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10.1161/ATVBAHA.120.314860 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.120.314860 32762443!7505138!32762443     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arterioscler+Thromb+Vasc+Biol 2020 ; 40 (10): 2404-2407 Nephropedia Template TP {{tp|p=32762443|t=2020. Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief Report |pdf=|usr=}}{{32762443}} gab.com Text Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief Report JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=32762443 #FOAvip OBJECTIVE: Alveolar-capillary endothelial cells can be activated by severe acute respiratory syndrome coronavirus 2 infection leading to cytokine release. This could trigger endothelial dysfunction, pyroptosis, and thrombosis, which are the vascular changes, commonly referred to as coronavirus disease 2019 (COVID-19) endotheliopathy. Thus, this study aimed to identify tissue biomarkers associated with endothelial activation/dysfunction and the pyroptosis pathway in the lung samples of patients with COVID-19 and to compare them to pandemic influenza A virus H1N1 subtype 2009 and control cases. Approach and Results: Postmortem lung samples (COVID-19 group =6 cases; H1N1 group =10 cases, and control group =11 cases) were analyzed using immunohistochemistry and the following monoclonal primary antibodies: anti-IL (interleukin)-6, anti-TNF (tumor necrosis factor)-alpha, anti-ICAM-1 (intercellular adhesion molecule 1), and anticaspase-1. From the result, IL-6, TNF-alpha, ICAM-1, and caspase-1 showed higher tissue expression in the COVID-19 group than in the H1N1 and control groups. CONCLUSIONS: Our results demonstrated endothelial dysfunction and suggested the participation of the pyroptosis pathway in the pulmonary samples. These conditions might lead to systemic thrombotic events that could impair the clinical staff's efforts to avoid fatal outcomes. One of the health professionals' goals should be to identify the high risk of thrombosis patients early to block endotheliopathy and its consequences. Twit Text FOAVip Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief Report ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=32762443 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32762443 #FOAvip English Wikipedia <ref>{{Cite pmid|32762443}}</ref> Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief Report #MMPMID32762443 Nagashima S; Mendes MC; Camargo Martins AP; Borges NH; Godoy TM; Miggiolaro AFRDS; da Silva Deziderio F; Machado-Souza C; de Noronha L Arterioscler Thromb Vasc Biol 2020[Oct]; 40 (10): 2404-2407 PMID32762443show ga OBJECTIVE: Alveolar-capillary endothelial cells can be activated by severe acute respiratory syndrome coronavirus 2 infection leading to cytokine release. This could trigger endothelial dysfunction, pyroptosis, and thrombosis, which are the vascular changes, commonly referred to as coronavirus disease 2019 (COVID-19) endotheliopathy. Thus, this study aimed to identify tissue biomarkers associated with endothelial activation/dysfunction and the pyroptosis pathway in the lung samples of patients with COVID-19 and to compare them to pandemic influenza A virus H1N1 subtype 2009 and control cases. Approach and Results: Postmortem lung samples (COVID-19 group =6 cases; H1N1 group =10 cases, and control group =11 cases) were analyzed using immunohistochemistry and the following monoclonal primary antibodies: anti-IL (interleukin)-6, anti-TNF (tumor necrosis factor)-alpha, anti-ICAM-1 (intercellular adhesion molecule 1), and anticaspase-1. From the result, IL-6, TNF-alpha, ICAM-1, and caspase-1 showed higher tissue expression in the COVID-19 group than in the H1N1 and control groups. CONCLUSIONS: Our results demonstrated endothelial dysfunction and suggested the participation of the pyroptosis pathway in the pulmonary samples. These conditions might lead to systemic thrombotic events that could impair the clinical staff's efforts to avoid fatal outcomes. One of the health professionals' goals should be to identify the high risk of thrombosis patients early to block endotheliopathy and its consequences. |Autopsy[MESH] |Biopsy, Needle[MESH] |COVID-19[MESH] |Cause of Death[MESH] |Coronavirus Infections/mortality/*pathology[MESH] |Endothelial Cells/*cytology/pathology[MESH] |Endothelium, Vascular/*pathology/physiopathology[MESH] |Female[MESH] |Humans[MESH] |Immunohistochemistry[MESH] |Male[MESH] |Pandemics[MESH] |Pneumonia, Viral/mortality/*pathology[MESH] |Risk Assessment[MESH] |Thrombosis/etiology/mortality/*pathology[MESH]Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief(epmc).pdf DeepDyve Pubget Overpricing