Bibliografías temáticas / Focal cerebral ischemia

Literatura académica sobre el tema "Focal cerebral ischemia"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 5 de febrero de 2022

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Artículos de revistas sobre el tema "Focal cerebral ischemia":

Hua, Y., G. Xi, G. M. de Courten-Myers, K. R. Wagner y R. E. Myers. "FOCAL CEREBRAL ISCHEMIA". Journal of Neuropathology and Experimental Neurology 55, n.º 5 (mayo de 1996): 663. http://dx.doi.org/10.1097/00005072-199605000-00240.

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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata y Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, n.º 5 (6 de marzo de 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.

Kinuta, Yuji, Haruhiko Kikuchi, Masatsune Ishikawa, Mieko Kimura y Yoshinori Itokawa. "Lipid peroxidation in focal cerebral ischemia". Journal of Neurosurgery 71, n.º 3 (septiembre de 1989): 421–29. http://dx.doi.org/10.3171/jns.1989.71.3.0421.

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✓ To verify whether lipid peroxidation is associated with focal cerebral ischemia, a unilateral middle cerebral artery occlusion was carried out in rats. The concentrations of various endogenous antioxidants in the ischemic center were measured, including α-tocopherol and ubiquinones as lipid-soluble antioxidants and ascorbate as a water-soluble antioxidant. At 30 minutes after ischemia, α-tocopherol decreased to 79% of baseline, reduced ubiquinone-9 to 73%, ubiquinone-10 to 66%, and reduced ascorbate to 76%. Six hours after ischemia, α-tocopherol decreased to 63% and reached a plateau, whereas reduced ubiquinones and reduced ascorbate declined further to 16% and 10%, respectively, 12 hours after ischemia and then reached plateau levels. These results suggest functional and durational differences between antioxidants and lipid peroxidation in this ischemic model. Although the reciprocal increase in oxidized ubiquinones during ischemia was not observed, that of oxidized ascorbate was noted. The complementary antioxidant system between cytoplasmic and membranous components, the combination α-tocopherol/ascorbate, was estimated from the calculated consumption ratio of these antioxidants on the basis that the loss of these reduced antioxidants is due to neutralization of free radicals. This system is suggested to play an important role in the early ischemic period. Urate also increased during ischemia. The possible involvement of the xanthine-xanthine oxidase system in initiating free radical reactions in cerebral ischemia is also discussed.

Pettigrew, L. Creed, Mary L. Holtz, Susan D. Craddock, Stephen L. Minger, Nathan Hall y James W. Geddes. "Microtubular Proteolysis in Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 16, n.º 6 (noviembre de 1996): 1189–202. http://dx.doi.org/10.1097/00004647-199611000-00013.

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Calpain, a neutral protease activated by calcium, may promote microtubular proteolysis in ischemic brain. We tested this hypothesis in an animal model of focal cerebral ischemia without reperfusion. The earliest sign of tissue injury was observed after no more than 15 min of ischemia, with coiling of apical dendrites immunolabeled to show microtubule-associated protein 2 (MAP2). After 6 h of ischemia, MAP2 immunoreactivity was markedly diminished in the infarct zone. Quantitative Western analysis demonstrated that MAP2 was almost unmeasurable after 24 h of ischemia. An increase in calpain activity, shown by an antibody recognizing calpain-cleaved spectrin fragments, paralleled the loss of MAP2 immunostaining. Double-labeled immunofluorescent studies showed that intraneuronal calpain activity preceded evidence of MAP2 proteolysis. Perikaryal immunolabeling of τ protein became increasingly prominent between 1 and 6 h in neurons located within the transition zone between ischemic and unaffected tissue. Western blot experiments confirmed that dephosphorylation of τ protein occurred during 24 h of ischemia, but was not associated with significant loss of τ antigen. We conclude that focal cerebral ischemia is associated with early microtubular proteolysis caused by calpain.

Han, Xue Mei, Hong Tao Wei y Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance". Advanced Materials Research 554-556 (julio de 2012): 1650–55. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1650.

