<strong>Objective:</strong> Coronavirus disease 2019 (COVID-19) spread throughout the world and caused hundreds of thousands of infected people to death. However, the pathogenesis of severe acute respirato...<strong>Objective:</strong> Coronavirus disease 2019 (COVID-19) spread throughout the world and caused hundreds of thousands of infected people to death. However, the pathogenesis of severe acute respiratory syndrome coronavirus-2 (SARS COV-2) is poorly understood. The objective of this study is to retrospectively explore the pathogenesis of COVID-19 from clinical laboratory findings, taking disease progression into account. <strong>Methods:</strong> A single-centered, retrospective study was carried out, which included moderate (n = 76) and severe COVID-19 cases (n = 22). The difference of laboratory findings from blood routine examination and hepatorenal function test were retrospectively evaluated between the state of moderate and severe. The disease progression was indicated by oxygenation index. <strong>Results: </strong>Age is a risk factor for disease progression from moderate to severe. Lymphocytopenia, neutrophilia, liver and kidney function decreasement occurred in severe patients on admission, compared with moderate patients. Lymphocytopenia and neutrophilia deteriorated at the lowest oxygenation index timepoint in the severe patients. And the oxygenation index was associated with ratio of lymphocyte and neutrophil in COVID-19 patients. <strong>Conclusions:</strong> Lymphocytopenia and neutrophilia, which deteriorate in the progression of severe patients, are the main pathogenesis of COVID-19. More measures need to be taken to control lymphocytopenia and neutrophilia in severe COVID-19. Oxygenation index presented potentiality as predictor on the progression of COVID-19.展开更多
Excessive fibrogenesis disrupts normal liver structure,impairs liver function,and precipitates the development of cirrhosis,an irreversible end-stage liver disease.A host of factors including nutrition surplus contrib...Excessive fibrogenesis disrupts normal liver structure,impairs liver function,and precipitates the development of cirrhosis,an irreversible end-stage liver disease.A host of factors including nutrition surplus contribute to liver fibrosis but the underlying mechanism is not fully understood.In the present study,we investigated the involvement of protein inhibitor for activated stat 4（PIAS4）in liver fibrosis in a mouse model of non-alcoholic steatohepatitis（NASH）.We report that PIAS4 silencing using short hairpin RNA（shRNA）attenuated high-fat high-carbohydrate（HFHC）diet induced liver fibrosis in mice.Quantitative PCR and Western blotting analyses confirmed that PIAS4 knockdown downregulated a panel of pro-fibrogenic genes including type I and type III collagens,smooth muscle actin,and tissue inhibitors of metalloproteinase.Mechanistically,PIAS4 silencing blocked the recruitment of SMAD3,a potent pro-fibrogenic transcription factor,to the promoter regions of pro-fibrogenic genes and dampened SMAD3 acetylation likely by upregulating SIRT1 expression.In conclusion,PIAS4 may contribute to liver fibrosis by modulating SIRT1-dependent SMAD3 acetylation.展开更多
文摘<strong>Objective:</strong> Coronavirus disease 2019 (COVID-19) spread throughout the world and caused hundreds of thousands of infected people to death. However, the pathogenesis of severe acute respiratory syndrome coronavirus-2 (SARS COV-2) is poorly understood. The objective of this study is to retrospectively explore the pathogenesis of COVID-19 from clinical laboratory findings, taking disease progression into account. <strong>Methods:</strong> A single-centered, retrospective study was carried out, which included moderate (n = 76) and severe COVID-19 cases (n = 22). The difference of laboratory findings from blood routine examination and hepatorenal function test were retrospectively evaluated between the state of moderate and severe. The disease progression was indicated by oxygenation index. <strong>Results: </strong>Age is a risk factor for disease progression from moderate to severe. Lymphocytopenia, neutrophilia, liver and kidney function decreasement occurred in severe patients on admission, compared with moderate patients. Lymphocytopenia and neutrophilia deteriorated at the lowest oxygenation index timepoint in the severe patients. And the oxygenation index was associated with ratio of lymphocyte and neutrophil in COVID-19 patients. <strong>Conclusions:</strong> Lymphocytopenia and neutrophilia, which deteriorate in the progression of severe patients, are the main pathogenesis of COVID-19. More measures need to be taken to control lymphocytopenia and neutrophilia in severe COVID-19. Oxygenation index presented potentiality as predictor on the progression of COVID-19.
基金supported by the Natural Science Foundation of China(No.81500441)
文摘Excessive fibrogenesis disrupts normal liver structure,impairs liver function,and precipitates the development of cirrhosis,an irreversible end-stage liver disease.A host of factors including nutrition surplus contribute to liver fibrosis but the underlying mechanism is not fully understood.In the present study,we investigated the involvement of protein inhibitor for activated stat 4（PIAS4）in liver fibrosis in a mouse model of non-alcoholic steatohepatitis（NASH）.We report that PIAS4 silencing using short hairpin RNA（shRNA）attenuated high-fat high-carbohydrate（HFHC）diet induced liver fibrosis in mice.Quantitative PCR and Western blotting analyses confirmed that PIAS4 knockdown downregulated a panel of pro-fibrogenic genes including type I and type III collagens,smooth muscle actin,and tissue inhibitors of metalloproteinase.Mechanistically,PIAS4 silencing blocked the recruitment of SMAD3,a potent pro-fibrogenic transcription factor,to the promoter regions of pro-fibrogenic genes and dampened SMAD3 acetylation likely by upregulating SIRT1 expression.In conclusion,PIAS4 may contribute to liver fibrosis by modulating SIRT1-dependent SMAD3 acetylation.
