Relevant bibliographies by topics / Ischemia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Ischemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "Ischemia"

1

Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, Soon Sung Lim, Il Jun Kang, Ji Hyeon Ahn, Joon Ha Park, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (May 3, 2022): 5096. http://dx.doi.org/10.3390/ijms23095096.

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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis.
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Park, Kwon Moo, Ang Chen, and Joseph V. Bonventre. "Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury and JNK, p38, and MAPK Kinase Activation by Remote Ischemic Pretreatment." Journal of Biological Chemistry 276, no. 15 (January 9, 2001): 11870–76. http://dx.doi.org/10.1074/jbc.m007518200.

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MAPK activities, including JNK, p38, and ERK, are markedly enhanced after ischemiain vivoand chemical anoxiain vitro. The relative extent of JNK, p38, or ERK activation has been proposed to determine cell fate after injury. A mouse model was established in which prior exposure to ischemia protected against a second ischemic insult imposed 8 or 15 days later. In contrast to what was observed after 30 min of bilateral ischemia, when a second period of ischemia of 30- or 35-min duration was imposed 8 days later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtration rate, or increase in fractional excretion of sodium. A shorter period of prior ischemia (15 min) was partially protective against subsequent ischemic injury 8 days later. Unilateral ischemia was also protective against a subsequent ischemic insult to the same kidney, revealing that systemic uremia is not necessary for protection. The ischemia-related activation of JNK and p38 and outer medullary vascular congestion were markedly mitigated by prior exposure to ischemia, whereas preconditioning had no effect on post-ischemic activation of ERK1/2. The phosphorylation of MKK7, MKK4, and MKK3/6, upstream activators of JNK and p38, was markedly reduced by ischemic preconditioning, whereas the post-ischemic phosphorylation of MEK1/2, the upstream activator of ERK1/2, was unaffected by preconditioning. Pre- and post-ischemic HSP-25 levels were much higher in the preconditioned kidney. In summary, post-ischemic JNK and p38 (but not ERK1/2) activation was markedly reduced in a model of kidney ischemic preconditioning that was established in the mouse. The reduction in JNK and p38 activation can be accounted for by reduced activation of upstream MAPK kinases. The post-ischemic activation patterns of MAPKs may explain the remarkable protection against ischemic injury observed in this model.
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Lee, H. Thomas, and Charles W. Emala. "Protective effects of renal ischemic preconditioning and adenosine pretreatment: role of A1 and A3receptors." American Journal of Physiology-Renal Physiology 278, no. 3 (March 1, 2000): F380—F387. http://dx.doi.org/10.1152/ajprenal.2000.278.3.f380.

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Renal ischemia and reperfusion during aortic and renal transplant surgery result in ischemic-reperfusion injury. Ischemic preconditioning and adenosine infusion before ischemia protect against ischemic-reperfusion injury in cardiac and skeletal muscle, but these protective phenomena have not been demonstrated in the kidney. Rats were randomized to sham operation, 45-min renal ischemia, ischemic preconditioning with four cycles of 8-min renal ischemia and 5-min reperfusion followed by 45-min renal ischemia, systemic adenosine pretreatment before 45-min renal ischemia, or pretreatments with selective adenosine receptor subtype agonists or antagonists before 45-min renal ischemia. Forty-five minutes of renal ischemia followed by 24 h of reperfusion resulted in marked rises in blood urea nitrogen and creatinine. Ischemic preconditioning and adenosine pretreatment protected renal function and improved renal morphology. A1 adenosine receptor activation mimics and A1 adenosine antagonism blocks adenosine-induced protection. In addition, A3 adenosine receptor activation before renal ischemia worsens renal ischemic-reperfusion injury, and A3 adenosine receptor antagonism protects renal function. We demonstrate for the first time that rat kidneys can be preconditioned to attenuate ischemic-reperfusion injury and adenosine infusion before ischemic insult protects renal function via A1 adenosine receptor activation. Our data suggest that an A1 adenosine agonist and A3 adenosine antagonist may have clinically beneficial implications where renal ischemia is unavoidable.
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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (March 6, 2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.

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The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models, although initial signals appear within hours of ischemia onset. Components of the neurovascular unit, its participation in new vessel formation, and the nature of the core and penumbra responses to experimental focal cerebral ischemia, are considered here. The potential co-localization of vascular remodeling and axonal outgrowth following focal cerebral ischemia based on the definition of tissue remodeling and the processes that follow ischemic stroke are also considered. The region of angiogenesis in the ischemic core and its surrounding tissue (ischemic periphery) may be a novel target for treatment. We summarize issues that are relevant to model studies of focal cerebral ischemia looking ahead to potential treatments.
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Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.

