Objective:To determine the correlations of single nucleotide polymorphisms (SNPs) with atrial fibrillation (AF) in the Chinese Han population from the central plains.Methods:A total of 168 hospitalized patients,including 56 AF and 112 controls,were recruited in this case-control study.The clinical data were obtained from the medical records.All 5 SNPs,rs337711 in KCNN2,rs11264280 near KCNN3,rs17042171 near PITX2,rs6771157 and rs6795970 in SCN10A,were genotyped using amplification refractory mutation system-polymerase chain reaction or direct sequencing.The x2 test was used to compare categorical variables and preliminarily examine correlations between the genotype frequencies and AF.Subsequently,a logistic regression model was constructed to determine the associations between the SNPs and AF based on the above screened results.Odds ratios (ORs) and 95％ confidence interval (CI) were calculated to assess the strength of the correlations.Moreover,we downloaded the genotype data from the HapMap Project for linkage disequilibrium analysis ofrs17042171.Results:AF patients were likely to be of older age and longer left atrial diameter and had more coronary artery disease and higher hypertension compared with the control group (P＜0.05).Among the 5 SNPs,the frequency distribution of genotype AA for rs17042171 was significantly different between the AF and control groups (P＜0.05).After adjusting for several covariates,there was still a high risk ratio in patients with the AA genotype compared with the AC+CC genotype (OR:5.591,95％CI 2.176 to 14.365,P-B＜0.008).Similarly,stratification analysis on the AA genotype demonstrated significant differences between rs17042171 and persistent AF.However,there were not significant correlations between AF and the control groups for the other 4 SNPs (P＜0.05).Conclusion:Rs17042171,near PITX2 on chromosome 4q25,is associated with AF susceptibility in the Chinese Han population from the central plains,suggesting that this SNP can provide a new strategy for clinical diagnosis in AF patients.

Background: Androgenetic alopecia (AGA) leads to thinning of scalp hair and affects 60%~70% of the adult population worldwide. Developing more effective treatments and studying its mechanism are of great significance. Previous clinical studies have revealed that hair growth is stimulated by 650-nm red light. Objective: This study aimed to explore the effect and mechanism of 650-nm red light on the treatment of AGA by using ex vivo hair follicle culture. Methods: Human hair follicles were obtained from hair transplant patients with AGA. Hair follicles were cultured in Williams E medium and treated with or without 650-nm red light.Real-time RT-PCR and immunofluorescence staining were used to detect the expression level of genes and proteins in hair follicles, respectively. RNA-sequencing analysis was carried out to reveal the distinct gene signatures upon 650 nm treatment. Results: Low-level 650 nm red light promoted the proliferation of human hair follicles in the experimental cultured-tissue model. Consistently, 650 nm red light significantly delayed the transition of hair cycle from anagen to catagen in vitro. RNA-seq analysis and gene clustering for the differentially expressed genes suggests that leukocyte transendothelial migration, metabolism, adherens junction and other biological process maybe involved in stimulation of hair follicles by 650-nm red light treatment. Conclusion The effect of 650-nm red light on ex vivo hair follicles and the transcriptome set which implicates the role of red light in promoting hair growth and reversing of miniaturization process of AGA were identified.