and Brain Damage After Focal Cerebral Ischemia in Rats: Involvement of PI3K/Akt and ERK1/2 Signaling Pathway.  

PubMed

Ischemic preconditioning (IPC) has been demonstrated to provide a neuroprotection against brain damage produced by focal cerebral ischemia. However, it is elusive whether ischemic preconditioning attenuates ischemic brain damage through modulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. In the present study, we first explored the best scheme of repetitive ischemic preconditioning (RIPC) to protect rat brain against ischemic damage and then further investigated the underlying mechanisms in RIPC's neuroprotection. Adult male Sprague-Dawley rats underwent ischemic preconditioning or (and) middle cerebral artery occlusion (MCAO). LY294002 or (and) PD98059 were injected intracerebroventricularly to selectively inhibit the activation of PI3K/Akt or ERK1/2. Neurological deficit scores, cerebral infarct volume, and morphological characteristic were detected at corresponding time after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was measured 24 h after cerebral ischemia. Expressions of p-Akt, t-Akt, p-ERK1/2, t-ERK1/2, nuclear factor-kappa B (NF-?B) p65, and cyclooxygenase-2 (COX-2) in ischemic brain were determined by Western blot. The release of tumor necrosis factor-? (TNF-?) in blood was examined by ELISA. In the various schemes of RIPC, IPC2?×?5 min causes less neuronal damage in the cortex and subcortex of ischemic brain and provides an obvious alleviation of cerebral infarction and neurological deficit after lethal ischemia. IPC2?×?5 min significantly reduces cerebral infarct volume, neurological deficit scores, and MPO activity; all of which were diminished by LY294002 or (and) PD98059. IPC2?×?5 min significantly upregulates the expressions of p-Akt and p-ERK1/2, which were inhibited by LY294002 or (and) PD98059. IPC2?×?5 min significantly downregulates the expressions of NF-?B p65 and COX-2 and attenuates the release of TNF-?; all of which were abolished by LY294002 or (and) PD98059. IPC2?×?5 min is the best scheme of RIPC to protect rat brain against cerebral ischemia. IPC2?×?5 min attenuates brain damage in rats subjected to lethal ischemia, and this neuroprotection is associated with inhibition of neuroinflammation through modulating PI3K/Akt and ERK1/2 signaling pathway. PMID:25338292

Tu, Xian-Kun; Yang, Wei-Zhong; Chen, Jian-Ping; Chen, Yan; Chen, Quan; Chen, Ping-Ping; Shi, Song-Sheng

2015-04-01

94

Phosphorylation of p38 MAPK mediates hypoxic preconditioning-induced neuroprotection against cerebral ischemic injury via mitochondria translocation of Bcl-xL in mice.  

PubMed

Hypoxic preconditioning (HPC) initiates intracellular signaling pathway to provide protection, but the role of p38 mitogen-activated protein kinase (p38 MAPK) in HPC-induced neuroprotection against cerebral ischemic injuries is a matter of debate. In this study, we found that HPC could reduce 6h middle cerebral artery occlusion (MCAO)-induced infarct volume, edema ratio and cell apoptosis, as well as enhancing the up-regulated p38 MAPK phosphorylation (P-p38 MAPK) levels in the peri-infarct region of mice after 6h MCAO. However, intracerebroventricular injection of p38 MAPK inhibitor SB203580 abolished this HPC-induced neuroprotection. HPC significantly increased the translocation of anti-apoptotic Bcl-2-related protein Bcl-xL from the cytosol to the mitochondria in the peri-infarct region of MCAO mice. Interestingly, the results of reciprocal immunoprecipitation showed that Bcl-xL and P-p38 MAPK were coimmunoprecipitated reciprocally only in the peri-infarct region of HPC and MCAO treated mice, while Bcl-xL and total p38 (T-p38 MAPK), not P-p38 MAPK, could be coimmunoprecipited by each other in the brain of normal control mice. In addition, we found SB203580 significantly decreased P-p38 MAPK levels, and inhibited HPC-induced mitochondria translocation of Bcl-xL in the brain of HPC and MCAO treated mice. Taken together, our findings suggested that P-p38 MAPK mediates HPC-induced neuroprotection against cerebral ischemic injury via mitochondria translocation of Bcl-xL, which might be a key anti-cell apoptotic mechanism of HPC. PMID:23399686

Zhao, Li; Liu, Xu; Liang, Jing; Han, Song; Wang, Yue; Yin, Yanling; Luo, Yanlin; Li, Junfa

2013-03-29

95

Effect of remote ischemic preconditioning in the elderly patients with coronary artery disease with diabetes mellitus undergoing elective drug-eluting stent implantation.  

PubMed

There is conflicting evidence regarding the effectiveness of remote ischemic preconditioning (RIPC) in patients undergoing elective percutaneous coronary intervention (PCI). Therefore, we prospectively enrolled elderly patients with coronary heart disease (CHD) with diabetes mellitus (DM) undergoing elective drug-eluting stent (DES) implantation. They were randomized to receive RIPC within 2 hours before PCI (n = 102) or not (controls, n = 98). Baseline clinical characteristics were similar between the 2 groups. Despite a trend toward decline, the median high-sensitivity cardiac troponin I (hscTnI) level (P = .256) and the incidence of myocardial infarction (MI) type 4a (P = .106) in the RIPC group 16 hours after PCI procedure was not significantly different from the control group. The RIPC could attenuate the release of a myocardial biomarker but failed to show a significant effect on hscTnI level or MI type 4a incidence after PCI procedure in elderly patients with CHD having DM undergoing elective DES implantation. PMID:24163121

Xu, Xiaohan; Zhou, Yujie; Luo, Shengjie; Zhang, Weijun; Zhao, Yingxin; Yu, Miao; Ma, Qian; Gao, Fei; Shen, Hua; Zhang, Jianwei

2014-09-01

96

Molecular mechanism of preconditioning.  

PubMed

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

Das, Manika; Das, Dipak K

2008-04-01

97

Intestinal ischemic preconditioning ameliorates hepatic ischemia/reperfusion injury in rats: role of heme oxygenase 1 in the second window of protection.  

PubMed

Preconditioning by brief ischemia protects not only the concerned organ but also other distant organs against subsequent lethal damage; this is called remote ischemic preconditioning (RIPC). This study was designed to investigate the impact of intestinal RIPC on hepatic ischemia/reperfusion injury (IRI) with a special interest in heme oxygenase 1 (HO-1) induction in the second window of protection (SWOP). Male Wistar rats were randomly assigned to 1 of 2 groups: an RIPC group or a sham group. Before hepatic IRI, either intestinal RIPC, consisting of 2 cycles of 4-minute superior mesenteric artery clamping separated by 11 minutes of declamping (RIPC group), or a sham procedure (sham group) was performed. After 48 hours of recovery, the rats were exposed to 30 minutes of total hepatic IRI. Transaminase releases and proinflammatory cytokines were determined at several time points after reperfusion. Histopathological analysis and animal survival were also investigated. Intestinal RIPC significantly lowered transaminase release (alanine aminotransferase at 2 hours: 873.3?±?176.4 IU/L for the RIPC group versus 3378.7?±?871.1 IU/L for the sham group, P?

Kageyama, Shoichi; Hata, Koichiro; Tanaka, Hirokazu; Hirao, Hirofumi; Kubota, Toyonari; Okamura, Yusuke; Iwaisako, Keiko; Takada, Yasutsugu; Uemoto, Shinji

2015-01-01

98

Ischemic preconditioning inhibits expression of Na(+)/H(+) exchanger 1 (NHE1) in the gerbil hippocampal CA1 region after transient forebrain ischemia.  

PubMed

The participation of Na(+)/H(+) exchanger (NHE) in neuronal damage/death in the hippocampal CA1 region (CA1) induced by transient forebrain ischemia has not been well established, although acidosis may be involved in neuronal damage/death. In the present study, we examined the effect of ischemic preconditioning (IPC) on NHE1 immunoreactivity following a 5min of transient forebrain ischemia in gerbils. The animals used in the study were randomly assigned to four groups (sham-operated-group, ischemia-operated-group, IPC plus (+) sham-operated-group and IPC+ischemia-operated-group). IPC was induced by subjecting animals to 2min of ischemia followed by 1day of recovery. A significant neuronal loss was found in the stratum pyramidale (SP) of the CA1, not the CA2/3, of the ischemia-operated-group at 5days post-ischemia. However, in the IPC+ischemia-operated-group, neurons in the SP of the CA1 were well protected. NHE1 immunoreactivity was not detected in any regions of the CA1-3 of the sham- and IPC+sham-operated-groups. However, the immunoreactivity was apparently expressed in the SP of the CA1-3 after ischemia, and the NHE1immunoreactivity was very weak 5days after ischemia; however, at this point in time, strong NHE1immunoreactivity was found in astrocytes in the CA1. In the CA2/3, NHE1immunoreactivity was slightly changed, although NHE1immunoreactivity was expressed in the SP. In the IPC+ischemia-operated-groups, NHE1 immunoreactivity was also expressed in the SP of the CA1-3; however, the immunoreactivity was more slightly changed than that in the ischemia-operated-groups. In brief, our findings show that IPC dramatically protected CA1 pyramidal neurons and strongly inhibited NHE1 expression in the SP of the CA1 after ischemia-reperfusion. These findings suggest that the inhibition of NHE1 expression may be necessary for neuronal survival from transient ischemic damage. PMID:25783008

Lee, Jae-Chul; Cho, Jeong-Hwi; Kim, In Hye; Ahn, Ji Hyeon; Park, Joon Ha; Cho, Geum-Sil; Chen, Bai Hui; Shin, Bich Na; Tae, Hyun-Jin; Park, Seung Min; Ahn, Ji Yun; Kim, Dong Won; Cho, Jun Hwi; Bae, Eun Joo; Yong, Jun-Hwan; Kim, Young-Myeong; Won, Moo-Ho; Lee, Yun Lyul

2015-04-15

99

Remote Ischemic Preconditioning Reduces Perioperative Cardiac and Renal Events in Patients Undergoing Elective Coronary Intervention: A Meta-Analysis of 11 Randomized Trials  

PubMed Central

Background Results from randomized controlled trials (RCT) concerning cardiac and renal effect of remote ischemic preconditioning(RIPC) in patients with stable coronary artery disease(CAD) are inconsistent. The aim of this study was to explore whether RIPC reduce cardiac and renal events after elective percutaneous coronary intervention (PCI). Methods and Results RCTs with data on cardiac or renal effect of RIPC in PCI were searched from Pubmed, EMBase, and Cochrane library (up to July 2014). Meta-regression and subgroup analysis were performed to identify the potential sources of significant heterogeneity(I2?40%). Eleven RCTs enrolling a total of 1713 study subjects with stable CAD were selected. Compared with controls, RIPC significantly reduced perioperative incidence of myocardial infarction (MI) [odds ratio(OR) ?=?0.68; 95% CI, 0.51 to 0.91; P?=?0.01; I2?=?41.0%] and contrast-induced acute kidney injury(AKI) (OR?=?0.61; 95% CI, 0.38 to 0.98; P?=?0.04; I2?=?39.0%). Meta-regression and subgroup analyses confirmed that the major source of heterogeneity for the incidence of MI was male proportion (coefficient ?=??0.049; P?=?0.047; adjusted R2?=?0.988; P?=?0.02 for subgroup difference). Conclusions The present meta-analysis of RCTs suggests that RIPC may offer cardiorenal protection by reducing the incidence of MI and AKI in patients undergoing elective PCI. Moreover, this effect on MI is more pronounced in male subjects. Future high-quality, large-scale clinical trials should focus on the long-term clinical effect of RIPC. PMID:25551671

Pei, Hanjun; Wu, Yongjian; Wei, Yingjie; Yang, Yuejin; Teng, Siyong; Zhang, Haitao

2014-01-01

100

Serum from patients undergoing remote ischemic preconditioning protects cultured human intestinal cells from hypoxia-induced damage: involvement of matrixmetalloproteinase-2 and -9.  

PubMed

Remote ischemic preconditioning (RIPC) can be induced by transient occlusion of blood flow to a limb with a blood pressure cuff and exerts multiorgan protection from ischemia/reperfusion injury. Ischemia/reperfusion injury in the intestinal tract leads to intestinal barrier dysfunction and can result in multiple organ failure. Here we used an intestinal cell line (CaCo-2) to evaluate the effects of RIPC-conditioned patient sera on hypoxia-induced cell damage in vitro and to identify serum factors that mediate RIPC effects. Patient sera (n = 10) derived before RIPC (T0), directly after RIPC (T1) and 1 h after RIPC (T2) were added to the culture medium at the onset of hypoxia until 48 h after hypoxia. Reverse transcription-polymerase chain reaction, lactate dehydrogenase (LDH) assays, caspase-3/7 assays, silver staining, gelatin zymography and Western blotting were performed. Hypoxia led to morphological signs of cell damage and increased the release of LDH in cultures containing sera T0 (P < 0.01) and T1 (P < 0.05), but not sera T2, which reduced the hypoxia-mediated LDH release compared with sera T0 (P < 0.05). Gelatin zymography revealed a significant reduction of activities of the matrixmetalloproteinase (MMP)-2 and MMP-9 in the protective sera T2 compared with the nonprotective sera T0 (MMP-2: P < 0.01; MMP-9: P < 0.05). Addition of human recombinant MMP-2 and MMP-9 to MMP-deficient culture media increased the sensitivity of CaCo-2 cells to hypoxia-induced cell damage (P < 0.05), but did not result in a reduced phosphorylation of prosurvival kinases p42/44 and protein kinase B (Akt) or increased activity of caspase-3/7. Our results suggest MMP-2 and MMP-9 as currently unknown humoral factors that may be involved in RIPC-mediated cytoprotection in the intestine. PMID:22009279

Zitta, Karina; Meybohm, Patrick; Bein, Berthold; Heinrich, Christin; Renner, Jochen; Cremer, Jochen; Steinfath, Markus; Scholz, Jens; Albrecht, Martin

2012-01-01

101

Liver Ischemic Preconditioning (IPC) Improves Intestinal Microbiota Following Liver Transplantation in Rats through 16s rDNA-Based Analysis of Microbial Structure Shift  

PubMed Central

Background Ischemia-reperfusion (I/R) injury is associated with intestinal microbial dysbiosis. The “gut-liver axis” closely links gut function and liver function in health and disease. Ischemic preconditioning (IPC) has been proven to reduce I/R injury in the surgery. This study aims to explore the effect of IPC on intestinal microbiota and to analyze characteristics of microbial structure shift following liver transplantation (LT). Methods The LT animal models of liver and gut IPC were established. Hepatic graft function was assessed by histology and serum ALT/AST. Intestinal barrier function was evaluated by mucosal ultrastructure, serum endotoxin, bacterial translocation, fecal sIgA content and serum TNF-?. Intestinal bacterial populations were determined by quantitative PCR. Microbial composition was characterized by DGGE and specific bacterial species were determined by sequence analysis. Principal Findings Liver IPC improved hepatic graft function expressed as ameliorated graft structure and reduced ALT/AST levels. After administration of liver IPC, intestinal mucosal ultrastructure improved, serum endotoxin and bacterial translocation mildly decreased, fecal sIgA content increased, and serum TNF-? decreased. Moreover, liver IPC promoted microbial restorations mainly through restoring Bifidobacterium spp., Clostridium clusters XI and Clostridium cluster XIVab on bacterial genus level. DGGE profiles indicated that liver IPC increased microbial diversity and species richness, and cluster analysis demonstrated that microbial structures were similar and clustered together between the NC group and Liver-IPC group. Furthermore, the phylogenetic tree of band sequences showed key bacteria corresponding to 10 key band classes of microbial structure shift induced by liver IPC, most of which were assigned to Bacteroidetes phylum. Conclusion Liver IPC cannot only improve hepatic graft function and intestinal barrier function, but also promote restorations of intestinal microbiota following LT, which may further benefit hepatic graft by positive feedback of the “gut-liver axis”. PMID:24098410

Lu, Haifeng; Chen, Xinhua; Jiang, Jianwen; Liu, Hui; He, Yong; Ding, Songming; Hu, Zhenhua; Wang, Weilin; Zheng, Shusen

2013-01-01

102

Liver ischemia preconditions the heart against ischemia-reperfusion arrhythmias  

PubMed Central

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

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

2015-01-01

103

Vector-Free and Transgene-Free Human iPS Cells Differentiate into Functional Neurons and Enhance Functional Recovery after Ischemic Stroke in Mice  

PubMed Central

Stroke is a leading cause of human death and disability in the adult population in the United States and around the world. While stroke treatment is limited, stem cell transplantation has emerged as a promising regenerative therapy to replace or repair damaged tissues and enhance functional recovery after stroke. Recently, the creation of induced pluripotent stem (iPS) cells through reprogramming of somatic cells has revolutionized cell therapy by providing an unlimited source of autologous cells for transplantation. In addition, the creation of vector-free and transgene-free human iPS (hiPS) cells provides a new generation of stem cells with a reduced risk of tumor formation that was associated with the random integration of viral vectors seen with previous techniques. However, the potential use of these cells in the treatment of ischemic stroke has not been explored. In the present investigation, we examined the neuronal differentiation of vector-free and transgene-free hiPS cells and the transplantation of hiPS cell-derived neural progenitor cells (hiPS-NPCs) in an ischemic stroke model in mice. Vector-free hiPS cells were maintained in feeder-free and serum-free conditions and differentiated into functional neurons in vitro using a newly developed differentiation protocol. Twenty eight days after transplantation in stroke mice, hiPS-NPCs showed mature neuronal markers in vivo. No tumor formation was seen up to 12 months after transplantation. Transplantation of hiPS-NPCs restored neurovascular coupling, increased trophic support and promoted behavioral recovery after stroke. These data suggest that using vector-free and transgene-free hiPS cells in stem cell therapy are safe and efficacious in enhancing recovery after focal ischemic stroke in mice. PMID:23717557

Mohamad, Osama; Faulkner, Ben; Chen, Dongdong; Yu, Shan Ping; Wei, Ling

2013-01-01

104

Preconditioning Balloons  

NSDL National Science Digital Library

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

Integrated Teaching and Learning Program,

105

Preconditioning Strategy in Stem Cell Transplantation Therapy  

PubMed Central

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

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

2013-01-01

106

Persimmon leaf flavonoid promotes brain ischemic tolerance  

PubMed Central

Persimmon leaf flavonoid has been shown to enhance brain ischemic tolerance in mice, but its mechanism of action remains unclear. The bilateral common carotid arteries were occluded using a micro clip to block blood flow for 10 minutes. After 10 minutes of ischemic preconditioning, 200, 100, and 50 mg/kg persimmon leaf flavonoid or 20 mg/kg ginaton was intragastrically administered per day for 5 days. At 1 hour after the final administration, ischemia/reperfusion models were estab-lished by blocking the middle cerebral artery for 2 hours. At 24 hours after model establishment, compared with cerebral ischemic rats without ischemic preconditioning or drug intervention, plasma endothelin, thrombomodulin and von Willebrand factor levels significantly decreased and intercel-lular adhesion molecule-1 expression markedly reduced in brain tissue from rats with ischemic pre-conditioning. Simultaneously, brain tissue injury reduced. Ischemic preconditioning combined with drug exposure noticeably improved the effects of the above-mentioned indices, and the effects of 200 mg/kg persimmon leaf flavonoid were similar to 20 mg/kg ginaton treatment. These results indicate that ischemic preconditioning produces tolerance to recurrent severe cerebral ischemia. However, persimmon leaf flavonoid can elevate ischemic tolerance by reducing inflammatory reactions and vascular endothelial injury. High-dose persimmon leaf flavonoid showed an identical effect to ginaton. PMID:25206573

Miao, Mingsan; Zhang, Xuexia; Bai, Ming; Wang, Linan

2013-01-01

107

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

Microsoft Academic Search

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

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

2012-01-01

108

Is longer sevoflurane preconditioning neuroprotective in permanent focal cerebral ischemia?  

PubMed Central

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

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

2013-01-01

109

Studying ischemic preconditioning in isolated cardiomyocyte models  

Microsoft Academic Search

Isolated cardiomyocytes, obtained by enzymatic digestion of whole hearts, have multiple advantages, most related to their accessibility to microscopic visualization, beyond the obvious elimination of other cell types that exist in the heart. Conversely, they cannot reproduce the mechanical disruption of reperfusion hypercontracture or the vascular phenomena of leukocyte plugging and compression from interstitial edema and contracture that can lead

Roberto J. Diaz; Gregory J. Wilson

2006-01-01

110

Myocardial ischemic protection in natural mammalian hibernation.  

PubMed

Hibernating myocardium is an important clinical syndrome protecting the heart with chronic myocardial ischemia, named for its assumed resemblance to hibernating mammals in winter. However, the effects of myocardial ischemic protection have never been studied in true mammalian hibernation, which is a unique strategy for surviving extreme winter environmental stress. The goal of this investigation was to test the hypothesis that ischemic stress may also be protected in woodchucks as they hibernate in winter. Myocardial infarction was induced by coronary occlusion followed by reperfusion in naturally hibernating woodchucks in winter with and without hibernation and in summer, when not hibernating. The ischemic area at risk was similar among groups. Myocardial infarction was significantly less in woodchucks in winter, whether hibernating or not, compared with summer, and was similar to that resulting after ischemic preconditioning. Whereas several genes were up or downregulated in both hibernating woodchuck and with ischemic preconditioning, one mechanism was unique to hibernation, i.e., activation of cAMP-response element binding protein (CREB). When CREB was upregulated in summer, it induced protection similar to that observed in the woodchuck heart in winter. The cardioprotection in hibernation was also mediated by endothelial nitric oxide synthase, rather than inducible nitric oxide synthase. Thus, the hibernating woodchuck heart is a novel model to study cardioprotection for two major reasons: (1) powerful cardioprotection occurs naturally in winter months in the absence of any preconditioning stimuli, and (2) it resembles ischemic preconditioning, but with novel mechanisms, making this model potentially useful for clinical translation. PMID:25613166

Yan, Lin; Kudej, Raymond K; Vatner, Dorothy E; Vatner, Stephen F

2015-03-01

111

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

Microsoft Academic Search

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

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

112

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

PubMed Central

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

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

2010-01-01

113

Preconditioning protects the heart in a prolonged uremic condition.  

