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10.1016/j.pneurobio.2013.09.002 http://scihub22266oqcxt.onion/10.1016/j.pneurobio.2013.09.002 C3961493!3961493!24076160     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Prog+Neurobiol 2014 ; ä (ä): 64-91 Nephropedia Template TP {{tp|p=24076160|t=2014. Controversies and Evolving New Mechanisms in Subarachnoid Hemorrhage |pdf=|usr=}}{{24076160}} gab.com Text Controversies and Evolving New Mechanisms in Subarachnoid Hemorrhage JO: Prog Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=24076160 #FOAvip Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms ?early brain injury? and ?delayed brain injury? are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications. Twit Text FOAVip Controversies and Evolving New Mechanisms in Subarachnoid Hemorrhage ????Prog Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=24076160 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24076160 #FOAvip English Wikipedia <ref>{{Cite pmid|24076160}}</ref> Controversies and Evolving New Mechanisms in Subarachnoid Hemorrhage #MMPMID24076160 Chen S; Feng H; Sherchan P; Klebe D; Zhao G; Sun X; Zhang J; Tang J; Zhang JH Prog Neurobiol 2014[Apr]; ä (ä): 64-91 PMID24076160show ga Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms ?early brain injury? and ?delayed brain injury? are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications. äControversies and Evolving New Mechanisms in Subarachnoid Hemorrhage (epmc).pdf DeepDyve Pubget Overpricing