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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral ischemia group, and diabetes mellitus+cerebral ischemia+PC group (in which the tree shrews with diabetic cerebral ischemia were treated with ischemic PC). H&E staining was used to examine the pathological changes in the retina, and immunohistochemistry was performed to determine the retinal expression of VEGF (vascular endothelial growth factor). The modeling resulted in 77% tree shrews with diabetes. Ischemic PC reduced the blood glucose levels in the tree shrews with diabetic cerebral ischemia. Tree shrews with diabetes had thinned retina with disordered structures, and these pathological changes were aggravated after cerebral ischemia. The retinopathy was alleviated after ischemic PC. Retina expression of VEGF was mainly distributed in the ganglion cell layer in tree shrews. Diabetes and cerebral ischemia increased retinal VEGF expression in a step-wise manner, while additional ischemic PC reduced retinal VEGF expression. Therefore, ischemic PC effectively alleviates retinopathy in tree shrews with diabetic cerebral ischemia, and this effect is associated with reduced retinal VEGF expression.
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Li, Chuanfu, Race L. Kao, Tuanzhu Ha, Jim Kelley, I. William Browder, and David L. Williams. "Early activation of IKKβ during in vivo myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1264.

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We have demonstrated that in vitro brief ischemia activates nuclear factor (NF)-κB in rat myocardium. We report in vivo ischemia-reperfusion (I/R)-induced NF-κB activation, IκB kinase -β (IKKβ) activity, and IκBα phosphorylation and degradation in rat myocardium. Rat hearts were subjected to occlusion of the coronary artery for up to 45 min or occlusion for 15 min followed by reperfusion for up to 3 h. Cytoplasmic and nuclear proteins were isolated from ischemic and nonischemic areas of each heart. NF-κB activation was increased in the ischemic area (680%) after 10 min of ischemia and in the nonischemic area (350%) after 15 min of ischemia and remained elevated during prolonged ischemia and reperfusion. IKKβ activity was markedly increased in ischemic (1,800%) and nonischemic (860%) areas, and phosphorylated IκBα levels were significantly elevated in ischemic (180%) and nonischemic (280%) areas at 5 min of ischemia and further increased after reperfusion. IκBα levels were decreased in the ischemic (45%) and nonischemic (36%) areas after 10 min of ischemia and remained low in the ischemic area during prolonged ischemia and reperfusion. The results suggest that in vivo I/R rapidly induces IKKβ activity and increases IκBα phosphorylation and degradation, resulting in NF-κB activation in the myocardium.
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Zhan, Xinhua, Bradley P. Ander, Glen Jickling, Renée Turner, Boryana Stamova, Huichun Xu, Dazhi Liu, Ryan R. Davis, and Frank R. Sharp. "Brief Focal Cerebral Ischemia That Simulates Transient Ischemic Attacks in Humans Regulates Gene Expression in Rat Peripheral Blood." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (September 9, 2009): 110–18. http://dx.doi.org/10.1038/jcbfm.2009.189.

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Blood gene expression profiles of very brief (5 and 10 mins) focal ischemia that simulates transient ischemic attacks in humans were compared with ischemic stroke (120 mins focal ischemia), sham, and naïve controls. The number of significantly regulated genes after 5 and 10 mins of cerebral ischemia was 39 and 160, respectively (fold change ⩾∣1.5∣ and P<0.05). There were 103 genes common to brief focal ischemia and ischemic stroke. Ingenuity pathway analysis showed that genes regulated in the 5 mins group were mainly involved in small molecule biochemistry. Genes regulated in the 10 mins group were involved in cell death, development, growth, and proliferation. Such genes were also regulated in the ischemic stroke group. Genes common to ischemia were involved in the inflammatory response, immune response, and cell death—indicating that these pathways are a feature of focal ischemia, regardless of the duration. These results provide evidence that brief focal ischemia differentially regulates gene expression in the peripheral blood in a manner that could distinguish brief focal ischemia from ischemic stroke and controls in rats. We postulate that this will also occur in humans.
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KAKOKI, MASAO, YASUNOBU HIRATA, HIROSHI HAYAKAWA, ETSU SUZUKI, DAISUKE NAGATA, AKIHIRO TOJO, HIROAKI NISHIMATSU, et al. "Effects of Tetrahydrobiopterin on Endothelial Dysfunction in Rats with Ischemic Acute Renal Failure." Journal of the American Society of Nephrology 11, no. 2 (February 2000): 301–9. http://dx.doi.org/10.1681/asn.v112301.

