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10.3390/ijms22105114 http://scihub22266oqcxt.onion/10.3390/ijms22105114 34066051!8151768!34066051     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34066051&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       Int+J+Mol+Sci 2021 ; 22 (10): ? Nephropedia Template TP {{tp|p=34066051|t=2021. Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management |pdf=|usr=}}{{34066051}} gab.com Text Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34066051 #FOAvip Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 degrees C and 36 degrees C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 degrees C produces a neuroprotective effect comparable to 33 degrees C, we performed an experiment using a rat model. We found that TTM at 36 degrees C and at 33 degrees C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 degrees C and 36 degrees C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 degrees C and 33 degrees C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest. Twit Text FOAVip Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34066051 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34066051 #FOAvip English Wikipedia <ref>{{Cite pmid|34066051}}</ref> Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management #MMPMID34066051 Hong DK; Park YS; Woo JS; Kim JH; Beom JH; Chung SP; You JS; Suh SW Int J Mol Sci 2021[May]; 22 (10): ? PMID34066051show ga Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 degrees C and 36 degrees C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 degrees C produces a neuroprotective effect comparable to 33 degrees C, we performed an experiment using a rat model. We found that TTM at 36 degrees C and at 33 degrees C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 degrees C and 36 degrees C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 degrees C and 33 degrees C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest. |*Body Temperature[MESH] |Animals[MESH] |Brain Diseases/etiology/pathology/*therapy[MESH] |Brain Ischemia/*complications[MESH] |Hypothermia, Induced/*methods[MESH] |Inflammation/etiology/pathology/*therapy[MESH] |Male[MESH] |Rats[MESH]Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuat(epmc).pdf DeepDyve Pubget Overpricing