PubMed

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

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

2012-11-15

114

Ischemic colitis  

Microsoft Academic Search

Ischemic colitis represents the most common form of gastrointestinal ischemia. The presumed etiologies are numerous; however, it typically develops “spontaneously,” in the absence of major vasculature occlusion, and in the presence of viable intestine elsewhere. It is most usefully classified into gangrenous and nongangrenous forms, the latter of which may be subdivided into transient and chronic types. Ischemic colitis may

Sanjiv K. Gandhi; Morin M. Hanson; Anthony M. Vernava; Donald L. Kaminski; Walter E. Longo

1996-01-01

115

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

PubMed

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

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

2014-03-01

116

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

Microsoft Academic Search

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

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

2008-01-01

117

Ischemic Postconditioning's Benefit on Reperfusion Ventricular Arrhythmias Is Maintained in the Senescent Heart  

Microsoft Academic Search

The purpose of this study is to determine if postconditioning's beneficial effect on ventricular arrhythmias is maintained in elderly hearts. In elderly populations, the cardioprotective effects of ischemic preconditioning are lost. Previously, the authors observed that ischemic postconditioning markedly reduced reperfusion-induced ventricular arrhythmias in adult rats. Whether this benefit is maintained in senescent hearts is unknown. Here, the authors study

Joan Dow; Anil Bhandari; Robert A. Kloner

2008-01-01

118

Immune mechanisms in cerebral ischemic tolerance  

PubMed Central

Stressor-induced tolerance is a central mechanism in the response of bacteria, plants, and animals to potentially harmful environmental challenges. This response is characterized by immediate changes in cellular metabolism and by the delayed transcriptional activation or inhibition of genetic programs that are not generally stressor specific (cross-tolerance). These programs are aimed at countering the deleterious effects of the stressor. While induction of this response (preconditioning) can be established at the cellular level, activation of systemic networks is essential for the protection to occur throughout the organs of the body. This is best signified by the phenomenon of remote ischemic preconditioning, whereby application of ischemic stress to one tissue or organ induces ischemic tolerance (IT) in remote organs through humoral, cellular and neural signaling. The immune system is an essential component in cerebral IT acting simultaneously both as mediator and target. This dichotomy is based on the fact that activation of inflammatory pathways is necessary to establish IT and that IT can be, in part, attributed to a subdued immune activation after index ischemia. Here we describe the components of the immune system required for induction of IT and review the mechanisms by which a reprogrammed immune response contributes to the neuroprotection observed after preconditioning. Learning how local and systemic immune factors participate in endogenous neuroprotection could lead to the development of new stroke therapies. PMID:24624056

Garcia-Bonilla, Lidia; Benakis, Corinne; Moore, Jamie; Iadecola, Costantino; Anrather, Josef

2014-01-01

119

Resveratrol pretreatment protects rat brain from cerebral ischemic damage via a sirtuin 1–uncoupling protein 2 pathway  

Microsoft Academic Search

Resveratrol is a natural polyphenol found in grapes and wine and has been associated with protective effects against cardiovascular diseases. In vitro, both resveratrol preconditioning (RPC) and ischemic preconditioning (IPC) require activation of sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, to induce neuroprotection against cerebral ischemia. In the present study, we tested two hypotheses: (a) that neuroprotection against

D. Della-Morte; K. R. Dave; R. A. DeFazio; Y. C. Bao; A. P. Raval; M. A. Perez-Pinzon

2009-01-01

120

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

SciTech Connect

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

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

2005-09-01

121

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

Microsoft Academic Search

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

Takayuki Okada; Hajime Otani; Yue Wu; Takamichi Uchiyama

2005-01-01

122

Pre-ischemic exercise alleviates oxidative damage following ischemic stroke in rats  

PubMed Central

Physical exercise has been proved to be neuroprotective in clinical trials and animal experiments. However, the exact mechanism underlying this neuroprotective effect remains unclear. The aim of the present study was to explore whether pre-ischemic treadmill training could act as a form of ischemic preconditioning in a rat following ischemic stroke by reducing oxidative damage. Fifty-four rats were randomly divided into three groups (n=18 per group): Sham surgery, middle cerebral artery occlusion (MCAO) without exercise and MCAO with exercise. Subsequent to treadmill training, ischemic stroke was induced by occluding the MCA for 1.5 h, followed by reperfusion. Six rats in each group were evaluated for neurological deficits and then sacrificed by decapitation to calculate the infarct volume. The remaining rats in each group were sacrificed to detect the level of superoxide dismutase (SOD) activity (n=6) and malondialdehyde (MDA) concentration (n=6). The results indicated that pre-ischemic exercise training reduced brain infarct volume and neurological deficits, increased SOD activity and decreased the concentration of MDA following ischemic stroke. In conclusion, treadmill exercise training prior to MCAO/reperfusion increased the antioxidant ability and decreased the oxidative damage in the brain subsequent to ischemic stroke. PMID:25187848

FENG, RUI; ZHANG, MIN; WANG, XIAO; LI, WEN-BIN; REN, SHI-QING; ZHANG, FENG

2014-01-01

123

Induction of ischemic tolerance as a promising treatment against diabetic retinopathy  

PubMed Central

Diabetic retinopathy is a leading cause of acquired blindness, and it is the most common ischemic disorder of the retina. Available treatments are not very effective. Efforts to inhibit diabetic retinopathy have focused either on highly specific therapeutic approaches for pharmacologic targets or using genetic approaches to change expression of certain enzymes. However, it might be wise to choose innovative treatment modalities that act by multiple potential mechanisms. The resistance to ischemic injury, or ischemic tolerance, can be transiently induced by prior exposure to a non-injurious preconditioning stimulus. A complete functional and histologic protection against retinal ischemic damage can be achieved by previous preconditioning with non-damaging ischemia. In this review, we will discuss evidence that supports that ischemic conditioning could help avert the dreaded consequences that results from retinal diabetic damage. PMID:25368643

Rosenstein, Ruth E.; Fernandez, Diego C.

2014-01-01

124

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

PubMed Central

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

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

2014-01-01

125

TOWARD THE OPTIMAL PRECONDITIONED EIGENSOLVER: LOCALLY OPTIMAL BLOCK PRECONDITIONED  

E-print Network

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

Knyazev, Andrew

126

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

PubMed

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

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

2001-07-01

127

SIP Server VoIP UA IP  

E-print Network

SIP Server UA UA IP VoIP UA IP 1 1 Transport Layer Security (TLS) SIP server TLS Client TLS TLS Client VoIP SRTP SIP server TLS Client TLS SRTP .2> Skype (Skype Trunk) skype server skype ( Skype Client ) skype 20 20 VoIP Option

128

Collateral recruitment and “warm-up” after first exercise in ischemic heart disease  

Microsoft Academic Search

Background Proposed mechanisms for “warm-up” after angina on first exercise include ischemic preconditioning and collateral recruitment. The aim of this study was to determine whether patients with ischemic heart disease and well-developed coronary collateral vessels have a greater warm-up response than those with no visible collateral vessels. Methods And Results Fifteen patients with a total coronary occlusion and collateral vessels

I. Patrick Kay; John Kittelson; Ralph A. H. Stewart

2000-01-01

129

Mobile IP  

Microsoft Academic Search

Mobile IP has been designed within the Internet Engineering Task Force (IETF) to serve the needs of the burgeoning population of mobile computer users who wish to connect to the Internet and maintain communications as they move from place to place. The basic protocol is described, with details given on the three major component protocols: agent advertisement, registration, and tunneling.

C. E. Perkins

1997-01-01

130

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

Microsoft Academic Search

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

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

2007-01-01

131

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

Microsoft Academic Search

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

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

2010-01-01

132

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

Microsoft Academic Search

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

K R Francis; L Wei

2010-01-01

133

PRECONDITIONING HIGHLY INDEFINITE AND NONSYMMETRIC MATRICES \\Lambda  

E-print Network

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

Tùma, Miroslav

134

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

PubMed

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

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

2015-04-01

135

The Mechanism by Which Ischemic Postconditioning Reduces Reperfusion Arrhythmias in Rats Remains Elusive  

Microsoft Academic Search

We have observed that ischemic postconditioning markedly reduces reperfusion-induced ventricular arrhythmias, but whether the mechanism is related to previously described pathways of preconditioning or postconditioning for infarct size reduction is unknown. The purpose of this study was to determine whether known pathways were involved in postconditioning's protective effect on arrhythmias.Anesthetized female rats were subjected to 5 minutes of proximal coronary

Joan Dow; Anil Bhandari; Robert A. Kloner

2009-01-01

136

IP switching for scalable IP services  

Microsoft Academic Search

Internet protocol (IP) switching is emerging as a critical technology for improving the speed and scalability of the Internet. This paper discusses IP Navigator, a form of IP switching developed specifically for use in core network backbones, such as Internet service provider networks and major corporate backbones. IP Navigator combines the high speed and quality of service capabilities of asynchronous

HASSAN M. AHMED; R. Gallon; ANDREW G. MALIS; JOHN MOY

1997-01-01

137

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

PubMed

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

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

2011-04-10

138

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

PubMed

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

Gniel, Helen M; Martin, Rosemary L

2013-06-01

139

Preconditioning Operators on Unstructured Grids  

NASA Technical Reports Server (NTRS)

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

Nepomnyaschikh, S. V.

1996-01-01

140

Tridermal tumorigenesis of induced pluripotent stem cells transplanted in ischemic brain  

Microsoft Academic Search

Stroke is a major neurologic disorder. Induced pluripotent stem (iPS) cells can be produced from basically any part of patients, with high reproduction ability and pluripotency to differentiate into various types of cells, suggesting that iPS cells can provide a hopeful therapy for cell transplantation. However, transplantation of iPS cells into ischemic brain has not been reported. In this study,

Hiromi Kawai; Toru Yamashita; Yasuyuki Ohta; Kentaro Deguchi; Shoko Nagotani; Xuemei Zhang; Yoshio Ikeda; Tohru Matsuura; Koji Abe

2010-01-01

141

Mild activation of poly(ADP-ribose) polymerase (PARP) is neuroprotective in rat hippocampal slice models of ischemic tolerance.  

PubMed

Ischemic tolerance is a phenomenon in which exposure to a mild preconditioning stress results in resistance to a subsequent lethal ischemic insult. Here we investigated the role of poly(ADP-ribose) polymerase (PARP) in the development of ischemic tolerance by using organotypic rat hippocampal slices exposed to 30 min oxygen-glucose deprivation (OGD), which leads to selective injury of the CA1 subregion 24 h later. We developed models of pharmacological preconditioning by exposing slices to subtoxic concentrations of either N-methyl-D-aspartate (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) and then, 24 h later, to 30 min OGD. Under these conditions, we observed a significant reduction in OGD-induced CA1 damage. Exposure of slices to the PARP-1 and -2 inhibitors TIQ-A, PJ-34 and UPF 1069 during preconditioning prevented the development of OGD tolerance in a concentration-dependent manner. NMDA and DHPG preconditioning increased the activity of PARP, as detected by immunoblots using antibodies against the poly(ADP-ribose) polymer product, but was not associated with consumption of cellular NAD(+) or ATP. Neuroprotection induced by preconditioning was also prevented by the caspase inhibitor Z-VAD-FMK. The modest but significant increase in caspase-3/7 induced by preconditioning, however, was not associated with PARP-1 cleavage, as occurred with staurosporine. Finally, TIQ-A prevented the activation of ERK1/2 and Akt induced by NMDA preconditioning, suggesting that the protective mechanism evoked by PARP requires activation of these prosurvival mediators. Our results suggest that preconditioning with appropriate pharmacological stimuli may promote neuroprotective mechanisms triggered by the sublethal activation of two otherwise deleterious executioners such as PARP and caspase-3/7. PMID:22639866

Gerace, Elisabetta; Scartabelli, Tania; Formentini, Laura; Landucci, Elisa; Moroni, Flavio; Chiarugi, Alberto; Pellegrini-Giampietro, Domenico E

2012-07-01

142

Ischemic tolerance induction in organotypic hippocampal slices: role for the GABA(A) receptor?  

PubMed

Ischemic preconditioning (IPC) refers to sublethal ischemic insults rendering brain tissue tolerant against subsequent ischemic insults. We investigated the role of the GABA(A) receptor (GABA(A)R) upon IPC induction. Rat organotypic hippocampal slices were subjected to IPC by 15 min of oxygen-glucose deprivation (OGD) followed by 40 min of OGD 48 h later, resulting in robust cell death reduction as assessed by the propidium iodide fluorescence method ('late' or 'second window' IPC). Superfusion with the GABA(A)R antagonist bicuculline during IPC ameliorated propidium iodide uptake at a high but not at low doses indicating that GABA(A)R activation may be assigned a limited role in neuroprotection. In previous studies, we found that increased neuronal excitability can promote IPC neuroprotection. We, therefore, tested the hypothesis that blockade of inhibitory GABAergic transmission conferred ischemic tolerance. However, temporary administration of bicuculline 48 h prior to ischemic challenge was not neuroprotective. In another approach, we tested whether preconditioning with the GABA(A)R agonist, 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) mediated ischemic tolerance and found no significant neuroprotection. The results are discussed in light of the intrinsic excitatory-inhibitory balance of glutamate and GABA. PMID:15908115

Lange-Asschenfeldt, Christian; Raval, Ami P; Pérez-Pinzón, Miguel A

143

Ischemic tolerance modulates TRAIL expression and its receptors and generates a neuroprotected phenotype  

PubMed Central

TNF-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily released by microglia, appears to be involved in the induction of apoptosis following focal brain ischemia. Indeed, brain ischemia is associated with progressive enlargement of damaged areas and prominent inflammation. As ischemic preconditioning reduces inflammatory response to brain ischemia and ameliorates brain damage, the purpose of the present study was to evaluate the role of TRAIL and its receptors in stroke and ischemic preconditioning and to propose, by modulating TRAIL pathway, a new therapeutic strategy in stroke. In order to achieve this aim a rat model of harmful focal ischemia, obtained by subjecting animals to 100?min of transient occlusion of middle cerebral artery followed by 24?h of reperfusion and a rat model of ischemic preconditioning in which the harmful ischemia was preceded by 30?mins of tMCAO, which represents the preconditioning protective stimulus, were used. Results show that the neuroprotection elicited by ischemic preconditioning occurs through both upregulation of TRAIL decoy receptors and downregulation of TRAIL itself and of its death receptors. As a counterproof, immunoneutralization of TRAIL in tMCAO animals resulted in significant restraint of tissue damage and in a marked functional recovery. Our data shed new light on the mechanisms that propagate ongoing neuronal damage after ischemia in the adult mammalian brain and provide new molecular targets for therapeutic intervention. Strategies aimed to repress the death-inducing ligands TRAIL, to antagonize the death receptors, or to activate the decoy receptors open new perspectives for the treatment of stroke. PMID:25032854

Cantarella, G; Pignataro, G; Di Benedetto, G; Anzilotti, S; Vinciguerra, A; Cuomo, O; Di Renzo, G F; Parenti, C; Annunziato, L; Bernardini, R

2014-01-01

144

PVM and IP multicast  

SciTech Connect

This report describes a 1994 demonstration implementation of PVM that uses IP multicast. PVM`s one-to-many unicast implementation of its pvm{_}mcast() function is replaced with reliable IP multicast. Performance of PVM using IP multicast over local and wide-area networks is measured and compared with the original unicast implementation. Current limitations of IP multicast are noted.

Dunigan, T.H.; Hall, K.A.

1996-12-01

145

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

146

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

PubMed

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

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

2014-09-17

147

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

PubMed Central

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

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

2015-01-01

148

Ischemic optic neuropathy  

Microsoft Academic Search

Ischemic optic neuropathy (ION), based on vascular anatomy of the optic nerve, pathogenesis and clinical picture, consists of two distinct entities: anterior (AION) and posterior (PION) ischemic optic neuropathies. AION is due to interference with posterior ciliary artery supply to the optic nerve head and retrolaminar part of the optic nerve; it initially presents with visual loss and optic disc

Sohan Singh Hayreh

1978-01-01

149

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

PubMed Central

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

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

2009-01-01

150

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

PubMed

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

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

2014-07-01

151

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

PubMed Central

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

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

2012-01-01

152

IP switching—ATM under IP  

Microsoft Academic Search

IP traffic on the Internet and private enterprise networks has been growing exponentially for some time. This growth is beginning to stress the traditional, processor based design of current day routers. Switching technology offers much higher aggregate bandwidth but presently only offers a layer-2 bridging solution. Various proposals are under way to support IP routing over an ATM network. However,

Peter Newman; Greg Minshall; Thomas L. Lyon

1998-01-01

153

Preconditioning the diabetic human myocardium  

PubMed Central

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

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

2010-01-01

154

Income Protection (IP) Insurance  

E-print Network

Income Protection (IP) Insurance Kenneth Stokes, G.A. ?Art? Barnaby, Mark Waller and Joe Outlaw* The Income Protection (IP) program insures the producer against lost income from reductions in yield or price. This policy pays when the harvested...

Stokes, Kenneth; Barnaby, G. A. Art; Waller, Mark L.; Outlaw, Joe

1999-06-09

155

IP puzzles, probabilistic networking,  

E-print Network

systems The nuclear weapon: scanrand Inverse SYN cookies and a single socket Statelessly scan large to fight problem #12;osit Puzzles must be placed in the IP layer to be effective #12;Why are IP puzzles

156

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

Microsoft Academic Search

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

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

2010-01-01

157

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

PubMed Central

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

Zhao, Xi; Zhang, Guangwei; Ma, Hong

2014-01-01

158

Ischemic Optic Neuropathies  

Microsoft Academic Search

? Ischemic optic neuropathy is classified by location as anterior or posterior and by etiology as arteritic or nonarteritic.\\u000a \\u000a \\u000a ? Anterior ischemic optic neuropathy (AION) presents with rapid, usually painless, monocular visual field loss in the presence\\u000a of optic disc edema. \\u000a \\u000a \\u000a \\u000a ? Arteritic AION is typically more severe and more frequently bilateral than nonarteritic AION, and is associated with severe

Anthony C. Arnold

159

The Protective Effects of Monophosphoryl Lipid A on the Ischemic Myocardium and Endothelium in Rats  

Microsoft Academic Search

Previous investigations have shown that a single dose of low-density lipoprotein (LDL) injection causes a marked decrease in endothelium-dependent relaxation, and that endothelial dysfunction aggravates myocardial injury due to ischemia-reperfusion in atherosclerotic animals. Monophosphoryl lipid A-induced delayed preconditioning preserves the ischemic myocardium and endothelial cells. The objective of the present study was to examine the effect of monophosphoryl lipid A

Hui-Qing Zhu; Jun-Lin Jiang; Rong Lu; Xiao-Hong Zhang; Han-Wu Deng; Yuan-Jian Li

2003-01-01

160

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

PubMed Central

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

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

2012-01-01

161

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

162

Immunizing Beef Calves: A Preconditioning Immunization Concept  

E-print Network

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

Faries Jr., Floron C.

2000-12-20

163

40 CFR 1065.518 - Engine preconditioning.  

Code of Federal Regulations, 2014 CFR

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

2014-07-01

164

Hardware\\/software IP protection  

Microsoft Academic Search

Design methodologies based on reuse of intellectual property (IP) components critically depend on techniques to protect IP ownership. IP protection is particularly challenging for hardware\\/software systems, where an IP core runs embedded software: both the software and the core are valuable IP that must be protected.We propose a new technique for protecting the IP of both processor cores and application

Marcello Dalpasso; Alessandro Bogliolo; Luca Benini

2000-01-01

165

Laser thermal preconditioning enhances dermal wound repair  

NASA Astrophysics Data System (ADS)

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

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

2008-02-01

166

Interplay between histone acetylation/deacetylation and poly(ADP-ribosyl)ation in the development of ischemic tolerance in vitro.  

PubMed

Ischemic tolerance is an endogenous defense program in which exposure to a subtoxic preconditioning insult results in resistance to a subsequent, otherwise lethal, episode of ischemia. Herein, we evaluated the role of histone acetylation/deacetylation in an in vitro model of preconditioning, using rat organotypic hippocampal slices exposed to 30 min oxygen-glucose deprivation (OGD), which leads to CA1 injury 24 h later: tolerance was induced by exposing the slices to preconditioning bouts of NMDA (3 ?M for 60 min) 24 h prior to the toxic OGD challenge. Under these conditions, CA1 damage induced by OGD was reduced. The induction of tolerance was prevented by incubating the slices with HDAC inhibitors. NMDA preconditioning was associated with a mild increase in poly(ADP-ribose) polymerase (PARP) activity that was apparently followed, 3 h later, by a mild increase in histone acetylation. Use of PARP and HDAC inhibitors suggests a possible interaction between PARP and HDAC activities in the development of ischemic tolerance. Finally, both PARP and HDAC inhibitors were able to prevent the increase in pERK1/2 induced by NMDA preconditioning. We propose a model in which mild histone acetylation and PARP activity cooperate in producing a neuroprotective response in the development of ischemic tolerance. PMID:25623965

Gerace, Elisabetta; Landucci, Elisa; Scartabelli, Tania; Moroni, Flavio; Chiarugi, Alberto; Pellegrini-Giampietro, Domenico E

2015-05-01

167

Ischemic ulcers - self-care  

MedlinePLUS

Ischemic ulcers (wounds) can occur when there is poor blood flow in your legs . Poor blood flow causes cells to die and damages tissue. Most ischemic ulcers occur on the feet and legs. These types ...

168

Optimal preconditioning of lattice Boltzmann methods  

NASA Astrophysics Data System (ADS)

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

Izquierdo, Salvador; Fueyo, Norberto

2009-09-01

169

Ischemic Stroke and Neuroprotection  

PubMed Central

Stroke is a major cause of morbidity and mortality in both developed and developing countries of the world. Greater understanding of the pathophysiology of neuronal damage in ischemic stroke has generated interest in neuroprotection as a management strategy. This paper aims to review the current concept and place of neuroprotection in ischemic stroke. An extensive search of all materials related to the topic was made using library sources including Pubmed and Medline searches. Current research findings were also included. The findings are as presented. Neuroprotection is an increasingly recognized management strategy in ischemic stroke that promises to assist clinicians in reducing stroke mortality rates and improving the quality of life of survivors. PMID:23439855

Onwuekwe, IO; Ezeala-Adikaibe, B

2012-01-01

170

Voice over IP Calculator  

NSDL National Science Digital Library

The Voice over IP Calculator Web site actually consists of four free online tools that can be used to estimate bandwidth requirements and voice paths for a planned VoIP system. The four tools are: Lines and IP Bandwidth Calculator, Erlangs and Bandwidth Calculator, Minutes and Lines Calculator, and Erlangs and Lines Calculator. Each utility is very easy to use, but is mainly intended for experienced IT workers.

171

Deploying VoIP in Existing IP Networks Khaled Salah  

E-print Network

1 Deploying VoIP in Existing IP Networks Khaled Salah Department of Information and Computer such as VoIP. VoIP requires timely packet delivery with low latency, jitter, packet loss, and sufficient bandwidth. To achieve this goal, an efficient deployment of VoIP must ensure these real-time traffic

Salah, Khaled Hamed

172

Remote ischemic conditioning: A novel way to treat ischemia-related injury of limbs.  

PubMed

Remote ischemic conditioning (RIC) including remote ischemic preconditioning (RIPC) and remote ischemic postconditioning (RIPostC) is widely reported to be able to prevent many organs, such as heart, brain, and skeletal muscle from ischemia-related injury. However, the clinical application of RIC is confined to treating myocardial infarction and stroke. Since RIC could prevent skeletal muscle from ischemia-related injury, and was effective in heart and brain treatments, we hypothesized RIC could treat ischemia-related injury of limbs, such as diabetic foot, Buerger's disease, plantation of severed limb, and crush injury. As we know, many researches not only proved the promising clinical applications of RIC, but also researched the mechanisms in animal models. Our hypothesis could be confirmed by these researches. PMID:25737337

Tengfei, Li; Jiangning, Wang

2015-05-01

173

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

174

Posterior Ischemic Optic Neuropathy  

Microsoft Academic Search

14 cases of posterior ischemic optic neuropathy (PION) were clinically analyzed, in whom we excluded known etiologies of optic nerve disturbances and confirmed the decreased blood supply to the posterior portion of the optic nerve. On the basis of our clinical findings, we have proposed the following criteria for the diagnosis of idiopathic PION: (1) sudden onset of unilateral visual

Y. Isayama; T. Takahashi; M. Inoue; T. Jimura

1983-01-01

175

Ischemic Nerve Block.  

ERIC Educational Resources Information Center

This experiment investigated the capability for movement and muscle spindle function at successive stages during the development of ischemic nerve block (INB) by pressure cuff. Two male subjects were observed under six randomly ordered conditions. The duration of index finger oscillation to exhaustion, paced at 1.2Hz., was observed on separate…

Williams, Ian D.