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The role of nitric oxide (NO) in ischemic renal injury is still controversial. NO release was measured in rat kidneys subjected to ischemia and reperfusion to determine whether (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), a cofactor of NO synthase (NOS), reduces ischemic injury. Twenty-four hours after bilateral renal arterial clamp for 45 min, acetylcholine-induced vasorelaxation and NO release were reduced and renal excretory function was impaired in Wistar rats. Administration of BH4 (20 mg/kg, by mouth) before clamping resulted in a marked improvement of those parameters (10-8 M acetylcholine, Δrenal perfusion pressure: sham-operated control -45 ± 5, ischemia -30 ± 2, ischemia + BH4 -43 ± 4%; ΔNO: control +30 ± 6, ischemia +10 ± 2, ischemia + BH4 +23 ± 4 fmol/min per g kidney; serum creatinine: control 23 ± 2, ischemia 150 ± 27, ischemia + BH4 48 ± 6 μM; mean ± SEM). Most of renal NOS activity was calcium-dependent, and its activity decreased in the ischemic kidney. However, it was restored by BH4 (control 5.0 ± 0.9, ischemia 2.2 ± 0.4, ischemia + BH4 4.3 ± 1.2 pmol/min per mg protein). Immunoblot after low-temperature sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that the dimeric form of endothelial NOS decreased in the ischemic kidney and that it was restored by BH4. These results suggest that the decreased activity of endothelium-derived NO may worsen the ischemic tissue injury, in which depletion of BH4 may be involved.
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Kim, Gyung W., Taku Sugawara, and Pak H. Chan. "Involvement of Oxidative Stress and Caspase-3 in Cortical Infarction after Photothrombotic Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1690–701. http://dx.doi.org/10.1097/00004647-200012000-00008.

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Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected by hydroethidine oxidation, and cytosolic cytochrome c were detected in early ischemic lesions. Western blot analysis showed the cleaved form and the level of the proform of caspase-3 in the ischemic lesion 24 hours after ischemia. Decreased caspase-3 immunoreactivity was detected in the antioxidant-treated group after ischemia. Decreased DNA fragmentation and laddering were detected and the lesion was smaller in the treated group after ischemia compared with the untreated group. Oxidative stress and cytochrome c release occur in the ischemic lesion after photothrombotic ischemia. The free radical scavenger attenuated caspase-3 up-regulation, DNA fragmentation, and the final lesion. The authors concluded that oxidative stress may mediate caspase-related apoptotic cell death and subsequent cortical infarction after photothrombotic ischemia.
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Pan, Hui-Lin, Shao-Rui Chen, Gloria M. Scicli, and Oscar A. Carretero. "Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H116—H121. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h116.

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Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 ± 2.8 vs. 7.3 ± 1.7 ng/ml, P < 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 ± 0.6 ng/ml during the control period to 23.1 ± 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 ± 0.6 to 13.4 ± 1.9 ng/ml, P < 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning.
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Dissertations / Theses on the topic "Ischemia"

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Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.

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Christensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /." Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Dowden, Jennifer. "Characterizing the neuroprotective efficacy of ischemic preconditioning (ischemic tolerance) : is age an important factor? /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ54834.pdf.

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Harhous, Zeina. "Deciphering the Interlink between STAT3 and MAPKs in Ischemia/Reperfusion and Ischemic Conditioning." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1145.