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Abstract Objective To investigate the expression of erythropoietin (EPO) after acupuncture preconditioning plus focal cerebral ischemia treatment. Methods Rat focal cerebral ischemia model and acupuncture preconditioning model were established. Animals were randomly assigned into different groups: control (focal cerebral ischemia) and acupuncture preconditioning plus focal cerebral ischemia, with 8 rats for each group. The expression of EPO after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein expressions of EPO could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Focal cerebral ischemia promoted the expression of EPO. Significant enhanced EPO level was found in the ischemic peripheral zone after acupuncture preconditioning (P < 0.05). Conclusion Our results demonstrated that acupuncture preconditioning enhanced the expression of EPO in neurons, glia and vascular endothelial cells the ischemic peripheral zone, suggesting the involvement of EPO in acupuncture preconditioning-induced neuroprotection following focal cerebral ischemia. EPO may exert neuroprotective effects through promoting neurotrophic support and angiogenesis.

Kitagawa, Kazuo, Masayasu Matsumoto, Takuma Mabuchi, Yoshiki Yagita, Toshiho Ohtsuki, Masatsugu Hori y Takehiko Yanagihara. "Deficiency of Intercellular Adhesion Molecule 1 Attenuates Microcirculatory Disturbance and Infarction Size in Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 18, n.º 12 (diciembre de 1998): 1336–45. http://dx.doi.org/10.1097/00004647-199812000-00008.

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Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against ICAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using ICAM-1–knockout mice. Ischemic lesions were significantly mitigated in knockout mice after permanent and transient focal ischemia, even though the number of granulocytes in the infarcted tissue was almost the same between knockout and wild-type mice. Depletion of granulocytes further decreased the size of ischemic lesions after transient focal ischemia in ICAM-1–knockout mice. Microcirculation was reduced after focal ischemia, but it was better preserved in the cerebral cortex of knockout mice than that of wild-type mice. The present study demonstrated that ICAM-1 played a role in microcirculatory failure and subsequent development and expansion of infarction after focal cerebral ischemia. However, it is highly unlikely that ICAM-1 played a key role in accumulation of granulocytes after focal cerebral ischemia.

Duarte, Sinésio Grace, Antônio Dorival Campos y Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model". Arquivos de Neuro-Psiquiatria 61, n.º 3B (septiembre de 2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.

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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.

del Zoppo, Gregory J. y Takuma Mabuchi. "Cerebral Microvessel Responses to Focal Ischemia". Journal of Cerebral Blood Flow & Metabolism 23, n.º 8 (agosto de 2003): 879–94. http://dx.doi.org/10.1097/01.wcb.0000078322.96027.78.

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Cerebral microvessels have a unique ultrastructure form, which allows for the close relationship of the endothelium and blood elements to the neurons they serve, via intervening astrocytes. To focal ischemia, the cerebral microvasculature rapidly displays multiple dynamic responses. Immediate events include breakdown of the primary endothelial cell permeability barrier, with transudation of plasma, expression of endothelial cell-leukocyte adhesion receptors, loss of endothelial cell and astrocyte integrin receptors, loss of their matrix ligands, expression of members of several matrix-degrading protease families, and the appearance of receptors associated with angiogenesis and neovascularization. These events occur pari passu with neuron injury. Alterations in the microvessel matrix after the onset of ischemia also suggest links to changes in nonvascular cell viability. Microvascular obstruction within the ischemic territory occurs after occlusion and reperfusion of the feeding arteries (“focal no-reflow” phenomenon). This can result from extrinsic compression and intravascular events, including leukocyte(-platelet) adhesion, platelet-fibrin interactions, and activation of coagulation. All of these events occur in microvessels heterogeneously distributed within the ischemic core. The panorama of acute microvessel responses to focal cerebral ischemia provide opportunities to understand interrelationships between neurons and their microvascular supply and changes that underlie a number of central nervous system neurodegenerative disorders.

Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 77, n.º 3 (septiembre de 1992): 337–54. http://dx.doi.org/10.3171/jns.1992.77.3.0337.

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✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.

Codaccioni, Jean-Laurent, Lionel J. Velly, Chahrazad Moubarik, Nicolas J. Bruder, Pascale S. Pisano y Benjamin A. Guillet. "Sevoflurane Preconditioning against Focal Cerebral Ischemia". Anesthesiology 110, n.º 6 (1 de junio de 2009): 1271–78. http://dx.doi.org/10.1097/aln.0b013e3181a1fe68.

