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10.1038/aps.2016.162 http://scihub22266oqcxt.onion/10.1038/aps.2016.162 C5386316!5386316!28260801     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28260801&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28260801.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Acta+Pharmacol+Sin 2017 ; 38 (4): 445-58 Nephropedia Template TP {{tp|p=28260801|t=2017. Regulation of microglial activation in stroke |pdf=|usr=}}{{28260801}} gab.com Text Regulation of microglial activation in stroke JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28260801 #FOAvip When ischemic stroke occurs, oxygen and energy depletion triggers a cascade of events, including inflammatory responses, glutamate excitotoxicity, oxidative stress, and apoptosis that result in a profound brain injury. The inflammatory response contributes to secondary neuronal damage, which exerts a substantial impact on both acute ischemic injury and the chronic recovery of the brain function. Microglia are the resident immune cells in the brain that constantly monitor brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce both detrimental and neuroprotective mediators, and the balance of the two counteracting mediators determines the fate of injured neurons. The activation of microglia is defined as either classic (M1) or alternative (M2): M1 microglia secrete pro-inflammatory cytokines (TNF?, IL-23, IL-1?, IL-12, etc) and exacerbate neuronal injury, whereas the M2 phenotype promotes anti-inflammatory responses that are reparative. It has important translational value to regulate M1/M2 microglial activation to minimize the detrimental effects and/or maximize the protective role. Here, we discuss various regulators of microglia/macrophage activation and the interaction between microglia and neurons in the context of ischemic stroke. Twit Text FOAVip Regulation of microglial activation in stroke ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28260801 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28260801 #FOAvip English Wikipedia <ref>{{Cite pmid|28260801}}</ref> Regulation of microglial activation in stroke #MMPMID28260801 Zhao Sc; Ma Ls; Chu Zh; Xu H; Wu Wq; Liu F Acta Pharmacol Sin 2017[Apr]; 38 (4): 445-58 PMID28260801show ga When ischemic stroke occurs, oxygen and energy depletion triggers a cascade of events, including inflammatory responses, glutamate excitotoxicity, oxidative stress, and apoptosis that result in a profound brain injury. The inflammatory response contributes to secondary neuronal damage, which exerts a substantial impact on both acute ischemic injury and the chronic recovery of the brain function. Microglia are the resident immune cells in the brain that constantly monitor brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce both detrimental and neuroprotective mediators, and the balance of the two counteracting mediators determines the fate of injured neurons. The activation of microglia is defined as either classic (M1) or alternative (M2): M1 microglia secrete pro-inflammatory cytokines (TNF?, IL-23, IL-1?, IL-12, etc) and exacerbate neuronal injury, whereas the M2 phenotype promotes anti-inflammatory responses that are reparative. It has important translational value to regulate M1/M2 microglial activation to minimize the detrimental effects and/or maximize the protective role. Here, we discuss various regulators of microglia/macrophage activation and the interaction between microglia and neurons in the context of ischemic stroke. äRegulation of microglial activation in stroke (epmc).pdf DeepDyve Pubget Overpricing