176

Imaging of Ischemic Stroke  

PubMed Central

This content discusses the individual components of multi-modal CT and multi-modal MRI, present the current status of neuroimaging for the evaluation of the acute ischemic stroke, and address the potential role of a combined multimodal stroke protocol. PMID:20974371

Leiva-Salinas, Carlos; Wintermark, Max

2010-01-01

177

SIMPLE MACHINE PERFUSION SIGNIFICANTLY ENHANCES HEPATOCYTE YIELDS OF ISCHEMIC AND FRESH RAT LIVERS  

PubMed Central

The scarcity of viable hepatocytes is a significant bottleneck in cell transplantation, drug discovery, toxicology, tissue engineering, and bioartificial assist devices, where trillions of high-functioning hepatocytes are needed annually. We took the novel approach of using machine perfusion to maximize cell recovery, specifically from uncontrolled cardiac death donors, the largest source of disqualified donor organs. In a rat model, we developed a simple 3 hour room temperature (20±2°C) machine perfusion protocol to treat non-premedicated livers exposed to 1 hour of warm (34°C) ischemia. Treated ischemic livers were compared to fresh, fresh-treated and untreated ischemic livers using viable hepatocyte yields and in vitro performance as quantitative endpoints. Perfusion treatment resulted in both a 25-fold increase in viable hepatocytes from ischemic livers, and a 40% increase from fresh livers. While cell morphology and function in suspension and plate cultures of untreated warm ischemic cells was significantly impaired, treated warm ischemic cells were indistinguishable from fresh hepatocytes. Further, a strong linear correlation between tissue ATP and cell yield enabled accurate evaluation of the extent of perfusion recovery. Maximal recovery of warm ischemic liver ATP content appears to be correlated with optimal flow through the microvasculature. These data demonstrate that the inclusion of a simple perfusion-preconditioning step can significantly increase the efficiency of functional hepatocyte yields and the number of donor livers that can be gainfully utilized. PMID:25431743

Izamis, Maria-Louisa; Calhoun, Candice; Uygun, Basak E.; Guzzardi, Maria Angela; Price, Gavrielle; Luitje, Martha; Saeidi, Nima; Yarmush, Martin L.; Uygun, Korkut

2014-01-01

178

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

179

Analytical IP Alias Resolution  

Microsoft Academic Search

IP alias resolution is an important step in generating sample Internet topologies from collected path traces. Inaccuracies in IP alias resolution may significantly affect the characteristics of the resulting sample topologies. This in turn affects the accuracy of measurement results obtained using such topologies. Existing tools for alias resolution use an active probing approach. They induce significant traffic overhead into

Mehmet Hadi Gunes; Kamil Sarac

2006-01-01

180

Ischemic conditioning: the challenge of protecting the diabetic heart  

PubMed Central

The successful clinical translation of novel therapeutic strategies to attenuate lethal myocardial ischemia-reperfusion injury and limit infarct size has been identified as a major unmet need, and is of particular importance in patients with type-2 diabetes. There is a wealth of preclinical evidence that ischemic conditioning (encompassing the three paradigms of preconditioning, postconditioning and remote conditioning) is profoundly cardioprotective and, via up-regulation of endogenous signaling cascades, renders the heart resistant to infarction. However, current phase II trials aimed at exploiting ischemic conditioning for the clinical treatment of myocardial ischemia-reperfusion injury have yielded mixed results, possibly reflecting the emerging concern that the efficacy of conditioning-induced cardioprotection may be compromised in the diabetic heart. Our goal in this review is to provide a summary of our present understanding of the effect of type-2 diabetes on the infarct-sparing effect of ischemic conditioning, and the challenges of limiting ischemia-reperfusion injury in the diabetic heart. PMID:25414825

Wider, Joseph

2014-01-01

181

Hypoxic-Ischemic Neonatal Encephalopathy: Animal Experiments for Neuroprotective Therapies  

PubMed Central

Hypoxic-ischemic neonatal encephalopathy and ensuing brain damage is still an important problem in modern perinatal medicine. In this paper, we would like to share some of the results of our recent studies on neuroprotective therapies in animal experiments, as well as some literature reviews. From the basic animal studies, we have now obtained some possible candidates for therapeutic measures against hypoxic-ischemic neonatal encephalopathy. For example, they are hypothermia, rehabilitation, free radical scavenger, neurotrophic factors and growth factors, steroid, calcium channel blocker, vagal stimulation, some anti apoptotic agents, pre- and post conditioning, antioxidants, cell therapy with stem cells, modulators of K(+)-ATP channels, and so on. Whether combination of these therapies may be more beneficial than any single therapy needs to be clarified. Hypoxia-ischemia is a complicated condition, in which the cause, severity, and time-course are different in each case. Likewise, each fetus has its own inherent potentials such as adaptation, preconditioning-tolerance, and intolerance. Therefore, further extensive studies are required to establish an individualized strategy for neuroprotection against perinatal hypoxic-ischemic insult. PMID:23533962

Ikenoue, Tsuyomu

2013-01-01

182

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

PubMed Central

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

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

2012-01-01

183

Advanced Networking Voice over IP  

E-print Network

.LoCigno@dit.unitn.it Advanced Networking ­ VoIP - 1 2 VoIP: Integrating Services !" # " $ $ # " % ! ! & # ' ( ) * Renato.LoCigno@dit.unitn.it Advanced Networking ­ VoIP - 1 3 Plain Old Telephone Service (POTS) #12;2 Renato.LoCigno@dit.unitn.it Advanced Networking ­ VoIP - 1 4 IP services Renato.LoCigno@dit.unitn.it Advanced Networking ­ VoIP - 1 5

Lo Cigno, Renato Antonio

184

Preconditioning 9.1 The General Approach  

E-print Network

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

John, Volker

185

[Painful ischemic neuropathy].  

PubMed

Chronic ischemia in patients with peripheral arterial disease (PAD) represents a common medical problem. Neuropathic changes and pain caused by chronic ischemia are often found in the lower extremities of these patients. Pain in patients with chronic critical limb ischemia fulfill the criteria of neuropathic pain. Diagnostic tools besides medical history and examination are questionnaires, quantitative sensory testing (QST) and measuring intraepidermal nerve fiber density (IENFD) when indicated. A pharmacological approach with non-opioids and opioids as well as antidepressive and anticonvulsive drugs (according to the recommendations for the therapy of neuropathic pain) seems to be indicated for treating painful ischemic neuropathy. Spinal cord stimulation (SCS) provides the best evidence for invasive procedures in treating chronic ischemic pain. PMID:25620734

Lang, P M

2015-02-01

186

[Genetics of ischemic stroke].  

PubMed

Stroke is one of the most widespread causes of mortality und disability worldwide. Around 80 % of strokes are ischemic and different forms of intracranial bleeding account for the remaining cases. Monogenic stroke disorders are rare but the diagnosis may lead to specific therapeutic consequences for the affected patients who are predominantly young. In common sporadic stroke, genetic factors play a role in the form of susceptibility genes. Their discovery may give rise to new therapeutic options in the future. PMID:23334453

Gschwendtner, A; Dichgans, M

2013-02-01

187

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

PubMed Central

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

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

2014-01-01

188

Ischemic tissue injury.  

PubMed Central

The subendocardial to subepicardial gradient in the severity of ischemia following acute coronary occlusion is described. The effects of mild, moderate, and severe ischemia on cell structure and function are compared in summary form, and special attention is given to the effects of severe ischemia on myocardial cells. The characteristics of reversible and irreversible ischemic injury are defined in biologic terms. The failure of cell volume regulation in cells which have entered an irreversible state of ischemic injury is demonstrated by the use of free-hand slices in vitro. Irreversibility is associated with structural defects in the plasma membrane and is reflected in an increased slice inulin-diffusible space, increased slice H2O and Na+ content, and failure of the tissue to maintain the high K+ and Mg2+ levels characteristic of normal left ventricular myocardium. Defective cell membrane function is an early feature of irreversible ischemic injury and may be a primary event in the genesis of the irreversible state. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 PMID:1180331

Jennings, R. B.; Ganote, C. E.; Reimer, K. A.

1975-01-01

189

Condition number estimation of preconditioned matrices.  

PubMed

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

Kushida, Noriyuki

2015-01-01

190

Condition Number Estimation of Preconditioned Matrices  

PubMed Central

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

Kushida, Noriyuki

2015-01-01

191

IPS User's Guide  

Microsoft Academic Search

IntroductionIPS[2] is an interactive, trace driven performance measurement system for parallel and distributedprograms. It runs on DECstation, Sun, Vax, Sequent Symmetry, and Cray Y-MP computers(or a heterogeneous combination of these computers). IPS provides a large amount of performancedata about the execution of a parallel program, and this information is organized hierarchicallyso that access to it is easy and intuitive.Performance data

Barton P. Miller; Bruce Irvin; Hi Low; Jeff Hollingsworth

1989-01-01

192

Mechanisms of ischemic brain injury  

Microsoft Academic Search

Stroke is the third leading cause of death and the leading cause of long-term disability in the United States. Approximately\\u000a 80% of all strokes are ischemic and there are limited therapies approved for the treatment of acute ischemic stroke. Understanding\\u000a the mechanisms of ischemic brain damage is necessary for the development of innovative treatment strategies. In this review,\\u000a we discuss

Vallabh Janardhan; Adnan I. Qureshi

2004-01-01

193

Hyperbaric oxygen preconditioning protects cortical neurons against oxygen-glucose deprivation injury: role of peroxisome proliferator-activated receptor-gamma.  

PubMed

Ischemic stroke is one of the leading causes of mortality and disability worldwide. Our previous studies have shown that hyperbaric oxygen (HBO) preconditioning can afford significant neuroprotection against cerebral ischemia-reperfusion (I/R) injury in rats. However, it is still unknown whether HBO preconditioning can directly protect primary cultured cortical neurons against oxygen-glucose deprivation (OGD). Peroxisome proliferator-activated receptor-gamma (PPAR ?) plays a central role in the regulation of apoptosis, oxidative stress and inflammation as well as affords significant neuroprotection against cerebral I/R injury. 15-deoxy-?(12,14)-prostaglandin J(2) (15d-PGJ(2)) is an endogenous ligand with a high affinity for PPAR ?. Recently, some studies demonstrate that activation of PPAR ? mediates lipopolysaccharide and anesthetic preconditioning. In the present study, we firstly found that OGD exposure caused the significant damage of cultured cortical neurons evaluated by cell viability, lactate dehydrogenase (LDH) release and caspase-3 activity, which were significantly ameliorated by HBO preconditioning. Furthermore, HBO preconditioning significantly increased the levels of PPAR ? mRNA and protein, PPAR ? DNA binding activity, 15d-PGJ(2) and antioxidant enzymatic activities in primary cultured cortical neurons with OGD exposure. Moreover, PPAR ? antagonist GW9662 dose-dependently abolished the protection of HBO preconditioning in OGD-exposed neurons. GW9662 blocked the increase of PPAR ? DNA binding activity and antioxidant enzymatic activities, but did not influence the 15d-PGJ(2) level in OGD-exposed neurons with HBO preconditioning. However, the cyclooxygenase (COX)-2 inhibitor NS-398 blocked the production of 15d-PGJ(2) in OGD-exposed neurons with HBO preconditioning. In addition, 15d-PGJ(2) preconditioning could also protect cultured neurons against OGD injury. These results demonstrate that HBO preconditioning has directly beneficial effects on ODG-exposed cortical neurons by the activation of PPAR ? subsequent to the production of 15d-PGJ(2), which in turn increases the downstream antioxidant enzymatic activities. PMID:22444276

Zeng, Yi; Xie, Keliang; Dong, Hailong; Zhang, Haopeng; Wang, Feng; Li, Yan; Xiong, Lize

2012-05-01

194

IP switching and gigabit routers  

Microsoft Academic Search

To cope with the growth in the Internet and corporate IP networks, we require IP routers capable of much higher performance than is possible with existing architectures. This article examines two approaches to the design of a high-performance router, the gigabit router and the IP switch, and then provides some detail on the implementation of an IP switch and the

P. Newman; G. Minshall; T. Lyon; L. Huston

1997-01-01

195

Ischemic postconditioning as a novel avenue to protect against brain injury after stroke  

PubMed Central

Ischemic postconditioning initially referred to a stuttering reperfusion performed immediately after reperfusion, for preventing ischemia/reperfusion injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers, and may even be performed as late as 6 h after focal ischemia and 2 days after transient global ischemia. The concept is thought to be derived from ischemic preconditioning or partial/gradual reperfusion, but in fact the first experiment for postconditioning was carried out much earlier than that of preconditioning or partial/gradual reperfusion, in the research on myocardial ischemia. This review first examines the protective effects and parameters of postconditioning in various cerebral ischemic models. Thereafter, it provides insights into the protective mechanisms of postconditioning associated with reperfusion injury and the Akt, mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and ATP-sensitive K+ (KATP) channel cell signaling pathways. Finally, some open issues and future challenges regarding clinical translation of postconditioning are discussed. PMID:19240739

Zhao, Heng

2009-01-01

196

Protein redox modification as a cellular defense mechanism against tissue ischemic injury.  

PubMed

Protein oxidative or redox modifications induced by reactive oxygen species (ROS) or reactive nitrogen species (RNS) not only can impair protein function, but also can regulate and expand protein function under a variety of stressful conditions. Protein oxidative modifications can generally be classified into two categories: irreversible oxidation and reversible oxidation. While irreversible oxidation usually leads to protein aggregation and degradation, reversible oxidation that usually occurs on protein cysteine residues can often serve as an "on and off" switch that regulates protein function and redox signaling pathways upon stress challenges. In the context of ischemic tolerance, including preconditioning and postconditioning, increasing evidence has indicated that reversible cysteine redox modifications such as S-sulfonation, S-nitrosylation, S-glutathionylation, and disulfide bond formation can serve as a cellular defense mechanism against tissue ischemic injury. In this review, I highlight evidence of cysteine redox modifications as protective measures in ischemic injury, demonstrating that protein redox modifications can serve as a therapeutic target for attenuating tissue ischemic injury. Prospectively, more oxidatively modified proteins will need to be identified that can play protective roles in tissue ischemic injury, in particular, when the oxidative modifications of such identified proteins can be enhanced by pharmacological agents or drugs that are available or to be developed. PMID:24883175

Yan, Liang-Jun

2014-01-01

197

Protein Redox Modification as a Cellular Defense Mechanism against Tissue Ischemic Injury  

PubMed Central

Protein oxidative or redox modifications induced by reactive oxygen species (ROS) or reactive nitrogen species (RNS) not only can impair protein function, but also can regulate and expand protein function under a variety of stressful conditions. Protein oxidative modifications can generally be classified into two categories: irreversible oxidation and reversible oxidation. While irreversible oxidation usually leads to protein aggregation and degradation, reversible oxidation that usually occurs on protein cysteine residues can often serve as an “on and off” switch that regulates protein function and redox signaling pathways upon stress challenges. In the context of ischemic tolerance, including preconditioning and postconditioning, increasing evidence has indicated that reversible cysteine redox modifications such as S-sulfonation, S-nitrosylation, S-glutathionylation, and disulfide bond formation can serve as a cellular defense mechanism against tissue ischemic injury. In this review, I highlight evidence of cysteine redox modifications as protective measures in ischemic injury, demonstrating that protein redox modifications can serve as a therapeutic target for attenuating tissue ischemic injury. Prospectively, more oxidatively modified proteins will need to be identified that can play protective roles in tissue ischemic injury, in particular, when the oxidative modifications of such identified proteins can be enhanced by pharmacological agents or drugs that are available or to be developed. PMID:24883175

Yan, Liang-Jun

2014-01-01

198

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

199

Preconditioning with endoplasmic reticulum stress ameliorates endothelial cell inflammation.  

PubMed

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

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

2014-01-01

200

SUMO and ischemic tolerance.  

PubMed

Hibernating squirrels slow blood flow to a crawl, but sustain no damage to brain or other tissues. This phenomenon provides an excellent model of natural tolerance to ischemia. Small ubiquitin-like modifier (SUMO) is a 100-residue peptide that modifies other proteins by being attached to the epsilon amino group of specific lysine residues. The discovery of massive SUMOylation (by both SUMO-1 and SUMO-2/3) occurring in the brains of 13-lined ground squirrels (Ictidomys tridecemlineatus) during hibernation torpor had opened the door to the studies on SUMO and ischemic tolerance reviewed here. Ischemic stress was shown to increase the levels of SUMO conjugation, especially SUMO-2/3, mostly during reperfusion in animal models and during restoration of oxygen and glucose in cell culture systems. Over-expression or depletion of SUMOs and/or Ubc9 (the SUMO E2 conjugating enzyme) increases or decreases (respectively) the levels of SUMO conjugates. Elevated global SUMO conjugations were shown to cytoprotect from ischemic insults; conversely, depressed SUMOylation sensitized cells. Global protein conjugation not only by SUMOs, but also by other ubiquitin-like modifiers (ULMs) including NEDD8, ISG15, UFM1 and FUB1 was shown to be significantly increased in the brains of hibernating ground squirrels during torpor. These increases in multiple ULM conjugations may orchestrate the cellular events in hibernating ground squirrels that induce a state of natural tolerance through their multipronged effects. Certain miRNAs such as the miR-200 family and the miR-182 family were shown, at least partly, to control the levels of these ULM conjugations. Lowering the levels of these miRNAs leads to an increase in global SUMOylation/ULM conjugation, thereby providing the tolerance to ischemia. This suggests that these miRNAs may be good targets for therapeutic intervention in stroke. PMID:23775726

Lee, Yang-ja; Hallenbeck, John M

2013-12-01

201

Lethal Myocardial Ischemic Injury  

PubMed Central

The biologic changes occurring in severely ischemic myocytes in vivo as the affected cells pass through the phase of reversible to the phase of lethal or irreversible injury are reviewed with special emphasis on the effect of ischemia on the production and utilization of highenergy phosphate, the destruction of the adenine nucleotide pool, and the appearance of signs of damage to the plasma membrane of the sarcolemma. Evidence is presented that indicates that the events occurring in severe ischemia in vivo are essentially identical to those found in total ischemia in vitro except that the biologic changes of ischemia develop more slowly in total ischemia in vitro than in severe ischemia in vivo. The slower time course of injury, together with the uniformity of injury provided by total ischemia in vitro, may allow for more precise identification of potential lethal cellular events in ischemic injury. The production of highenergy phosphates (HEP) from anaerobic glycolysis have been estimated in both in vivo and in vitro ischemia by the measurement of lactate accumulation, and total HEP utilization has been estimated from the depletion of stores of preformed HEP. The results show that between 80% and 90% of the HEP utilized by ischemic dog left ventricle is produced by anaerobic glycolysis. The onset of irreversibility is associated with marked depletion of the HEP and adenine nucleotide pools of the tissue and the cessation of energy production via glycolysis. The cessation of anaerobic glycolysis may be caused by the low sarcoplasmic, adenosine triphosphate (ATP) concentration of the dying myocyte. In addition to the foregoing changes, irreversibly injured tissue exhibits both ultrastructural and functional evidence of disruption of the plasmalemma of the sarcolemma. The possible relationships, causal and otherwise, between severe HEP depletion and membrane damage are discussed. Both HEP depletion (ATP < 3-8% of control) and membrane damage are considered to be objective signs of the presence of irreversible myocardial ischemic injury. However, at the present time, there is no proof that these changes are causally related either to each other or to cell death in severe in vivo ischemia. ImagesFigure 3Figure 4 PMID:7008621

Jennings, Robert B.; Reimer, Keith A.

1981-01-01

202

Preserving Symmetry in Preconditioned Krylov Subspace Methods  

NASA Technical Reports Server (NTRS)

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

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

1996-01-01

203

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

204

Preconditioned Multigrid Methods for Unsteady Incompressible Flows  

Microsoft Academic Search

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

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

1998-01-01

205

On polynomial preconditioning for indefinite Hermitian matrices  

NASA Technical Reports Server (NTRS)

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

Freund, Roland W.

1989-01-01

206

Approximate polynomial preconditioning applied to biharmonic equations on vector supercomputers  

NASA Technical Reports Server (NTRS)

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

Wong, Yau Shu; Jiang, Hong

1987-01-01

207

Voice Over IP Curriculum  

NSDL National Science Digital Library

The Convergence Technology Center has made Voice over IP curriculum available online. The site includes a syllabus and learning activities related to the topic. If you are an educator who would like to gain full access to the complete curriculum, you may email convergence_technology@collin.edu (further instructions for access are available on the site).

208

Remote ischemic conditioning.  

PubMed

In remote ischemic conditioning (RIC), brief, reversible episodes of ischemia with reperfusion in one vascular bed, tissue, or organ confer a global protective phenotype and render remote tissues and organs resistant to ischemia/reperfusion injury. The peripheral stimulus can be chemical, mechanical, or electrical and involves activation of peripheral sensory nerves. The signal transfer to the heart or other organs is through neuronal and humoral communications. Protection can be transferred, even across species, with plasma-derived dialysate and involves nitric oxide, stromal derived factor-1?, microribonucleic acid-144, but also other, not yet identified factors. Intracardiac signal transduction involves: adenosine, bradykinin, cytokines, and chemokines, which activate specific receptors; intracellular kinases; and mitochondrial function. RIC by repeated brief inflation/deflation of a blood pressure cuff protects against endothelial dysfunction and myocardial injury in percutaneous coronary interventions, coronary artery bypass grafting, and reperfused acute myocardial infarction. RIC is safe and effective, noninvasive, easily feasible, and inexpensive. PMID:25593060

Heusch, Gerd; Bøtker, Hans Erik; Przyklenk, Karin; Redington, Andrew; Yellon, Derek

2015-01-20

209

CISCO IP 7902 FONCTIONS TLPHONIQUES  

E-print Network

CISCO IP 7902 FONCTIONS T�L�PHONIQUES FONCTIONS DE BASE FAIRE UN APPEL Soulever le combiné et participants. Mettre un terme à une conférence Raccrocher le combiné. . Cisco_IP_7902_FR_CM%207.0_2009324[1].doc 1 de 2 #12;CISCO IP 7902 FONCTIONS T�L�PHONIQUES Cisco_IP_7902_FR_CM%207.0_2009324[1].doc 2 de 2

Charette, André

210

ISOFLURANE PRECONDITIONING AND POSTCONDITIONING IN RAT HIPPOCAMPAL NEURONS  

PubMed Central

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

McMurtrey, Richard J.; Zuo, Zhiyi

2010-01-01

211

Time-derivative preconditioning for viscous flows  

NASA Technical Reports Server (NTRS)

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

Choi, Yunho; Merkle, Charles L.

1991-01-01

212

Cryoglobulins in Acute Ischemic Stroke  

NASA Astrophysics Data System (ADS)

Cryoglobulins (Cgs) are pathogenic immune complexes, non specific markers of the inflammatory and autoimmune responses. In this study we for the first time, revealed Cgs in the blood of ischemic stroke patients and analyze their composition.

Manukyan, L. A.; Ayvazyan, V. A.; Boyajyan, A. S.

213

Intravenous Thrombolytics for Ischemic Stroke  

Microsoft Academic Search

For many decades, intravenous (IV) thrombolytics have been delivered to treat acute thrombosis. Although these medications\\u000a were originally effective for coronary thrombosis, their mechanisms have proven beneficial for many other disease processes,\\u000a including ischemic stroke. Treatment paradigms for acute ischemic stroke have largely followed those of cardiology. Specifically,\\u000a the aim has been to recanalize the occluded artery and to restore

Andrew D. Barreto

214

Downregulation of miR199a may play a role in 3-nitropropionic acid induced ischemic tolerance in rat brain  

Microsoft Academic Search

MicroRNAs (miR) are single-stranded short RNA molecules that regulate gene expression by degradation or translational repression of mRNA. It has been reported that the downregulation of miR-199a plays an important role in cardiac ischemic tolerance. We examined the expression of miR-199a after 3-nitropropionic acid (3-NPA) preconditioning in rat brain. 3-NPA (20mg\\/kg), an irreversible inhibitor of succinate dehydrogenase, was injected intraperitoneally

Wei-Hai Xu; Xiao-Ying Yao; Hao-Jie Yu; Ji-Wei Huang; Li-Ying Cui

215

TRPV1 and TRPV4 channels: potential therapeutic targets for ischemic conditioning-induced cardioprotection.  

