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10.31083/j.rcm.2020.03.126 http://scihub22266oqcxt.onion/10.31083/j.rcm.2020.03.126 33070537!ä!33070537 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Rev+Cardiovasc+Med 2020 ; 21 (3): 315-319 Nephropedia Template TP {{tp|p=33070537|t=2020. Endothelial dysfunction contributes to COVID-19-associated vascular inflammation and coagulopathy |pdf=|usr=}}{{33070537}} gab.com Text Endothelial dysfunction contributes to COVID-19-associated vascular inflammation and coagulopathy JO: Rev Cardiovasc Med http://www.kidney.de/pget.php?&tw=1&pmid=33070537 #FOAvip Great attention has been paid to endothelial dysfunction (ED) in coronavirus disease 2019 (COVID-19). There is growing evidence to suggest that the angiotensin converting enzyme 2 receptor (ACE2 receptor) is expressed on endothelial cells (ECs) in the lung, heart, kidney, and intestine, particularly in systemic vessels (small and large arteries, veins, venules, and capillaries). Upon viral infection of ECs by severe acute respiratory syndrome coronarvirus 2 (SARS-CoV-2), ECs become activated and dysfunctional. As a result of endothelial activation and ED, the levels of pro-inflammatory cytokines (interleukin -1, interleukin-6 (IL-6), and tumor necrosis factor-alpha), chemokines (monocyte chemoattractant protein-1), von Willebrand factor (vWF) antigen, vWF activity, and factor VIII are elevated. Higher levels of acute phase reactants (IL-6, C-reactive protein, and D-dimer) are also associated with SARS-CoV-2 infection. Therefore, it is reasonable to assume that ED contributes to COVID-19-associated vascular inflammation, particularly endotheliitis, in the lung, heart, and kidney, as well as COVID-19-associated coagulopathy, particularly pulmonary fibrinous microthrombi in the alveolar capillaries. Here we present an update on ED-relevant vasculopathy in COVID-19. Further research for ED in COVID-19 patients is warranted to understand therapeutic opportunities. Twit Text FOAVip Endothelial dysfunction contributes to COVID-19-associated vascular inflammation and coagulopathy ????Rev Cardiovasc Med http://www.kidney.de/pget.php?&tw=1&pmid=33070537 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33070537 #FOAvip English Wikipedia <ref>{{Cite pmid|33070537}}</ref> Endothelial dysfunction contributes to COVID-19-associated vascular inflammation and coagulopathy #MMPMID33070537 Zhang J; Tecson KM; McCullough PA Rev Cardiovasc Med 2020[Sep]; 21 (3): 315-319 PMID33070537show ga Great attention has been paid to endothelial dysfunction (ED) in coronavirus disease 2019 (COVID-19). There is growing evidence to suggest that the angiotensin converting enzyme 2 receptor (ACE2 receptor) is expressed on endothelial cells (ECs) in the lung, heart, kidney, and intestine, particularly in systemic vessels (small and large arteries, veins, venules, and capillaries). Upon viral infection of ECs by severe acute respiratory syndrome coronarvirus 2 (SARS-CoV-2), ECs become activated and dysfunctional. As a result of endothelial activation and ED, the levels of pro-inflammatory cytokines (interleukin -1, interleukin-6 (IL-6), and tumor necrosis factor-alpha), chemokines (monocyte chemoattractant protein-1), von Willebrand factor (vWF) antigen, vWF activity, and factor VIII are elevated. Higher levels of acute phase reactants (IL-6, C-reactive protein, and D-dimer) are also associated with SARS-CoV-2 infection. Therefore, it is reasonable to assume that ED contributes to COVID-19-associated vascular inflammation, particularly endotheliitis, in the lung, heart, and kidney, as well as COVID-19-associated coagulopathy, particularly pulmonary fibrinous microthrombi in the alveolar capillaries. Here we present an update on ED-relevant vasculopathy in COVID-19. Further research for ED in COVID-19 patients is warranted to understand therapeutic opportunities. |*Betacoronavirus[MESH] |Blood Coagulation Disorders/*etiology/physiopathology[MESH] |COVID-19[MESH] |Coronavirus Infections/*complications/epidemiology[MESH] |Endothelium, Vascular/*physiopathology[MESH] |Humans[MESH] |Inflammation/etiology/physiopathology[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications/epidemiology[MESH] |SARS-CoV-2[MESH] |Vascular Diseases/*etiology/physiopathology[MESH]Endothelial dysfunction contributes to COVID-19-associated vascular in(epmc).pdf DeepDyve Pubget Overpricing