Inhibition of miR-148b ameliorates myocardial ischemia/reperfusion injury via regulation of Wnt/ß-catenin signaling pathway.

Our work aims to elucidate the effect how microRNA-148b (miR-148b) participated in myocardial ischemia/reperfusion (I/R) injury via regulation of Wnt/ß-catenin signaling pathway. The in vivo myocardial I/R models of SD rats and in vitro hypoxia/reoxygenation (H/R) models of H9C2 cells were established. The heart function and infarction area of rats and lactic dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), and superoxide dismutase (SOD) levels were evaluated. Myocardial cell viability was measured using positron emission tomography combined with computer tomography and (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, and the apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated nick-end labeling method and flow cytometry; quantitative reverse-transcription polymerase chain reaction and western blot were used to detect the related molecules expressions. The myocardial infarction area of rats was significantly increased with reductions in LVSP, + dp/dtmax, - dp/dtmax, LVFS%, LVEF% and standardized uptake value and elevation in left ventricular developed pressure after ischemia/reperfusion (I/R), and the LDH, CK, and MDA levels were enhanced with the decreased SOD. The apoptotic rates were higher in I/R rats and H/R H9C2 cells with upregulated miR-148b and cleaved caspase-3, but decreased Bcl-2/Bax ratio; and meanwhile, the Wnt/ß-catenin pathway was inhibited. Additionally, the H/R-induced H9C2 cells also exhibited decreased cell viability. MiR-148b overexpression further aggravated I/R injury of rats, whereas inhibition of miR-148b reduced I/R and H/R injury through activation of Wnt/ß-catenin pathway. In addition, Wnt-1 small interfering RNA exposure abolished the effect of miR-148b inhibitor on H/R injury of H9C2 cells. Inhibition of miR-148b improved the antioxidative ability and myocardial cell survival to suppress its apoptosis by activating Wnt/ß-catenin signaling pathway, thus ameliorating the myocardial I/R injury.

[AIDS-related knowledge among adult males in Chongqing City].

OBJECTIVE: To evaluate AIDS-related knowledge among adult men in Chongqing City, and provide some evidence for AIDS-related health education. METHODS: Using the randomized multistage stratified cluster sampling method, we investigated AIDS-related knowledge among the adult males in Chongqing City. RESULTS: Of the 1502 adult men, those who knew the three major transmitting routes of AIDS (blood-borne, vertical transmission and sexual contact) constituted 85.35, 83.16 and 66.11%, respectively, and 22.70% did not know the proper use of condoms. Those who thought that AIDS could be transmitted by mosquito bite, kissing, dining together, handshake or embracing made up 54.86, 50.6, 30.29 and 19.11%, respectively. The floating population scored significantly lower than the resident population in total AIDS knowledge, HIV transmission knowledge and HIV non-transmission knowledge (P<0.01). CONCLUSION: AIDS-related knowledge among the adult men in Chongqing City needs to be improved by enhancing targeted AIDS-related health education.

Adropin inhibits the phenotypic modulation and proliferation of vascular smooth muscle cells during neointimal hyperplasia by activating the AMPK/ACC signaling pathway.

In-stent restenosis (ISR) remains an inevitable problem for some patients receiving drug-eluting stent (DES) implantation. Intimal hyperplasia is an important biological cause of ISR. It has been previously reported that adropin is a potentially protective factor in cardiovascular disease. Therefore, the present study investigated the function of adropin in inhibiting smooth muscle cell (SMC) phenotype modulation and proliferation, causing intimal hyperplasia. A total of 56 patients who visited the hospital consecutively (25 with ISR and 31 without ISR), who were followed up between April 2016 and March 2019, 1 year following DES, were analyzed to evaluate the association between in-stent neointimal volume and adropin serum levels. Rat aorta smooth muscle cells (RASMCs) were used to determine the effects of adropin on their phenotypic modulation and proliferation using western blot, MTT, PCR and immunofluorescence analyses. Adropin serum levels in the ISR group were significantly lower than those in the non-ISR group. Furthermore, linear regression analysis revealed that only adropin levels were negatively associated with neointimal volume in both groups. The overall adropin levels of the 56 patients and the percentages of neointimal volume revealed a strong negative association. In vitro, adropin suppressed angiotensin II (Ang II)-induced phenotypic modulation in RASMCs by restoring variations of osteopontin and α-smooth muscle actin. Furthermore, compared with the Ang II group, adropin markedly decreased the percentage of G2/M-phase cells. Finally, adropin negatively regulated the phenotypic modulation and proliferation of RASMCs via the AMP-activated protein kinase/acetyl-CoA carboxylase (AMPK/ACC) signaling pathway. In conclusion, an independent, negative association was revealed between adropin and intimal hyperplasia; specifically, adropin inhibited the phenotypic modulation and proliferation of RASMCs by activating the AMPK/ACC signaling pathway. Therefore, adropin may be used as a potential predictor and therapeutic target for intimal hyperplasia and ISR.