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Les maladies cardiovasculaires sont une des principales causes de morbidité et de mortalité au monde. La plus courante est l’infarctus du myocarde définit pathologiquement par la mortalité cellulaire dû à une ischémie prolongée d’une partie du ventricule gauche. L'ischémie est caractérisée par un apport sanguin insuffisant causé par une obstruction d’une artère coronaire. La restauration, en clinique, du flux sanguin, appelée reperfusion, est considérée comme la méthode la plus efficace contre les dommages ischémiques. Paradoxalement, cette restauration du flux sanguin est associée à une exacerbation de la lésion tissulaire, entraînant alors des lésions d'ischémie-reperfusion (I/R). Dans le but de limiter ces lésions, le conditionnement ischémique myocardique est une avancée majeure dans le domaine de la cardioprotection. Ce protocole confère ses effets cardioprotecteurs via le recrutement de divers mécanismes endogènes suivant l’activation de deux voies intracellulaires : la voie RISK (Reperfusion Injury Salvage Kinase) et/ou la voie SAFE (Survivor Activator Factor Enhancer). Ces voies impliquent l'activation de différentes cascades de signalisation et de protéines kinases. En particulier, concernant la voie SAFE, le transducteur de signal et l'activateur de transcription-3 STAT3, a été identifié comme un acteur clé dans le postconditionnement ischémique (PostCI). Il est suggéré que les effets cardioprotecteurs attribués à STAT3 soient liés à ses effets en tant que facteur de transcription et en tant que régulateur de l’activité mitochondriale, mais tout n’est pas encore connu. En revanche, il est admis que STAT3 est activé par la phosphorylation ciblant les résidus tyrosine 705 et sérine 727. Dans nos travaux actuels, nous avions initialement pour objectif d’étudier les rôles cardioprotecteurs mitochondriaux de STAT3 après une I/R et un PostCI. Cependant, nous n'avons pas été en mesure de détecter STAT3 dans les mitochondries de cardiomyocytes adultes de souris, dans des conditions basales et de stress, en utilisant différentes approches. Fait intéressant, nous avons montré une localisation exclusive de STAT3 dans les myocytes cardiaques adultes, le long des tubules T, et nous avons mis en évidence les inconvénients des techniques précédemment utilisées.Outre les rôles putatifs de STAT3 dans les mitochondries, nous avons ciblé ses effets dans la signalisation et la génomique au cours de l'I/R et du PostCI. Nous avons tout d’abord cherché à déterminer, pendant l’I/R et le PostCI, la cinétique temporelle d’activation de STAT3 et des autres kinases de la voie RISK, notamment Akt et les MAPK ERK1 / 2, JNK et p38. En outre, nous avions pour objectif d’étudier les liens entre les voies SAFE et RISK en déchiffrant les liens entre STAT3 et les kinases RISK au cours du PostCI. Nous avons montré qu’après une ischémie et un temps court de reperfusion, STAT3 et ERK1/2 sont activés, et que l’utilisation d’un PostCI active d’autant plus STAT3 en induisant exclusivement la phosphorylation de sa tyrosine. Nous avons également montré que l’interconnexion entre les voies SAFE et RISK, dans le protocole PostCI utilisé, se fait par STAT3 et ERK1/2. À partir de ces résultats, nous nous sommes dirigés vers la génomique grâce à laquelle nous avons étudié l'activité de STAT3 au cours de l'IPoC. À cet égard, nous avons montré que STAT3 est impliqué dans la régulation de la réponse inflammatoire au cours de la PostCI. Dans l’ensemble, cette étude présente une approche globale des fonctions mitochondriales, de signalisation et génomiques de STAT3 dans le contexte de la protection cardiaque
Cardiovascular diseases are leading causes of morbidity and mortality worldwide. Among the mostly prevailing cardiovascular diseases is myocardial infarction, which is pathologically defined as myocardial death due to a prolonged ischemia. Ischemia is an insufficient supply of blood caused by a blockade in the coronary arteries. The early restoration of blood flow is considered the most effective method against the ischemic lesions. Paradoxically, this blood flow restoration is associated with an exacerbation of the tissue injury, leading to the ischemia-reperfusion (I/R) injury. To avoid this injury, the myocardial ischemic conditioning protocol has rejuvenated the field of cardioprotection. This protocol confers its cardioprotective effects via recruiting various endogenous mechanisms following the activation of two intracellular pathways: the reperfusion injury salvage kinase (RISK) or survivor activator factor enhancer (SAFE) pathways. These pathways involve the activation of different signaling cascades and protein kinases. Zooming in through the SAFE pathway, the signal transducer and activator of transcription-3, STAT3, has been identified as a prominent key player in ischemic postconditioning (IPoC). The cardioprotective effects attributed to STAT3 are suggested to be linked to its roles as a transcription factor and as a regulator of the mitochondrial activity, but these are not well studied and elaborated. STAT3 is activated by phosphorylation, which targets the tyrosine 705 and serine 727 residues. In our current work, we initially aimed to investigate the mitochondrial cardioprotective roles of STAT3 following I/R and IPoC. However, we were not able to detect STAT3 in the mitochondria of adult mouse cardiomyocytes under variousbasal and stress conditions using different approaches. Interestingly, we showed an exclusive STAT3 pattern in adult cardiac myocytes, along the T-tubules, and highlighted drawbacks of previously used techniques. Aside from the mitochondrial roles of STAT3, we targeted its signaling and genomic roles during I/R and IPoC. We first aimed to determine, during I/R and IPoC, the temporal kinetics of activation of STAT3 and the other kinases of the RISK pathway including Akt and the MAPKs ERK1/2, JNK and p38. In addition, we aimed to decipher the interlink between the SAFE and RISK pathways through deciphering the interlink between STAT3 and the RISK kinases following IPoC. We showed that a short reperfusion time activates STAT3 and ERK1/2 following ischemia, and that the application of IPoC further activates STAT3 through inducing its tyrosine phosphorylation. We also showed that the interlink between SAFE and RISK pathways, in the IPoC protocol we used, is through STAT3 and ERK1/2. From this signaling level, we moved toward the genomic level whereby we investigated the genomic activity of STAT3 during IPoC. In this regard, we have shown that STAT3 is involved in the regulation of the inflammatory response during IPoC. Overall, this study presents a global approach of STAT3’s mitochondrial, signaling and genomic functions in the context of cardiac protection
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Zhang, Jitian. "Nebulized phosphodiesterase 3 inhibitor during warm ischemia attenuates pulmonary ischemia-reperfusion injury." Kyoto University, 2009. http://hdl.handle.net/2433/126442.

