Neuronal signaling together with synapse activity in the central nervous system requires a precisely regulated microenvironment. Recently, the blood-brain barrier is considered as a “neuro-glia-vascular unit,” a structural and functional compound composed of capillary endothelial cells, glial cells, pericytes, and neurons, which plays a pivotal role in maintaining the balance of the microenvironment in and out of the brain. Tight junctions and adherens junctions, which function as barriers of the blood-brain barrier, are two well-known kinds in the endothelial cell junctions. In this review, we focus on the less-concerned contribution of gap junction proteins, connexins in blood-brain barrier integrity under physio-/pathology conditions. In the neuro-glia-vascular unit, connexins are expressed in the capillary endothelial cells and prominent in astrocyte endfeet around and associated with maturation and function of the blood-brain barrier through a unique signaling pathway and an interaction with tight junction proteins. Connexin hemichannels and connexin gap junction channels contribute to the physiological or pathological progress of the blood-brain barrier; in addition, the interaction with other cell-cell-adhesive proteins is also associated with the maintenance of the blood-brain barrier. Lastly, we explore the connexins and connexin channels involved in the blood-brain barrier in neurological diseases and any programme for drug discovery or delivery to target or avoid the blood-brain barrier.

Guidelines divide patients with heart failure (HF) into 3 distinct groups based on left ventricular ejection fraction (LVEF) We used the Minnesota Living with Heart Failure Questionnaire (MLHFQ) to quantify the health-related quality of life in patients with HF. Patients were stratified into three cohorts: preserved LVEF (>50%), mid-range LVEF (40–49%) and reduced LVEF (<40%). The MLHFQ scores were evaluated using one-way ANOVA, and differences were observed among the groups. The association of New York Heart Association (NYHA) class with the physical scores was analyzed by Spearman’s correlation analysis. The predictive utility of the total MLHFQ scores was assessed with Kaplan-Meier curves for death and HF-related hospitalization. The Cox proportional hazards model was used to identify the risk factors for prognosis. Internal reliability was assessed with Cronbach’s α. There were significant differences in the total MLHFQ scores and the MLHFQ subscale scores among the three groups (p<0.05). MLHFQ domains demonstrated high internal consistency among the three groups (Cronbach’s α = 0.92, 0.96 and 0.93). The MLHFQ physical subscale scores were significantly associated with NYHA class in HFrEF (r = 0.59, p<0.001) and HFmrEF patients (r = 0.537, p<0.001). The survival analysis indicated that there was a significant difference among the three groups regarding high MLHFQ scores (p = 0.038). In the groups with low MLHFQ scores, the HFmrEF group exhibited significantly increased rates of death and HF-related hospitalization compared with the HFpEF group (p = 0.035). The features and clinical outcomes varied among heart failure patients with different EF values. The MLHFQ appears to be a valid and reliable measurement of health status and offers excellent prognostic ability.

Aims/Introduction: Obesity plays a central role in metabolic syndrome. Obesity indexes are important in clinical work. In the present study, we sought to determine the relationships between obesity indexes and metabolic risk factors.Materials and Methods: We studied 11,568 participants over 35 years. Body mass index, waist circumference (WC), waist‐to‐height ratio (WHtR) and waist‐to‐hip ratio were measured and calculated. To compare the predictive ability of the obesity indexes in diagnosing multiple metabolic risk factors, the areas under receiver operating characteristic curves were calculated, and cut‐off values were determined. A partial correlation coefficient was used to assess the intercorrelations between the obesity indexes, and to evaluate the correlations between each index and each metabolic risk factor.Results: The partial correlation coefficient for WHtR and WC was 0.947. In diagnosing multiple metabolic risk factors, the WHtR areas under receiver operating characteristic curves was greater than that for the other obesity indexes in both sexes. The cut‐off point for the WHtR was 0.50 in men and 0.52 in women. The cut‐off point for WC was 85 cm in men and 80 cm in women.Conclusions: WHtR strongly correlates with WC. The WHtR might show the same predictive ability as the WC in diagnosing multiple metabolic risk factors.

Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensin II receptor-like 1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarction‑induced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin‑13 during myocardial infarction‑induced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin‑13. Apelin‑13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Masson's trichrome staining and western blotting showed that apelin‑13 attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzyme‑linked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin‑13 inhibited the activation of nuclear factor (NF)‑κB signaling in vitro and in vivo. To the best of our knowledge, the present study was the first to demonstrate that apelin‑13 may attenuate myocardial infarction‑induced myocardial fibrosis, and that this protective function may be mediated by inhibition of NF‑κB signaling. The present study suggests a theoretical basis for the effects of apelin‑13 and provides insight into the potential clinical application of apelin-13.