PubMed

Besides the involvement of TRPV channels in exhibiting various cellular functions including thermoregulation, pain perception, maintenance of bone homeostasis and gastrointestinal function; certain studies have also implicated the putative role of these channels in mediating ischemic conditioning-induced cardioprotection. The potential role of TRPV1 channels in different forms of ischemic conditioning (pre/post/remote)-induced cardioprotection has been described by employing TRPV1 knockout mice and various pharmacological modulators. The cardioprotective effects of TRPV1 activation during ischemic conditioning have been linked with increased CGRP, substance P release and augmented ALOX expression. Furthermore, the role of TRPV4 channels in mediating preconditioning-induced preservation of vascular function in terms restoring NO- and further improving EDH(F)-mediated endothelial relaxation has been described. The present review discusses the putative role of TRPV1 and TRPV4 channels in mediating different forms of conditioning (pre/post/remote)-induced cardioprotection along with the possible mechanisms. Future perspectives have also been described to fully understand the cascade of signaling and contribution of TRPV channel activation during myocardial ischemic conditioning. PMID:25449039

Randhawa, Puneet Kaur; Jaggi, Amteshwar Singh

2015-01-01

216

Equivalent operator preconditioning for elliptic problems  

NASA Astrophysics Data System (ADS)

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

Axelsson, O.; Karátson, J.

2009-03-01

217

Involvement of SIRT1 in hypoxic down-regulation of c-Myc and ?-catenin and hypoxic preconditioning effect of polyphenols  

SciTech Connect

SIRT1 has been found to function as a Class III deacetylase that affects the acetylation status of histones and other important cellular nonhistone proteins involved in various cellular pathways including stress responses and apoptosis. In this study, we investigated the role of SIRT1 signaling in the hypoxic down-regulations of c-Myc and ?-catenin and hypoxic preconditioning effect of the red wine polyphenols such as piceatannol, myricetin, quercetin and resveratrol. We found that the expression of SIRT1 was significantly increased in hypoxia-exposed or hypoxic preconditioned HepG2 cells, which was closely associated with the up-regulation of HIF-1? and down-regulation of c-Myc and ?-catenin expression via deacetylation of these proteins. In addition, blockade of SIRT1 activation using siRNA or amurensin G, a new potent SIRT1 inhibitor, abolished hypoxia-induced HIF-1? expression but increased c-Myc and ?-catenin expression. SIRT1 was also found to stabilize HIF-1? protein and destabilize c-Myc, ?-catenin and PHD2 under hypoxia. We also found that myricetin, quercetin, piceatannol and resveratrol up-regulated HIF-1? and down-regulated c-Myc, PHD2 and ?-catenin expressions via SIRT1 activation, in a manner that mimics hypoxic preconditioning. This study provides new insights of the molecular mechanisms of hypoxic preconditioning and suggests that polyphenolic SIRT1 activators could be used to mimic hypoxic/ischemic preconditioning. -- Graphical abstract: Polyphenols mimicked hypoxic preconditioning by up-regulating HIF-1? and SIRT1 and down-regulating c-Myc, PHD2, and ?-catenin. HepG2 cells were pretreated with the indicated doses of myricetin (MYR; A), quercetin (QUR; B), or piceatannol (PIC; C) for 4 h and then exposed to hypoxia for 4 h. Levels of HIF-1?, SIRT1, c-Myc, ?-catenin, and PHD2 were determined by western blot analysis. The data are representative of three individual experiments. Highlights: ? SIRT1 expression is increased in hypoxia-exposed or hypoxic preconditioned cells. ? SIRT1 deacetylates c-Myc and ?-catenin ? HIF-1? is up-regulated by down-regulation of c-Myc and ?-catenin expression. ? Polyphenolic SIRT1 activators mimics hypoxic preconditioning.

Hong, Kyung-Soo [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Park, Jun-Ik [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of)] [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Mi-Ju; Kim, Hak-Bong; Lee, Jae-Won [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Dao, Trong Tuan; Oh, Won Keun [BK21 Project Team, College of Pharmacy, Chosun University, Gwangju (Korea, Republic of)] [BK21 Project Team, College of Pharmacy, Chosun University, Gwangju (Korea, Republic of); Kang, Chi-Dug, E-mail: kcdshbw@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of)] [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Sun-Hee, E-mail: ksh7738@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of) [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of)

2012-03-01

218

Pharmacological Induction of Ischemic Tolerance by Glutamate Transporter1 (EAAT2) Upregulation  

Microsoft Academic Search

Background and Purpose—Astrocytic glutamate transporter protein, GLT-1 (EAAT2), recovers extracellular glutamate and ensures that neurons are protected from excess stimulation. Recently, -lactam antibiotics, like ceftriaxone (CTX), were reported to induce the upregulation of GLT-1. Here, we investigated ischemic tolerance induction by CTX in an experimental model of focal cerebral ischemia. Methods—CTX (200 mg\\/kg per day, IP) was administered for 5

Kon Chu; Soon-Tae Lee; Dong-In Sinn; Song-Yi Ko; Eun-Hee Kim; Jeong-Min Kim; Se-Jeong Kim; Keun-Hwa Jung; Eun-Cheol Song; Sang Kun Lee; Manho Kim; Jae-Kyu Roh

2010-01-01

219

Role of protein kinase C in ischemic "conditioning": from first evidence to current perspectives.  

PubMed

Since the discovery of ischemic preconditioning (IPC) 26 years ago, numerous studies attempted to determine the mechanism of this powerful form of cardioprotection. One of the first proposed pathways of IPC suggested that the preconditioning stimulus activated phospholipase C via G-protein, and diacylglycerol released from phospholipid moieties activated protein kinase C (PKC) by translocating it from the cytosol to the sarcolemmal membranes. The major protective isoform of PKC was found to be the PKC-?. Despite some contradictions and controversies, today even the most skeptical opponents acknowledge that PKC plays a significant role in the mechanism of IPC. During recent years, both the role and the place of PKC-? in the mechanism of IPC have been revised. The current review presents the evolution of the "PKC theory" and summarizes the most recent data regarding the role of PKC in IPC. In addition to classical IPC, PKC appears to play a role in the mechanisms of newer conditioning protocols, that is, remote IPC and ischemic postconditioning. PMID:23872508

Simkhovich, Boris Z; Przyklenk, Karin; Kloner, Robert A

2013-11-01

220

IP-10 in autoimmune thyroiditis.  

PubMed

The interferon-?-inducible protein 10 (IP-10) was initially identified as a chemokine that is induced by interferon (IFN)-?. IP-10 exerts its function through binding to chemokine (C-X-C motif) receptor 3 (CXCR3). IP-10 and its receptor, CXCR3, appear to contribute to the pathogenesis of many autoimmune diseases, organ specific (such as type 1 diabetes, Graves' disease and ophthalmopathy), or systemic (such as systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren syndrome, or systemic sclerosis). The secretion of IP-10 by (CD)4+, CD8+, and natural killer is dependent on IFN-?. Under the influence of IFN-?, IP-10 is secreted by thyrocytes. Determination of high level of IP-10 in peripheral fluids is therefore a marker of a T helper 1 orientated immune response. High levels of circulating IP-10, have been shown in patients with autoimmune thyroiditis (AT). Among patients with AT, IP-10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern, which is a sign of a more severe lympho-monocytic infiltration, and in those with hypothyroidism. For these reasons, it has been postulated that IP-10 could be a marker of a stronger and more aggressive inflammatory response in the thyroid, subsequently leading to thyroid destruction and hypothyroidism. Further studies are needed to investigate whether IP-10 is a novel therapeutic target in AT. PMID:24977661

Ruffilli, I; Ferrari, S M; Colaci, M; Ferri, C; Fallahi, P; Antonelli, A

2014-08-01

221

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

222

Mitochondria: The Missing Link Between Preconditioning and Neuroprotection  

PubMed Central

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

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

2010-01-01

223

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

224

Simple characterizations for commutativity of quantum weakest preconditions  

E-print Network

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

T. Lin

2013-12-02

225

Maneesh Bakshi The paper discusses the implementation of Voice over IP (VoIP) and IP Multimedia Subsystem services (IMS)  

E-print Network

Maneesh Bakshi The paper discusses the implementation of Voice over IP (VoIP) and IP Multimedia addressed are : Introduction to the working of VoIP and multimedia transmission over wireless, and the impact of these developments on the existing Telecom and Satellite/CableTV industry. Keywords - WiMAX, VoIP

Jain, Raj

226

iPS cell sheets created by a novel magnetite tissue engineering method for reparative angiogenesis  

PubMed Central

Angiogenic cell therapy represents a novel strategy for ischemic diseases, but some patients show poor responses. We investigated the therapeutic potential of an induced pluripotent stem (iPS) cell sheet created by a novel magnetite tissue engineering technology (Mag-TE) for reparative angiogenesis. Mouse iPS cell-derived Flk-1+ cells were incubated with magnetic nanoparticle-containing liposomes (MCLs). MCL-labeled Flk-1+ cells were mixed with diluted extracellular matrix (ECM) precursor and a magnet was placed on the reverse side. Magnetized Flk-1+ cells formed multi-layered cell sheets according to magnetic force. Implantation of the Flk-1+ cell sheet accelerated revascularization of ischemic hindlimbs relative to the contralateral limbs in nude mice as measured by laser Doppler blood flow and capillary density analyses. The Flk-1+ cell sheet also increased the expressions of VEGF and bFGF in ischemic tissue. iPS cell-derived Flk-1+ cell sheets created by this novel Mag-TE method represent a promising new modality for therapeutic angiogenesis. PMID:23475393

Kito, Tetsutaro; Shibata, Rei; Ishii, Masakazu; Suzuki, Hirohiko; Himeno, Tatsuhito; Kataoka, Yoshiyuki; Yamamura, Yumiko; Yamamoto, Takashi; Nishio, Naomi; Ito, Sachiko; Numaguchi, Yasushi; Tanigawa, Tohru; Yamashita, Jun K.; Ouchi, Noriyuki; Honda, Hiroyuki; Isobe, Kenichi; Murohara, Toyoaki

2013-01-01

227

Ischemic penumbra in acute stroke: Demonstration by PET with fluorine-18 fluoromisonidazole  

SciTech Connect

Ischemic penumbra (IP) in acute stroke has gained clinical interest since tissue functions may be recovered if perfusion can be reestablished. However, such therapeutic intervention is {open_quotes}blind{close_quotes} since clinical examination can not distinguish IP from developing infarction. In vivo demonstration of IP may have significance for stroke patient management. This study was a preliminary evaluation of detecting IP in vivo by F-18 fluoromisonidazole ([F-18]-FMISO), a hypoxic imaging agent. Static PET imaging was performed after IV injection of 370 MBq of [F-18]-FMISO at 20 and 120 min. Tomograms were reconstructed and evaluated visually in correlation with CT or MR scans. In acute stroke, patients (pts) were called back for the second PET study one month after the initial study. CT was used for confirming infarction. In 6 pts with acute cerebral infarction, three of them had intense [F-18]-FMISO retention in the penumbra surrounding the central, eclipse-like zone of absent radio-activity (infarction) at 2 hr in the acute state, and the penumbra disappeared in association with increased area of infarction on CT in one case in the chronic state. In five pts with chronic infarction, all had no penumbra of [F-18]-FMISO retention. In summary, our preliminary results demonstrate the feasibility of using [F-18]-FMISO PET to detect ischemic penumbra in vivo.

Yeh, S.H.; Liu, R.S.; Hu, H.H. [National Yang-Ming Medical College (Taiwan, Province of China)] [and others

1994-05-01

228

Progress in Parallel Schur Complement Preconditioning for Computational Fluid Dynamics  

NASA Technical Reports Server (NTRS)

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

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

1997-01-01

229

Pharmacological preconditioning to improve outcome in free tissue transfer   

E-print Network

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

Edmunds, Marie-Claire

2013-11-29

230

Behavioral/Systems/Cognitive Octopamine Mediates Thermal Preconditioning of the  

E-print Network

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

Robertson, Meldrum

231

40 CFR 1065.516 - Sample system decontamination and preconditioning.  

Code of Federal Regulations, 2014 CFR

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

2014-07-01

232

Hash-based IP traceback  

Microsoft Academic Search

The design of the IP protocol makes it difficult to reliably identify the originator of an IP packet. Even in the absence of any deliberate attempt to disguise a packet's origin, wide-spread packet forwarding techniques such as NAT and encapsulation may obscure the packet's true source. Techniques have been developed to determine the source of large packet flows, but, to

Alex C. Snoeren; Craig Partridge; Luis A. Sanchez; Christine E. Jones; Fabrice Tchakountio; Stephen T. Kent; W. Timothy Strayer

2001-01-01

233

Single-packet IP traceback  

Microsoft Academic Search

The design of the IP protocol makes it difficult to reliably identify the originator of an IP packet. Even in the absence of any deliberate attempt to disguise a packet's origin, widespread packet forwarding techniques such as NAT and encapsulation may obscure the packet's true source. Techniques have been developed to determine the source of large packet flows, but, to

Alex C. Snoeren; Craig Partridge; Luis A. Sanchez; Christine E. Jones; Fabrice Tchakountio; Beverly Schwartz; Stephen T. Kent; W. Timothy Strayer

2002-01-01

234

IP Addresses in Email Clients  

Microsoft Academic Search

Abstract. IP addresses are an important tool for fighting spam, used for safe lists, blackhole lists, anti-spoofing and related purposes. While it is trivial to find the sender's IP address in most email server software, it turns out to be surprisingly di cult to do so in email client software: we explain why. This implies that either alternative approaches are

Joshua Goodman

2004-01-01

235

Voice Over IP Reference Page  

NSDL National Science Digital Library

This site is a collection of architectural specifications, network and signaling protocols, and technical papers related to virtually every aspect of VoIP. Detailed articles and standards information are regularly updated on the site. There is also a collection of documents containing VoIP references, and in this sections, visitors will find an H.323 tutorial.

236

1 Introduction Voice over IP (VoIP) systems are gaining in popularity as the  

E-print Network

1 Introduction Voice over IP (VoIP) systems are gaining in popularity as the technology for transmitting voice traffic over IP networks. Along with the anticipated widespread adoption of VoIP systems by the architecture of VoIP systems. VoIP applications have soft real time requirements. Second, the attacks can span

Bagchi, Saurabh

237

Myocardial ischemic reperfusion induces de novo Nrf2 protein translation.  

PubMed

Nrf2 is a bZIP transcription factor regulating the expression of antioxidant and detoxification genes. We have found that Nrf2 knockout mice have an increased infarction size in response to regional ischemic reperfusion and have a reduced degree of cardiac protection by means of ischemic preconditioning. With cycles of brief ischemia and reperfusion (5'I/5'R) that induce cardiac protection in wild type mice, an elevated Nrf2 protein was observed without prior increases of Nrf2 mRNA. When an mRNA species is being translated into a protein, it is occupied by multiple ribosomes. The level of ribosome-associated Nrf2 mRNA increased following cycles of 5'I/5'R, supporting de novo Nrf2 protein translation. A dicistronic reporter assay indicated a role of the 5' untranslated region (5' UTR) of Nrf2 mRNA in oxidative stress induced Nrf2 protein translation in isolated cardiomyocytes. Western blot analyses after isolation of proteins binding to biotinylated Nrf2 5' UTR from the myocardium or cultured cardiomyocytes demonstrated that cycles of 5'I/5'R or oxidants caused an increased association of La protein with Nrf2 5' UTR. Ribonucleoprotein complex immunoprecipitation assays confirmed such association indeed occurring in vivo. Knocking down La using siRNA was able to prevent Nrf2 protein elevation by oxidants in cultured cardiomyocytes and by cycles of 5'I/5'R in the myocardium. Our data point out a novel mechanism of cardiac protection by de novo Nrf2 protein translation involving interaction of La protein with 5' UTR of Nrf2 mRNA in cardiomyocytes. PMID:24915518

Xu, Beibei; Zhang, Jack; Strom, Joshua; Lee, Sang; Chen, Qin M

2014-09-01

238

Transient ischemic attack induced by melted solid lipid microparticles protects rat brains from permanent focal ischemia.  

PubMed

This study aims to develop a transient ischemic attack (TIA) model in conscious animals and uses this model to investigate the effect of TIA on subsequent permanent ischemia. TIA was induced by injecting designed temperature-sensitive melted solid lipid microparticles with a melting point around body temperature into male Wistar rats via arterial cannulation. Neurologic deficit was monitored immediately after the injection without anesthesia. According to the clinical definition of TIA, rats were divided into neurologic symptom durations <24-h, 24-48-h and ?48-h groups. The lipid microparticle-induced infarct volumes were small in the <24-h and 24-48-h groups, while the volumes were five times larger in the ?48-h group. Permanent ischemic stroke was induced 3d after the induction of TIA by injecting a different kind of embolic particle manufactured by blending chitin and PLGA. The <24-h group had less severe neurologic deficits and smaller infarct volumes than that of 24-48-h and control (without prior lipid microparticle treatment) rats. Taken together, we successfully develop a TIA animal model which allows us to monitor the neurologic deficit in real-time. By adopting this model, we validate that TIA (<24h) preconditioning protects the brain from subsequent permanent ischemic stroke. PMID:24937754

Tsai, M-J; Kuo, Y-M; Tsai, Y-H

2014-09-01

239

A Weakest Precondition Approach to Robustness  

NASA Astrophysics Data System (ADS)

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

Balliu, Musard; Mastroeni, Isabella

240

Reduction in postsystolic wall thickening during late preconditioning.  

PubMed

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

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

2007-01-01

241

Fetal asphyctic preconditioning alters the transcriptional response to perinatal asphyxia  

PubMed Central

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

2014-01-01

242

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

PubMed

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

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

2014-01-01

243

Hyperbaric oxygen preconditioning attenuates hemorrhagic transformation through increasing PPAR? in hyperglycemic MCAO rats.  

PubMed

Hyperbaric oxygen preconditioning (HBO-PC) has been demonstrated to attenuate hemorrhagic transformation (HT) after middle cerebral artery occlusion (MCAO) in hyperglycemic rats. However, the mechanisms remain to be illustrated. Recently, HBO-PC has been shown to activate peroxisome proliferator-activated receptor-gamma (PPAR?) by increasing 15d-PGJ2 in primary cultured neurons. We hypothesize that HBO-PC reduces HT by suppressing inflammation through increasing 15d-PGJ2 and activating PPAR? in hyperglycemic MCAO rats. HBO (2.5ATA) was administered for 1h daily for 5 consecutive days. The PPAR? inhibitor GW9662 was administered intraperitoneally to designated animals. Infarction volume, hemorrhage volume, neurological scores and mortality were analyzed. The levels of 15d-PGJ2, PPAR?, TNF-? and IL-1?, tight junction proteins as well as the activity of MMP-2 and MMP-9 were evaluated 24h after MCAO. HBO-PC reduced HT, improved neurological function, down-regulated inflammatory molecules and inhibited the activation of MMP-9 by increasing 15d-PGJ2 and PPAR? at 24h after MCAO. The results suggested that HBO-PC might be an alternative measure to decrease HT in ischemic stroke. PMID:25542160

Bian, Hetao; Hu, Qin; Liang, Xiping; Chen, Di; Li, Bo; Tang, Jiping; Zhang, John H

2015-03-01

244

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

PubMed Central

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

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

2012-01-01

245

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

246

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats.  

PubMed

Hyperglycemia dramatically aggravates brain infarct and hemorrhagic transformation (HT) after ischemic stroke. Oxidative stress and matrix metalloproteinases (MMPs) play an important role in the pathophysiology of HT. Hyperbaric oxygen preconditioning (HBO-PC) has been proved to decrease oxidative stress and has been demonstrated to be neuroprotective in experimental stroke models. The present study determined whether HBO-PC would ameliorate HT by a pre-ischemic increase of reactive oxygen species (ROS) generation, and a suppression of MMP-2 and MMP-9 in hyperglycemic middle cerebral artery occlusion (MCAO) rats. Rats were pretreated with HBO (100% O?, 2.5 atmosphere absolutes) 1 h daily for 5 days before MCAO. Acute hyperglycemia was induced by an injection of 50% dextrose. Neurological deficits, infarction volume and hemorrhagic volume were assessed 24 h and 7 days after ischemia. ROS scavenger n-acetyl cysteine (NAC), hypoxia-inducible factor-1? (HIF-1?), inhibitor 2-methoxyestradiol (2ME2) and activator cobalt chloride (CoCl?), and MMP inhibitor SB-3CT were administrated for mechanism study. The activity of MMP-2 and MMP-9, and the expression HIF-1? were measured. HBO-PC improved neurological deficits, and reduced hemorrhagic volume; the expression of HIF-1? was significantly decreased, and the activity of MMP-2 and MMP-9 was reduced by HBO-PC compared with vehicle group. Our results suggested that HBO-PC attenuated HT via decreasing HIF-1? and its downstream MMP-2 and MMP-9 in hyperglycemic MCAO rats. PMID:23537951

Soejima, Yoshiteru; Hu, Qin; Krafft, Paul R; Fujii, Mutsumi; Tang, Jiping; Zhang, John H

2013-09-01

247

Nanoparticle Pre-Conditioning for Enhanced Thermal Therapies in Cancer  

PubMed Central

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

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

2011-01-01

248

Fast curve estimation using preconditioned generalized Radon transform.  

PubMed

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

Hansen, K V; Toft, P A

1996-01-01

249

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

250

Soluble Thrombomodulin Protects Ischemic Kidneys  

PubMed Central

Altered coagulation and inflammation contribute to the pathogenesis of ischemic renal injury. Thrombomodulin is a necessary factor in the anticoagulant protein C pathway and has inherent anti-inflammatory properties. We studied the effect of soluble thrombomodulin (sTM) in a hypoperfusion model of ischemic kidney injury. To markedly reduce infrarenal aortic blood flow and femoral arterial pressures, we clamped the suprarenal aorta of rats, occluding them 90%, for 60 min. Reversible acute kidney injury (AKI) occurred at 24 h in rats subjected to hypoperfusion. Histologic analysis at 24 h revealed acute tubular necrosis (ATN), and intravital two-photon microscopy showed flow abnormalities in the microvasculature and defects of endothelial permeability. Pretreatment with rat sTM markedly reduced both I-R-induced renal dysfunction and tubular histologic injury scores. sTM also significantly improved microvascular erythrocyte flow rates, reduced microvascular endothelial leukocyte rolling and attachment, and minimized endothelial permeability to infused fluorescence dextrans, assessed by intravital quantitative multiphoton microscopy. Furthermore, sTM administered 2 h after reperfusion protected against ischemia-induced renal dysfunction at 24 h and improved survival. By using an sTM variant, we also determined that the protective effects of sTM were independent of its ability to generate activated protein C. These data suggest that sTM may have therapeutic potential for ischemic AKI. PMID:19176699

Sharfuddin, Asif A.; Sandoval, Ruben M.; Berg, David T.; McDougal, Grant E.; Campos, Silvia B.; Phillips, Carrie L.; Jones, Bryan E.; Gupta, Akanksha; Grinnell, Brian W.; Molitoris, Bruce A.

2009-01-01

251

IP Version 6, Online Version  

NSDL National Science Digital Library

This page offers five videos of lectures from Sam Bowne's IP Version 6 course. Each video varies in length from ten minutes to an hour. These materials would be most useful for individuals with some experience with IP technology; the end goal of the course was for individuals enrolled to gain IPv6 certification and be able to set up IPv6 on a router. Flash is required to view the videos.

