Interactions between ALDH2 rs671 polymorphism and lifestyle behaviors on coronary artery disease risk in a Chinese Han population with dyslipidemia: A guide to targeted heart health management.

BACKGROUND: Both aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism and lifestyle behaviors are involved in coronary artery disease (CAD), while the interaction between them is currently unknown. METHODS: A nested case-control study was conducted in 161 patients with CAD and 495 controls in dyslipidemia population in Yinzhou District, Ningbo, Zhejiang Province, China, in August 2013. Anthropometric data and blood samples were collected, demographic characteristics and lifestyle behaviors information were obtained by a face-to-face interview, dietary intake was assessed by a food frequency questionnaire, and genomic DNA was genotyped. RESULTS: Carriers with increasing number of A alleles had an elevated CAD risk compared with G allele carriers (adjusted OR = 1.483, 95% CI = 1.114-1.974). Carriers of rs671 A/G and A/A genotypes had a higher CAD risk than carriers of G/G genotype (adjusted OR = 1.492, 95% CI = 1.036-2.148). Similarly, individuals with rs671 A/A genotype had a higher CAD risk than individuals with A/G and G/G genotypes (adjusted OR = 2.161, 95% CI = 1.139-4.101). We found a borderline additive interaction between regular fried food intake and A/A and A/G genotypes, and a significantly additive interaction between sedentary/light physical activity and A/A and A/G genotypes. CONCLUSIONS: Individuals with A/A or A/G genotypes of rs671 have a higher CAD risk, if they lack physical activity and take fried food regularly, than individuals with G/G genotypes. These findings can help to provide a guide to targeted heart health management.

Associations of genetic variation in CASP3 gene with noise-induced hearing loss in a Chinese population: a case-control study.

BACKGROUND: Noise-induced hearing loss (NIHL) is a complex disease caused by environmental and genetic risk factors. This study explored the relationship between the genetic variations in the CASP gene and the risk of developing NIHL among Chinese workers exposed to occupational noise. METHODS: A case-control study of 272 NIHL workers and 272 normal-hearing workers matched for age, sex and years of noise exposure was conducted. Fifteen single-nucleotide polymorphisms (SNP) in the CASP1, CASP3, CASP4, CASP5, CASP6, CASP8, CASP9, CASP10 and CASP14 genes were genotyped using the polymerase chain reaction-ligase detection reaction method. Using conditional logistic regression models, the adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of genetic variations associated with NIHL risk were calculated. RESULTS: Two SNPs in the CASP3 gene were associated with NIHL risk. For rs1049216, TT genotype was associated with a decreased risk of NIHL (OR = 0.246, 95% CI = 0.069-0.886) when compared with the CC genotype. For rs6948, the AC and CC genotype were associated with a decreased NIHL risk (OR = 0.568, 95% CI = 0.352-0.916) compared with AA genotype. There were joint effects of working time and CASP3 polymorphisms on NIHL risk (P < 0.05). CONCLUSIONS: Genetic variations in the CASP3 gene and the joint effects of working time and CASP3 polymorphisms may modify the risk of developing NIHL.

Genetic variations in protocadherin 15 and their interactions with noise exposure associated with noise-induced hearing loss in Chinese population.

OBJECTIVES: The purpose of this study was to examine the associations between genetic variations in the Protocadherin 15 gene (PCDH15) and the risk to noise induced hearing loss (NIHL) in a Chinese population. METHODS: A case-control study was conducted with 476 noise-sensitive workers (NIHL) and 475 noise-resistant workers (normal) matched for gender, years of noise exposure, and intensity of noise exposure. 13 tag single-nucleotide polymorphisms in PCDH15 were genotyped using nanofluidic dynamic arrays on the Fluidigm platform. Multiple logistic regression was used to analyze the associations of genetic variations of PCDH15 with NIHL adjusted by age, smoking/drinking status, and cumulative noise exposure and their interactions with noise exposure. RESULTS: The allele frequency and genotypes of rs1104085 were significantly associated with the risk of NIHL(P=0.009 and 0.005 respectively ). The subjects carrying variant alleles (CT or CC) of rs11004085 had a decreased the risk for NIHL (adjusted odds ratio=0.587, 95% confidence interval 0.409-0.842) compared with subjects who had the wild-type (TT) homozygotes. The interactions were found between the SNPs of rs1100085, rs10825122, rs1930146, rs2384437, rs4540756, and rs2384375 and noise exposure. CONCLUSIONS: Genetic variations of PCDH15 and their interactions with occupational noise exposure are associated with genetic susceptibility to NIHL and modify the risk of noise induced hearing loss.