OBJECTIVE To study the influence of micro ribonucleic acid (miR)-155 on depression-like behaviors of depression mice, and to explore the role of Wnt/b-catenin signaling pathway in behavioral regulation of depression mice. MATERIALS AND METHODS The mouse model of depression was established via chronic unpredictable mild stress (CUMS). All mice were randomly divided into control group (n=12), model group (n=12), and fluoxetine group (n=12). The expression level of miR-155 in the hippocampus of mice in each group was detected via quantitative Polymerase Chain Reaction (qPCR). The changes in the behaviors of mice in each group were evaluated via behavioral experiments. The apoptosis level in the hippocampus of mice in each group was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, the content of inflammatory factors in the hippocampus of mice in each group was detected using the enzyme-linked immunosorbent assay (ELISA) kits. The expression levels of W apoptosis of hippocampal neurons. Its mechanism may be related to the inhibition of the Wnt/b-catenin signaling pathway.OBJECTIVE This review analyzes the prevalence of the most important comorbidities associated with atrial fibrillation (AF) in the growing population of patients with Cushing's syndrome (CS). MATERIALS AND METHODS The review is arranged in a way to list important risk factors for AF and the references, which suggest the significant prevalence of these particular risk factors in CS. The search is conducted on PubMed, Science Direct, Springer, Wiley, SAGE, Oxford Press, and Google Scholar. PubMed search for "Cushing's syndrome atrial fibrillation" on 8/7/2019 revealed 4 papers only. None of them either analyzed or implicated high risk for AF in CS. RESULTS Arterial hypertension (AHT) can be found in approximately 80% of adult individuals with endogenous CS and in 20% of patients with exogenous CS. The reported prevalence of diabetes mellitus (DM) is from 13% to 47% in CS patients and the risk for de novo DM is approximately two-fold higher in individuals treated with glucocorticoids. High risk for myocardial infarction (MI) with hazard ratio (HR) 3.7 (95% confidence intervals, CI 2.4-5) in patients with endogenous CS was found. In CS patients the obesity can be detected in up to 41% and overweight in 21-48%. Left ventricular hypertrophy (LVH), pulmonary thromboembolism (PTE), infections, and hypokalemia are also more prevalent in CS as compared to healthy population. All cited comorbidities have been associated with AF. Therefore, clustering of the important factors associated with AF is confirmed repeatedly in CS. CONCLUSIONS The prevalence of AF in CS should be studied more precisely, both in a scientific way and at the individual patient's level.OBJECTIVE Arsenic trioxide (As2O3) an evident effect in the treatment of acute promyelocytic leukemia and other malignant tumors in recent years. However, more and more studies have found that the cardiac toxicity of As2O3 was increased, limiting its wide clinical application. This study aims to explore the molecule mechanisms of As2O3 on cardiomyocyte injury. MATERIALS AND METHODS The cardiomyocyte injury under As2O3 was detected by MTT assay. The levels of NEAT1 and miR-124 were examined by RT-PCR. The functions of NEAT1 and miR-124 at H9c2 cell injury under As2O3 were detected by cell transfection of the overexpression or repression. The expression levels of inflammation factors, apoptosis genes and NF-κB signals were measured by Western blot in H9c2 cell lines under As2O3. The luciferase assay detected the direct interaction between NEAT1 and miR-124. RESULTS The overexpression of NEAT1 decreased the H9c2 cells injury under As2O3. The levels of IL-1β, IL-6, TNF-α were upregulated after NEAT1 overexpression. Moreover, the luciferase assay results showed NEAT1 was directly interacting with miR-124. Silencing of miR-124 significantly increased the H9c2 cell survival under As2O3 by repressing NF-κB signaling pathway. Furthermore, the overexpression of NEAT1 markedly increased H9c2 cells survival under As2O3, while the miR-124 could reverse the effects. Finally, NEAT1 regulated the H9c2 cells As2O3 injury by repressing the miR-124, NF-kappa B expressions and inflammatory response. CONCLUSIONS According to the results, we found that long non-coding RNA NEAT1 regulated the expression of inflammatory factors to protect cardiomyocytes from As2O3 damage by inhibiting miR-124/NF-kappa B signaling pathway. It provides a novel potential treatment strategy for As2O3 cardiomyocytes injury.OBJECTIVE The role of NEAT1 in cancers has been demonstrated. But the role of NEAT1 in cardiac hypertrophy still remains unknown. This study aimed to elucidate the specific function of long non-coding RNA (lncRNA) NEAT1 in cardiac hypertrophy and its underlying mechanism. PATIENTS AND METHODS In this study, the in vivo and in vitro cardiac hypertrophy models were constructed by transverse aortic coarctation (TAC) procedure in rats and phenylephrine (PE) induction in primary cardiomyocytes, respectively. The expression levels of NEAT1, microRNA-19a-3p, SMYD2, and cardiac hypertrophic markers were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cardiac hypertrophy was evaluated as calculating the surface area of hypertrophic cardiomyocyte by fluorescein isothiocyanate (FITC)-Phalloidin staining. Luciferase Reporter Gene Assay was conducted to detect the binding of NEAT1, SMYD2, and microRNA-19a-3p. RESULTS The results showed that NEAT1 and SMYD2 were highly expressed in myocardium of ratby binding to microRNA-19a-3p.OBJECTIVE Acute myocardial infarction (AMI) contributes to long-term cardiac ischemia induced by hypoxia.  https://www.selleckchem.com/products/gsk2879552-2hcl.html  Long non-coding RNAs (lncRNAs) affect the development and progression of heart diseases. This study explored the role and mechanism of lncRNA X inactive specific transcript (XIST) in H9c2 cells with hypoxia-induced injury. MATERIALS AND METHODS Methyl-thiazolyl-tetrazolium (MTT), transwell, and flow cytometry assays were employed to analyze the survival, invasion, migration, and apoptosis of H9c2 cells under different conditions, respectively. Expression of related genes was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot. RESULTS XIST was over-expressed in H9c2 cells with hypoxia-induced injury, and the silence of XIST alleviated cell injury. Up-regulation of XIST promoted the expression of B-cell lymphoma 2-Associated X (Bax) through competitive binding to miR-150-5p. CONCLUSIONS XIST protects cardiomyocytes from hypoxia-induced injury by mediating miR-150-5p/Bax axis, suggesting that XIST is an important target for AMI treatment.