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Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.

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Thesis (Ph.D.)--Indiana University, 2009.
Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).
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Keasey, Matthew P. "MicroRNAs in Cerebral Ischemia." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526014.

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Lipšic, Erik. "Erythropoietin in cardiac ischemia." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/293076030.

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Aoyama, Akihiro. "Post-ischemic Infusion of Atrial Natriuretic Peptide Attenuates Warm Ischemia-Reperfusion Injury in Rat Lung." Kyoto University, 2011. http://hdl.handle.net/2433/142544.

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Hultgren, Rebecka. "Lower limb ischemia in women /." Stockholm, 2004. http://diss.kib.ki.se/2003/91-7349-798-3.

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Books on the topic "Ischemia"

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Walz, Wolfgang. Cerebral Ischemia. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/0896035409.

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Hacke, Werner, Herman J. Gelmers, Michael Hennerici, and Günter Krämer. Cerebral Ischemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75548-4.

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Gusev, Eugene, and Veronica I. Skvortsova. Brain Ischemia. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9248-2.

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v. Arnim, Th, and A. Maseri, eds. Silent Ischemia. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-12997-5.

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Walz, Wolfgang, ed. Cerebral Ischemia. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5.

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Dhalla, Naranjan S., Ian R. Innes, and Robert E. Beamish, eds. Myocardial Ischemia. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5.

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Caplan, Louis R., ed. Brain Ischemia. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5.

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Cokkinos, Dennis V., Constantinos Pantos, Gerd Heusch, and Heinrich Taegtmeyer, eds. Myocardial Ischemia. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6.

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Gusev, E. I. Brain ischemia. New York: Kluwer Academic/Plenum Publishers, 2003.

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10

J, Boley Scott, and Brandt Lawrence J, eds. Intestinal ischemia. Philadelphia: Saunders, 1992.

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Book chapters on the topic "Ischemia"

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Hasan, Aliya G., and Joel S. Levine. "Ischemia/Ischemic Colitis." In Textbook of Clinical Gastroenterology and Hepatology, 417–20. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118321386.ch55.

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Romano, Stefania, and Luigia Romano. "Ischemia (Acute Mesenteric Ischemia and Ischemic Colitis)." In CT of the Acute Abdomen, 183–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/174_2010_82.

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Roth, Elliot J. "Ischemia." In Encyclopedia of Clinical Neuropsychology, 1862. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2186.

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Roth, Elliot J. "Ischemia." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2186-2.

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Mirzakhani, Hooman, and Ala Nozari. "Ischemia." In Chemistry and Biochemistry of Oxygen Therapeutics, 145–58. Chichester, UK: John Wiley & Sons, Ltd, 2011. http://dx.doi.org/10.1002/9781119975427.ch10.

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Cheung, Raymond T. F., and Vladimir Hachinski. "Ischemia." In Molecular Mechanisms of Dementia, 271–91. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-471-9_17.

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Mehlhorn, Heinz. "Ischemia." In Encyclopedia of Parasitology, 1361. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3974.

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Mehlhorn, Heinz. "Ischemia." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3974-1.

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Urbach, Horst. "Ischemia." In MRI in Epilepsy, 193–206. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/174_2012_781.

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Gooch, Jan W. "Ischemia." In Encyclopedic Dictionary of Polymers, 902. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14054.

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Conference papers on the topic "Ischemia"

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Lee, Gija, Seokkeun Choi, Sungwook Kang, Samjin Choi, Jeonghoon Park, Dong Hyun Park, Youngho Park, Kyungsook Kim, Bermseok Oh, and Hunkuk Park. "Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206602.

