Titlebook: Brain Injury; Robert S. B. Clark,Patrick Kochanek Book 2001 Springer Science+Business Media New York 2001 Alzheimer.Neurointensiv.Trauma.a

Helmet

书目名称Brain Injury影响因子(影响力)




书目名称Brain Injury影响因子(影响力)学科排名




书目名称Brain Injury网络公开度




书目名称Brain Injury网络公开度学科排名




书目名称Brain Injury被引频次




书目名称Brain Injury被引频次学科排名




书目名称Brain Injury年度引用




书目名称Brain Injury年度引用学科排名




书目名称Brain Injury读者反馈




书目名称Brain Injury读者反馈学科排名

天赋

openSAP – der Enterprise-MOOC-Pioniersent novel targets for therapies aimed at limiting damage after acute or chronic CNS injury. This chapter will provide a general review of death receptors and their signaling mechanisms, focusing on the two best characterized death receptors, Fas and TNF-α.

jocular

Machen elektromagnetische Felder krank?l disintegration, nuclear condensation, and digestion of DNA. Finally, the engulfment of the dead cell or cell fragments by phagocytosis peacefully terminates the death program. Incomplete execution of programmed cell death may redirect the cell to necrosis, which is an unfavorable event for the org

杠杆支点

Machiavelli in Contemporary Media neurocytoskeletal elements sustain damage as a result of trauma, potentially contributing to neuronal dysfunction. Some of the major neurocytoskeletal proteins include neurofilaments (NFs), tubulin, microtubule-associated proteins (MAPs) such as MAP2 and tau, actin, and spectrin. Because cytoskelet

焦虑

偶像

The Multifaceted Role of Adenosine in Experimental and Clinical Traumatic Brain Injury,thermia—putative pharmacological agents that might simultaneously or sequentially confer multiple beneficial effects in the injured brain. One endogenous mediator that fits this category is adenosine—which has the potential to favorably influence excitotoxicity, energy failure, hypoperfusion, calciu

instructive

Death Receptors in Acute Brain Injury,sent novel targets for therapies aimed at limiting damage after acute or chronic CNS injury. This chapter will provide a general review of death receptors and their signaling mechanisms, focusing on the two best characterized death receptors, Fas and TNF-α.

PANIC

遗传学

Neurocytoskeletal Changes Following Traumatic Brain Injury, neurocytoskeletal elements sustain damage as a result of trauma, potentially contributing to neuronal dysfunction. Some of the major neurocytoskeletal proteins include neurofilaments (NFs), tubulin, microtubule-associated proteins (MAPs) such as MAP2 and tau, actin, and spectrin. Because cytoskelet

注意力集中

Reproductive Hormones as Neuroprotectants in Brain Injury,d molecular mechanisms by which estrogen salvages brain are detailed. We focus on estrogen’s mechanisms since there is a large, and rapidly developing, understanding of this hormone’s neuroprotective potential. Limited data are available at present for progesterone or testosterone (reviewed in .; .)