Bowne, Sam

252

IP Reassembly The ip_local_deliver() function, defined in net/ipv4/ip_input.c, is called by ip_rcv_finish.(). Its  

E-print Network

_HOOK() call specifying the NF_IP_LOCAL_IN chain. 269 if (skb->nh.iph->frag_off & htons: A timer used for cleaning up an old incomplete fragments queue. 4 #12;The variable, ip_frag_mem, is used/ip_fragment.c and initialized to 0. /* Memory used for fragments */ 130 atomic_t ip_frag

Westall, James M.

253

IP routing issues in satellite constellation networks  

Microsoft Academic Search

SUMMARY The growth in use of Internet-based applications in recent years has led to telecommunication networks transporting an increasingly large amount of Internet Protocol (IP)-based traffic. Proposed broadband satellite constellation networks, currently under development, will be required to transport IP traffic. A case can be made for implementing IP routing directly within the constellation network, in order to transport IP

L. Wood; A. Clerget; I. Andrikopoulos; G. Pavlou; W. Dabbous

2001-01-01

254

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

Code of Federal Regulations, 2010 CFR

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

2010-07-01

255

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

Code of Federal Regulations, 2011 CFR

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

2011-07-01

256

40 CFR 85.2218 - Preconditioned idle test-EPA 91.  

Code of Federal Regulations, 2011 CFR

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

2011-07-01

257

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

Code of Federal Regulations, 2011 CFR

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

2011-07-01

258

On adaptive weighted polynomial preconditioning for Hermitian positive definite matrices  

NASA Technical Reports Server (NTRS)

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

Fischer, Bernd; Freund, Roland W.

1992-01-01

259

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

260

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

NASA Technical Reports Server (NTRS)

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

Wong, G. S.

1973-01-01

261

Voix sur IP Julien Vey Gil Noirot  

E-print Network

L'architecture VoIP Les protocoles Les limites de la VoIP Ce dont nous n'allons pas parler Le fonctionnement détaillé du RTC Le traitement du signal JulienVey - Gil Noirot 2VoIP Introduction #12;Introduction au RTC Les enjeux de la VoIP L'architecture VoIP Les protocoles de communication Les protocoles de

Perronnin, Florence

262

Performance of VoIP on HSDPA  

Microsoft Academic Search

This paper provides packet scheduler design and performance simulations for running VoIP services over high-speed downlink packet access (HSDPA) in WCDMA. The main challenge of supporting VoIP service on HSDPA is the tight delay requirement combined with the small VoIP packet size. A packet scheduler design incorporating VoIP packet aggregation and user multiplexing is proposed and the VoIP capacity is

Bang Wang; Klaus I. Pedersen; Troels E. Kolding; Preben E. Mogensen

2005-01-01

263

Voice over IP Measurements Radu Dudici Ruscior  

E-print Network

problems for a future installation of a VoIP system and to troubleshoot existing VoIP systems. The tool is structured in 7 sections. Section 1 presents the general problem of QoS in a VoIP system and shows a possible, and some VoIP termi- nology. Keywords VoIP, Packets, Round Trip Delay, H.323, Jitter, Network, Measure

264

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

265

Inflammation in the pathogenesis of ischemic stroke.  

PubMed

Ischemic stroke is a common cause of permanent disability in adults worldwide. Inflammation plays a significant role in the pathogenesis of ischemic stroke and its mechanism is complex. Both pro-inflammatory and anti-inflammatory mediators are involved in the pathogenesis of ischemic stroke, an imbalance of which leads to inflammation. Inflammatory cells from both the innate and acquired immune systems are involved in ischemic stroke-related inflammation; processes that are linked by the action of interleukin-17A (IL-17A). Although most inflammatory cells promote inflammation, T regulatory cells (Tregs) may have a protective function at the early stages of an ischemic injury, but a negative role during later stages. However, the precise mechanism of inflammation in ischemic stroke remains elusive; further understanding of it may provide new ideas for the prevention and treatment of ischemic stroke. In this review, we discuss the role of pro-inflammatory and anti-inflammatory mediators and related immune cells in the pathogenesis of ischemic stroke. PMID:25553478

Pei, Jian; You, Xiaoxin; Fu, Qinghui

2015-01-01

266

Preconditioning Eigenvalues and Some Comparison of Ronald B. Morgan  

E-print Network

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

Morgan, Ron

267

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

E-print Network

that their solution constitutes a challenging test for nonlinear elliptic solvers. The flame sheet model adds only onePreconditioned Multigrid Simulation of an Axisymmetric Laminar Diffusion Flame \\Lambda Samir Karaa of an elliptic flame sheet problem. By selecting the generalized minimum residual method as the linear smoother

Zhang, Jun

268

Preconditioning Indefinite Systems in Interior Point Methods for Optimization  

Microsoft Academic Search

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

Luca Bergamaschi; Jacek Gondzio; Giovanni Zilli

2004-01-01

269

Preconditioning with cobalt chloride modifies pain perception in mice  

PubMed Central

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

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

2015-01-01

270

Dexmedetomidine Preconditioning Attenuates Cisplatin-Induced Ototoxicity in Zebrafish  

PubMed Central

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

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

2014-01-01

271

Modern Preconditioned Eigensolvers for Spectral Image Segmentation and Graph Bisection  

E-print Network

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

Knyazev, Andrew

272

Learning Controller Preconditions for Physics-Based Character Animation  

E-print Network

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

Faloutsos, Petros

273

Cisco 7900 Series IP Phone Cisco 7900 Series IP Phone  

E-print Network

a party from a Conference 13. Idivert 14. Call Forward All 15. Call Park 16. Cisco Call Manager Web Page Unanswered Call Green (Steady) = Connected Call Green (Flashing) = Call on Hold Red (Steady) = Coverage line;Cisco 7900 Series IP Phone Speaker Key (Green when activated) The Speaker is located under the "Handset

274

IP Layer Transmission Functions The ip_build_xmit() function  

E-print Network

to be used and the flags from the msg structure. When called by UDP the frag pointer is set to point(const void*, char*, unsigned int, unsigned int), const void *frag, unsigned length, struct ipcm_cookie *ipc. */ 654 if (length > rt->u.dst.pmtu || ipc->opt != NULL) 655 return ip_build_xmit_slow(sk,getfrag,frag

Westall, James M.

275

Continuously Connected With Mobile IP  

NASA Technical Reports Server (NTRS)

Cisco Systems developed Cisco Mobile Networks, making IP devices mobile. With this innovation, a Cisco router and its connected IP devices can roam across network boundaries and connection types. Because a mobile user is able to keep the same IP address while roaming, a live IP connection can be maintained without interruption. Glenn Research Center jointly tested the technology with Cisco, and is working to use it on low-earth-orbiting research craft. With Cisco's Mobile Networks functionality now available in Cisco IOS Software release 12.2(4)T, the commercial advantages and benefits are numerous. The technology can be applied to public safety, military/homeland security, emergency management services, railroad and shipping systems, and the automotive industry. It will allow ambulances, police, firemen, and the U.S. Coast Guard to stay connected to their networks while on the move. In the wireless battlefield, the technology will provide rapid infrastructure deployment for U.S. national defense. Airline, train, and cruise passengers utilizing Cisco Mobile Networks can fly all around the world with a continuous Internet connection. Cisco IOS(R) Software is a registered trademark of Cisco Systems.

2002-01-01

276

IP Address Passing for VANETs  

Microsoft Academic Search

In Vehicular Ad-hoc Networks (VANETs), vehicles can gain short connections to the Internet by using wireless ac- cess points (AP). A significant part of the connection time is the time required for acquiring an IP address via Dynamic Host Configuration Protocol (DHCP). Depending on a ve- hicle's speed and the AP coverage area, DHCP can con- sume up to 100

Todd Arnold; Wyatt Lloyd; Jing Zhao; Guohong Cao

2008-01-01

277

Yeasts from ips sexdentatus (scolytidae)  

Microsoft Academic Search

Yeasts from the digestive tract of Ips sexdentatus were isolated. Four strains, representing the different identified yeast species, were chosen. Their enzymatic activity on oligosaccharides, heterosides and polysaccharides was measured. Moreover, we showed that they excrete some B group vitamins which are necessary for the insect, unable to synthesize them.

Marie-Claire Pignal; C. Chararas; Michèle Bourgeay-Causse

1988-01-01

278

Erythropoietin: Powerful Protection of Ischemic and Post-Ischemic Brain  

PubMed Central

Ischemic brain injury inflicted by stroke and cardiac arrest ranks among the leading causes of death and long-term disability in the United States. The brain consumes large amounts of metabolic substrates and oxygen to sustain its energy requirements. Consequently, the brain is exquisitely sensitive to interruptions in its blood supply, and suffers irreversible damage after 10–15 minutes of severe ischemia. Effective treatments to protect the brain from stroke and cardiac arrest have proven elusive, due to the complexities of the injury cascades ignited by ischemia and reperfusion. Although recombinant tissue plasminogen activator and therapeutic hypothermia have proven efficacious for stroke and cardiac arrest, respectively, these treatments are constrained by narrow therapeutic windows, potentially detrimental side effects and the limited availability of hypothermia equipment. Mounting evidence demonstrates the cytokine hormone erythropoietin (EPO) to be a powerful neuroprotective agent and a potential adjuvant to established therapies. Classically, EPO originating primarily in the kidneys promotes erythrocyte production by suppressing apoptosis of proerythroid progenitors in bone marrow. However, the brain is capable of producing EPO, and EPO’s membrane receptors and signaling components also are expressed in neurons and astrocytes. EPO activates signaling cascades that increase the brain’s resistance to ischemia-reperfusion stress by stabilizing mitochondrial membranes, limiting formation of reactive oxygen and nitrogen intermediates, and suppressing pro-inflammatory cytokine production and neutrophil infiltration. Collectively, these mechanisms preserve functional brain tissue and, thus, improve neurocognitive recovery from brain ischemia. This article reviews the mechanisms mediating EPO-induced brain protection, critiques the clinical utility of exogenous EPO to preserve brain threatened by ischemic stroke and cardiac arrest, and discusses the prospects for induction of EPO production within the brain by the intermediary metabolite, pyruvate. PMID:24595981

Nguyen, Anh Q.; Cherry, Brandon H.; Scott, Gary F.; Ryou, Myoung-Gwi; Mallet, Robert T.

2015-01-01

279

Villains and Voice Over IP Heather Bonin  

E-print Network

......................................................................................................................... 3 How VOIP Works............................................................................................... 3 VoIP: The New Baby on the Block......................................................................................................................... 13 #12;3 Introduction Vonage, Skype, Verizon, SpeakEasy, Yak, 3Com. The list of VoIP (Voice Over

280

Detecting Spam in VoIP Networks  

Microsoft Academic Search

Voice over IP (VoIP) is a key enabling technology for the migration of circuit-switched PSTN architectures to packet- based networks. The problem of spam in VoIP networks has to be solved in real time compared to e-mail systems. Many of the techniques devised for e-mail spam detection rely upon content analysis and in the case of VoIP it is too

Ram Dantu; Prakash Kolan

2005-01-01

281

IP 3 receptors: the search for structure  

Microsoft Academic Search

Inositol (1,4,5)-trisphosphate receptors (IP3R) are intracellular Ca2+ channels that are regulated by Ca2+ and IP3, and are modulated by many additional signals. They thereby allow both receptors that stimulate IP3 formation and Ca2+ to control release of Ca2+ from intracellular stores. IP3Rs share many features with their close relatives, ryanodine receptors; each provides insight into the structure and function of

Colin W. Taylor; Paula C. A. da Fonseca; Edward P. Morris

2004-01-01

282

Adenosine kinase determines the degree of brain injury after ischemic stroke in mice.  

PubMed

Adenosine kinase (ADK) is the major negative metabolic regulator of the endogenous neuroprotectant and homeostatic bioenergetic network regulator adenosine. We used three independent experimental approaches to determine the role of ADK as a molecular target for predicting the brain's susceptibility to ischemic stroke. First, when subjected to a middle cerebral artery occlusion model of focal cerebral ischemia, transgenic fb-Adk-def mice, which have increased ADK expression in striatum (164%) and reduced ADK expression in cortical forebrain (65%), demonstrate increased striatal infarct volume (126%) but almost complete protection of cortex (27%) compared with wild-type (WT) controls, indicating that cerebral injury levels directly correlate to levels of ADK in the CNS. Second, we demonstrate abrogation of lipopolysaccharide (LPS)-induced ischemic preconditioning in transgenic mice with brain-wide ADK overexpression (Adk-tg), indicating that ADK activity negatively regulates LPS-induced tolerance to stroke. Third, using adeno-associated virus-based vectors that carry Adk-sense or -antisense constructs to overexpress or knockdown ADK in vivo, we demonstrate increased (126%) or decreased (51%) infarct volume, respectively, 4 weeks after injection into the striatum of WT mice. Together, our data define ADK as a possible therapeutic target for modulating the degree of stroke-induced brain injury. PMID:21427729

Shen, Hai-Ying; Lusardi, Theresa A; Williams-Karnesky, Rebecca L; Lan, Jing-Quan; Poulsen, David J; Boison, Detlev

2011-07-01

283

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?ischemic hemisphere, RHP increased B cell representation by attenuating the diapedesis of monocyte, macrophage, neutrophil and T cells, to quantities indistinguishable from the uninjured, contralateral hemisphere. Pre-stroke splenic B cells isolated from RHP-treated mice had >1,900 genes differentially expressed by microarray analysis. Genes related to B-T cell interactions, including antigen presentation, B cell differentiation and antibody production, were profoundly downregulated. Maturation and activation were arrested in a cohort of B cells from pre-stroke RHP-treated mice while regulatory B cells, a subset implicated in neurovascular protection from stroke, were upregulated. Conclusions Collectively, our data characterize an endogenous neuroprotective phenotype that utilizes adaptive immune mechanisms pre-stroke to protect the brain from injury post-stroke. Future studies to validate the role of B cells in minimizing injury and promoting central nervous system recovery, and to determine whether B cells mediate an adaptive immunity to systemic hypoxia that protects from subsequent stroke, are needed. PMID:24485041

2014-01-01

284

Growth factors in ischemic stroke  

PubMed Central

Abstract Data from pre-clinical and clinical studies provide evidence that colony-stimulating factors (CSFs) and other growth factors (GFs) can improve stroke outcome by reducing stroke damage through their anti-apoptotic and anti-inflammatory effects, and by promoting angiogenesis and neurogenesis. This review provides a critical and up-to-date literature review on CSF use in stroke. We searched for experimental and clinical studies on haemopoietic GFs such as granulocyte CSF, erythropoietin, granulocyte-macrophage colony-stimulating factor, stem cell factor (SCF), vascular endothelial GF, stromal cell-derived factor-1? and SCF in ischemic stroke. We also considered studies on insulin-like growth factor-1 and neurotrophins. Despite promising results from animal models, the lack of data in human beings hampers efficacy assessments of GFs on stroke outcome. We provide a comprehensive and critical view of the present knowledge about GFs and stroke, and an overview of ongoing and future prospects. PMID:20015202

Lanfranconi, S; Locatelli, F; Corti, S; Candelise, L; Comi, G P; Baron, P L; Strazzer, S; Bresolin, N; Bersano, A

2011-01-01

285

RESEARCH & INNOVATION OFFICE EASY ACCESS IP  

E-print Network

for free to those who can develop it and put it to use. In return for a free license to UTS Easy Access IP on the development of the Easy Access IP agree that if the IP is not exploited within three years, the licence regardless of how successful the end product is You gain easy access to cutting edge science, technology

University of Technology, Sydney

286

CISCO IP 7905-7912 FONCTIONS TLPHONIQUES  

E-print Network

CISCO IP 7905-7912 FONCTIONS T�L�PHONIQUES FONCTIONS DE BASE FAIRE UN APPEL · Soulever le combiné numéros erronés. Cisco_IP_7905_7912_Fr_CUCM_V7.0_20090320[1].doc 1 de 6 #12;CISCO IP 7905-7912 FONCTIONS

Charette, André

287

CISCO IP 7906/7911 FONCTIONS TLPHONIQUES  

E-print Network

CISCO IP 7906/7911 FONCTIONS T�L�PHONIQUES FONCTIONS DE BASE FAIRE UN APPEL · Soulever le combiné sur la touche Cisco_IP_7906_7911_Fr_CUCM_V7.0_20090320[1].doc 1 de 6 #12;CISCO IP 7906/7911 FONCTIONS T�L�PHONIQUES CONF�RENCE LISTE Lorsque vous êtes en appel

Charette, André

288

Cisco IP 7935/7936 FONCTIONS TLPHONIQUES  

E-print Network

Cisco IP 7935/7936 FONCTIONS T�L�PHONIQUES Légende des touches de fonctions 1 Modèle de l surbrillance dans le menu. 6 Touches interactives Permet de sélectionner les touches interactives. #12;Cisco IP la sonnerie et le contraste. #12;Cisco IP 7935/7936 FONCTIONS T�L�PHONIQUES Légende des touches

Charette, André

289

VoIP in a Campus Environment  

ERIC Educational Resources Information Center

Internet Protocol (IP) Telephony, or voice-over IP (VoIP), has proved to be a wise decision for many organizations. This technology crosses the boundaries of public and private networks, enterprise and residential markets, voice and data technologies, as well as local and long-distance services. The convergence of voice and data into a single,…

Young, Dan

2005-01-01

290

Strategies for Study of Neuroprotection from Cold-preconditioning  

PubMed Central

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

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

2010-01-01

291

Prevention of ischemic stroke: surgery.  

PubMed

The last 15 years have witnessed a resurgence of the role of surgical options for prevention of ischemic stroke. The landmark randomized trials including NASCET and ECST were published and explored the role of carotid endarterectomy in this regard. Patients with high grade stenosis of the internal carotid artery (> or = 70%) with prior TIA or minor non disabling stroke in the same territory were shown to have significant benefit of the procedure compared to best medical treatment. Benefit was comparatively less in patients with moderate grade stenosis of the ICA (50-69%). Surgical treatment of patients with <50% stenosis of the ICA resulted in worse outcomes compared to medical therapy and is consequently not recommended. These studies also standardized the method for measuring the degree of ICA stenosis. The ACAS and ACST studies attempted to resolve the rather vexing issue of surgical treatment of patients with asymptomatic ICA stenosis. The risk benefit ratio in asymptomatic patients is low and depends to a large extent on a low perioperative complication rate. Studies have also attempted to identify the best medical treatment in the perioperative period during CEA. Low dose aspirin has been shown to be beneficial, but the role of statins and betablockers is promising but yet uncertain. Ischemic stroke is a common complication after CABG. In this regard surgeons have differed in their approaches to performing CEA, some preferring to do it during the bypass surgery, while others prefer a two staged procedure. The surgical treatment of complete carotid occlusion by EC-IC bypass surgery has also enjoyed renewed interest and results of the COSS study are awaited keenly. The EC-IC bypass surgical procedure is also beneficial in moya-moya disease. PMID:17630940

Rajamani, Kumar; Chaturvedi, Seemant

2007-07-01

292

Shape reanalysis and sensitivities utilizing preconditioned iterative boundary solvers  

NASA Technical Reports Server (NTRS)

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

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

1992-01-01

293

Mobile-ip Aeronautical Network Simulation Study  

NASA Technical Reports Server (NTRS)

NASA is interested in applying mobile Internet protocol (mobile-ip) technologies to its space and aeronautics programs. In particular, mobile-ip will play a major role in the Advanced Aeronautic Transportation Technology (AATT), the Weather Information Communication (WINCOMM), and the Small Aircraft Transportation System (SATS) aeronautics programs. This report presents the results of a simulation study of mobile-ip for an aeronautical network. The study was performed to determine the performance of the transmission control protocol (TCP) in a mobile-ip environment and to gain an understanding of how long delays, handoffs, and noisy channels affect mobile-ip performance.

Ivancic, William D.; Tran, Diepchi T.

2001-01-01

294

Neuroprotective Mechanisms of Taurine against Ischemic Stroke  

PubMed Central

Ischemic stroke exhibits a multiplicity of pathophysiological mechanisms. To address the diverse pathophysiological mechanisms observed in ischemic stroke investigators seek to find therapeutic strategies that are multifaceted in their action by either investigating multipotential compounds or by using a combination of compounds. Taurine, an endogenous amino acid, exhibits a plethora of physiological functions. It exhibits antioxidative properties, stabilizes membrane, functions as an osmoregulator, modulates ionic movements, reduces the level of pro-inflammators, regulates intracellular calcium concentration; all of which contributes to its neuroprotective effect. Data are accumulating that show the neuroprotective mechanisms of taurine against stroke pathophysiology. In this review, we describe the neuroprotective mechanisms employed by taurine against ischemic stroke and its use in clinical trial for ischemic stroke. PMID:24961429

Menzie, Janet; Prentice, Howard; Wu, Jang-Yen

2013-01-01

295

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

PubMed

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

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

2015-04-01

296

Can preconditioning reduce laparoscopy-induced tissue injury?  

Microsoft Academic Search

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

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

2003-01-01

297

Exercise and Cardiac Preconditioning Against Ischemia Reperfusion Injury  

PubMed Central

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

Quindry, John C; Hamilton, Karyn L

2013-01-01

298

Preconditioning effects of intermittent stream flow on leaf litter decomposition  

Microsoft Academic Search

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

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

299

Preconditioned Alternating Projection Algorithms for Maximum a Posteriori ECT Reconstruction  

PubMed Central

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

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

2012-01-01

300

Effect of preconditioning unconditioned stimulus experience on learned taste aversions  

Microsoft Academic Search

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

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

1975-01-01

301

Chemogenetic Silencing of Neurons in Retrosplenial Cortex Disrupts Sensory Preconditioning  

PubMed Central

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

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

2014-01-01

302

The Spacelab IPS Star Simulator  

NASA Technical Reports Server (NTRS)

The cost of doing business in space is very high. If errors occur while in orbit the costs grow and desired scientific data may be corrupted or even lost. The Spacelab Instrument Pointing System (IPS) Star Simulator is a unique test bed that allows star trackers to interface with simulated stars in a laboratory before going into orbit. This hardware-in-the-loop testing of equipment on earth increases the probability of success while in space. The IPS Star Simulator provides three fields of view 2.55 x 2.55 deg each for input into star trackers. The fields of view are produced on three separate monitors. Each monitor has 4096 x 4096 addressable points and can display 50 stars (pixels) maximum at a given time. The pixel refresh rate is 1000 Hz. The spectral output is approximately 550 nm. The available relative visual magnitude range is two to eight visual magnitudes. The star size is less than 100 arcsec. The minimum star movement is less than 5 arcsec and the relative position accuracy is approximately 40 arcsec. The purpose of this paper is to describe the IPS Star Simulator design and to provide an operational scenario so others may gain from the approach and possible use of the system.

Wessling, Francis C., III

1993-01-01

303

IP Profiling via Service Cluster Membership Vectors  

SciTech Connect

This study investigates the feasibility of establishing and maintaining a system of compact IP behavioral profiles as a robust means of computer anomaly definition and detection. These profiles are based upon the degree to which a system's (IP's) network traffic is distributed among stable characteristic clusters derived of the aggregate session traffic generated by each of the major network services. In short, an IP's profile represents its degree of membership in these derived service clusters. The goal is to quantify and rank behaviors that are outside of the statistical norm for the services in question, or present significant deviation from profile for individual client IPs. Herein, we establish stable clusters for accessible features of common session traffic, migrate these clusters over time, define IP behavior profiles with respect to these clusters, migrate individual IP profiles over time, and demonstrate the detection of IP behavioral changes in terms of deviation from profile.

