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.

10.1007/s12975-020-00818-9 http://scihub22266oqcxt.onion/10.1007/s12975-020-00818-9 32378030!7202903!32378030     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32378030&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       Transl+Stroke+Res 2020 ; 11 (3): 322-325 Nephropedia Template TP {{tp|p=32378030|t=2020. COVID-19-Related Stroke |pdf=|usr=}}{{32378030}} gab.com Text COVID-19-Related Stroke JO: Transl Stroke Res http://www.kidney.de/pget.php?&tw=1&pmid=32378030 #FOAvip The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a "sepsis-induced coagulopathy" and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the "harmful" ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy. Twit Text FOAVip COVID-19-Related Stroke ????Transl Stroke Res http://www.kidney.de/pget.php?&tw=1&pmid=32378030 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32378030 #FOAvip English Wikipedia <ref>{{Cite pmid|32378030}}</ref> COVID-19-Related Stroke #MMPMID32378030 Hess DC; Eldahshan W; Rutkowski E Transl Stroke Res 2020[Jun]; 11 (3): 322-325 PMID32378030show ga The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a "sepsis-induced coagulopathy" and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the "harmful" ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy. |Angiotensin-Converting Enzyme 2[MESH] |Betacoronavirus/metabolism[MESH] |COVID-19[MESH] |Coronavirus Infections/blood/*complications/drug therapy/epidemiology[MESH] |Disseminated Intravascular Coagulation/drug therapy/virology[MESH] |Female[MESH] |Humans[MESH] |Male[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/administration & dosage/metabolism[MESH] |Pneumonia, Viral/blood/*complications/drug therapy/epidemiology[MESH] |Recombinant Proteins/administration & dosage[MESH] |SARS-CoV-2[MESH] |Stroke/drug therapy/*virology[MESH]COVID-19-Related Stroke (epmc).pdf DeepDyve Pubget Overpricing