The authors performed a meta-analysis of observational studies to estimate the magnitude of spousal concordance for hypertension and to examine whether the concordance varied by important study methodological aspects. PubMed and Embase were searched up to June 2017 for cross-sectional, case-control, and cohort studies that investigated the concordance/association of hypertension between spouse pairs. A meta-analysis with random-effects models was performed by pooling adjusted odds ratios. Eight studies with a total number of 81 928 spouse pairs were eligible. The pooled results showed that spouses of individuals with hypertension had 41% (odds ratio, 1.41; 95% confidence interval, 1.21-1.64) increased odds of having hypertension themselves. The association applied to both men and women, and was not significantly different between studies with adjustment for body mass index and those without. The findings highlighted the importance of environmental factors in the development of hypertension. | INTRODUCTIONHypertension is the leading risk factor for morbidities and mortalities caused by cardiovascular and kidney diseases. The Global Burden Project estimated that hypertension accounts for 9.4 million deaths each year worldwide.1 Hypertension is a complex disorder resulting from both genetic and environmental determinants. and body mass index (BMI), spousal diagnosis of hypertension was the strongest risk factor of hypertension for men and second strongest risk factor for women, with adjusted risk estimates at two-to three-fold. 7 In another community-based population study in Brazil, however, the spousal association was not significant after adjusting for age. 9 Therefore, these inconsistencies and uncertainties need to be addressed using quantitative and comparative methods.Previous meta-analyses have observed a significant positive spousal concordance for diabetes mellitus and the majority of main coronary risk factors. 15,16 However, no meta-analysis has summarized the available evidence of spousal concordance for hypertension. In addition, the mechanism through which spousal concordance operates was not known. The concordance may operate through the Zhancheng Wang and Wenhui Ji contributed equally to this work.

It has been hypothesized that flowering plants at high elevation could be pollinated by local passerine birds given that low temperature limits insect activity. In particular, species with large flowers are likely to be pollinated by large-body animals because a morphological fit between floral morphology and pollinator body could facilitate pollen transfer. Huang et al. investigated pollinator species and their visitation frequency in 15 Rhododendron species from East Himalayas. The pollinator experiments excluding all pollinators, or just birds in the 15 species demonstrated that birds acted as pollinators in 2/3 studied Rhododendron species, in support of the hypotheses.

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Background Inflammation in epicardial adipose tissue (EAT) may contribute to coronary atherosclerosis. Myocardial bridge is a congenital anomaly in which the left anterior descending coronary artery takes a “tunneled” course under a bridge of myocardium: while atherosclerosis develops in the proximal left anterior descending coronary artery, the bridged portion is spared, highlighting the possibility that geographic separation from inflamed EAT is protective. We tested the hypothesis that inflammation in EAT was related to atherosclerosis by comparing EAT from proximal and bridge depots in individuals with myocardial bridge and varying degrees of atherosclerotic plaque. Methods and Results Maximal plaque burden was quantified by intravascular ultrasound, and inflammation was quantified by pericoronary EAT signal attenuation (pericoronary adipose tissue attenuation) from cardiac computed tomography scans. EAT overlying the proximal left anterior descending coronary artery and myocardial bridge was harvested for measurement of mRNA and microRNA (miRNA) using custom chips by Nanostring; inflammatory cytokines were measured in tissue culture supernatants. Pericoronary adipose tissue attenuation was increased, indicating inflammation, in proximal versus bridge EAT, in proportion to atherosclerotic plaque. Individuals with moderate‐high versus low plaque burden exhibited greater expression of inflammation and hypoxia genes, and lower expression of adipogenesis genes. Comparison of gene expression in proximal versus bridge depots revealed differences only in participants with moderate‐high plaque: inflammation was higher in proximal and adipogenesis lower in bridge EAT. Secreted inflammatory cytokines tended to be higher in proximal EAT. Hypoxia‐inducible factor 1a was highly associated with inflammatory gene expression. Seven miRNAs were differentially expressed by depot: 3192‐5P, 518D‐3P, and 532‐5P were upregulated in proximal EAT, whereas miR 630, 575, 16‐5P, and 320E were upregulated in bridge EAT. miR 630 correlated directly with plaque burden and inversely with adipogenesis genes. miR 3192‐5P, 518D‐3P, and 532‐5P correlated inversely with hypoxia/oxidative stress, peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PCG1a), adipogenesis, and angiogenesis genes. Conclusions Inflammation is specifically elevated in EAT overlying atherosclerotic plaque, suggesting that EAT inflammation is caused by atherogenic molecular signals, including hypoxia‐inducible factor 1a and/or miRNAs in an “inside‐to‐out” relationship. Adipogenesis was suppressed in the bridge EAT, but only in the presence of atherosclerotic plaque, supporting cross talk between the vasculature and EAT. miR 630 in EAT, expressed differentially according to burden of atherosclerotic plaque, and 3 other miRNAs appear to inhibit key genes related to adipogenesis, angiogenesis, hypoxia/oxidative stress, and thermogenesis in EAT, highlighting a role for miRNA in mediating cross talk between the coronary vasculature and EAT.

Background/Aims: Hyperlipidemia is a risk factor for various cardiovascular and metabolic disorders. And it is tightly related to chronic inflammation. Interleukin-38 (IL-38) represents a new member of anti-inflammatory cytokines. Thus we studied the important role of IL-38 in hyperlipidemia development and treatment. Methods: The mRNA level of IL-38 in PBMCs (peripheral blood mononuclear cells) and serum IL-38 levels in hyperlipidemia patients and healthy controls were measured by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunoassay (ELISA). The hyperlipidemia patients were further divided into two groups (Sensitive and Resistant Group) according to their clinical response to Atorvastatin therapy. Finally, the effects of IL-38 on hyperlipidemia was evaluated in the mice model. Results: Data showed that the IL-38 mRNA and serum protein levels were higher in patients with hyperlipidemia compared with healthy controls. And the IL-38 mRNA and serum protein levels were higher in patients sensitive to Atorvastatin therapy than the resistant group. In vitro, IL-38 inhibited the production of IL-6, IL-1β and CRP in PBMCs of patients with hyperlipidemia. In the mice model of hyperlipidemia, IL-38 was also elevated during the hyperlipidemia development. Furthermore, the IL-38 over-expressed by adeno-associated virus significantly inhibited the hyperlipidemia development, inflammatory factor secretion and also the atherosclerosis process. Conclusion: Thus our data showed that IL-38 might present protective effects on hyperlipidemia treatment.