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Titlebook: Maturation Phenomenon in Cerebral Ischemia III; Defensive Mechanisms Umeo Ito,Cesare Fieschi,Igor Klatzo Conference proceedings 1999 Spring

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书目名称Maturation Phenomenon in Cerebral Ischemia III
副标题Defensive Mechanisms
编辑Umeo Ito,Cesare Fieschi,Igor Klatzo
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图书封面Titlebook: Maturation Phenomenon in Cerebral Ischemia III; Defensive Mechanisms Umeo Ito,Cesare Fieschi,Igor Klatzo Conference proceedings 1999 Spring
描述The Maturation Phenomenon, described by Ito et al. in 1975 [3) on the basis of his to­ logical observations in the hippocampus as well as other portions of the cerebral hemisphere, refers to the hours or days of delay in the development of pathological changes in various parameters of ischemic injury following the restoration of blood flow to the ischemic brain. There is a direct relationship between the intensity of ischemic insult and the speed and rate of maturation of ischemic injury, a lesser intensity being associated with slower and less severe development of the lesions. The delayed neuronal death of CAl pyramidal cells of the hippocampus [8) is a classic example. In the cerebral cortex, with increasing intensity of the ischemic insult, the maturation phenomenon of ischemic injuries intensifies, seamlessly, from less exten­ sive to more extensive disseminated selective neuronal necrosis (DSNN), and then further to cerebral infarction upon reaching a critical threshold [1,2,4,6,7). We also have found that following ischemic insults just under the threshold level required to induce infarction, only disseminated selective neuronal necrosis (DSNN) progresses, while following is
出版日期Conference proceedings 1999
关键词Cerebral ischemia; adenosine; apoptosis; cerbral infarction; delayed neuronal death; forebrain; neuronal n
版次1
doihttps://doi.org/10.1007/978-3-642-58602-6
isbn_softcover978-3-540-65023-2
isbn_ebook978-3-642-58602-6
copyrightSpringer-Verlag Berlin Heidelberg 1999
The information of publication is updating

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Conference proceedings 1999ns of the cerebral hemisphere, refers to the hours or days of delay in the development of pathological changes in various parameters of ischemic injury following the restoration of blood flow to the ischemic brain. There is a direct relationship between the intensity of ischemic insult and the speed
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Delayed Gene Expression and Ischemic Brain Injurynd that the products of their reaction contribute to the delayed progression of ischemic brain damage. Administration of iNOS and COX-2 inhibitors may be a useful therapeutic strategy to selectively target the progression of the brain damage that takes place during the post-ischemic period.
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Upregulation of Vascular Endothelial Growth Factor Protein Levels in Global Ischemia Induced by Cardoccurs in the brain stem after 24 h. We found that vascular endothelial growth factor (VEGF) protein levels are significantly elevated in brain after 24 h and 48 h of reperfusion. We propose that increased VEGF expression is responsible for blood-brain barrier breakdown and vasogenic edema.
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Multiple Molecular Penumbras Associated with Focal Ischemia in Brained as an area outside of the infarction that is electrophysiologically silent [119], is depolarized, demonstrates decreased perfusion [38], increased oxygen extraction [30], decreased protein metabolism [46] and decreased glucose metabolism [35] as well as other parameters [7, 28, 40]. The applicati
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