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During the operation, surgeons in neurosurgical area usually performed the multiple temporary occlusions of parental artery which may induce the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this experiment, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model during repeated within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. During ischemia, the peak level of glutamate release was gradually decreased as 112.38±26.21 μM in first period, 82.63±18.50 μM in second period, and 48.58±11.89 μM in third period. The time interval between the ischemia induction and the beginning of glutamate release was increased as 106.7 ± 10.89 (sec) at first attack, 139.11 ± 3.87 (sec) in second attack, 169.00 ± 14.56 (sec) in third ischemic period. From the results of real-time monitoring about glutamate release in 11-VO model during repetitive ischemic episode, it was demonstrated that repetitive ischemia induced less glutamate release from neuronal cell than single ischemia due to endogeneous protective mechanism which delayed glutamate release time in later ischemic injury.
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Fisher, M., and R. Francis. "ALTERED COAGULATION IN CEREBRAL ISCHEMIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644345.

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We investigated coagulation changes in a group of patients with cerebral ischemia, ranging from transient ischemic attacks to cerebral infarction. Patients were studied acutely (within 72 hours of onset of ischemia) and again approximately 2 months following the initial examination. We evaluated platelet activation, fibrin generation, and fibrinolysis by measuring plasma beta-thromboglobulin (BTG), fibrinopeptide A (FPA), and fibrinopeptide B-beta 1-42 (FPB), respectively. We compared measurements in cerebral ischemia patients with a group of age -and sex-matched neurological inpatients without vascular disease ("patient controls") and a similarly matched group of normal volunteers ("normal controls"). BTG levels for 90 patients studied acutely were not significantly different compared to 58 of the same patients studied 2 months later, 16.4 ± 11.3 ng/ml (mean ± SD) versus 17.5 ± 10.2 ng/ml. Both values were significantly increased (p< .05) compared to normal controls (12.2 ± 6.5 ng/ml, n = 44); patient controls (13.2 ± 7.6 ng/ml, n = 18) were not significantly different from normals. In contrast, FPA measurements were significantly increased in acute patients compared to normals (3.3 ± 5.8 versus 1.0 ± 1.7 ng/ml, p< .05) while FPA levels 2 months post-ischemia (0.6 ± 0.9 ng/ml) were no different than normals. FPB measurements were not significantly different among either acute patients (6.5 ± 2.4 pmol/ml) or patients 2 months post-ischemia (4.8 ± 1.5 pmol/ml) compared to normals (6.5 ± 1.8 pmol/ml).In summary, we have found, among cerebral ischemia patients, sustained increases in BTG, acute increases in FPA, and normal FPB. These findings are compatible with a model of cerebral ischemia consisting of acutely increased fibrin generation without concomitant increased fibrinolytic activity, superimposed on a background of increased platelet activation.
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Xia, Cao, Ma Kewei, Han Bing, Yu Xiaofeng, Qu Shaochun, Sui Dayuan, Pei Jin, and Gu Xinquan. "Protective effects of ischemic preconditioning on myocardial ischemia reperfusion injury." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027906.

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Шварц, Владислав Александрович, Марина Станиславовна Кудабаева, Илья Леонидович Губский, Дарья Дмитриевна Наместникова, and Марина Юрьевна Ходанович. "LONG-TERM DYNAMIC OF ISCHEMIC LESION VOLUME AND THE BRAIN HEMISPHERES’ VOLUME IN THE MODEL OF FOCAL ISCHEMIA MODEL IN RAT." In Высокие технологии и инновации в науке: сборник избранных статей Международной научной конференции (Санкт-Петербург, Сентябрь 2020). Crossref, 2020. http://dx.doi.org/10.37539/vt187.2020.52.45.003.

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В исследовании изучалась динамика объема ишемического очага и объемов полушарий мозга у животных с локальной ишемией в течении 2 месяцев после ишемии при помощи ручной сегментации. Были выявлены значимые различия между объемами полушарий на 1, 3, 14, 21, 30, 42 день исследования (p<0,01-0,05),, а также резкий рост объема ишемического поражения в течение 1-3 суток, после чего его объем монотонно уменьшался. Ischemic lesion volume and the brain hemisphere volume long-term changes were evaluated during 2 month after focal ischemia in rats using manual segmentation,. Significant differences were identified between hemisphere volumes on the 1st, 3rd, 14th, 21st, 30th, 42nd day after ischemia (p<0,01-0,05). A sharp increase in volume ischemic lesion was identified from the 1st till the 3rd day, then lesion volume constantly decreased.
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Breton, Michael E., Graham E. Quinn, Sara S. Keene, Janet C. Dahmen, and Alexander J. Brucker. "Analysis of ERG Parameters in Central Retinal Vein Occlusion." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/navs.1988.wa1.

