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10.1172/jci.insight.138070 http://scihub22266oqcxt.onion/10.1172/jci.insight.138070 32427582!7406259!32427582     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2020 ; 5 (12): ä Nephropedia Template TP {{tp|p=32427582|t=2020. Clinical and pathological investigation of patients with severe COVID-19 |pdf=|usr=}}{{32427582}} gab.com Text Clinical and pathological investigation of patients with severe COVID-19 JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=32427582 #FOAvip BACKGROUND: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), has become a pandemic. This study addresses the clinical and immunopathological characteristics of severe COVID-19. METHODS: Sixty-nine patients with COVID-19 were classified into severe and nonsevere groups to analyze their clinical and laboratory characteristics. A panel of blood cytokines was quantified over time. Biopsy specimens from 2 deceased cases were obtained for immunopathological, ultrastructural, and in situ hybridization examinations. RESULTS: Circulating cytokines, including IL-8, IL-6, TNF-alpha, IP10, MCP1, and RANTES, were significantly elevated in patients with severe COVID-19. Dynamic IL-6 and IL-8 were associated with disease progression. SARS-CoV-2 was demonstrated to infect type II and type I pneumocytes and endothelial cells, leading to severe lung damage through cell pyroptosis and apoptosis. In severe cases, lymphopenia, neutrophilia, depletion of CD4+ and CD8+ T lymphocytes, and massive macrophage and neutrophil infiltrates were observed in both blood and lung tissues. CONCLUSIONS: A panel of circulating cytokines could be used to predict disease deterioration and inform clinical interventions. Severe pulmonary damage was predominantly attributed to both cytopathy caused by SARS-CoV-2 and immunopathologic damage. Strategies that prohibit pulmonary recruitment and overactivation of inflammatory cells by suppressing cytokine storm might improve the outcomes of patients with severe COVID-19. Twit Text FOAVip Clinical and pathological investigation of patients with severe COVID-19 ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=32427582 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32427582 #FOAvip English Wikipedia <ref>{{Cite pmid|32427582}}</ref> Clinical and pathological investigation of patients with severe COVID-19 #MMPMID32427582 Li S; Jiang L; Li X; Lin F; Wang Y; Li B; Jiang T; An W; Liu S; Liu H; Xu P; Zhao L; Zhang L; Mu J; Wang H; Kang J; Li Y; Huang L; Zhu C; Zhao S; Lu J; Ji J; Zhao J JCI Insight 2020[Jun]; 5 (12): ä PMID32427582show ga BACKGROUND: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), has become a pandemic. This study addresses the clinical and immunopathological characteristics of severe COVID-19. METHODS: Sixty-nine patients with COVID-19 were classified into severe and nonsevere groups to analyze their clinical and laboratory characteristics. A panel of blood cytokines was quantified over time. Biopsy specimens from 2 deceased cases were obtained for immunopathological, ultrastructural, and in situ hybridization examinations. RESULTS: Circulating cytokines, including IL-8, IL-6, TNF-alpha, IP10, MCP1, and RANTES, were significantly elevated in patients with severe COVID-19. Dynamic IL-6 and IL-8 were associated with disease progression. SARS-CoV-2 was demonstrated to infect type II and type I pneumocytes and endothelial cells, leading to severe lung damage through cell pyroptosis and apoptosis. In severe cases, lymphopenia, neutrophilia, depletion of CD4+ and CD8+ T lymphocytes, and massive macrophage and neutrophil infiltrates were observed in both blood and lung tissues. CONCLUSIONS: A panel of circulating cytokines could be used to predict disease deterioration and inform clinical interventions. Severe pulmonary damage was predominantly attributed to both cytopathy caused by SARS-CoV-2 and immunopathologic damage. Strategies that prohibit pulmonary recruitment and overactivation of inflammatory cells by suppressing cytokine storm might improve the outcomes of patients with severe COVID-19. |Adult[MESH] |Aged[MESH] |Betacoronavirus/isolation & purification[MESH] |Biopsy[MESH] |CD8-Positive T-Lymphocytes[MESH] |COVID-19[MESH] |Chemokine CCL2/blood[MESH] |Chemokine CCL5/blood[MESH] |China/epidemiology[MESH] |Coronavirus Infections/blood/*diagnosis/epidemiology/*pathology[MESH] |Cytokines/blood[MESH] |Disease Progression[MESH] |Endothelial Cells/pathology[MESH] |Female[MESH] |Humans[MESH] |Lung/diagnostic imaging/pathology[MESH] |Lymphocyte Count[MESH] |Lymphopenia/pathology/virology[MESH] |Male[MESH] |Middle Aged[MESH] |Pandemics[MESH] |Pneumonia, Viral/blood/*diagnosis/epidemiology/*pathology[MESH]Clinical and pathological investigation of patients with severe COVID-(epmc).pdf DeepDyve Pubget Overpricing