The effect of remote health intervention based on internet or mobile communication network on hypertension patients: Protocol for a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: To systematically review the impact of remote health interventions based on an internet or mobile communication network on patients with hypertension and to provide a theoretical basis for hypertension patients with the implementation of remote health interventions. METHODS: Data were retrieved from a total of 4 Chinese databases and 3 foreign databases. The Chinese databases included: China National Knowledge Infrastructure (CNKI), WanFang Data, Chinese Biomedical Database (SinoMed), and Chongqing Chinese Science and Technology Journey database (VIP). The foreign language databases included PubMed, The Cochrane Library, and EMbase, and the date range for the search was from the date the database became active to December 1, 2018. After screening and extracting the materials and evaluating the risk of bias in each study (conducted by 2 researchers), the quality of the selected literature was evaluated by Review Manager (RevMan) [Computer program]. Version 5.3. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2014, and the statistical analysis was applied by Stata 12.0 software. RESULT: This study will provide high-quality evidence-based medicine research evidence for remote health interventions on hypertensive patients based on the Internet and mobile communication network using systematic evaluation and meta-analysis methods. CONCLUSION: This systematic review will provide a scientific conclusion as to whether the remote health intervention model based on an internet or mobile communication network can better control blood pressure and improve patient compliance than the traditional nursing intervention model for hypertensive patients. ETHICS AND DISSEMINATION: This protocol for a systematic review and meta-analysis of randomized controlled trials does not require ethical approval and the results of this paper will be published in an open form in internationally influential academic journals. PROTOCOL AND REGISTRATION: A protocol had been registered in PROSPERO CRD42019122404.

Regulation of airway inflammation and remodeling in asthmatic mice by TLR3/TRIF signal pathway.

This paper aims to investigate the effect of Toll-like receptors 3 (TLR3)/TIR-domain-containing adapter-inducing interferon-ß (TRIF) signal pathway on the airway inflammation and remodeling in asthmatic mice. C57BL/6 and TLR3-/- mice were randomly divided into three groups (10 mice per group), including Control group (mice inhaled phosphate buffer saline (PBS)), Asthma group (mice inhaled ovalbumin (OVA)) and polyriboinosinic-ribocytidylic acid (poly (I: C)) group (asthmatic mice were injected intraperitoneally with TLR3 agonist poly (I: C)). Hematoxylin-eosin (HE) staining, Wright-Giemsa staining, Enzyme-linked immunosorbent assay (ELISA), Immunohistochemistry, Hydroxyproline assay, quantitative real time polymerase chain reaction (qRT-PCR) and Western blot were used to assess for the indices of airway inflammation and remodeling. In terms of WT mice, all asthma groups with or without the addition of poly (I: C) showed exaggerated inflammation and remodeling in the airways as compared to Control group, which were more seriously in poly (I: C) group than Asthma group. Furthermore, we observed the significant inhibition of airway inflammation and remodeling in the TLR3-/- mice in both Asthma no matter with or without addition of poly (I: C) than the WT mice. TLR3 knockout could obviously relieve the airway inflammation and remodeling in asthma through inhibiting TLR3/TRIF signaling pathway.

Association between serum corin levels and risk of acute myocardial infarction.

BACKGROUND: Accumulating evidence has indicated that corin plays critical roles in regulating salt-water balance, blood pressure and cardiac function by activating natriuretic peptides. The present case-control study was designed to evaluate the association of serum soluble corin with acute myocardial infarction (AMI). METHODS: We enrolled 856 consecutive AMI patients and 856 control subjects and explored the possible relation between serum corin levels and AMI risk using logistic regression model. RESULTS: Patients with AMI had higher BMI, were less physically active, and were more likely to have histories of hypertension, diabetes, hyperlipidemia and smoking compared with the controls. Serum levels of corin were remarkably reduced in AMI patients (825±263pg/ml) compared with those in healthy controls (1246±425pg/ml). Odds ratios of ST elevation (STEMI) and non-ST elevation myocardial infarction (NSTEMI) were significantly decreased with the increasing levels of serum corin in both men and women (P for trend, <0.001) after adjustment for body mass index, hypertension, diabetes, hyperlipidemia, smoking, and physical activity. CONCLUSIONS: Our study demonstrates that serum levels of corin are significantly decreased in AMI patients, and it is inversely associated with the incidences of STEMI and NSTEMI in both men and women.

Plasma Corin as a Predictor of Cardiovascular Events in Patients With Chronic Heart Failure.

