Survival Analysis and Risk Factors in COVID-19 Patients.

OBJECTIVE: The aim of this study is to evaluate the clinical characteristics and outcomes in 2019 coronavirus disease (COVID-19) patients and to help clinicians perform correct treatment and evaluate prognosis and guide the treatment. METHODS: Patients totaling 239 were diagnosed with COVID-19 and were included in this study. Patients were divided into the improvement group and the death group according to their outcome (improvement or death). Clinical characteristics and laboratory parameters were collected from medical records. Continuous variables were tested by an independent sample T test, and categorical variables were analyzed by the chi-square test or Fisher's exact test. The Cox proportional hazard regression model was used for survival analysis in death patients. The time-dependent area under curves (AUC) based on white blood cell count, lymphocyte count, neutrophil count by age, blood urea nitrogen, and C-reactive protein were plotted. RESULTS: Efficacy evaluation indicated that 99 (41.4%) patients had deteriorated, and 140 (58.6%) patients had improved. Oxygen saturation, hemoglobin levels, infection-related indicators, lymphocyte and platelet counts, C-reactive protein, serum albumin, liver and kidney function, and lactate dehydrogenase in improvement group were statistically significant between the improvement and death groups. A survival analysis revealed that comorbidities, lymphocyte counts, platelet count, serum albumin, C-reactive protein level, and renal dysfunction may be risk factors in patients with COVID-19. CONCLUSION: Patients with comorbidities, lower lymphocyte counts in hemogram, platelet count and serum albumin, high C-reactive protein level, and renal dysfunction may have higher risk for death. More attention should be given to risk management in the progression of COVID-19.

MicroRNA-18 promotes apoptosis of islet ß-cells via targeting NAV1.

The detailed pathogenesis of diabetes mellitus (DM) remains to be fully elucidated. The purpose of the present study was to explore the role of microRNA (miR)-18 in DM and its underlying mechanisms, providing novel ideas for the treatment of the disease. After inflammatory factor-mediated induction, miR-18 expression in the islet ß-cell line MIN6 was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). miR-18 mimics and miR-18 inhibitor were then constructed and transfected into MIN6 cells. The mRNA levels of pro-insulin in MIN6 cells were also detected by RT-qPCR. Released insulin levels and insulin secretion function of MIN6 cells were accessed by ELISA and glucose-stimulated insulin secretion assay, respectively. Apoptosis of MIN6 cells was detected by a terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick end labeling assay and western blot analysis of apoptotic proteins. The binding interaction of miR-18 and neuron navigator 1(NAV1), a constituent of the phosphoinositide 3-kinase (PI3K)/AKT pathway, was assessed using a dual-luciferase reporter gene assay. Finally, the regulatory effect of miR-18 on the PI3K/AKT pathway was determined by western blot analysis. After induction of inflammatory factors in MIN6 cells, miR-18 expression was markedly upregulated. Transfection with miR-18 mimics inhibited pro-insulin levels, as well as insulin production and secretion capacity. miR-18 knockdown partially abrogated the inhibited insulin secretion capacity induced by interleukin-1ß (IL-1ß) treatment. In addition, apoptosis of MIN6 cells was increased by miR-18 mimics. The dual-luciferase reporter gene assay confirmed the direct binding of miR-18 to NAV1. Western blot analysis suggested that miR-18 markedly inhibited the PI3K/AKT pathway in MIN6 cells. In conclusion, miR-18 expression is upregulated by IL-1ß induction in islet ß-cells. It was demonstrated that miR-18 promotes apoptosis of islet ß-cells at least partially by inhibiting NAV1 expression and insulin production via suppression of the PI3K/AKT pathway.