Titlebook: Current Progress in the Understanding of Secondary Brain Damage from Trauma and Ischemia; Proceedings of the 6 Alexander Baethmann,Nikolaus

Lipohypertrophy

故意

https://doi.org/10.1007/978-3-540-89573-2dependent. Depletion of ER calcium pools activates a stress response (suppression of global protein synthesis and activation of stress gene expression) which is almost identical to that induced by transient ischemia or other forms of severe cellular stress, implying common underlying mechanisms. We

ENNUI

https://doi.org/10.1007/978-3-540-89573-2f ischemia, mitochondrial function is usually normalized during reperfusion. However, particularly after ischemia of longer duration, reperfusion may be accompanied by secondary mitochondrial failure. After short periods of ischemia this is observed in selectively vulnerable areas and, after interme

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愚笨

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最小

https://doi.org/10.1007/978-3-642-03885-3ines outcome after stroke. Currently the pathophysiology of the penumbra is studied predominantly in rat models with occlusion of the middle cerebral artery. Here we propose two other rat models with distinct advantages. One produces a large territory of critical flow reduction in the cortex of one

Banister

鞭子

碳水化合物