The IL-1beta (-511) and (-31) polymorphisms were significantly associated with BP in women. The other genetic polymorphisms of cytokine genes that we analysed do not appear to be associated with BP susceptibility in our Chinese population.

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Objective: This review summarizes the advances in the study of ncRNAs and atrial remodeling mechanisms to explore potential therapeutic targets and strategies for AF.Background: Atrial fibrillation (AF) is one of the most common arrhythmias, and its morbidity and mortality rates are gradually increasing. Non-coding ribonucleic acid RNAs (ncRNAs) are transcribed from the genome and do not have the ability to be translated into proteins. A growing body of evidence has shown ncRNAs are extensively involved in the pathophysiological processes underlying AF. However, the precise molecular mechanisms of these associations have not been fully elucidated. Atrial remodeling plays a key role in the occurrence and development of AF, and includes electrical remodeling, structural remodeling, and autonomic nerve remodeling. Research has shown that ncRNA expression is altered in the plasma and tissues of AF patients that mediate cardiac excitation and arrhythmia, and is closely related to atrial remodeling.Methods: Literatures about ncRNAs and atrial fibrillation were extensively reviewed to discuss and analyze. Conclusions:The biology of ncRNAs represents a relatively new field of research and is still in an emerging stage. Recent studies have laid a foundation for understanding the molecular mechanisms of AF, future studies aimed at identifying how ncRNAs act on atrial fibrillation to provide potentially promising therapeutic targets for the treatment of atrial fibrillation.

Aim: To assess the epistatic relationships of nitric oxide (NO) biosynthesis pathway genes in susceptibility to coronary heart disease (CHD). Methods: A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms (SNP) within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction (GMDR) analyses, respectively. Results: Two alleles (rs1049255*C and rs841*A) were identified that were significantly associated with increased risk of CHD after adjusting for all confounders (OR=1.21, 95% CI: 1.06−1.39, combined P=0.001, P corr =0.007 and OR=1.30, 95% CI 1.12−1.50, combined P<0.001, P corr <0.001, respectively). Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polymorphisms, affecting the risk of CHD (P<0.001 for both). No significant high-order interactions were identified. Conclusion:The results suggested that two-way SNP-SNP interactions of polymorphisms within NO biosynthesis pathway genes contribute to CHD risk.

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