Introduction: Increasing evidence indicate that coronavirus disease 2019 (COVID-19) is companied by renal dysfunction. However, the association of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2)-induced renal dysfunction with prognosis remains unclear.Materials and methods: This prospective case-cohort study analyzed 154 COVID-19 patients from the Second People’s Hospital of Fuyang City in Anhui Province. Clinical and demographic information were collected. Renal function was evaluated and its prognosis was followed up. Results: Of 154 hospitalized patients with COVID-19, 125 were common and 29 were severe patients. On admission, 16 (10.4%) patients were with renal dysfunction. Serum creatinine and cystatin C were increased, eGFR was decreased in severe patients compared with those in common patients. Renal dysfunction was more common in severe patients. By multivariate logistic regression, male, higher age and hypertension were three importantly independent risk factors of renal dysfunction in COVID-19 patients. Follow-up study found that at least one renal function marker of 3.33% patients remained abnormal in two weeks after discharge. Conclusion: Male elderly COVID-19 patients with hypertension elevates the risk of renal dysfunction. SARS-CoV-2-induced renal dysfunction are not fully recovered in two weeks after discharge.
Background and Objectives Limited studies suggested that calprotectin may take part in the pathophysiology of community-acquired pneumonia (CAP). Nevertheless, there is no clinical study to analyze the role of S100A8 in CAP patients. The objective of this study was to analyze the association of serum S100A8 with the severity of CAP based on a cross-sectional study. Methods Entire 200 CAP patients and 100 normal subjects were recruited. Demographic data, clinical information and serum were collected on admission. Serum S100A8 and inflammatory cytokines were detected. Results Serum S100A8 was increased in CAP patients on admission. Serum S100A8 was gradually increased in parallel with the CAP severity scores. Serum S100A8 was positively correlated with CAP severity scores (CURB-65, CRB-65, PSI, CURXO and SMART-COP), blood routine parameters (WBC, neutrophil-lymphocyte ratio and monocyte-lymphocyte ratio) and inflammatory cytokines (TNFα, IL-1β and CRP). Furtherly, univariate and multivariate logistical regression analysis revealed that there was a positive association between serum S100A8 with CRB-65, PSI and CURXO. Moreover, the predictive capacity of serum S100A8 was performed by receiver operating characteristic area under the curve (AUC) analysis. The AUCs of S100A8 for CAP and CAP severity were 0.855 and 0.893, respectively. Mechanistic analysis found that S100A8 knockdown alleviated streptococcus pneumoniae-evoked inflammatory cytokines in A549 cells. Conclusion Serum S100A8 on admission was positively associated with the severity of CAP. S100A8 knockdown alleviates streptococcus pneumoniae- evoked inflammatory cytokines in A549 cells, indicating that S100A8 may exert an important role in the pathophysiology of CAP and be an early serum diagnostic biomarker for CAP.
The tumor suppressor p53 has been implicated in the pathogenesis of liver fibrosis. HERC5-mediated posttranslational ISG modification of the p53 protein is critical for controlling its activity. Here, we demonstrated that the expression of HERC5 and ISG15 is highly elevated, whereas p53 is downregulated, in fibrotic liver tissues of mice and transforming growth factor-β1 (TGF-β1)induced LX2 cells. HERC5 siRNA clearly increased the protein expression of p53, but the mRNA expression of p53 was not obviously changed. The inhibition of lincRNA-ROR (ROR) downregulated HERC5 expression and elevated p53 expression in TGF-β1stimulated LX-2 cells. Furthermore, the expression of p53 was almost unchanged after TGF-β1stimulated LX-2 cells were co-transfected with a RORexpressing plasmid and HERC5 siRNA. We further confirmed that miR-145 is a target gene of ROR. In addition, we also showed that ROR regulates the HERC5mediated ISGylation of p53 through mir-145/ZEB2. Together, we propose that ROR/miR-145/ZEB2 might be involved in the course of liver fibrosis by regulating ISGylation of the p53 protein.
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