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10.1007/s12325-020-01399-7 http://scihub22266oqcxt.onion/10.1007/s12325-020-01399-7 32504450!7274265!32504450     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32504450&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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Adv+Ther 2020 ; 37 (7): 3033-3039 Nephropedia Template TP {{tp|p=32504450|t=2020. Dysfunctional Coagulation in COVID-19: From Cell to Bedside |pdf=|usr=}}{{32504450}} gab.com Text Dysfunctional Coagulation in COVID-19: From Cell to Bedside JO: Adv Ther http://www.kidney.de/pget.php?&tw=1&pmid=32504450 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which can induce multisystem disease. Human angiotensin-converting enzyme 2 (ACE2) widely expressing in arterial and venous endothelial cells and arterial smooth muscle cells has been identified as a functional receptor for SARS-CoV-2. Dysfunction of ACE2 leads to abnormal activation of the renin-angiotensin system and a systemic endotheliitis that may relate to abnormal coagulation and sepsis. Meanwhile, innate immune response and inflammation activation participate in dysfunctional coagulation. Previous research indicated that dysfunctional coagulation was one of the important risk factors accountable for a high risk of severe disease and death in patients with COVID-19. Understanding the possible mechanisms of dysfunctional coagulation and appropriate anticoagulation therapeutic strategies are important to prevent disease deterioration and reduce fatality rates during the ongoing COVID-19 pandemic. Twit Text FOAVip Dysfunctional Coagulation in COVID-19: From Cell to Bedside ????Adv Ther http://www.kidney.de/pget.php?&tw=1&pmid=32504450 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32504450 #FOAvip English Wikipedia <ref>{{Cite pmid|32504450}}</ref> Dysfunctional Coagulation in COVID-19: From Cell to Bedside #MMPMID32504450 Wang J; Saguner AM; An J; Ning Y; Yan Y; Li G Adv Ther 2020[Jul]; 37 (7): 3033-3039 PMID32504450show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which can induce multisystem disease. Human angiotensin-converting enzyme 2 (ACE2) widely expressing in arterial and venous endothelial cells and arterial smooth muscle cells has been identified as a functional receptor for SARS-CoV-2. Dysfunction of ACE2 leads to abnormal activation of the renin-angiotensin system and a systemic endotheliitis that may relate to abnormal coagulation and sepsis. Meanwhile, innate immune response and inflammation activation participate in dysfunctional coagulation. Previous research indicated that dysfunctional coagulation was one of the important risk factors accountable for a high risk of severe disease and death in patients with COVID-19. Understanding the possible mechanisms of dysfunctional coagulation and appropriate anticoagulation therapeutic strategies are important to prevent disease deterioration and reduce fatality rates during the ongoing COVID-19 pandemic. äDysfunctional Coagulation in COVID-19: From Cell to Bedside (epmc).pdf DeepDyve Pubget Overpricing