Objective: To observe the anxiety and depression experienced by patients with suspected and confirmed COVID-19 during hospitalization and isolation.Methods: A cross-sectional survey was performed with 66 patients with suspected and confirmed COVID-19 who were admitted to the Fifth Affiliated Hospital of Sun Yat-sen University from February 9, 2020, to February 22, 2020. The data collected including sex, age, education level, and nucleic acid test results. Anxiety, depression, and sleep disorders were evaluated using the Self-Rating Anxiety Scale (SAS), Self-Rating Depression Scale (SDS) and Pittsburgh Sleep Quality Index Scale (PSQI), respectively. Statistical analysis: SPSS 23.0 software was used for data processing, and multifactor logistic regression analysis was used to identify the independent risk factors. Spearman correlation analysis was used to study the correlations among the observed indicators; P <0.05 was considered statistically significant.Results: The incidences of anxiety, depression, and sleep disorders in the suspected case group were 18.2%, 18.2%, and 39.4%; the incidences of anxiety, depression, and sleep disorders in the diagnosed group were 42.4%, 57.6%, and 69.7%. The incidence of sleep disorders was higher than the domestic norm, and the difference was statistically significant (P <0.05). Logistic regression analysis adjusted for multiple factors showed that the main factor affecting anxiety was age; the main factors affecting depression were age and a positive nucleic acid test; and the main factor affecting sleep disorders was age. The anxiety, depression and sleep disorder scores were significantly positively correlated (P <0.05).Conclusion: Patients with suspected and confirmed COVID-19, especially people aged 50 years and over, have significant anxiety, depression and sleep disorders. Anxiety, depression and sleep disorders in patients with confirmed cases are more serious than those in patients with suspected cases. It is necessary to focus on the psychological state of such patients, actively conduct psychological counseling, and reduce their anxiety and depression.
Background/Aims: The purpose of this study is to analyze the expression and biological function of lncRNA ANRIL, microRNA-199a, TLR4, and nuclear factor-kappa B (NF-κB) in acute renal injury (AKI) induced by lipopolysaccharide (LPS). Methods: The levels of ANRIL and microRNA-199a in mouse cells and kidneys were detected by quantitative-polymerase chain reaction. Western blot analysis was used for the NF-κB pathway protein. MTT assay was used for cell viability. Enzyme-linked immunosorbent assay was used for the secretion of inflammatory factors in mouse kidney tissue. Apoptosis was measured by flow cytometry and Western blotting. The potential binding region between ANRIL and miR-199a was verified by luciferase reporter assay. Results: The upregulation of ANRIL can reduce the expression of microRNA-199a and increases the number of apoptotic cells. The expression levels of ANRIL in LPS-induced AKI mice and LPS-treated HK2 cells were upregulated compared with the control group. Overexpression of ANRIL increased apoptosis and promoted TLR4 (Toll-like receptor 4), NF-κB phosphorylation, and downstream transcription factor production. Conclusion: ANRIL/NF-κB pathway in LPS-induced apoptosis provided theoretical guidance for ANRIL in the treatment of AKI.
Background: Anti-inflammatory cytokine polymorphisms in the transforming growth factor-b1 (TGF-b1), interleukin-4 (IL-4), and IL-10 genes have been implicated as risk factors for chronic kidney disease (CKD), but the results from published studies are inconsistent. Our meta-analysis reviews and summarizes the cumulative evidence for these associations. Methods: A systematic literature search of five databases was performed up to October 2019. Two authors independently extracted data and evaluated the quality of included studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were generated from random-effects or fixed-effects models using Stata 12.0. Results: Nineteen studies from 10 countries satisfied our inclusion criteria and were included in the meta-analysis. Overall, the pooled analysis showed that TGF-b1 rs1800469 was associated with decreased susceptibility to CKD (CC + TC vs. TT, OR = 0.33, 95% CI: 0.15-0.76, P = 0.009; CC vs. TT, OR = 0.33, 95% CI: 0.15-0.73, P = 0.006), whereas TGF-b1 rs1800471 was associated with increased CKD susceptibility (CC vs. CG + GG, OR = 1.68, 95% CI: 1.02-2.77, P = 0.041). In stratified analyses based on ethnicity, TGF-b1 rs1800469 was associated with CKD susceptibility in Asians and Caucasians, and there was an association of TGF-b1 rs1800470 and IL-4 rs8179190 with CKD in Asians. Stratified analyses also associated TGF-b1 rs1800471 with CKD susceptibility in Caucasians. Neither overall meta-analyses nor stratified analyses identified an association of the IL-10 rs1800869 and rs1800871 polymorphisms with susceptibility to CKD. Conclusions: Available data suggest that common polymorphisms in the TGF-b1 and IL-4 genes including rs1800469, rs1800470, rs1800471, and rs8179190 may be important genetic contributors to CKD susceptibility.
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