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Effective treatment of the complications resulting from an ischemic condition such as central retinal vein occlusion (CRVO) may depend on the accuracy of early diagnosis. In CRVO, relative ischemia of a significant proportion of retina has been associated with ocular morbidity in the form of rubeosis iridis and neovascular glaucoma (1,2,3). Fluorescein angiography (FA) has been used routinely to determine the degree of retinal ischemia in CRVO as in other occlusive vascular diseases of the retina. However, FA interpretation, based on non-quantitative visual judgements, may lack sufficient sensitivity to detect early ischemic changes (4). The purposes of this report are: 1) to characterize the ERG parameters for CRVO and fellow eyes as to their ability to identify functionally distinct sub-groups, and 2) to compare the ERG characterization of CRVO eyes to a variety of FA caracteristics.
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La Barck, Anthony J., Jennifer E. Akers, and Thomas L. Merrill. "Tissue Oxygen Transfer During Reperfusion and Post-Conditioning." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53064.

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Heart disease is the leading cause of death in the United States. Ischemic heart disease occurs when coronary blood flow to the heart is reduced, limiting the amount of oxygen and nutrients the heart receives. When blood flow is restored after a percutaneous transluminal coronary intervention (PCI), rapid reperfusion from sudden balloon deflation can cause further injury to oxygen-starved tissue, leading to increased cell injury and cell death. Studies in animal models with ischemic heart disease have shown that reperfusion injury may account for up to 50% of the final infarct size [1]. Post-conditioning (PC) may reduce the amount of reperfusion injury by applying intermittent periods of ischemia during the early moments of reperfusion. This procedure periodically occludes blood vessels during reperfusion by periodically inflating and deflating an angioplasty balloon according to a specific algorithm. Zhao et al. showed that PC reduced reperfusion injury in a canine model by applying 3 cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia (re-occlusion) at the onset of reperfusion. PC in this study reduced tissue AN/AAR (area of necrosis/area at risk) by 48% [2]. In 2008, Gao et al. demonstrated that the effectiveness of PC in rats was dependent on the number of cycles in the PC algorithm, as well as the durations of the ischemia/reperfusion phases [3].
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Parsons, J., H. Hirzallah, and F. M. Zeid. "Vasopressor Induced Limb Ischemia." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6557.

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Emam, A., H. Tonekabonipour, M. Teshnelab, and M. Aliyari Shoorehdeli. "Ischemia prediction using ANFIS." In 2010 IEEE International Conference on Systems, Man and Cybernetics - SMC. IEEE, 2010. http://dx.doi.org/10.1109/icsmc.2010.5642197.

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Zahavi, J., R. Schafer, A. Zelikos-ki, E. Firsteter, M. Zahavi, and E. Avrahami. "EFFICACY OF INTRAVENOUS PENTOXIFYLLINE IN THE MANAGEMENT OF PATIENTS WITH CRITICAL LEG ISCHEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644824.

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The xantine derivative pentoxifylline (P) can promote blood flow in the macro-and-micro circulation of ischemic tissues by improvement of red cell rigidity and by enhancing PGI2 release from the vascular endothelium. 35 patients (mean age 71±1.2 1SE years) suffering from critical leg ischemia due to advanced peripheral vascular disease (PVD) were treated by continuous I.V. drip of P (mean dose 22.2 g. during a mean period of 22.2 days). 19 patients were diabetics and 16 non-diabetics. Severity of PVD was assessed by the walking distance (WD), the presence of ischemic rest pain (IRP), leg ulcers or gangrene (doccumented photographically), hemodynamic evaluation using Doppler auscultation andby an arteriography of the lower limbs. The most common lesion on arteriography was occlusion or severe stenosis of the superficial femoral artery. All the patients suffered from IRP, 20 of them from leg ulcers and or gangrene. Following treatment of the diabetics, the WD was considerably improved (p≺0.01) in 7patients, the IRP disappeared in 11 and was milder in another 4 patients. Leg ulcers were healed in 5.out of 11 patients and gangrene subsided in 2 out of 9 patients. It was partially healed in another3 patients. Thus only in 4 patients the leg ischemia was worse and required bellow-knee amputation. In the non-diabetics, WD was improved considerably in 12 patients, the IRP disappeared in 11 and was milder in another 4 ' patients. Gangrene subsided in 2 out of 4 patients andwasimproved in the remaining 2 patients. None of these patients underwent amputation. The resting ankle pressure index(on Doppler auscultation) values were similar in the 2 groups and were increased after treatment (p≺0.01).Our results indicate that P ia a useful drug in the management of patients with advanced PVD and critical leg ischemia particularly in non-diabetics. It should be considered in inoperable patients in whom leg amputation is imminent. P can induce both subjective and objective improvement in the WD and the hemodynamicprofile of these patients and promote the blood flow in the microcicul-ation of the ischemic tissues in the lower limbs.
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Gaudette, Glenn R., Irvin B. Krukenkamp, Joseph Todaro, Fu-Pen Chiang, and E. Guan. "Using Computer Aided Speckle Interferometry to Measure Deformation in the Nonbeating Perfused Rabbit Heart." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2547.

