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Titlebook: Brain Ischemia; Eugene Gusev,Veronica I. Skvortsova Book 2003 Springer Science+Business Media New York 2003 brain.death.depression.glutama

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發(fā)表于 2025-3-21 19:25:40 | 只看該作者 |倒序瀏覽 |閱讀模式
期刊全稱Brain Ischemia
影響因子2023Eugene Gusev,Veronica I. Skvortsova
視頻videohttp://file.papertrans.cn/191/190209/190209.mp4
圖書封面Titlebook: Brain Ischemia;  Eugene Gusev,Veronica I. Skvortsova Book 2003 Springer Science+Business Media New York 2003 brain.death.depression.glutama
影響因子Ischemia is localized tissue anemia due to obstruction of the inflow of arterial blood, thus brain ischemia is the condition where insufficient blood is delivered to the brain. Many physiological processes occurring in the brain critically depend on the state of its energy metabolism. The state of brain energy metabolism in turn depends on the delivery of oxygen and glucose to the brain via the bloodstream. Although it comprises only 2% of the total body weight, the human brain consumes 20-25% of the oxygen and up to 70% of the free glucose taken in by the body. The brain respires more intensively than any other organ of the body. The intensity of oxygen consumption by cortical brain tissue much exceeds the demands of other tissues (5.43 mmol 02/g per h versus 3.06 and 4.02 mmol for heart at rest and intensively working, respectively, 2.4 mmol for kidneys, and 1.8 mmol for liver). Oxidative phosphorylation in mitochondria generates 95% of the adenosine triphosphate (ATP) that is formed in the brain. Thus, it is clear why insufficiency of oxygen delivery to brain cells adversely affects brain function. Glucose is the main energy-providing substrate in the brain. The basic pathway of
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書目名稱Brain Ischemia影響因子(影響力)




書目名稱Brain Ischemia影響因子(影響力)學(xué)科排名




書目名稱Brain Ischemia網(wǎng)絡(luò)公開度




書目名稱Brain Ischemia網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Brain Ischemia被引頻次




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發(fā)表于 2025-3-21 21:48:24 | 只看該作者
Energy Failure Induced by Brain Ischemia a substrate for cytochrome oxidase, the terminal enzyme of the respiratory chain. The resulting state of hypoxia is the consequence of a complicated multi-stage process involving sequential changes in the properties of the mitochondrial enzyme complexes [.].
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發(fā)表于 2025-3-22 00:35:38 | 只看該作者
Metabolic Acidosis and Ischemic Damagey activation of anaerobic glycolysis and to increased production of lactate and H. that causes the development of lactic acidosis. Modest increase in H. concentration in early stages of ischemia plays a compensatory and adaptive role as it promotes the improvement of perfusion in the penumbral area
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發(fā)表于 2025-3-22 07:21:15 | 只看該作者
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發(fā)表于 2025-3-22 09:30:42 | 只看該作者
Autoimmune Mechanisms of Trophic Dysfunction and Ischemic Brain Damagethey interact via mutual regulation involving neuromediators, neuropeptides, cytokines, trophic factors, and hormones and the corresponding receptor systems [.]. Mutual regulation of the nervous, endocrine, and immune systems determines the reliability of their common functioning. However, this enta
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發(fā)表于 2025-3-22 16:50:23 | 只看該作者
Reaction of the Stress-Mediating Endocrine System in Response to Acute Brain Ischemiastem caused by the expression of immediate-early genes—by the synthesis of heat-shock (or stress) proteins (HSP) and cytokines, which are immune mediators [., ., ., .] (see Chapters 7 and 8; Fig. 8.1). The stress-mediating response provides the metabolie basis for compensatory and adaptive changes t
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發(fā)表于 2025-3-22 20:52:00 | 只看該作者
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發(fā)表于 2025-3-22 22:01:50 | 只看該作者
Reparative Therapyin tissue. Thus, from the first hours after stroke onset it is necessary to proceed with treatment aimed at the improvement of reparative and regenerative processes, plasticity of brain tissue, and the formation of new associative pathways, along with neuroprotection aimed at prevention of further b
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發(fā)表于 2025-3-23 03:48:21 | 只看該作者
Vimal K. Shrivastava,Monoj K. Pradhanant to mention not only its therapeutic, but also preventive value. Correction of delayed consequences of ischemia can lead to retardation of vascular encephalopathy development in the post-stroke period.
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發(fā)表于 2025-3-23 08:20:26 | 只看該作者
Secondary Neuroprotectionant to mention not only its therapeutic, but also preventive value. Correction of delayed consequences of ischemia can lead to retardation of vascular encephalopathy development in the post-stroke period.
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