Bartoletti, A

2009-02-23

304

Preconditioned alternating projection algorithms for maximum a posteriori ECT reconstruction  

NASA Astrophysics Data System (ADS)

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

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

2012-11-01

305

The Ischemic Stroke Genetics Study (ISGS) Protocol  

PubMed Central

Background The molecular basis for the genetic risk of ischemic stroke is likely to be multigenic and influenced by environmental factors. Several small case-control studies have suggested associations between ischemic stroke and polymorphisms of genes that code for coagulation cascade proteins and platelet receptors. Our aim is to investigate potential associations between hemostatic gene polymorphisms and ischemic stroke, with particular emphasis on detailed characterization of the phenotype. Methods/Design The Ischemic Stroke Genetic Study is a prospective, multicenter genetic association study in adults with recent first-ever ischemic stroke confirmed with computed tomography or magnetic resonance imaging. Patients are evaluated at academic medical centers in the United States and compared with sex- and age-matched controls. Stroke subtypes are determined by central blinded adjudication using standardized, validated mechanistic and syndromic classification systems. The panel of genes to be tested for polymorphisms includes ?-fibrinogen and platelet glycoprotein Ia, Iba, and IIb/IIIa. Immortalized cell lines are created to allow for time- and cost-efficient testing of additional candidate genes in the future. Discussion The study is designed to minimize survival bias and to allow for exploring associations between specific polymorphisms and individual subtypes of ischemic stroke. The data set will also permit the study of genetic determinants of stroke outcome. Having cell lines will permit testing of future candidate risk factor genes. PMID:12848902

Meschia, James F; Brott, Thomas G; Brown, Robert D; Crook, Richard JP; Frankel, Michael; Hardy, John; Merino, José G; Rich, Stephen S; Silliman, Scott; Worrall, Bradford Burke

2003-01-01

306

Vulnerabilities of the Real-Time Transport (RTP) Protocol for Voice over IP (VoIP) Traffic  

E-print Network

Vulnerabilities of the Real-Time Transport (RTP) Protocol for Voice over IP (VoIP) Traffic Mike IP (VoIP) has revolutionalized the telecommunications industry. VoIP has be- come more prevalent than the analogue Public Switched Telephone Network (PSTN). One challenge, though, is to secure and protect these VoIP

Kwon, Minseok "James"

307

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

PubMed Central

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

Schipper, Casey; Church, Terry; Harris, Brian

1989-01-01

308

Radionuclide imaging in ischemic stroke.  

PubMed

Ischemic stroke is caused by interruption or significant impairment of blood supply to the brain, which leads to a cascade of metabolic and molecular alterations resulting in functional disturbance and morphologic damage. The changes in regional cerebral blood flow and regional metabolism can be assessed by radionuclide imaging, especially SPECT and PET. SPECT and PET have broadened our understanding of flow and metabolic thresholds critical for maintenance of brain function and morphology: PET was essential in the transfer of the concept of the penumbra to clinical stroke and thereby had a great impact on developing treatment strategies. Receptor ligands can be applied as early markers of irreversible neuronal damage and can predict the size of the final infarcts, which is important for decisions on invasive therapy in large ("malignant") infarction. With SPECT and PET, the reserve capacity of the blood supply can be tested in obstructive arteriosclerosis, which is essential for planning interventions. The effect of a stroke on surrounding and contralateral primarily unaffected tissue can be investigated, helping to understand symptoms caused by disturbance in functional networks. Activation studies are useful to demonstrate alternative pathways to compensate for lesions and to test the effect of rehabilitative therapy. Radioisotope studies help to detect neuroinflammation and its effect on extension of tissue damage. Despite the limitations of broad clinical application of radionuclide imaging, this technology has a great impact on research in cerebrovascular diseases and still has various applications in the management of stroke. PMID:25300599

Heiss, Wolf-Dieter

2014-11-01

309

[Ischemic stroke in young age].  

PubMed

We studied 203 patients (116 male, 87 female, mean age 34,6±8,2 years) with ischemic stroke (IS). The study was carried out in one week - 14 months after the development of stroke. All patients underwent MRT/CT of the brain, cerebral angiography (MRA, rarely - CTA or conventional angiography), duplex ultrasound and echocardiography. Antiphospholipid antibodies, homocysteine, platelet aggregation, blood clotting, methylenetetrahydrofolate reductase, prothrombin and factor V Leiden gene mutations were also studied along with routine clinical and biochemical blood tests. When it was indicated, antinuclear antibodies, DNA antibodies, antibodies to some viruses were studied and muscle biopsy was performed. The causes of IS were as follows: cerebral artery dissections (25%), cardioembolism (12%), antiphospholipid syndrome (11%), coagulography (7%), arterial hypertension (8%), atherosclerosis (3%), mitochondrial cytopathy (3%), cerebral vasculitis (1%), Moya-moya disease (0,5%), cerebral artery spasm after the aneurysm disruption (0,5%). The cause of IS remained unknown (cryptogenic stroke) in 29%. In a half of these cases, clinical presentations suggest the cerebral artery dissection as a cause of IS. However in the acute period the diagnosis was not verified by angiography which was conducted only in the late stage of stroke (3 months or more after stroke development). PMID:21423109

Dobrynina, L A; Kalashnikova, L A; Pavlova, L N

2011-01-01

310

Applying a gaming approach to IP strategy.  

PubMed

Adopting an appropriate IP strategy is an important but complex area, particularly in the pharmaceutical and biotechnology sectors, in which aspects such as regulatory submissions, high competitive activity, and public health and safety information requirements limit the amount of information that can be protected effectively through secrecy. As a result, and considering the existing time limits for patent protection, decisions on how to approach IP in these sectors must be made with knowledge of the options and consequences of IP positioning. Because of the specialized nature of IP, it is necessary to impart knowledge regarding the options and impact of IP to decision-makers, whether at the level of inventors, marketers or strategic business managers. This feature review provides some insight on IP strategy, with a focus on the use of a new 'gaming' approach for transferring the skills and understanding needed to make informed IP-related decisions; the game Patentopolis is discussed as an example of such an approach. Patentopolis involves interactive activities with IP-related business decisions, including the exploitation and enforcement of IP rights, and can be used to gain knowledge on the impact of adopting different IP strategies. PMID:20127561

Gasnier, Arnaud; Vandamme, Luc

2010-02-01

311

Caspase 3 activation is essential for neuroprotection in preconditioning  

Microsoft Academic Search

Sublethal insults can induce tolerance to subsequent stressors in neurons. As cell death activators such as ROS generation and decreased ATP can initiate tolerance, we tested whether other cellular elements normally associated with neuronal injury could add to this process. In an in vivo model of ischemic tolerance, we were surprised to observe widespread caspase 3 cleavage, without cell death,

Bethann McLaughlin; Karen A. Hartnett; Joseph A. Erhardt; Jeffrey J. Legos; Ray F. White; Frank C. Barone; Elias Aizenman

2003-01-01

312

Prevention of experimental stroke by hypercapnic-hypoxic preconditioning.  

PubMed

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

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

2008-09-01

313

Prevention of experimental stroke by hypercapnic-hypoxic preconditioning  

Microsoft Academic Search

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

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

2008-01-01

314

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

PubMed Central

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

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

2015-01-01

315

Cardiac preconditioning with 4-h, 17 degrees C ischemia reduces [Ca(2+)](i) load and damage in part via K(ATP) channel opening.  

PubMed

Brief ischemia before normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear whether it protects against long-term moderate hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia before 4 h, 17 degrees C hypothermic ischemia on cardiac cytosolic [Ca(2+)], mechanical and metabolic function, and infarct size, and 2) the potential role of K(ATP) channels in eliciting cardioprotection. We found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca(2+)] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36 +/- 2 (SE)% to 15 +/- 1% with IPC. Bracketing ischemic pulses with 200 microM 5-hydroxydecanoic acid or 10 microM glibenclamide increased infarct size to 28 +/- 3% and 26 +/- 4%, respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia and that this is associated with decreased cytosolic [Ca(2+)] loading and enhanced ATP-sensitive K channel opening. PMID:12003799

Chen, Qun; Camara, Amadou K S; An, Jianzhong; Riess, Matthias L; Novalija, Enis; Stowe, David F

2002-06-01

316

Analysis of Handoff Mechanisms in Mobile IP  

NASA Astrophysics Data System (ADS)

One of the most important challenges in mobile Internet Protocol (IP) is to provide service for a mobile node to maintain its connectivity to network when it moves from one domain to another. IP is responsible for routing packets across network. The first major version of IP is the Internet Protocol version 4 (IPv4). It is one of the dominant protocols relevant to wireless network. Later a newer version of IP called the IPv6 was proposed. Mobile IPv6 is mainly introduced for the purpose of mobility. Mobility management enables network to locate roaming nodes in order to deliver packets and maintain connections with them when moving into new domains. Handoff occurs when a mobile node moves from one network to another. It is a key factor of mobility because a mobile node can trigger several handoffs during a session. This paper briefly explains on mobile IP and its handoff issues, along with the drawbacks of mobile IP.

Jayaraj, Maria Nadine Simonel; Issac, Biju; Haldar, Manas Kumar

2011-06-01

317

Cyclooxygenase-2 Mediates Hyperbaric Oxygen Preconditioning Induced Neuroprotection in the Mouse Model of Surgical Brain Injury  

PubMed Central

Background and Purpose: We investigated the role of cyclooxygenase-2 (COX-2) in mechanisms of hyperbaric oxygen preconditioning (HBO-PC) in the mouse model of surgical brain injury (SBI). Methods: C57BL mice were administered 100% oxygen for 1 hr at 2.5 ATA for 5 consecutive days and subjected to SBI. Neurological status and brain edema were evaluated at 24 hrs and 72 hrs after the brain insult. Fluorescent immunostaining and Western blotting were performed to study hypoxia inducible factor-1? (HIF-1?) and COX-2, respectively. Two doses of COX-2 inhibitor, NS398 (3mg/kg and 10mg/kg) were used to verify the role of COX-2 signaling pathway in the mechanism of HBO-PC. Results: HBO-PC improved neurological status and decreased brain edema at 24hrs and 72hrs after SBI. HBO-PC by itself and SBI independently increased COX-2 levels by 2-fold and 4-fold respectively. HBO-PC however reduced increase in HIF-1? and COX-2 expression after SBI. The HBO-PC-induced improvement in neurological status and brain edema was reversed by suboptimal dose of COX-2 inhibitor, NS398 (10mg/kg, i.p; 1/4th of dose shown to provide neuroprotection), which itself had no effect on investigated endpoints. Conclusions: HBO-PC attenuates post-operative brain edema and improves neurological outcomes following SBI. The HBO-PC induced neuroprotection is mediated via COX-2 signaling pathways. PMID:19628811

Jadhav, Vikram; Ostrowski, Robert P.; Tong, Wenni; Matus, Brenden; Jesunathadas, Rachel; Zhang, John H.

2009-01-01

318

Small vessel hematocrit in ischemic myocardium  

SciTech Connect

As blood enters the microvasculature of normally perfused myocardium, there is a progressive decrease in small vessel hematocrit (SV Hct) due to RBC streaming in smaller branching vessels and the Fahraeus-Lindqvist effect. We hypothesized that if the coronary collateral circulation was composed of very small vessels branching from large parent vessels, plasma streaming would result in a further decrease of SV Hct in ischemic myocardium. Six open chest anesthetized dogs were studied. Plasma was labelled with /sup 59/FeCl siderophilin and RBC's with /sup 99/mTc to estimate SV Hct from myocardial biopsies. The LAD was occluded and cannulated for measurement of retrograde flow (arising presumably from proximal collaterals). The ischemic region was identified using the microsphere shadow technique. Collateral flow after LAD occlusion was 30 +- 12 ml/min 100g (x +- SE). Systemic Hct was 40 +- 1%. The Hct of blood from retrograde flow was 39 +- 1% (p = NS). Activity of /sup 59/FeCl and /sup 99/mTc in known quantities of blood were compared to myocardial biopsies to estimate SV Hct. Ischemic SV Hct was 23 +- 2% and non-ischemic SV Hct was 21 +- 1% (p = NS). We conclude that the size and branching pattern of coronary collaterals is such that plasma streaming in collaterals does not result in an additional decrease in SV Hct in ischemic myocardium.

Gumm, D.C.; Cooper, S.M.; Marcus, M.L.; Chilian, W.M.; Harrison, D.G.

1986-03-01

319

CISCO IP 7941-7961 FONCTIONS TLPHONIQUES  

E-print Network

CISCO IP 7941-7961 FONCTIONS T�L�PHONIQUES FONCTIONS DE BASE BOUTON DE LIGNE (DESCRIPTION DES raccrocher pour effectuer le transfert de l'appel. Cisco_IP_7941_7961_Fr_CUCM_V7.0_20090320[1].doc 1 de 7 #12;CISCO IP 7941-7961 FONCTIONS T�L�PHONIQUES APPEL CONF�RENCE Vous pouvez établir un appel conférence

Charette, André

320

CISCO IP 7940-7960 FONCTIONS TLPHONIQUES  

E-print Network

CISCO IP 7940-7960 FONCTIONS T�L�PHONIQUES FONCTIONS DE BASE FAIRE UN APPEL · Soulever le combiné navigation; · appuyer sur la touche Joindre (tous les intervenants seront en communication). Cisco_IP_7940_7960_Fr_CUCM_V7.0_20090320[1].doc 1 de 7 #12;CISCO IP 7940-7960 FONCTIONS T�L�PHONIQUES APPEL CONF�RENCE

Charette, André

321

The Spacelab IPS Star Simulator  

NASA Technical Reports Server (NTRS)

The cost of doing business in space is very high. If errors occur while in orbit the costs grow and desired scientific data may be corrupted or even lost. The Spacelab Instrument Pointing System (IPS) Star Simulator is a unique test bed that allows star trackers to interface with simulated stars in a laboratory before going into orbit. This hardware-in-the loop testing of equipment on earth increases the probability of success while in space. The IPS Star Simulator provides three fields of view 2.55 x 2.55 degrees each for input into star trackers. The fields of view are produced on three separate monitors. Each monitor has 4096 x 4096 addressable points and can display 50 stars (pixels) maximum at a given time. The pixel refresh rate is 1000 Hz. The spectral output is approximately 550 nm. The available relative visual magnitude range is 2 to 8 visual magnitudes. The star size is less than 100 arc seconds. The minimum star movement is less than 5 arc seconds and the relative position accuracy is approximately 40 arc seconds. The purpose of this paper is to describe the LPS Star Simulator design and to provide an operational scenario so others may gain from the approach and possible use of the system.

Wessling, Francis C., III

1993-01-01

322

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

PubMed Central

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

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

2010-01-01

323

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

PubMed

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

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

2010-01-01

324

Risk factors of young ischemic stroke in Qatar  

Microsoft Academic Search

ObjectivesThere is limited information about risk factors of young ischemic stroke in Qatar. The aim of this study was to describe the risk factors and subtypes of young ischemic stroke among Qatari and non-Qatari residents.

Fahmi Yousef Khan

2007-01-01

325

Dual Antiplatelet Therapy after Noncardioembolic Ischemic Stroke or Transient Ischemic Attack: Pros and Cons  

PubMed Central

Dual antiplatelet therapy simultaneously blocks different platelet activation pathways and might thus be more potent at inhibiting platelet activation and more effective at reducing major ischemic vascular events compared to antiplatelet monotherapy. Aspirin plus clopidogrel dual therapy is now the standard therapy for patients with acute coronary syndrome and for those undergoing percutaneous coronary intervention. However, dual antiplatelet therapy carries an increased risk of bleeding. Patients with ischemic stroke or transient ischemic attack (TIA) are generally older and likely to have a fragile cerebrovascular bed, which further increases the risk of systemic major bleeding events and intracranial hemorrhage. Clinical trials and meta-analyses suggest that in comparison to antiplatelet monotherapy, dual antiplatelet therapy initiated early after noncardioembolic ischemic stroke or TIA further reduces the rate of recurrent stroke and major vascular events without significantly increasing the rate of major bleeding events. In contrast, studies of long-term therapy in patients with noncardioembolic ischemic stroke or TIA have yielded inconsistent data regarding the benefit of dual antiplatelet therapy over monotherapy. However, the harm associated with major bleeding events, including intracranial hemorrhage, which is generally more disabling and more fatal than ischemic stroke, is likely to increase with dual antiplatelet therapy. Physicians should carefully assess the benefits and risks of dual antiplatelet therapy versus antiplatelet monotherapy when managing patients with ischemic stroke or TIA. PMID:25045370

2014-01-01

326

Mobility management for VoIP service: Mobile IP vs. SIP  

Microsoft Academic Search

Wireless Internet access has gained significant attention as wireless\\/mobile communications and networking become widespread. The voice over IP service is likely to play a key role in the convergence of IP-based Internet and mobile cellular networks. We explore different mobility management schemes from the perspective of VoIP services, with a focus on Mobile IP and session initiation protocol. After illustrating

TED TAEKYOUNG KWON; MARIO GERLA; S. Das

2002-01-01

327

A preconditioned fast decoupled power flow method for contingency screening  

SciTech Connect

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

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

1995-12-31

328

A preconditioned fast decoupled power flow method for contingency screening  

SciTech Connect

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

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

1996-02-01

329

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

330

Preconditioning of the Navier-Stokes equations with multiple constraints  

NASA Astrophysics Data System (ADS)

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

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

2013-10-01

331

Spectroscopic Monitoring of Kidney Tissue Ischemic Injury  

SciTech Connect

Noninvasive evaluation of tissue viability of donor kidneys used for transplantation is an issue that current technology is not able to address. In this work, we explore optical spectroscopy for its potential to assess the degree of ischemic damage in kidney tissue. We hypothesized that ischemic damage to kidney tissue will give rise to changes in its optical properties which in turn may be used to asses the degree of tissue injury. The experimental results demonstrate that the autofluorescence intensity of the injured kidney is decreasing as a function of time exposed to ischemic injury. Changes were also observed in the NIR light scattering intensities most probably arising from changes due to injury and death of the tissue.

Demos, S G; Fitzgerald, J T; Michalopoulou, A P; Troppmann, C

2004-03-11

332

Spectroscopic monitoring of kidney tissue ischemic injury  

NASA Astrophysics Data System (ADS)

Noninvasive evaluation of tissue viability of donor kidneys used for transplantation is an issue that current technology is not able to address. In this work, we explore optical spectroscopy for its potential to assess the degree of ischemic damage in kidney tissue. We hypothesized that ischemic damage to kidney tissue will give rise to changes in its optical properties which in turn may be used to asses the degree of tissue injury. The experimental results demonstrate that the autofluorescence intensity of the injured kidney is decreasing as a function of time exposed to ischemic injury. Changes were also observed in the NIR light scattering intensities most probably arising from changes due to injury and death of the tissue.

Fitzgerald, Jason T.; Michalopoulou, Andromachi P.; Troppmann, Christoph; Demos, Stavros G.

2004-07-01

333

Population Genetics of Spruce Bark Beetle Ips typographus (Col., Scolytidae) and Related Ips Species1  

E-print Network

Population Genetics of Spruce Bark Beetle Ips typographus (Col., Scolytidae) and Related Ips method to study population genetic aspects in Ips typographus (L.) be- cause of three highly polymorphic to be regionally different. A genetic basis of these differences was assumed. Seventeen European populations

Standiford, Richard B.

334

A UML-Based Approach for Heterogeneous IP Integration Abstract -With increasing availability of predefined IP  

E-print Network

for heterogeneous IP would benefit designers working through a top-down design process. UML-based approa the time to market. However, as the IP blocks are provided by different vendors, they differ to customize them to comply with the OCP standard. The process of IP integration also suffers from mis

Wong, Weng Fai

335

ENABLING PARTIALLY RECONFIGURABLE IP CORES PARAMETERISATION AND INTEGRATION USING MARTE AND IP-XACT  

E-print Network

ENABLING PARTIALLY RECONFIGURABLE IP CORES PARAMETERISATION AND INTEGRATION USING MARTE AND IP) methodology, which exploits two widely used standards for Systems-on-Chip specification, MARTE and IP a case study in which a complete DPR platform is modeled in MARTE and implemented in a FPGA. Index Terms

Paris-Sud XI, Université de

336

Drug Delivery to the Ischemic Brain  

PubMed Central

Cerebral ischemia occurs when blood flow to the brain is insufficient to meet metabolic demand. This can result from cerebral artery occlusion that interrupts blood flow, limits CNS supply of oxygen and glucose, and causes an infarction/ischemic stroke. Ischemia initiates a cascade of molecular events inneurons and cerebrovascular endothelial cells including energy depletion, dissipation of ion gradients, calcium overload, excitotoxicity, oxidative stress, and accumulation of ions and fluid. Blood-brain barrier (BBB) disruption is associated with cerebral ischemia and leads to vasogenic edema, a primary cause of stroke-associated mortality. To date, only a single drug has received US Food and Drug Administration (FDA) approval for acute ischemic stroke treatment, recombinant tissue plasminogen activator (rt-PA). While rt-PA therapy restores perfusion to ischemic brain, considerable tissue damage occurs when cerebral blood flow is re-established. Therefore, there is a critical need for novel therapeutic approaches that can “rescue” salvageable brain tissue and/or protect BBB integrity during ischemic stroke. One class of drugs that may enable neural cell rescue following cerebral ischemia/reperfusion injury is the HMG-CoA reductase inhibitors (i.e., statins). Understanding potential CNS drug delivery pathways for statins is critical to their utility in ischemic stroke. Here, we review molecular pathways associated with cerebral ischemia and novel approaches for delivering drugs to treat ischemic disease. Specifically, we discuss utility of endogenous BBB drug uptake transporters such as organic anion transporting polypeptides (OATPs/Oatps) and nanotechnology-based carriers for optimization of CNS drug delivery. Overall, this chapter highlights state-of-the-art technologies that may improve pharmacotherapy of cerebral ischemia. PMID:25307217

Thompson, Brandon J.; Ronaldson, Patrick T.

2014-01-01

337

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

Code of Federal Regulations, 2010 CFR

... 2010-07-01 false PM sampling media (e.g., filters) preconditioning and...Duty Cycles § 1065.590 PM sampling media (e.g., filters) preconditioning and...the following steps to prepare PM sampling media (e.g., filters) and equipment...

2010-07-01

338

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

E-print Network

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

Wojcik, Edward J.

339

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

Code of Federal Regulations, 2011 CFR

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

2011-07-01

340

Inositol phosphates: Does IP(4) run a protection racket?  

PubMed

The phosphorylation of IP(3) by IP(3) 3-kinase leads to a number of physiological events, most of which are poorly understood. Recent findings about a hitherto unsuspected action of the IP(3) 3-kinase product, IP(4), suggest that the evolution of IP(3) 3-kinase may have even more far-reaching consequences than we thought. PMID:11267885

Irvine, R

2001-03-01

341

Voice over IP (VoIP) systems are gaining in popularity as the technology for transmitting voice traffic over IP networks. As the popularity of VoIP systems increases, they are being subjected to different kinds of  

E-print Network

1 Abstract Voice over IP (VoIP) systems are gaining in popularity as the technology for transmitting voice traffic over IP networks. As the popularity of VoIP systems increases, they are being a general pattern. VoIP systems pose several new challenges to Intrusion Detection System (IDS) designers

Bagchi, Saurabh

342

Sex shapes experimental ischemic brain injury  

PubMed Central

Biologic sex and sex steroids are important factors in clinical and experimental stroke. This review evaluates key evidence that biological sex strongly alters mechanisms and outcomes from cerebral ischemia. The role of androgens in male stroke is understudied and important to pursue given that male sex is a well known risk factor for human stroke. To date, male sex steroids remain largely evaluated at the bench rather than the bedside. We review recent advances in our understanding of androgens in the context of ischemic cell death and neuroprotection. We also highlight some possible molecular mechanisms by which androgens impact ischemic outcomes. PMID:19903490

Cheng, Jian; Hurn, Patricia D.