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Background Preconditioning the brain with volatile anesthetics seems to be a viable option for reducing ischemic cerebral injury. However, it is uncertain whether this preconditioning effect extends over a longer period of time. The purpose of this study was to determine if sevoflurane preconditioning offers durable neuroprotection against cerebral ischemia. Methods Rats (Sprague-Dawley) were randomly allocated to two groups: nonpreconditioned control group (n = 44) and preconditioned group (n = 45) exposed to 2.7 vol% sevoflurane (45 min) 60 min before surgery. Animals in both groups were anesthetized with 3.0 vol% sevoflurane and subjected to transient middle cerebral artery occlusion. After 60 min of awake focal ischemia, the filament was removed. Functional neurologic outcome (range 0-18; 0 = no deficit), cerebral infarct size (Nissl staining), and apoptosis (Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling; cleaved caspase-3 staining) were evaluated at 3, 7, and 14 days after ischemia. Results Sevoflurane preconditioning significantly improved functional outcome and reduced infarct volume (109 +/- 43 vs. 148 +/- 56 mm(3)) 3 days after ischemia compared to the control group. However, after 7- and 14-day recovery periods, no significant differences were observed between groups. The number of apoptotic cells was significantly lower in the preconditioned group than in the control group after 3- and 7-day recovery periods. Fourteen days after ischemia, no differences were observed between groups. Conclusion In this model of transient focal cerebral ischemia, sevoflurane preconditioning induced effective but transient neuroprotective effects. Sevoflurane preconditioning also decreased ischemia-induced apoptosis in a more sustained way because it was observed up to 7 days after injury.

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Tesis sobre el tema "Focal cerebral ischemia":

Thorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /". Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.

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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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Ng, Kit-ying. "Neuroprotective effects of adiponectin in focal cerebral ischemia". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634371.

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Ng, Kit-ying y 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.

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Ward, Nicholas M. "The assessment of behavioural deficits following focal cerebral ischemia". Thesis, University of St Andrews, 1997. http://hdl.handle.net/10023/14698.

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Evaluating the efficacy of neuroprotective drugs in rat models of focal cerebral ischemia has involved histological and behavioural batteries to examine pathology and sensorimotor function. However, the behavioural tests used provide little insight into the nature of the neurological impairments. In an effort to gain further insight into the behavioural impairment following ischemic lesions, a battery of tasks were used. The tasks included tests of sensorimotor, motor (paw use), motivation, sensory and attentional function. The use of the potent vasoconstrictor endothelin-1 has allowed cerebral arteries to be occluded. This can be used to occlude the MCA (which is a common target of ischemia research), as well as other arteries, such as the ACA. Typically quantitative volumetric analysis has used nissl stains to assess lesion extent. However, alternative markers of tissue dysfunction are available including GFAP to assess the astroglial response to ischemia. Consequently cresyl violet and GFAP were compared along with different methods for calculating lesion volume. The boundaries of the lesion identified using the two stains corresponded closely providing care was taken when calculating lesion volume to avoid distortion from histological procedures and edema. Following MCA occlusion the rats displayed unilateral somatosensory and motor deficits, however there was no evidence of attentional dysfunction. Performance in the covert orienting task was compared with striatal dopamine depletion and with a posterior parietal cortical lesion. Neither of these manipulations resulted in deficits of covert orienting. Furthermore, the behavioural consequences of ACA occlusion were studied in two experiments using reaction time tasks designed to dissociate response impairments from dysfunction of motivation and attention. The ACA ischemic damage did not disrupt motivation or attention, however, the results were consistent with an impairment in selecting and initiating responses.

Thomas, Sunu Samuel. "Murine models of cerebral ischemia, development of a mouse model of global cerebral ischemia; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50439.pdf.

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Davis, Stephanie. "Leukemia Inhibitory Factor as a Neuroprotective Agent against Focal Cerebral Ischemia". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6218.

