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Background: Few studies are available on the relationship of androstenedione with inflammation and obesity and the effect of androstenedione and inflammation on the association between testosterone and obesity. This study intended to examine the mediation effect of inflammatory markers on the association of testosterone with obesity and the moderation effect of androstenedione on the association of testosterone with inflammation and obesity in Chinese rural men. Materials and methods: This cross‐sectional research enrolled 2536 male rural inhabitants from the Henan Rural Cohort study. The serum concentrations of testosterone and androstenedione were determined by liquid chromatography–tandem mass spectrometry. Linear and logistic regression were used to examine the relationships between testosterone, inflammatory markers, and obesity. Mediation and moderation analyses were carried out to evaluate the potential effects of inflammatory markers on the relationship between testosterone and obesity, as well as androstenedione on the relationships of testosterone with inflammation and obesity. Results: After adjusting for confounding factors, the results showed that testosterone and androstenedione were negatively related to obesity, and inflammatory markers were positively associated with obesity. Besides, testosterone and androstenedione were negatively associated with inflammatory markers. Mediation analysis showed that white blood cell, neutrophil, monocyte, and high‐sensitivity C‐reactive protein had mediating effects on the association between testosterone and obesity. The most vital mediator was high‐sensitivity C‐reactive protein, and its proportion of the effect was 11.02% (defined by waist circumference), 11.15% (defined by waist‐to‐hip ratio), 12.92% (defined by waist‐to‐height ratio), and full mediating effect (defined by body mass index). Moreover, androstenedione played negative moderation effects on the associations of testosterone with inflammation and obesity. Conclusion: Inflammatory markers and androstenedione were first found to have modifying effects on the association of testosterone with obesity. Higher levels of testosterone and androstenedione could reduce the inflammation level and risk of obesity, indicating their potential roles in the prevention and treatment of chronic diseases. [ABSTRACT FROM AUTHOR]

It is worth paying attention to the level of worry and fear of students during the normalization of the epidemic. We conducted the cross‐sectional study that included 182,991 high school students using an online survey to assess worry and fear levels and its influencing factors in three cities in Henan Province, China, from May 21 to May 27, 2021. Worry and fear levels were measured using a five‐item Likert‐type scale. Multinomial logistic regression was used to analyze the risk factors. Approximately 65.42% of students reported being high worry about the coronavirus disease 2019 (COVID‐19) epidemic, and about 41.44% of students reported being high fear about the COVID‐19 epidemic. In addition, compared with female, male had lower odds of suffering from a high worry, and compared with senior high school students, junior high school students were more likely to suffer from a high worry. Students lived in rural had highest odds increased likelihood of high worry. Similar results in fear levels. During the normalization period of the COVID‐19 epidemic, many students have high levels of worry and fear. This study has implications for potential influencers of worry and fear levels in follow‐up work. Practitioner Points: Approximately 65.42% of students reported being high worry about the coronavirus disease 2019 (COVID‐19) epidemic, and about 41.44% of students reported being high fear about the COVID‐19 epidemic.Students lived in rural had highest odds increased likelihood of high level of worry and fear.Compared with senior high school students, junior high school students were more likely to suffer from a high worry. [ABSTRACT FROM AUTHOR]