2010-01-01

343

Incidental Unruptured Intracranial Aneurysms in Patients with Acute Ischemic Stroke  

Microsoft Academic Search

Background: The management and clinical prognosis of incidental intracranial aneurysms in acute ischemic stroke patients have been understudied. We investigated the clinical outcome of acute ischemic stroke subjects with incidentally found intracranial aneurysms. Methods: We consecutively included acute ischemic stroke patients within 7 days of onset. Their demographics, risk factors, stroke subtypes, antithrombotics use and modified Rankin scale (mRS) at

Yoon-Sang Oh; Seung-Jae Lee; Young-Min Shon; Dong Won Yang; Beum Saeng Kim; A-Hyun Cho

2008-01-01

344

Resource management for IP telephony networks  

Microsoft Academic Search

The two key resources in an IP telephony network are the Internet telephony gateways (ITGs) and the IP network. These resources must be effectively managed to simultaneously provide good QoS to calls and maximize network resource utilization. This paper presents two main contributions. First, we design a call admission policy based on congestion sensitive pricing. As the load increases, this

Matthew Chapman Caesar; Dipak Ghosal; Randy H. Katz

2002-01-01

345

IPS - Instrument pointing system for Spacelab payloads  

Microsoft Academic Search

An instrument pointing system (IPS) will be flown for the first time with Spacelab 2 in Oct. 1984. The IPS is a three-axis gimbal system with payload clamp units for mounting on the Spacelab pallets. Power to drive the units comes from an integrated electronic power and digital control system and Spacelab subsystems. Control originates in either Spacelab, the Shuttle,

A. Hammesfahr

1982-01-01

346

IP Traceback in a Switched Ethernet Network  

Microsoft Academic Search

IP traceback is the generic term given to systems that allow the tracing of IP packets back to their originating machine. A common shortcoming shared by existing traceback proposals is that they are able to identify the source network, but not the source host. Our work extends the traceback process by allowing the tracing of frames within the origi- nating

Marios S. Andreou; Aad van Moorsel

2007-01-01

347

VoIP to the Rescue  

ERIC Educational Resources Information Center

Voice over Internet Protocol (VoIP) is everywhere. The technology lets users make and receive phone calls over the Internet, transporting voice traffic alongside data traffic such as instant messages (IMs) and e-mail. While the number of consumer customers using VoIP increases every week, the technology is finding its way into K-12 education as…

Milner, Jacob

2005-01-01

348

Quality VoIP — An Engineering Challenge  

Microsoft Academic Search

Initial impressions of VoIP quality have not always been favourable. This paper discusses the issues behind delivering an 'appropriate' quality of service, specifically voice quality, by showing how design choices ultimately affect, and potentially limit, a customer's perception of VoIP quality.

RJB Reynolds; AW Rix

2001-01-01

349

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

PubMed

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

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

2014-07-25

350

Sound preconditioning therapy inhibits ototoxic hearing loss in mice  

PubMed Central

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

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

2013-01-01

351

Ischemic Burden and Clinical Outcome: Is One ‘Culprit’ Ischemic Segment by Dobutamine Stress Magnetic Resonance Predictive?  

PubMed Central

Aims We sought to evaluate the impact of ischemic burden for the prediction of hard cardiac events (cardiac death or nonfatal myocardial infarction) in patients with known or suspected CAD who undergo dobutamine stress cardiac magnetic resonance imaging (DCMR) Methods We included 3166 patients (pts.), mean age 63±12 years, 27% female, who underwent DCMR in 3 tertiary cardiac centres (University Hospital Heildelberg, German Heart Institute and Kings College London). Pts. were separated in groups based on the number of ischemic segments by wall motion abnormalities (WMA) as follows: 1. no ischemic segment, 2. one ischemic segment, 3. two ischemic segments and 4. ?three ischemic segments. Cardiac death and nonfatal myocardial infarction were registered as hard cardiac events. Pts. with an “early” revascularization procedure (in the first three months after DCMR) were not included in the final survival analysis. Results Pts. were followed for a median of 3.1 years (iqr 2–4.5 years). 187 (5.9%) pts. experienced hard cardiac events. 2349 (74.2%) had no inducible ischemia, 189 (6%) had ischemia in 1 segment, 292 (9.2%) in 2 segments and 336 (10.6%) ?3 segments. Patients with only 1 ischemic segment showed a high rate of hard cardiac events of ?6% annually, which was 10-fold higher compared to those without ischemia (0.6% annually, p<0.001) but similar to those with 2 and ?3ischemic segments (?5.5% and ?7%, p?=?NS). Conclusions The presence of inducible ischemia even in a single ‘culprit’ myocardial segment during DCMR is enough to predict hard cardiac events in patients with known or suspected CAD. PMID:25517506

Nagel, Eike; Buss, Sebastian Johannes; Puntmann, Valentina; Wellnhofer, Ernst; Fleck, Eckart; Katus, Hugo Albert; Korosoglou, Grigorios

2014-01-01

352

Pioglitazone Improves Insulin Sensitivity Among Nondiabetic Patients With a Recent Transient Ischemic Attack or Ischemic Stroke  

Microsoft Academic Search

Background and Purpose—The aim of this study was to determine the effectiveness of pioglitazone compared with placebo for improving insulin sensitivity among nondiabetic patients with a recent transient ischemic attack (TIA) or nondisabling ischemic stroke and impaired insulin sensitivity. Methods—Eligible subjects were men and women 45 years of age who had no history of diabetes, fasting glucose 7.0 mmol\\/L, and

Walter N. Kernan; Silvio E. Inzucchi; Catherine M. Viscoli; Lawrence M. Brass; Dawn M. Bravata; Gerald I. Shulman; James C. McVeety; Ralph I. Horwitz

2010-01-01

353

An Introduction to Voice over the IP: Laboratory Exercise  

NSDL National Science Digital Library

This document provides a sample laboratory exercise which may be used in classes studying Voice over IP. The exercise includes three parts: 1. Configure the classroom network; 2. Simulate VoIP calls; and 3. VoIP Network configuration.

Cherri, Mona

354

Inflammatory mechanisms in ischemic stroke: therapeutic approaches  

Microsoft Academic Search

Acute ischemic stroke is the third leading cause of death in industrialized countries and the most frequent cause of permanent disability in adults worldwide. Despite advances in the understanding of the pathophysiology of cerebral ischemia, therapeutic options remain limited. Only recombinant tissue-plasminogen activator (rt-PA) for thrombolysis is currently approved for use in the treatment of this devastating disease. However, its

Shaheen E Lakhan; Annette Kirchgessner; Magdalena Hofer

2009-01-01

355

Primary and Secondary Prevention of Ischemic Stroke  

Microsoft Academic Search

Prevention of stroke and transient ischemic attack includes both conventional approaches to vascular risk factor management (blood pressure lowering, cholesterol reduction with statins, smoking cessation and antiplatelet therapy) and more specific interventions, such as carotid revascularization or anticoagulation for atrial fibrillation. The objective of this review is to discuss effective interventions for optimal primary and secondary stroke prevention.

Maurizio Paciaroni; Julien Bogousslavsky

2010-01-01

356

Neovascular Glaucoma in Ocular Ischemic Syndrome  

E-print Network

We report a case of ocular ischemic syndrome accompanied by neovascular glaucoma that was successfully treated with Bevacizumab. A 70-year-old male patient diagnosed with neovascular glaucoma of the left eye 3-4 years prior complained of continuous left eye pain and declining visual acuity despite

unknown authors

357

Systemic corticosteroids in nonarteritic ischemic optic neuropathy  

PubMed Central

Nonarteritic ischemic optic neuropathy (NAION) is one of the most prevalent optic nerve disorders seen in ophthalmic practice. The role of corticosteroid therapy in NAION remains a highly controversial area of debate in ophthalmology. This brief review will provide an overview of the current clinical evidence on this topic as well as some comment on the medical debate. PMID:25449939

Al-Zubidi, Nagham; Zhang, Jason; Spitze, Arielle; Lee, Andrew G

2014-01-01

358

Cell Based Therapies for Ischemic Tissue Repair  

Cancer.gov

As the population ages and the acute mortality from cardiovascular disease decreases, a large population of patients is emerging who have symptomatic chronic ischemic cardiac and vascular disease, many of whom remain severely symptomatic despite exhausting conventional medical therapy and mechanical revascularization. Mounting evidence suggests that microvascular insufficiency plays a significant role in the pathophysiology of ischemia.

359

Ischemic stroke penumbra and extracorporeal ozone treatment.  

PubMed

The course of events in ischemic strokes is normally seen from a point in which the penumbra is already in place. Since there is no known treatment for edema reduction, mainstream medicine focuses on re-opening the occluded vessel. Here we show that reducing the penumbra saves neuronal units from undergoing apoptosis. PMID:23859279

Wasser, G

2013-06-01

360

Conversational Model Based VoIP Traffic Generation  

Microsoft Academic Search

VoIP (voice over IP) traffic generation has significant meaning for the measurement of VoIP quality in networks, but existing generation methods are insufficient both in reality and interactivity, and thus affect the accuracy of VoIP quality measurement. This paper proposes a conversational model based VoIP traffic generation algorithm, which simulates the behavior of two users in a VoIP session, and

Li Ji; Xingang Shi; Zhiliang Wang

2007-01-01

361

Ischemic tolerance is associated with VEGF-C and VEGFR-3 signaling in the mouse hippocampus.  

PubMed

The functions of vascular endothelial growth factor C (VEGF-C) and the VEGF receptor 3 (VEGFR-3) in the nervous system are not well known. In this study, we examined the role of VEGF-C and VEGFR-3 in ischemic preconditioning (IPC)-induced tolerance in the mouse hippocampus. Adult male C57BL/6 mice were subjected to either severe ischemia (SI) induced by 40min of bilateral common carotid artery occlusion (BCCAO) with or without IPC (5-min BCCAO) or IPC only. Cerebral blood flow was measured during ischemic periods using laser Doppler flowmetry. Neuronal damage was assessed histologically, and VEGF-C and VEGFR-3 expression levels were assessed through immunostaining. Fluoro-Jade B-labeled cells were abundant in the CA1 area 7days after SI without IPC (sham+SI group), whereas cells were rarely labeled in mice subjected to IPC followed by SI (IPC+SI group). Similarly, the number of neuronal nuclei (NeuN)-positive cells in the CA1 area was significantly lower in the sham+SI group than in the IPC+SI group. Interestingly, we found that sublethal IPC treatment induced prominent VEGF-C expression in the CA1 pyramidal neurons and VEGFR-3 expression in the stratum radiatum and stratum lacunosum moleculare after 3days of reperfusion that were sustained for 7days. Moreover, VEGF-C immunoreactivity was also markedly increased, whereas VEGFR-3 expression was sustained in tolerance-acquired CA1 neurons after SI. Application of a VEGFR-3 inhibitor, SAR131675, abolished the IPC-induced neuroprotection in a dose-dependent manner in the mouse hippocampus. These results suggest that VEGF-C/VEGFR-3 signaling is associated with IPC-induced hippocampal tolerance to lethal ischemia. PMID:25637798

Bhuiyan, M I H; Kim, J-C; Hwang, S-N; Lee, M-Y; Kim, S Y

2015-04-01

362

Impact of Severe Extracranial ICA Stenosis on MRI Perfusion and Diffusion Parameters in Acute Ischemic Stroke  

PubMed Central

Purpose: The aim of this study was to investigate the impact of a coexisting internal carotid artery (ICA) stenosis on lesion volumes as well as diffusion and perfusion parameters in acute ischemic stroke resulting from middle cerebral artery (MCA) occlusion. Material and methods: Magnetic resonance imaging data of 32 patients with MCA occlusion with or without additional ICA stenosis imaged within 4.5?h of symptom onset were analyzed. Both groups consisted of 16 patients. Acute diffusion lesions were semi-automatically segmented in apparent diffusion coefficient (ADC) MRI datasets. Perfusion maps of cerebral blood volume (CBV), cerebral blood flow, mean transit time and Tmax were calculated using perfusion-weighted MRI datasets. Tissue-at-risk (TAR) volumes were generated by subtracting the ADC lesion from the hypoperfusion lesion defined by Tmax >6?s. Median ADC and perfusion parameter values were extracted separately for the diffusion lesion and TAR and used for statistical analysis. Results: No significant differences were found between the groups regarding the diffusion lesion and TAR volumes. Statistical analysis of diffusion and perfusion parameters revealed CBV as the only parameter with a significant difference (p?=?0.009) contributing a small effect (?2?=?0.11) to the group comparison with higher CBV values for the patient group with a coexisting ICA stenosis, while no significant effects were found for the other diffusion and perfusion parameters analyzed. Conclusion: The results of this study suggest that a coexisting ICA stenosis does not have a strong effect on tissue status or perfusion parameters in acute stroke patients except for a moderate elevation of CBV. This may reflect improved collateral circulation or ischemic preconditioning in patients with a pre-existing proximal stenosis balancing impaired perfusion from the stenosis. PMID:25538674

Kaesemann, Philipp; Thomalla, Götz; Cheng, Bastian; Treszl, Andras; Fiehler, Jens; Forkert, Nils Daniel

2014-01-01

363

What are suspicious VoIP delays?  

E-print Network

Voice over IP (VoIP) is unquestionably the most popular real-time service in IP networks today. Recent studies have shown that it is also a suitable carrier for information hiding. Hidden communication may pose security concerns as it can lead to confidential information leakage. In VoIP, RTP (Real-time Transport Protocol) in particular, which provides the means for the successful transport of voice packets through IP networks, is suitable for steganographic purposes. It is characterised by a high packet rate compared to other protocols used in IP telephony, resulting in a potentially high steganographic bandwidth. The modification of an RTP packet stream provides many opportunities for hidden communication as the packets may be delayed, reordered or intentionally lost. In this paper, to enable the detection of steganographic exchanges in VoIP, we examined real RTP traffic traces to answer the questions, what do the "normal" delays in RTP packet streams look like? and, is it possible to detect the use of know...

Mazurczyk, Wojciech; Szczypiorski, Krzysztof

2010-01-01

364

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

PubMed Central

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

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

2013-01-01

365

Uniform communications software using TCP/IP  

SciTech Connect

Data acquisition applications at Fermilab require a reliable, distributed communication system for downloading, diagnostics, control, and data distribution. TCP/IP over Ethernet was chosen because of its uniform user interface and commercial availability for a number of processors and operating systems. This paper describes the authors software and hardware support for TCP/IP on VAX/VMS, VME/rhoSOS, FASTBUS/rhoSOS, and Unix systems. It includes plans to provide a portable, hardware independent implementation of TCP/IP based on Berkeley BSD software.

Bernett, M.; Oleynik, G. (Fermi National Accelerator Lab., Batavia, IL (USA))

1989-10-01

366

Uniform communications software using TCP/IP  

SciTech Connect

Data acquisition applications at Fermilab require a reliable, distributed communication system for downloading, diagnostics, control, and data distribution. TCP/IP over Ethernet was chosen because of its uniform user interface and commercial availability for a number of processors and operating systems. This paper describes our software and hardware support for TCP/IP on VAX/VMS, VME/pSOS, FASTBUS/pSOS, and Unix systems. It includes plans to provide a portable, hardware independent implementation of TCP/IP based on Berkeley BSD software. 8 refs., 3 figs.

Bernett, M.; Oleynik, G.

1989-05-01

367

IPS guidestar selection for stellar mode (ASTRO)  

NASA Technical Reports Server (NTRS)

This report describes how guide stars are selected for the Optical Sensor Package (OSP) for the Instrument Pointing System (IPS) when it is operating in the stellar mode on the ASTRO missions. It also describes how the objective loads are written and how the various roll angles are related; i.e., the celestial roll or position angle, the objective load roll angles, and the IPS gimbal angles. There is a brief description of how the IPS operates and its various modes of operation; i.e., IDOP, IDIN, and OSPCAL.

Mullins, Larry; Wooten, Lewis

1988-01-01

368

International Experience Approval Form INSTRUCTIONS: In order for international experience to count toward IP requirements, IP students must  

E-print Network

SAVANT). Updated 5/6/13 1) All students must first meet with the IP Assistant Director to discuss Savant). Signature_______________________________________________ Date____________________ IP Assistant

Li, Mo

369

Can endurance exercise preconditioning prevention disuse muscle atrophy?  

PubMed Central

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

Wiggs, Michael P.

2015-01-01

370

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

371

A frequency dependent preconditioned wavelet method for atmospheric tomography  

NASA Astrophysics Data System (ADS)

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

Yudytskiy, Mykhaylo; Helin, Tapio; Ramlau, Ronny

2013-12-01

372

ChIP-PED enhances the analysis of ChIP-seq and ChIP-chip data  

PubMed Central

Motivation: Although chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) or tiling array hybridization (ChIP-chip) is increasingly used to map genome-wide–binding sites of transcription factors (TFs), it still remains difficult to generate a quality ChIPx (i.e. ChIP-seq or ChIP-chip) dataset because of the tremendous amount of effort required to develop effective antibodies and efficient protocols. Moreover, most laboratories are unable to easily obtain ChIPx data for one or more TF(s) in more than a handful of biological contexts. Thus, standard ChIPx analyses primarily focus on analyzing data from one experiment, and the discoveries are restricted to a specific biological context. Results: We propose to enrich this existing data analysis paradigm by developing a novel approach, ChIP-PED, which superimposes ChIPx data on large amounts of publicly available human and mouse gene expression data containing a diverse collection of cell types, tissues and disease conditions to discover new biological contexts with potential TF regulatory activities. We demonstrate ChIP-PED using a number of examples, including a novel discovery that MYC, a human TF, plays an important functional role in pediatric Ewing sarcoma cell lines. These examples show that ChIP-PED increases the value of ChIPx data by allowing one to expand the scope of possible discoveries made from a ChIPx experiment. Availability: http://www.biostat.jhsph.edu/?gewu/ChIPPED/ Contact: hji@jhsph.edu Supplementary information: Supplementary data are available at Bioinformatics online. PMID:23457041

Wu, George; Yustein, Jason T.; McCall, Matthew N.; Zilliox, Michael; Irizarry, Rafael A.; Zeller, Karen; Dang, Chi V.; Ji, Hongkai

2013-01-01

373

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

NASA Technical Reports Server (NTRS)

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

Darmofal, David L.

1998-01-01

374

Iterated preconditioned LSQR method for inverse problems on unstructured grids  

NASA Astrophysics Data System (ADS)

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

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

2014-06-01

375

On the development of Voice over IP  

E-print Network

problems in the Session Initiation Protocol (SIP) call setup process. To support product line development and enable product evolution in the quickly growing VoIP market, I have proposed a generic development framework for SIP application servers...

Yang, Xu

2009-05-15

376

75 FR 13235 - IP-Enabled Services  

Federal Register 2010, 2011, 2012, 2013, 2014

...SUMMARY: The Commission amended part 63 in order to extend to providers of interconnected Voice over Internet Protocol (VoIP) service the discontinuance obligations that apply to domestic non-dominant telecommunications carriers under section...

2010-03-19

377

VoIP, Asterisk, and Emerging Technology  

NSDL National Science Digital Library

This Power Point presentation provides some information on Voice over IP, Asterisk and related emerging technologies. The fourth slide of the presentation includes a number of useful links on these topics.

Dâ??Ingianni, Vincente

378

VoIP technology comes of age.  

PubMed

Cabling specialist Connectix examines the growing potential for healthcare sector use of VoIP technology and highlights the importance of correct cabling infrastructure as a carrier of both voice and high-speed data traffic. PMID:18494421

2008-04-01

379

SIM-IP card benefits for a profitable business model in emerging VoIP technologies  

Microsoft Academic Search

This paper suggests introducing smartcards in emerging I.T systems, like Voice over IP (VoIP). First we shortly review performances evolution for next years in terms of computing capacities, memory size, and communication resources. Then we list some security issues in VoIP technology. Finally we describe an original experimental platform including an H323 software for win32, and a dedicated javacard (named

Pascal Urien; Adel Tizraoui; Marc Loutrel

2002-01-01

380

Voice Over IP Curriculum, Option II  

NSDL National Science Digital Library

The Convergence Technology Center has made Voice over IP curriculum available online. This set of curriculum is one of two available on VoIP. The site includes a syllabus and learning activities related to the topic. If you are an educator who would like to gain full access to the complete curriculum, you may email convergence_technology@collin.edu (further instructions for access are available on the site).

381

Multidimensional DFT IP Generator for FPGA Platforms  

Microsoft Academic Search

Multidimensional (MD) discrete Fourier transform (DFT) is a key kernel algorithm in many signal processing ap- plications. In this paper we describe an MD-DFT intellectual property (IP) generator and a bandwidth-efficient MD DFT IP for high performance implementations of 2-D and 3-D DFT on field-programmable gate array (FPGA) platforms. The proposed architecture is generated automatically and is based on a

Chi-Li Yu; Kevin Irick; Chaitali Chakrabarti; Vijaykrishnan Narayanan

2011-01-01

382

LACK - a VoIP Steganographic Method  

E-print Network

The paper presents a new steganographic method called LACK (Lost Audio PaCKets Steganography) which is intended mainly for VoIP. The method is presented in a broader context of network steganography and of VoIP steganography in particular. The analytical results presented in the paper concern the influence of LACK's hidden data insertion procedure on the method's impact on quality of voice transmission and its resistance to steganalysis.

Mazurczyk, Wojciech

2008-01-01

383

ERK5/KLF4 signaling as a common mediator of the neuroprotective effects of both nerve growth factor and hydrogen peroxide preconditioning.  

PubMed

Oxidative stress has long been implicated in the pathogenesis of various neurodegenerative disorders such as Alzheimer's disease and stroke. While high levels of oxidative stress are generally associated with cell death, a slight rise of reactive oxygen species (ROS) levels can be protective by "preconditioning" cells to develop a resistance against subsequent challenges. However, the mechanisms underlying such preconditioning (PC)-induced protection are still poorly understood. Previous studies have supported a role of ERK5 (mitogen-activated protein [MAP] kinase 5) in neuroprotection and ischemic tolerance in the hippocampus. In agreement with these findings, our data suggest that ERK5 mediates both hydrogen peroxide (H2O2)-induced PC as well as nerve growth factor (NGF)-induced neuroprotection. Activation of ERK5 partially rescued pheochromocytoma PC12 cells as well as primary hippocampal neurons from H2O2-caused death, while inhibition of ERK5 abolished NGF or PC-induced protection. These results implicate ERK5 signaling as a common downstream pathway for NGF and PC. Furthermore, both NGF and PC increased the expression of the transcription factor, KLF4, which can initiate an anti-apoptotic response in various cell types. Induction of KLF4 by NGF or PC was blocked by siERK5, suggesting that ERK5 is required in this process. siKLF4 can also attenuate NGF- or PC-induced neuroprotection. Overexpression of active MEK5 or KLF4 in H2O2-stressed cells increased Bcl-2/Bax ratio and the expression of NAIP (neuronal apoptosis inhibitory protein). Taken together, our data suggest that ERK5/KLF4 cascade is a common signaling pathway shared by at least two important mechanisms by which neurons can be protected from cell death. PMID:25015774

Su, Chang; Sun, Fen; Cunningham, Rebecca L; Rybalchenko, Nataliya; Singh, Meharvan

2014-01-01

384

Risk factors for ischemic stroke and transient ischemic attack in patients under age 50  

PubMed Central

To analyze risk factors for ischemic stroke and transient ischemic attack (TIA) in young adults under the age of 50. To make recommendations for additional research and practical consequences. From 97 patients with ischemic stroke or TIA under the age of 50, classical cardiovascular risk factors, coagulation disorders, history of migraine, use of oral contraceptives, cardiac abnormalities on ECG and echocardiography, and the results of duplex ultrasound were retrospectively analyzed. Literature was reviewed and compared to the results. 56.4% of the patients had hypertension, 12.1% increased total cholesterol, 20% hypertriglyceridemia, 31.5% an increased LDL-level, 32.6% a decreased HDL-level and 7.2% a disturbed glucose tolerance. Thrombophilia investigation was abnormal in 21 patients and auto-immune serology was abnormal in 15 patients. Ten of these patients were already known with a systemic disease associated with an increased risk for ischemic stroke (i.e. systemic lupus erythematosus). The ECG was abnormal in 16.7% of the cases, the echocardiography in 12.1% and duplex ultrasound of the carotid arteries was in 31.8% of the cases abnormal. Conventional cardiovascular risk factors are not only important in patients over the age of 50 with ischemic stroke or TIA, but also in this younger population under the age of 50. Thrombophilia investigation and/ or autoimmune serology should be restricted to patients without conventional cardiovascular risk factors and a history or other clinical symptoms associated with hypercoagulability and/ or autoimmune diseases. PMID:20532956

Janssen, A. W. M.; de Leeuw, F. E.