OBJECTIVES: The aim of this study was to determine the prognostic value of plasma corin in patients with chronic heart failure (CHF). BACKGROUND: In recent years, accumulating evidence has indicated that corin plays a critical role in regulating blood pressure and cardiac function. METHODS: We enrolled 1,148 consecutive CHF patients in a prospective cohort study and explored the association between plasma corin levels and clinical prognosis using multivariate Cox regression analysis. RESULTS: Patients with low corin levels (<458 pg/ml) were more likely to be women and to be hypertensive. Low corin was found to be associated with an increase in New York Heart Association (NYHA) functional class and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, and a decrease in left ventricular ejection fraction (LVEF) and the estimated glomerular filtration rate (eGFR). Multivariate Cox regression analysis suggested that log corin was an independent predictor of major adverse cardiac event(s) (MACE) (hazard ratio: 0.62; 95% confidence interval: 0.39 to 0.95), together with age, diabetes, NYHA functional class, LVEF, eGFR, and log NT-proBNP. In addition, log corin was also a significant predictor for cardiovascular death (p = 0.041) and heart failure rehospitalization (p = 0.015) after adjustment for clinical variables and established biomarkers of adverse prognosis. The Kaplan-Meier survival curves showed that low corin was a significant predictor of MACE in patients with NT-proBNP levels above and below the median. CONCLUSIONS: Our study demonstrates that plasma corin is a valuable prognostic marker of MACE in patients with CHF, independent of established conventional risk factors.

Adropin is associated with hyperhomocysteine and coronary atherosclerosis.

Homocysteine has been recognized as a risk factor for atherosclerosis and cardiovascular diseases. Adropin is a newly-identified energy homeostasis protein with a potential protective effect against coronary artery disease (CAD). This study attempted to measure the correlation between serum homocysteine and adropin levels in patients with CAD, and to ascertain how the two hormones could affect the severity of coronary atherosclerosis. A cohort of CAD patients who had undergone coronary angiography was prospectively recruited. The serum homocysteine and adropin levels of the patients were measured and the severity of coronary atherosclerosis was quantified with the SYNTAX score. The data were analyzed with a generalized structural equation model. In total, 170 consecutive patients were recruited with a mean serum homocysteine level of 15.9±8.3 µmol/l, and 76 (44.7%) patients were identified as hyperhomocysteinemic with a serum homocysteine level >15 µmol/l. Serum homocysteine level was found to be significantly negatively correlated with serum adropin level (r=-0.169, P=0.028). Patients with hyperhomocysteinemia had lower serum adropin levels and higher SYNTAX scores than patients without hyperhomocysteinemia. Further analysis with a generalized structural equation model showed that adropin was significantly associated with hyperhomocysteinemia (adjusted odds ratio: 0.95, 95% confidence interval: 0.93 to 0.98; P=0.002), which in turn was significantly associated with the SYNTAX score (coefficient: 4.71, 95% confidence interval: 1.39 to 8.03; P=0.005). In conclusion, the serum homocysteine level was inversely correlated with the serum adropin level in patients with CAD. A low serum adropin level was associated with hyperhomocysteinemia and more severe coronary atherosclerosis, as reflected by a higher SYNTAX score.

Vitamin D Supplementation in the Treatment of Chronic Heart Failure: A Meta-analysis of Randomized Controlled Trials.

BACKGROUND: In recent years, there has been growing evidence that vitamin D deficiency is associated with the development and progression of chronic heart failure (CHF). HYPOTHESIS: Additional supplementation of vitamin D may have protective effects in patients with CHF. METHODS: We searched PubMed, Embase, and Cochrane databases through June 2015 and included 7 randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in patients with CHF. Then, we performed a meta-analysis of clinical trials to confirm whether vitamin D supplementation is beneficial in CHF patients. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated using fixed- or random-effects models. RESULTS: Our pooled results indicated that additional supplementation of vitamin D was not superior to conventional treatment in terms of left ventricular ejection fraction, N-terminal pro-B-type natriuretic peptide, and 6-minute walk distance. Moreover, vitamin D supplementation was associated with significant decreases in the levels of tumor necrosis factor-α (WMD: -2.42 pg/mL, 95% CI: -4.26 to -0.57, P < 0.05), C-reactive protein (WMD: -0.72 mg/L, 95% CI: -1.42 to -0.02, P < 0.05), and parathyroid hormone (WMD: -13.44 pg/mL, 95% CI: -21.22 to -5.67, P < 0.05). CONCLUSIONS: Vitamin D supplementation may decrease serum levels of parathyroid hormone and inflammatory mediators in CHF patients, whereas it has no beneficial effects on improvement of left ventricular function and exercise tolerance.

[An assistant artificial hip joint].

The assistant artificial hip joint (AAHJ) is a new impermanent hip support implanted in the body. It is used for treatment of ischemic necrosis of the femoral head at the early stage. It reserves the natural femoral head, increases its containment and decreases its load, thus makes the recovery of the necrosed femoral head. The AAHJ's moving axis center is the same as that of the femoral head. Therefore, the moving range of the hip joint is very close to the normal postoperatively. The patient can walk with loading in 3 weeks after the surgical operation, and can regain his (or her) daily work and life in 2 to 3 months of the operation. The AAHJ's structure is simple and the price is cheap.