Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1172/jci.insight.90777 http://scihub22266oqcxt.onion/10.1172/jci.insight.90777 C5374066!5374066 !28405617     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28405617 &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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28405617 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       JCI+Insight 2017 ; 2 (7 ): e90777 Nephropedia Template TP {{tp|p=28405617 |t=2017. Inhibition of neuronal ferroptosis protects hemorrhagic brain |pdf=|usr=}}{{28405617 }} gab.com Text Inhibition of neuronal ferroptosis protects hemorrhagic brain JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell-derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies. Twit Text FOAVip Inhibition of neuronal ferroptosis protects hemorrhagic brain ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip English Wikipedia <ref>{{Cite pmid|28405617 }}</ref> Inhibition of neuronal ferroptosis protects hemorrhagic brain #MMPMID28405617 Li Q ; Han X ; Lan X ; Gao Y ; Wan J ; Durham F ; Cheng T ; Yang J ; Wang Z ; Jiang C ; Ying M ; Koehler RC ; Stockwell BR ; Wang J JCI Insight 2017[Apr]; 2 (7 ): e90777 PMID28405617 show ga Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell-derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies. |Animals [MESH] |Apoptosis/*drug effects [MESH] |Biomarkers/metabolism [MESH] |Brain/*metabolism [MESH] |Cells, Cultured [MESH] |Cerebral Hemorrhage/*prevention & control [MESH] |Cyclohexylamines/*pharmacology [MESH] |Cyclooxygenase 2/metabolism [MESH] |Hippocampus [MESH] |Humans [MESH] |In Vitro Techniques [MESH] |Iron/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neurons/cytology/*drug effects [MESH] |Neuroprotective Agents/*pharmacology [MESH] |Phenylenediamines/*pharmacology [MESH]Inhibition of neuronal ferroptosis protects hemorrhagic brain (epmc).pdf DeepDyve Pubget Overpricing