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Long-term exposure to ambient ozone links to aging biomarkers and increased risk for atherosclerotic cardiovascular diseases (ASCVD). However, the roles of aging biomarkers in the association of long-term exposure to ambient ozone with ASCVD are unclear.A total of 5298 participants completed the questionnaire and physical examination and provided biological specimens. Aging biomarkers (telomere length [TL] and mitochondrial copy number [mtDNA-CN]) were measured by using a real-time polymerase chain reaction method. The concentration of ambient ozone was assessed using a random forest model. Associations of ambient ozone or aging biomarkers with 10-year ASCVD risk were analyzed using logistic regression models. The roles of aging biomarkers in the association of ambient ozone exposure with 10-year ASCVD risk were explored by mediation analysis.The adjusted odds ratios and 95% confidence interval of high 10-year ASCVD risk were 1.16 (1.08, 1.25), 0.71 (0.60, 0.85), and 0.78 (0.64, 0.96) in association with each 1-unit increment in ambient ozone (1 μg/mLong-term exposure to ambient ozone was associated with increased 10-year ASCVD risk, and the association was partially mediated by aging biomarkers (shortened TL and decreased mtDNA-CN). This study indicated that ambient ozone pollution-related ASCVD risk might be partially explained by the telomere-mitochondrial axis of aging.

Growing evidence suggests that travel may serve as an effective intervention of subjective well-being (SWB). This study develops and empirically tests a psychological model that describes the links of travel experience and SWB. This study also compared the short- and long-term effects of the tourist experience on SWB. Our results identified 3 dimensions of cruise experience, namely, emotional experience, relational experience, and thinking experience. In the short term, happiness from cruise travel is created mainly through emotional and relational experiences. The long-term effect of cruising travel is largely derived from thinking experience. Theoretical and management implications were discussed.

Increasing evidence indicates that bisphenol A (BPA), a widely manufactured environmental pollutant, can induce changes in DNA methylation paatterns, which is a potential mechanism linking this environmental exposure to disease development. We investigated the influence of developmental exposure to BPA on pancreatic DNA methylation patterns and whether maternal folate supplementation can modify the epigenetic status and pancreatic impairment induced by BPA. Our results showed that maternal dietary folate supplementation in rats exposed to BPA counteracted the observed BPA-induced pancreatic impairments in the offspring, which included disrupted insulin secretion and glucose intolerance, and impaired morphology and ultrastructure of β cells. Moreover, these pancreatic dysfunctions were shown to be associated with low expression and DNA hypermethylation of insulin-like growth factor-2 (Igf2) in islets induced by exposure to BPA during the developmental period. Importantly, maternal dietary folate supplementation was demonstrated to negate this Igf2 DNA hypermethylation in the offspring, which was consistent with the upregulation of Igf2 expression. Overall, our results suggest that early developmental exposure to BPA alters the DNA methylation of Igf2, that these altered methylation patterns are associated with impaired β-cell function in the offspring and that these effects can be counteracted by maternal folate supplementation. Copyright © 2017 John Wiley & Sons, Ltd.

BACKGROUND: Taqman fluorescent probe was frequently applied in single nucleotide polymorphism (SNP) genotyping. However, the characteristic of calling error and the influencing factors remain unclear. METHOD: Calling errors of Taqman genotyping was evaluated systematically based on Mendelian inheritance. Twenty‐two SNPs were genotyped by Taqman probe for 419 pedigrees. Mendelian genetic errors were counted for every SNP and pedigree. Cluster analysis was applied to investigate the compatibility between Taqman probes and DNA sample. RESULTS: On one hand, errors were found for all the SNPs. The error number ranged from 4 to 33 with median of 10.5. On the other hand, Mendelian genetic errors showed features of both randomness and cluster. Half of the pedigrees containing errors had only 1 Mendelian genetic error. But there was also a pedigree containing up to 10 Mendelian genetic errors. Furthermore, cluster analysis indicated that errors of different SNPs took place in different pedigree cluster. CONCLUSION: It could be concluded that calling error is inevitable for Taqman genotyping of large samples. The quality of Taqman probe and DNA sample, as well as their compatibility, may account for the error incidence.

Perfluorooctane sulfonate (PFOS) is a widespread environmental contaminant that is detected in the lung of mammals. The mechanisms underlying PFOS-induced lung cytotoxicity remain unclear. The main purpose of this study was to evaluate the cytotoxic effects of PFOS on human lung cancer A549 cells and its possible molecular mechanism. A549 cells were treated with PFOS (0, 25, 50, 100 and 200 μm) and the cellular apoptosis, mitochondrial membrane potential as well as intracellular reactive oxygen species were determined. In this study, PFOS induced a dose-dependent increase in A549 cell toxicity via an apoptosis pathway as characterized by increased percentage of sub-G1, activation of caspase-3 and -9, and increased ratio of Bax/bcl-2 mRNA expression. In addition, there was obvious oxidative stress, represented by decreased glutathione level, increased malondialdehyde level and superoxide dismutase activity. N-Acetylcysteine, as an antioxidant that is a direct reactive oxygen species scavenger, can effectively block PFOS-induced reactive oxygen species generation, mitochondrial membrane potential loss and cell apoptosis. These data indicate that PFOS induces apoptosis in A549 cells through a reactive oxygen species-mediated mitochondrial dysfunction pathway mechanism.