Anxiety and depression and its correlates in patients with coronavirus disease 2019 in Wuhan.

OBJECTIVES: Coronavirus disease 2019 (COVID-19) first broke-out in Wuhan China in December 2019, and spread throughout the entire country within a short time. This cross-sectional study investigated the prevalence of depression and anxiety and associated risk factors were analysed in patients with COVID-19. METHODS: This single-center cross-sectional study focussed on measuring depression and anxiety using self-report scales. Linear regression was used to determine independent predictors for depression and anxiety. RESULTS: A total of 78 patients who were confirmed to have COVID-19 were enrolled in the study. Prevalence of depression and anxiety symptoms were diagnosed in 35.9% and 38.5% of the patients, respectively. Multivariate linear regression analysis found female gender was an independent predictor for higher depression severity index. Having family members who were diagnosed with COVID-19 and family members who died from COVID-19 were independently associated with higher depression severity index and anxiety score. CONCLUSIONS: Patients with COVID-19 especially those who had family members diagnosed with COVID-19 or died from COVID-19 were more susceptible to depression and anxiety than were other patients. Effective strategies should be pursued to improve the mental health of this patient population.Key pointsPatients with COVID-19 showed a significantly high prevalence of depression and anxiety.Female patients were associated with higher risk of depression.Patients with family members diagnosed as COVID-19 or died from this disease were associated with higher risk of depression and anxiety.

Identification of key candidate genes and pathways revealing the protective effect of liraglutide on diabetic cardiac muscle by integrated bioinformatics analysis.

BACKGROUND: Diabetes mellitus is becoming a significant health problem with the International Diabetes Federation (IDF) expecting a startling 642 million diabetes patients by 2040. Liraglutide, a glucagon-like peptide-1 (GLP-1) analog, is reported to protect against diabetic cardiomyopathy by binding to the receptor, GLP-1R. However, the underlying mechanism has yet to be clarified. This study aimed to investigate the underlying mechanisms and the effects of liraglutide on diabetic patient's cardiac muscles. METHODS: GSE102194 genetic expression profiles were extracted from the Gene Expression Omnibus (GEO) database. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were carried out. Next, Cytoscape software was used to construct the protein-protein interaction (PPI) network of the differentially expressed genes (DEGs). DEGs were mapped onto a protein-protein interaction (PPI) network that comprised 249 nodes and 776 edges. RESULTS: A total of 520 DEGs were discovered, including 159 down-regulated genes and 361 up-regulated genes. DEGs that were upregulated were notably enriched in biological processes (BP) such as muscle system process, muscle system process, muscle structure development and anatomical structure morphogenesis while DEGs that were downregulated were rich in detection of chemical stimulus and neurological system process. KEGG pathway analysis showed the up-regulated DEGs were enriched in adrenergic signaling for cardiomyocytes, dopaminergic synapse, and circadian entrainment, while the down-regulated DEGs were enriched for factory transduction in 249 of the 520 tested samples. The modular analysis identified 4 modules that participated in some pathways associated with cardiac muscle contraction, hypertrophic cardiomyopathy (HCM), and MAPK signaling pathway. CONCLUSIONS: Our data showed that Glp-1 could decrease the protein expression of p38, JNK, ERK1/2, and MARS proteins induced by high glucose (22 mM, 72 h). This study highlights the potential physiological processes that take place in diabetic cardiac muscles exposed to liraglutide. Our findings elucidated the regulatory network in diabetic cardiomyopathy and might provide a novel diagnostic and therapeutic target for diabetic cardiomyopathy.

MicroRNA-34a contributes to the protective effects of glucagon-like peptide-1 against lipotoxicity in INS-1 cells.

BACKGROUND: Glucagon-like peptide-1 (GLP-1) reduces fatty acid-induced beta-cell lipotoxicity in diabetes; however, the explicit mechanisms underlying this process are not fully understood. This study was designed to investigate the involvement of microRNA, which regulates gene expression by the sequence-specific inhibition of mRNA transcription in the GLP-1 mediation of beta-cell function. METHODS: The cell viability and apoptosis were determined using an methyl thiazoleterazolium (MTT) assay and flow cytometry. The expression of genes involved in beta-cell function, including microRNA-34a and sirtuin 1, were investigated using real-time PCR. The underlying mechanisms of microRNA-34a were further explored using cell-transfection assays. RESULTS: A 24-hours incubation of INS-1 cells with palmitate significantly decreased cell viability, increased cell apoptosis and led to the activation of microRNA-34a and the suppression of sirtuin 1. A co-incubation with GLP-1 protected the cells against palmitate-induced toxicity in association with a reduction in palmitate-induced activation of microRNA-34a. Furthermore, palmitate-induced apoptosis was significantly increased in cells that were infected with microRNA-34a mimics and decreased in cells that were infected with microRNA-34a inhibitors. CONCLUSION: MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.