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Titlebook: Clinical Pharmacology of Cerebral Ischemia; Gert J. Horst,Jakob Korf Book 1997 Springer Science+Business Media New York 1997 brain.brain i

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发表于 2025-3-21 16:34:47 | 显示全部楼层 |阅读模式
书目名称Clinical Pharmacology of Cerebral Ischemia
编辑Gert J. Horst,Jakob Korf
视频video
丛书名称Contemporary Neuroscience
图书封面Titlebook: Clinical Pharmacology of Cerebral Ischemia;  Gert J. Horst,Jakob Korf Book 1997 Springer Science+Business Media New York 1997 brain.brain i
描述A distinguished international panel ofauthors define our current understanding ofneuronal damage after ischemia and critically review the significant recent developments and progress in cerebrovascular accident (CVA) drug trials, both in animal models and in the clinical setting. These leading basic and fundamental authorities survey such important new drugs as calcium-influx inhibitors, free-radical scavenging drugs, glutamate and glycinergic antagonists, and immune suppressors. They also evaluate all the latest findings concerning calcium homeostasis, glutamate toxicity, gene activation, and the role of free radicals, glycine, and hormones. Chapters devoted to the neuroimaging of stroke, clinical trials, and the role of cerebral immune activation complete this informative collection of cutting-edge reviews.
出版日期Book 1997
关键词brain; brain injury; calcium; cerebral ischemia; clinical trial; death; drug; hypoxia; neuroimaging; neurotox
版次1
doihttps://doi.org/10.1007/978-1-59259-472-6
isbn_softcover978-1-4757-4783-6
isbn_ebook978-1-59259-472-6
copyrightSpringer Science+Business Media New York 1997
The information of publication is updating

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发表于 2025-3-21 21:46:54 | 显示全部楼层
Glutamate Neurotoxicity and Stroke,otropic receptors might mediate inositol phosphate metabolism, release of arachidonic acid, or changes in cyclic adenosine monophosphate (cAMP) levels .. Glutamate is removed from the synaptic cleft and extracellular space by Na.-dependent, high-affinity mono-carboxylic acid carriers located in both
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Animal Models Used in Cerebral Ischemia and Stroke Research,to very slight neurological deficits. Rational therapies for cerebral ischemia should be established on a detailed understanding of the pathomechanisms involved. This is why we need experimental stroke models.
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https://doi.org/10.1057/9781137012715otropic receptors might mediate inositol phosphate metabolism, release of arachidonic acid, or changes in cyclic adenosine monophosphate (cAMP) levels .. Glutamate is removed from the synaptic cleft and extracellular space by Na.-dependent, high-affinity mono-carboxylic acid carriers located in both
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Glycine Antagonists for Treatment of Ischemic Brain Injury,
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ation, and the role of free radicals, glycine, and hormones. Chapters devoted to the neuroimaging of stroke, clinical trials, and the role of cerebral immune activation complete this informative collection of cutting-edge reviews.978-1-4757-4783-6978-1-59259-472-6
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