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Previous publications from this laboratory demonstrated that administration of leukemia inhibitory factor (LIF) (125 µg/kg) to young, male Sprague-Dawley rats at 6, 24, and 48 h after middle cerebral artery occlusion (MCAO) reduced infract volume, improved sensimotor skills, and alleviated damage to white matter at 72 h after the injury. In vitro studies using cultured oligodendrocytes (OLs) showed that LIF (200 ng/ml) also protects against 24 h of oxygen-glucose deprivation through activation of Akt signaling and upregulation of the antioxidant enzymes peroxiredoxin IV and metallothionein III. Other groups have demonstrated that LIF reduces neurodegeneration in animal models of disease, but the neuroprotective mechanisms of LIF during permanent ischemia have not yet been examined. The overall hypothesis to be tested in this project is whether LIF exerts similar protective mechanisms against neurons during ischemia through increased antioxidant enzyme expression in neurons. In the first set of experiments, superoxide dismutase (SOD) activity was significantly increased in the ipsilateral hemisphere of LIF-treated rats compared to rats that received PBS treatment at 72 h after MCAO. Western blot and immunohistochemical analysis revealed that SOD3 was upregulated in brain tissue and induced specifically in cortical neurons tissue at this time point. Neurons that expressed high levels of SOD3 at 72 h after MCAO also showed high levels of phosphorylated Akt (Ser473). LIF (200 ng/ml) reduced necrotic and apoptotic cell death against 24 h of OGD as measured by lactate dehydrogenase (LDH) release and caspase-3 activation. Quantitative real-time PCR analysis showed that LIF treatment upregulated SOD3 gene expression in vitro during OGD. Treatment with 10 µM Akt Inhibitor IV and transfection with SOD3 siRNA counteracted the neuroprotective effects of LIF in vitro, showing that upregulation of SOD3 and activation of Akt signaling are necessary for LIF-mediated neuroprotection. Several transcription factors that regulated Akt-inducible genes were previously identified by this lab, including myeloid zinc finger-1 (MZF-1) and specificity protein-1 (Sp1). The goal of the second set of experiments was to determine whether LIF exerted protective actions through MZF-1 and Sp1. According to analysis with Genomatix, MZF-1 and Sp1 have multiple binding sites in the promoter for the rat SOD3 gene. Western blot analysis showed that there was a trend towards increased MZF-1 protein expression in the brains of LIF-treated rats that approached significance. Immunohistochemical analysis and quantitative real-time PCR showed a significant in vitro upregulation in MZF-1 expression among LIF-treated neurons compared to PBS-treated neurons. Sp1 gene expression was not changed by LIF treatment, but there was a trend towards increased protein expression. In addition, there was a significant correlation between Sp1 and MZF-1 among brain samples from LIF-treated rats but not PBS-treated or sham rats at 72 h after MCAO. Immunohistochemical analysis revealed that Sp1 and MZF-1 co-localized with neuronal nuclei and SOD3 at 72 h after MCAO. Neurons that were transfected with MZF-1 or Sp1 siRNA following isolation did not show a significant decrease in LDH release after 24 h OGD that was observed among neurons transfected with scrambled siRNA. These data demonstrate that Sp1 and MZF-1 are involved with the neuroprotective signaling of LIF under ischemia. This laboratory has demonstrated that LIF activates transcription of protective genes and increases the activity of transcription factors through modulation of intracellular signaling. However, the upstream signaling mechanisms of LIF during ischemia had not previously been investigated. Previous investigators found that the LIF-specific subunit of the heterodimeric LIF receptor (LIFR) is induced by CNS injury. Western blot analysis was used to determine whether LIFR was induced in the brain and the spleen, which plays a role in the peripheral immune response, after MCAO. According to these results, LIF treatment significantly upregulates LIF in the brain compared to PBS treatment or sham injury at 72 h after MCAO. Genomatix analysis of the LIFR promoter region revealed a binding site for Sp1, which is one of the transcription factors responsible for neuroprotection by LIF. At this same time point, splenic LIFR expression is significantly reduced after MCAO compared to sham injury. LIF treatment did not significantly increase LIFR expression, but did significantly increase spleen size compared to PBS treatment at 72 h after MCAO. Although there was a trend towards increased LIFR expression in the spleen from 24 h to 72 h after MCAO, this increase was not statistically significant. However, there was a significant positive correlation between spleen weight and LIFR expression among rats euthanized 24-72 h after MCAO/sham injury. In addition, there was a significant negative correlation between LIFR expression in the brain and the spleen weight, thus showing that LIFR is upregulated following the splenic response. According to findings from other groups, JAK1 has been shown to associate with the heterodimeric LIF receptor (LIFR/gp130) and directly activate PI3K/Akt signaling. To test whether JAK1 contributes neuroprotection during ischemia, cultured neurons were treated with several concentrations (2.5-50 nM) of GLPG0634, a JAK1-specific inhibitor prior to 24 h of OGD. With the exception of the 2.5 nM concentration, all concentrations of GLPG0634 significantly decreased LDH release compared to DMSO treatment, with the 5 nM concentration having the most potent effect on reducing cytotoxicity. However, the 5 nM concentration had no significant did not significantly reduce LDH release compared to DMSO treatment under 24 h of normoxic conditions. These results indicate that JAK1 activity is primarily detrimental to neurons during ischemia. Although it is possible that LIF signaling activates JAK1, it is unlikely that JAK1 is responsible for LIF-mediated neuroprotection during ischemia. The results of these experiments allowed us to determine several molecular mechanisms for LIF-mediated neuroprotection. LIF, which binds to its heterodimeric receptor, activates Akt signaling during ischemia. The transcription factors Sp1 and MZF-1, which are located downstream of Akt, bind to the promoter of the SOD3 gene. In addition, Sp1 also regulates the LIFR gene. SOD3 upregulation increases total SOD activity, which decreases apoptotic and necrotic cell death during apoptosis. Due to its ability to promote antioxidant expression and survival signaling in multiple neural cell types, LIF shows promise as a novel treatment for permanent focal cerebral ischemia.