2010-01-01

385

Aspirin resistant patients with recent ischemic stroke.  

PubMed

Some patients with a recent ischemic stroke who are being treated with aspirin as an antiaggregant suffer a new ischemic stroke. These patients (15-25%) have been called unresponsive to aspirin or aspirin resistant. The aspirin-resistant patients have a four-time greater risk of suffering a stroke. Furthermore, these strokes are generally more severe, with increased infarct volume and greater risk of recurrence. There is currently no ideal laboratory test to detect the resistance to the antiaggregant effect of aspirin. The study of resistance to aspirin would only be indicated in selected cases. In these patients, one should first rule out any "pseudo-resistance" to aspirin (lack of compliance, concomitant treatments that interfere with the action of the aspirin). PMID:24211052

Castilla-Guerra, L; Navas-Alcántara, M S; Fernández-Moreno, M C

2014-04-01

386

Neuroprotection in acute ischemic stroke – current status  

PubMed Central

Abstract With the growing understanding of the mechanism of cell death in ischemia, new approaches for treatment such as neuroprotection have emerged. The basic aim of this strategy is to interfere with the events of the ischemic cascade, blocking the pathological processes and preventing the death of nerve cells in the ischemic penumebra. This concept involves inhibition of the pathological molecular events which eventually leads to the influx of calcium, activation of free radicals and neuronal death. Despite encouraging data from experimental animal models, all clinical trials of neuroprotective therapies have to date been unsuccessful. This article reviews some of the reasons for the failure of neuroprotection in the clinical trials so far. Despite all the negative reports, we believe it would be wrong to give up at this point, since there is still reasonable hope of finding an effective neuroprotection for stroke. PMID:20716132

Auriel, E; Bornstein, NM

2010-01-01

387

Ventricular tachycardia in ischemic heart disease substrates  

PubMed Central

Advances in the treatment of myocardial infarction (MI) have improved survival after ischemic cardiac injury. Post-infarct structural and functional remodeling results in electrophysiologic substrates at risk for monomorphic ventricular tachycardia (MMVT). Characterization of this substrate using a variety of clinical and investigative tools has improved our understanding of MMVT circuits, and has accelerated the development of device and catheter-based therapies aimed at identification and elimination of this arrhythmia. This review will discuss the central role of the ischemic heart disease substrate in the development MMVT. Electrophysiologic characterization of the post-infarct myocardium using bipolar electrogram amplitudes to delineate scar border zones will be reviewed. Functional electrogram determinants of reentrant circuits such as isolated late potentials will be discussed. Strategies for catheter ablation of reentrant ventricular tachycardia, including structural and functional targets will also be examined, as will the role of the epicardial mapping and ablation in the management of recurrent MMVT. PMID:24568826

Ajijola, Olujimi A.; Tung, Roderick; Shivkumar, Kalyanam

2014-01-01

388

Ischemic stroke: carotid and vertebral artery disease.  

PubMed

Ischemic strokes may have distinct aetiologies, including several different intrinsic arterial pathological disorders. The diagnosis and understanding of these arterial diseases is critical for the correct management of stroke as different treatment approaches are undertaken according to the aetiology. Atherosclerosis is by far the most common arterial disease among adults, and other pathological processes include arterial dissection, small vessel disease, inflammatory and non-inflammatory vasculopathy and vasomotor disorders. In children, there are several vasculopathies responsible for vaso-occlusive disease such as sickle-cell anemia, acute regressive angiopathy and Moya-Moya disease, neurofibromatosis, dissections, vasculitis associated with intracranial and systemic infections. An overview of the major carotid and vertebral pathological diseases responsible for ischemic stroke in adults and children, highlighting the accuracy of the different imaging modalities for its diagnosis and the imaging appearance of these diseases, is given. PMID:15657789

Vilela, P; Goulão, A

2005-03-01

389

[Cryoglobulinemia and the ?-chemokine IP-10].  

PubMed

IFN-?-induced protein 10 (IP-10) and its receptor, CXCR3 chemokine (C-X-C motif) receptor 3 (CXCR3), appear to contribute to the pathogenesis of HCV related mixed cryoglobulinemia (HCV+MC). The secretion of IP-10 by CD4+, CD8+ and natural killer (NK)-T cells is dependent on interferon (IFN)-?, which is itself mediated by the interleukin (IL)-12 cytokine family. Under the influence of IFN-?, IP-10 is secreted by several cell types including lymphocytes, hepatocytes, endothelial cells, fibroblasts, etc. In tissues, recruited T helper (Th) 1 lymphocytes may be responsible for enhanced IFN-? and tumor necrosis factor (TNF)-? production, which in turn stimulates IP-10 secretion from the cells, therefore creating an amplification feedback loop, and perpetuating the autoimmune process. High levels circulation of IP-10 have been found in HCV+MC, especially in patients with clinically active vasculitis. Furthermore, HCV+MC patients with autoimmune thyroiditis (AT), have higher levels than those without AT. Further studies are needed to investigate interactions between chemokines and cytokines in the pathogenesis, and to evaluate whether IP-10 is a novel therapeutic target in HCV+MC. PMID:25203349

Corrado, A; Mazzi, V; Ferrari, S M; Politti, U; Giuggioli, D; Antonelli, A; Fallahi, P; Ferri, C

2014-01-01

390

Antioxidant Enzyme Gene Transfer for Ischemic Diseases  

PubMed Central

The balance of redox is pivotal for normal function and integrity of tissues. Ischemic insults occur as results of a variety of conditions, leading to an accumulation of reactive oxygen species (ROS) and an imbalanced redox status in the tissues. The oxidant stress may activate signaling mechanisms provoking more toxic events, and eventually cause tissue damage. Therefore, treatments with antioxidants, free radical scavengers and their mimetics, as well as gene transfer approaches to overexpress antioxidant genes represent potential therapeutic options to correct the redox imbalance. Among them, antioxidant gene transfer may enhance the production of antioxidant scavengers, and has been employed to experimentally prevent or treat ischemic injury in cardiovascular, pulmonary, hepatic, intestinal, central nervous or other systems in animal models. With improvements in vector systems and delivery approaches, innovative antioxidant gene therapy has conferred better outcomes for myocardial infarction, reduced restenosis after coronary angioplasty, improved the quality and function of liver grafts, as well as outcome of intestinal and cerebral ischemic attacks. However, it is crucial to be mindful that like other therapeutic armentarium, the efficacy of antioxidant gene transfer requires extensive preclinical investigation before it can be used in patients, and that it may have unanticipated short- or long-term adverse effects. Thus, it is critical to balance between the therapeutic benefits and potential risks, to develop disease-specific antioxidant gene transfer strategies, to deliver the therapy with an optimal time window and in a safe manner. This review attempts to provide the rationale, the most effective approaches and the potential hurdles of available antioxidant gene transfer approaches for ischemic injury in various organs, as well as the possible directions of future preclinical and clinical investigations of this highly promising therapeutic modality. PMID:19233238

Wu, Jian; Hecker, James G.; Chiamvimonvat, Nipavan

2009-01-01

391

Intensive care management of ischemic stroke  

Microsoft Academic Search

The practice of neurointensive care was initially developed to manage postoperative neurosurgical patients and expanded thereafter\\u000a to the management of patients with primary head trauma, intracranial hemorrhage, vasospasm after subarachnoid hemorrhage,\\u000a elevated intracranial pressure, and unstable pulmonary or cardiovascular medical conditions in neurologic patients. Can neurointensive\\u000a care with its advanced medical and neurologic resources improve the outcome of the ischemic

Thanh Nguyen; Walter J. Koroshetz

2003-01-01

392

Thrombolytic therapy in acute ischemic stroke  

Microsoft Academic Search

Opinion statement  The use of intravenous thrombolytic therapy for the treatment of patients with acute ischemic stroke is now approved in the\\u000a United States, Canada, Germany, and the European Union. Guidelines published in 1996 from the American Heart Association and\\u000a American Academy of Neurology committees recommended intravenous administration of recombinant tissue-plasminogen activator\\u000a (rt-PA) (0.9 mg\\/kg; maximum of 90 mg) given in

Anthony J. Furlan; Irene L. Katzan; Louis R. Caplan

2003-01-01

393

Hypoxic Ischemic Encephalopathy in the Term Infant  

PubMed Central

Synopsis Hypoxia-ischemia in the perinatal period is an important cause of cerebral palsy and associated disabilities in children. There has been significant research progress in hypoxic-ischemic encephalopathy over the last two decades and many new molecular mechanisms have been identified. Despite all these advances, therapeutic interventions are still limited. In this review paper, we discuss a number of molecular pathways involved in hypoxia-ischemia, and potential therapeutic targets. PMID:19944838

Fatemi, Ali; Wilson, Mary Ann; Johnston, Michael V.

2010-01-01

394

Network Provisioning & Resource Management for IP Telephony1  

Microsoft Academic Search

The rapid growth of IP-based packet switched network and the overall bandwidth efficiency of an inte- grated IP network make it an attractive candidate to transport real time voice connections. However, high quality voice over IP (VoIP) remains a challenge because interactive voice imposes many performance requirements (such as loss rate and latency) on the transport network. This cannot be

Chen-Nee Chuah; Randy H. Katz

395

Integration of IPs into the M8051 microcontroller  

Microsoft Academic Search

This paper presents the implementation and integration the AES 128 data encryption IP and the I2C serial communication interface IP, into the IP of the M8051 microcontroller. We detail each block and validate them though testbench simulation. We performed functionality testing in FPGA to verify the correct functioning of the IPs and their integration.

Thiago P Mussolini; Leonardo B Zoccal; Tales C Pimenta; Paulo C Crepaldi; Robson L Moreno

2012-01-01

396

Online Pairing of VoIP Conversations Michail Vlachos  

E-print Network

Online Pairing of VoIP Conversations Michail Vlachos Aris Anagnostopoulos Olivier Verscheure conversations over VoIP networks. We achieve this by exploiting the ape- riodic inter-departure time of VoIP packets, hence trivializ- ing each VoIP stream into a binary time-series, indicating the voice activity

Leonardi, Stefano

397

An Overlay Architecture for High Quality VoIP Streams  

E-print Network

An Overlay Architecture for High Quality VoIP Streams Yair Amir, Member, IEEE, ACM, Claudiu Danilov features associated with Voice over IP (VoIP) are driving its adoption by service providers. Unfortunately and jitter is the key requirement for supporting high quality interactive conversations, VoIP applications

Amir, Yair

398

VoIP Deployment Committee Version 1.6  

E-print Network

VoIP Deployment Committee Version 1.6 Prepared by William Green, ITS Last Edited October 30, 2012 1 VoIP Deployment Committee the deployment of the Voice Over IP (VoIP) telephony system on campus. IT Governance

Texas at Austin, University of

399

An Overlay Architecture for High Quality VoIP Streams  

E-print Network

An Overlay Architecture for High Quality VoIP Streams Yair Amir, Claudiu Danilov, Stuart Goose://www.cnds.jhu.edu Abstract-- The cost savings and novel features associated with Voice over IP (VoIP) are driving its requirement for supporting high quality interactive conversations, VoIP applications use UDP to transfer data

Amir, Yair

400

Error correctie in VoIP Frank van der Loo  

E-print Network

Error correctie in VoIP Frank van der Loo 0314005 20 juni 2007 #12;Inhoudsopgave 1 Inleiding 3 1.1 Probleemstelling . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 VoIP 4 2.1 VoIP protocollen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 2.2 VoIP Problemen . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 2.2.1 Firewalls

Lucas, Peter

401

VoIP Aggregation in Wireless Backhaul Networks Yongzhen Zhuang  

E-print Network

VoIP Aggregation in Wireless Backhaul Networks Yongzhen Zhuang , Kun Tan , Vincent Shen , Yunhao over IP (VoIP) ap- plications due to the MAC overheads introduced by huge amounts of small packets. As a result, they fail to ensure the VoIP quality in terms of delay and loss. The major contribution

Liu, Yunhao

402

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

403

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

404

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

E-print Network

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

Jimack, Peter

405

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

PubMed

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

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

2008-01-01

406

A Novel Therapy to Attenuate Acute Kidney Injury and Ischemic Allograft Damage after Allogenic Kidney Transplantation in Mice  

PubMed Central

Ischemia followed by reperfusion contributes to the initial damage to allografts after kidney transplantation (ktx). In this study we tested the hypothesis that a tetrapeptide EA-230 (AQGV), might improve survival and attenuate loss of kidney function in a mouse model of renal ischemia/reperfusion injury (IRI) and ischemia-induced delayed graft function after allogenic kidney transplantation. IRI was induced in male C57Bl/6N mice by transient bilateral renal pedicle clamping for 35 min. Treatment with EA-230 (20–50mg/kg twice daily i.p. for four consecutive days) was initiated 24 hours after IRI when acute kidney injury (AKI) was already established. The treatment resulted in markedly improved survival in a dose dependent manner. Acute tubular injury two days after IRI was diminished and tubular epithelial cell proliferation was significantly enhanced by EA-230 treatment. Furthermore, CTGF up-regulation, a marker of post-ischemic fibrosis, at four weeks after IRI was significantly less in EA-230 treated renal tissue. To learn more about these effects, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) at 28 hours after IRI. EA-230 improved both GFR and RBF significantly. Next, EA-230 treatment was tested in a model of ischemia-induced delayed graft function after allogenic kidney transplantation. The recipients were treated with EA-230 (50 mg/kg) twice daily i.p. which improved renal function and allograft survival by attenuating ischemic allograft damage. In conclusion, EA-230 is a novel and promising therapeutic agent for treating acute kidney injury and preventing IRI-induced post-transplant ischemic allograft injury. Its beneficial effect is associated with improved renal perfusion after IRI and enhanced regeneration of tubular epithelial cells. PMID:25617900

Gueler, Faikah; Shushakova, Nelli; Mengel, Michael; Hueper, Katja; Chen, Rongjun; Liu, Xiaokun; Park, Joon-Keun; Haller, Hermann

2015-01-01

407

Arterial Spin Label Imaging of Acute Ischemic Stroke and Transient Ischemic Attack  

PubMed Central

Since acute ischemic stroke and transient ischemic attack (TIA) are fundamentally disruptions of brain hemodynamics, neuroimaging of brain perfusion might be expected to be of clinical utility. Recently, a noncontrast method of measuring CBF using arterial spin labeling (ASL) has become feasible in the clinical setting. It has advantages when compared to dynamic susceptibility contrast (DSC) bolus contrast perfusion-weighted imaging (PWI) that include lack of exposure to gadolinium-based contrast materials, improved quantitation, and decreased sensitivity to susceptibility artifacts and motion. Drawbacks of ASL include reduced signal-to-noise (SNR) and high sensitivity to arterial transit delays. While deleterious for quantitative perfusion measurements, the sensitivity of ASL to late arriving blood can be beneficial to visualize collateral flow. This chapter will discuss ASL imaging findings in patients presenting with acute ischemic stroke and TIA, focusing on typical appearances, common artifacts, and comparisons with bolus contrast PWI. PMID:21640300

Zaharchuk, Greg

2011-01-01

408

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

PubMed Central

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

Xing, Dongmei

2009-01-01

409

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

NSDL National Science Digital Library

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

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

2005-07-05

410

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

PubMed

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

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

2015-02-01

411

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

NASA Technical Reports Server (NTRS)

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

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

1996-01-01

412

Billing Attacks on SIP-Based VoIP Systems  

Microsoft Academic Search

Billing is fundamental to any commercial VoIP services and it has direct impact on each individual VoIP sub- scriber. One of the most basic requirements of any VoIP billing function is that it must be reliable and trustwor- thy. From the VoIP subscriber's perspective, VoIP billing should only charge them for the calls they have really made and for the

Ruishan Zhang; Xinyuan Wang; Xiaohui Yang; Xuxian Jiang

413

Artificial muscle technology applied towards treating ischemic mitral regurgitation caused by left ventricular remodeling  

E-print Network

Ischemic Mitral Regurgitation (MR) affects a large portion of patients suffering from ischemic heart disease. Significant MR develops in one quarter to one third of patients who suffer from ischemic heart disease and doubles ...

Sabourin, Nicaulas A. (Nicaulas Alexandre), 1978-

2004-01-01

414

POPULATION ECOLOGY Population Dynamics of Ips pini and Ips grandicollis in Red Pine  

E-print Network

POPULATION ECOLOGY Population Dynamics of Ips pini and Ips grandicollis in Red Pine PlantationsÐ1051 (2002) ABSTRACT We sampled bark beetle (Coleoptera: Scolytidae) populations in 17 declining and healthy red pine plantations in Wisconsin over 3 yr. We tested for potential relationships among numbers

Erbilgin, Nadir

415

Positive Indian Ocean Dipole events precondition southeast Australia bushfires  

NASA Astrophysics Data System (ADS)

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

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

2009-10-01

416

Hyperbaric oxygen preconditioning protects skin from UV-A damage.  

PubMed

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

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

2013-01-01

417

Utility of ischemic scores in the differential diagnosis of Alzheimer's disease and ischemic vascular dementia.  

PubMed

Despite new developments in the concept of vascular dementia, the Hachinski Ischemic Score (HIS) and its modified versions continue to be widely used in the clinical differentiation of Alzheimer's disease (AD) and ischemic vascular dementia (IVD). The sensitivity of the HIS and two modified versions in the diagnosis of AD, IVD, and single infarcts in a large, geriatric population with mild cognitive impairment (N = 100) was evaluated. Sensitivity for identification of AD was greater than 90% but was less than 70% for IVD. Over one third of patients with one or more infarcts on computed tomographic brain scans and 63% of mixed cases were classified as having probable AD. It is concluded that ischemic scores may be useful at predicting prevalence rates if individual case accuracy is ignored. Despite being sensitive to identifying AD, ischemic scores are insensitive to both cerebral infarction and IVD and cannot reliably exclude IVD. Finally, patients with mixed dementia should not be expected to have intermediate scores. PMID:9116177

Swanwick, G R; Coen, R F; Lawlor, B A; O'Mahony, D; Walsh, J B; Coakley, D

1996-01-01

418

A survey of IP over ATM architectures  

SciTech Connect

Over the past decade, the Internet has burgeoned into a worldwide information highway consisting of approximately 5 million hosts on over 45,000 interconnected networks. This unprecedented growth, together with the introduction of multimedia workstations, has spurred the development of innovative applications that require high speed, low latency, and real-time transport. Today`s Internet can neither scale in its bandwidth nor guarantee the Quality of Services (QoS) necessary to meet these performance requirements. Many network researchers propose to use the Asynchronous Transfer Mode (ATM) technology as the underlying infrastructure for the next generation of workgroup, campus, and enterprise IP networks. Since ATM is significantly different from today`s legacy network technologies, efficient implementation of IP over ATM is especially challenging. This tutorial paper covers several existing proposals that integrate IP over ATM.

Chen, H.; Tsang, R.; Brandt, J.; Hutchins, J.

1997-07-01

419

Simulink based VoIP Analysis  

E-print Network

Voice communication over internet not be possible without a reliable data network, this was first available when distributed network topologies were used in conjunction with data packets. Early network used single centre node network in which a single workstation (Server) is responsible for the communication. This posed problems as if there was a fault with the centre node, (workstation) nothing would work. This problem was solved by the distributed system in which reliability increases by spreading the load between many nodes. The idea of packet switching & distributed network were combined, this combination were increased reliability, speed & responsible for voice communication over internet, Voice-over-IP (VoIP)These data packets travel through a packet-switched network such as the Internet and arrive at their destination where they are decompressed using a compatible Codec (audio coder/decoder) and converted back to analogue audio. This paper deals with the Simulink architecture for VoIP network.

Singh, Hardeep; Mian, M

2010-01-01

420

Antithrombotic and Thrombolytic Therapy for Ischemic Stroke  

PubMed Central

Objectives: This article provides recommendations on the use of antithrombotic therapy in patients with stroke or transient ischemic attack (TIA). Methods: We generated treatment recommendations (Grade 1) and suggestions (Grade 2) based on high (A), moderate (B), and low (C) quality evidence. Results: In patients with acute ischemic stroke, we recommend IV recombinant tissue plasminogen activator (r-tPA) if treatment can be initiated within 3 h (Grade 1A) or 4.5 h (Grade 2C) of symptom onset; we suggest intraarterial r-tPA in patients ineligible for IV tPA if treatment can be initiated within 6 h (Grade 2C); we suggest against the use of mechanical thrombectomy (Grade 2C) although carefully selected patients may choose this intervention; and we recommend early aspirin therapy at a dose of 160 to 325 mg (Grade 1A). In patients with acute stroke and restricted mobility, we suggest the use of prophylactic-dose heparin or intermittent pneumatic compression devices (Grade 2B) and suggest against the use of elastic compression stockings (Grade 2B). In patients with a history of noncardioembolic ischemic stroke or TIA, we recommend long-term treatment with aspirin (75-100 mg once daily), clopidogrel (75 mg once daily), aspirin/extended release dipyridamole (25 mg/200 mg bid), or cilostazol (100 mg bid) over no antiplatelet therapy (Grade 1A), oral anticoagulants (Grade 1B), the combination of clopidogrel plus aspirin (Grade 1B), or triflusal (Grade 2B). Of the recommended antiplatelet regimens, we suggest clopidogrel or aspirin/extended-release dipyridamole over aspirin (Grade 2B) or cilostazol (Grade 2C). In patients with a history of stroke or TIA and atrial fibrillation we recommend oral anticoagulation over no antithrombotic therapy, aspirin, and combination therapy with aspirin and clopidogrel (Grade 1B). Conclusions: These recommendations can help clinicians make evidence-based treatment decisions with their patients who have had strokes. PMID:22315273

Lansberg, Maarten G.; O’Donnell, Martin J.; Khatri, Pooja; Lang, Eddy S.; Nguyen-Huynh, Mai N.; Schwartz, Neil E.; Sonnenberg, Frank A.; Schulman, Sam; Vandvik, Per Olav; Spencer, Frederick A.; Alonso-Coello, Pablo; Guyatt, Gordon H.

2012-01-01

421

Intravenous thrombolysis for acute ischemic stroke.  

PubMed

Intravenous thrombolysis (IVT) with alteplase remains the standard treatment for acute ischemic stroke. Although IVT can be started up to 4.5 hours after symptoms' onset, it is all the more effective and safe when started early. It allows a 10% absolute reduction in the risk of handicap or death at 3 months, despite a 2-7% risk of symptomatic intracranial hemorrhage. Current research efforts involve firstly trying