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Abstract Many diseases result in a heterogeneous distribution of regional function. This results in the need for a technique that can accurately measure deformation with high spatial resolution. We have developed computer aided speckle interferometry (CASI) to accomplish this task. Instead of tracking individual particles, CASI tracks clusters of particles. An isolated rabbit heart was arrested, and data was acquired in the perfused state, globally ischemic (15 min) state and reperfused state (10 min). CASI was used to determine the simultaneous deformation of over 1,000 points located in a region approximately 5.5 × 5.5 mm. A balloon was inserted into the left ventricle, and balloon pressure was increased from 5 to 20 mmHg. Ischemia and reperfusion resulted in a change in the epicardial deformation, leading to a change in principle strain from 2.8% to 4.5% (ischemia) to 2.8% (reperfused). A change in principle angle was also seen, with a 43° increase with 15 minutes of ischemia, and only a 10° change with reperfusion. In summary, we have a novel technique to measure regional deformation with high spatial resolution and found differences in the perfusion status of the heart.
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Reports on the topic "Ischemia"

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Li, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li, and Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.

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Review question / Objective: Whether acupuncture is effective for infarction size on myocardial ischemia rat models. Condition being studied: Myocardial ischemia is a typical pathological condition of coronary heart disease (CHD), which has been a global issue with high incidence and mortality. Myocardial infarction caused by myocardial ischemia leads to cardiac dysfunction, and the size of myocardial infarction also determines the recovery and prognosis of cardiac function. Acupuncture, a long history of traditional Chinese medicine, is widely used to treat symptoms like thoracalgia and palpitation. Many researches based on rat experiments have shown that acupuncture affects infarction size, cardiac function, myocardial enzyme or arrhythmias severity on myocardial ischemia models; nevertheless, few literatures have systematically reviewed these studies, assessing the risk of bias, quality of evidence, validity of results, and summarizing potential mechanisms. A systematic review of animal studies can benefit future experimental designs, promote the conduct and report of basic researches and provide some guidance to translate the achievements of basic researches to clinical application in acupuncture for myocardial ischemia. Therefore, we will conduct this systematic review and meta analysis to evaluate effects of acupuncture on infarction size on myocardial ischemia rat models.
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Axford, T., J. Dearani, I. Khait, S. Khuri, and C. R. Valeri. On-Line Metabolic Monitoring of Tissue Ischemia. Fort Belvoir, VA: Defense Technical Information Center, June 1991. http://dx.doi.org/10.21236/ada360147.

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Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568392.

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Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada579994.

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chen, yaru, kai wang, jin yan, and zhenghua zhu. Comparison of the protective effect of ischemic preconditioning and remote ischemic preconditioning against ischemia reperfusion injury after hepatectomy: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2023. http://dx.doi.org/10.37766/inplasy2023.7.0007.

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Oeltgen, Peter R. Neuroprotective Effects of Opioid-Like Hibernation Factors in Cerebral Ischemia. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada424443.

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Merrill, Alfred H., and Jr. Subcellular Signal Transduction Systems in the Cellular Trauma of Ischemia. Fort Belvoir, VA: Defense Technical Information Center, November 1990. http://dx.doi.org/10.21236/ada229876.

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Zafirovski, Aleksandar, Marija Zafirovska, Dimitrij Kuhelj, and Tadeja Pintar. The impact of biomarkers in early detection of acute mesenteric ischemia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2023. http://dx.doi.org/10.37766/inplasy2023.12.0087.

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Zheng, Jinghui. Quercetin for Myocardial Ischemia/Reperfusion Injury: A Preclinical Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0162.

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Lu, Liying, Xiaocong Ma, Jinghui Zheng, Lijuan Li, Wenna Yang, Yixuan Kong, and Jie Wang. Quercetin for Myocardial Ischemia Reperfusion Injury: A Protocol for Systematic Review and Meta Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0067.

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