Leung, Wai-chung. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634127.

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Leung, Wai-chung y 梁偉聰. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634127.

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Fujimoto, Motoaki. "Tissue inhibitor of metalloproteinases protect blood?brain barrier disruption in focal cerebral ischemia". Kyoto University, 2009. http://hdl.handle.net/2433/124303.

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Libros sobre el tema "Focal cerebral ischemia":

Dirnagl, Ulrich, Bruce R. Ransom y Josef Priller. Focal Cerebral Ischemia: The Multifaceted Role of Glial Cells. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0058.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...

Murine models of cerebral ischemia: Development of a mouse model of global cerebral ischemia ; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia. Ottawa: National Library of Canada, 2000.

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Capítulos de libros sobre el tema "Focal cerebral ischemia":

Kuroda, S., P. Siesjö y B. K. Siesjö. "Focal Cerebral Ischemia". En Yearbook of Intensive Care and Emergency Medicine, 727–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-13450-4_60.

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Braeuninger, Stefan, Christoph Kleinschnitz, Bernhard Nieswandt y Guido Stoll. "Focal Cerebral Ischemia". En Methods in Molecular Biology, 29–42. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-307-3_3.

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Kushner, M., C. Fieschi, M. Reivich, A. Alavi, F. Silver, J. Chawluk y J. Greenberg. "Focal and Remote Dysmetabolism in Stroke". En Cerebral Ischemia and Hemorheology, 326–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71787-1_36.

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del Zoppo, Gregory J. "Compartmentalization in Focal Cerebral Ischemia". En Maturation Phenomenon in Cerebral Ischemia V, 81–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_8.

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Chopp, Michael y Y. Li. "Apoptosis in Focal Cerebral Ischemia". En Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma, 21–26. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-9465-2_4.

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Hayashi, Nariyuki y Dalton W. Dietrich. "Global and Focal Cerebral Ischemia". En Brain Hypothermia Treatment, 7–8. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7_2.

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Selman, Warren R., Joseph C. Lamanna, Robert A. Ratcheson y W. David Lust. "Metabolic Correlates of Focal Ischemia". En Neurochemical Correlates of Cerebral Ischemia, 9–39. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3312-2_2.

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McCulloch, J., D. I. Graham, A. M. Harper y G. M. Teasdale. "Calcium Antagonists and Experimental Focal Cerebral Ischemia". En Cerebral Ischemia and Calcium, 177–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_23.

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del Zoppo, G. J. "Fibrinolysis and its Relevance to Acute Focal Cerebral Ischemia". En Brain Ischemia, 105–19. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5_14.

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Sampaolo, S., N. Heye y J. Cervos-Navarro. "Blood-Brain Barrier Permeability to Micromolecules After Focal Cerebral Ischemia". En Cerebral Ischemia and Calcium, 52–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_7.

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Actas de conferencias sobre el tema "Focal cerebral ischemia":

Deng, Xiaolu, Fayi Liu, Yucheng Wang, Ming Li, Yadong Liu y Dewen Hu. "Focal cerebral ischemia in rats by photothrombosis of cortical microvessels". En 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381785.

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Кудабаева, Марина Станиславовна, Андрей Евгеньевич Акулов, Анна Олеговна Пищелко, Михаил Васильевич Светлик y Марина Юрьевна Ходанович. "SUTURE SIZE OPTIMIZATION IN THE MODEL OF FOCAL ISCHEMIA IN RATS". En Высокие технологии и инновации в науке: сборник избранных статей Международной научной конференции (Санкт-Петербург, Сентябрь 2020). Crossref, 2020. http://dx.doi.org/10.37539/vt187.2020.38.57.004.