Background: 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. Methods: 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. Results: 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/m3) concentration, relative TL, and mtDNA‐CN, respectively. The mediated proportion of the association between ambient ozone exposure and high 10‐year ASCVD risk by TL or mtDNA‐CN was 21.13% or 7.75%, respectively. The total proportion of association between ambient ozone exposure and high 10‐year ASCVD risk mediated by TL plus mtDNA‐CN was 21.02%. Conclusions: Long‐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. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aims/Introduction: Studies have found that a plant‐based diet was associated with a lower risk of type 2 diabetes, but evidence is scarce on such associations in China. The aim of this study was to investigate whether a plant‐based diet is related to a lower risk of type 2 diabetes among Chinese adults. Materials and Methods: A total of 37,985 participants were enrolled from the Henan Rural Cohort Study. An overall plant‐based diet index (PDI) was created by assigning positive and reverse scores to 12 commonly consumed food groups. Multivariate logistic regression models and restricted cubic spline analysis were performed to estimate the odds ratio (OR) and 95% confidence interval (95% CI). Results: After multivariable adjustment, the risk of type 2 diabetes was inversely associated with the PDI (extreme‐quartile OR = 0.88, 95% CI: 0.79–0.98; P = 0.027), the risk associated with a 1 standard deviation (SD) increase in PDI was 4% lower (95% CI, 0.93–1.00; P trend = 0.043) for type 2 diabetes. Moreover, the odds of type 2 diabetes was decreased with an increment of PDI after fitting restricted cubic splines (Ptrend < 0.01). Conclusions: Among Chinese populations, diets higher in plant foods and lower in animal foods were associated with a reduced risk of type 2 diabetes. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Maternal overweight has been associated with increasing offspring birth weight, but epidemiological data on potential biological mechanisms are limited. This study aimed to examine whether steroid hormones mediate the association between maternal prepregnancy BMI (pre-BMI) and birth weight.Methods: This study involving 2,039 participants was conducted from an ongoing cohort study in Wuhan, China. Mediation analysis was used to identify the extent to which steroid hormones mediated associations.Results: Each one-unit increase in pre-BMI was significantly associated with lower log2 -transformed cord blood levels of cortisol and corticosterone. Levels of cortisol and corticosterone were also negatively associated with birth weight. It was estimated that corticosterone mediated 3.48% of the association between pre-BMI and birth weight, and no significant mediation effect was observed in cortisol. After stratification by maternal gestational weight gain (GWG; within or in excess of the Institute of Medicine [IOM] guidelines), the associations of pre-BMI with cortisol and corticosterone levels were significant in the women with GWG > IOM but not in women with GWG ≤ IOM. When the mediation analysis in the women with GWG > IOM was limited, the mediation effects of cord blood cortisol and corticosterone were both significant (P < 0.05).Conclusions: Cord blood cortisol and corticosterone partially mediate the association of increased maternal pre-BMI with higher birth weight. [ABSTRACT FROM AUTHOR]

Conflicting evidence exists regarding the magnitude of the association between adult height and risk of stroke, and it is unclear whether this association is different between men and women. The authors carried out a meta-analysis to assess the sex-specific effect of adult height on the risk of stroke and its subtypes. Prospective cohort studies reporting sex-specific risk estimates of height with stroke or reported in a certain sex were included. Summary relative risks for 5-unit increments in height were calculated using random-effects, and dose-response relationships were performed using a restricted cubic spline model. Subgroup analyses, sensitivity analyses, and tests for publication bias were also performed. In all, 20 prospective studies were identified in this study. The summary of relative risks (95% CIs) of stroke for a 5 cm increase in adult height were 0.93 (0.90-0.95) for men and 0.88 (0.83-0.93) for women. There was no significant difference in the effect of height on future stroke risk between men and women (Pinteraction  = 0.085). There was evidence of a nonlinear association between adult height and stroke risk, with steeper inverse associations at lower level of height, but further reductions in risk were observed at greater heights. Subgroup and sensitivity analyses showed that the significant associations were consistent in most stratifications and with various inclusion criteria. In conclusion, higher adult height was significantly associated with lower risk of stroke in both men and women. [ABSTRACT FROM AUTHOR]

Abstract: 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

ABSTRACT 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 μ m) 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. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Aims: We aimed to investigate the association of serum testosterone with impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM) and calculate the proportion explained by obesity status on the relationship.Materials and Methods: A case-control study including 2775 participants was performed. Serum testosterone was quantified by liquid chromatography-tandem mass spectrometry. Conditional logistic regression and multivariable linear regression were performed to estimate the relationships between testosterone and different glucose status. Waist circumference (WC) was used as a mediator to estimate the mediation effect.Results: After adjusting for multiple variables, serum testosterone levels were negatively associated with T2DM in males (per 1 unit natural log-transformed, odd ratio (OR) = 0.73, 95% confidence interval (CI): 0.56, 0.96; Tertile 3 vs Tertile 1, OR = 0.46, 95% CI:0.29, 0.72) while were positively in females (per 1 unit natural log-transformed, OR = 1.56, 95% CI:1.32, 1.84; Tertile 3 vs Tertile 1, OR = 3.55, 95% CI: 2.22, 5.66). In males, a higher testosterone tended to be associated with a lower fasting plasma glucose level and a weaker HOMA2-IR but a stronger HOMA2-β. Opposite findings were observed in females. Furthermore, WC played a full and partial mediating role in the relationship between testosterone and IFG and T2DM both in males and females.Conclusion: Serum testosterone levels had opposite effects on IFG and T2DM in males and females. With higher serum testosterone levels, the dysglycemia progression was decreased among males while increased among females. In addition, WC played a full and partial mediating role in the relationship between testosterone and IFG and T2DM. [ABSTRACT FROM AUTHOR]