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На модели окклюзии срединой церебральной артерии (MCAO) у крыс исследовано влияние параметров монофиламента, используемого для проведения операции, на объем ишемического поражения мозга. Установлена оптимальная длина наконечника филамента, обеспечивающая такой объем ишемического поражения, который позволяет обеспечить хорошую выживаемость животных в сочетании с другими инвазивными процедурами в хроническом эксперименте. In middle cerebral artery occlusion model (MCAO) in rats surgical suture characteristics were analyzed as parameters that can effect on ischemic lesion size. Optimal suture lenght was assigned for inducing ischemic lesion size that facilitates animal survival in long-term experiment, if MCAO and other invasive procedures are combined.

Гиганова, Анастасия Александровна, Татьяна Викторовна Ананьина, Алёна Андреевна Кисель y Марина Юрьевна Ходанович. "MICROGLYOCYTES MORPHOLOGY AFTER FOCAL ISCHEMIC STROKE IN A MOUSE BRAIN". En Высокие технологии и инновации в науке: сборник избранных статей Международной научной конференции (Санкт-Петербург, Сентябрь 2020). Crossref, 2020. http://dx.doi.org/10.37539/vt187.2020.56.18.005.

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Проведен цитологический анализ изменения морфологии микроглиоцитов в мозге мышей, перенесших локальную ишемию головного мозга посредством окклюзии средней мозговой артерии (MCAO). Описана специфика изменения морфологии микроглиоцитов в белом и сером веществе головного мозга в ипсилатеральном полушарии. It was performed the cytological analysis of microglia morphology in mice underwent focal ischemia by means of middle cerebral artery occlusion (MCAO). The features of morphological microglyocyte changes in a white and gray matter of ipsilateral lesioned hemisphere was described.

Aguilera, Penélope, Perla D. Maldonado, Alma Ortiz-Plata, Diana Barrera, María Elena Chánez-Cárdenas, Leonardo Dagdug y Leopoldo Gracía-Colin S. "Evaluation of Aged Garlic Extract Neuroprotective Effect in a Focal Model of Cerebral Ischemia". En COMPLIFE 2007: The Third International Symposium on Computational Life Science. AIP, 2008. http://dx.doi.org/10.1063/1.2891417.

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YAN, Xiaoli, Huisu WU, Xiaoyan FANG y Minsan MIAO. "Effects of Total Flavonoids of Rosa Chinensis on Focal Cerebral Ischemia Reperfusion Model in Mice". En International Conference on Biological Engineering and Pharmacy 2016 (BEP 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/bep-16.2017.5.

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Miao, Mingsan, Lin Guo, Ming Bai y Shuai Shao. "Effect of Blushred rabdosia leaf total flavonoids on focal cerebral ischemia reperfusion model of mice". En International Conference on Modern Engineering Soultions for the Industry. Southampton, UK: WIT Press, 2014. http://dx.doi.org/10.2495/mesi141492.

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AMIR, LIVNAT, BARBIRO-MICHAELY EFRAT y MAYEVSKY AVRAHAM. "REAL-TIME MONITORING OF MITOCHONDRIAL FUNCTION AND CEREBRAL BLOOD FLOW FOLLOWING FOCAL ISCHEMIA IN RATS". En Proceedings of the 6th International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2007). WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812832344_0041.

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Culver, Joseph P., Daisuke Furuya, Joel H. Greenberg, Turgut Durduran, Cecil Cheung y Arjun G. Yodh. "Diffuse optical tomography of hemoglobin concentrations, and cerebral blood flow in rat brain during focal ischemia." En Biomedical Topical Meeting. Washington, D.C.: OSA, 2002. http://dx.doi.org/10.1364/bio.2002.sud42.

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Denisova, Alina, Ivan Filippenkov, Vasily Stavchansky, Vadim Yuzhakov, Larisa Sevan’kaeva, Nikolai Myasoedov, Svetlana Limborska, Lyudmila Dergunova y Leonid Gubsky. "PHARMACOTRANSCRIPTOME ANALYSIS OF THE PEPTIDE DRUGS ACTIONS UNDER EXPERIMENTAL MODEL CONDITION OF FOCAL CEREBRAL ISCHEMIA IN RATS". En XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2110.sudak.ns2021-17/133-134.

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Chen, Shangbin, Zhe Feng, Shaoqun Zeng, Qingming Luo y Pengcheng Li. "Evaluation the development of focal cerebral ischemia in rats by optical imaging based on the spreading depression signals". En Biomedical Optics (BiOS) 2007, editado por Valery V. Tuchin. SPIE, 2007. http://dx.doi.org/10.1117/12.701636.

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