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Parenting style has been associated with children's weight-related outcomes and health behaviors, but this relationship may be confounded by genetic influences. Using a twin design to better control for genetics and shared home environments, this study aimed to estimate the longitudinal parental effects on obesity, smoking, and drinking in children and adolescents.Data were retrieved from the first two waves of the German Twin Family Panel. A total of 631 pairs of same-sex monozygotic twins were analyzed, including three birth cohorts aged 5, 11, and 17 years. Self-reported parenting styles were measured in five dimensions: emotional warmth, psychological control, negative communication, monitoring, and inconsistent parenting. Outcome variables included children's body mass index z-score (BMIz) and smoking and alcohol drinking frequency. The differencing method was used to examine the relationship between within-monozygotic pair differences in parenting styles and health outcomes, controlling for differences at baseline, genetic influences, and other shared characteristics between twins.Controlling for genetics, shared environmental effects, and body weight status at baseline, the twin who received harsher parenting in communication had lower BMI than their cotwin. Subgroup analyses found that negative communication had a stronger impact on the youngest cohort and female twins. Paternal parenting differentially relates to child weight compared to maternal parenting. No concurrent and long-lasting effects of paternal parenting on smoking and drinking were found.The twin study design is a unique epidemiological tool to measure the contribution of genetics as opposed to the environment, to a given health trait. This study found that negative communication was associated with lower BMI in German twin families. However, it failed to identify strong evidence for the causal link between other parenting dimensions and child's weight status and alcohol and tobacco use. More twin studies with objective measurements are warranted to understand the critical role of parenting, especially family communication, in predicting children's BMIs and their health behaviors across cultures.

Rationale: Both genetic and environmental factors contribute to lung cancer, but the degree to which air pollution modifies the impact of genetic susceptibility on lung cancer remains unknown. Objectives: To investigate whether air pollution and genetic factors jointly contribute to incident lung cancer. Methods: We analyzed data from 455,974 participants (53% women) without previous cancer at baseline in the UK Biobank. The concentrations of particulate matter (PM) (PM ⩽2.5 μm in aerodynamic diameter [PM2.5], coarse PM between 2.5 μm and 10 μm in aerodynamic diameter [PMcoarse], and PM ⩽10 μm in aerodynamic diameter [PM10]), nitrogen dioxide (NO2), and nitrogen oxides (NOx) were estimated by using land-use regression models, and the association between air pollutants and incident lung cancer was investigated by using a Cox proportional hazard model. Furthermore, we constructed a polygenic risk score and evaluated whether air pollutants modified the effect of genetic susceptibility on the development of lung cancer. Measurements and Main Results: The results showed significant associations between the risk of lung cancer and PM2.5 (hazard ratio [HR], 1.63; 95% confidence interval [CI], 1.33-2.01; per 5 μg/m3), PM10 (HR, 1.53; 95% CI, 1.20-1.96; per 10 μg/m3), NO2 (HR, 1.10; 95% CI, 1.05-1.15; per 10 μg/m3), and NOx (HR, 1.13; 95% CI, 1.07-1.18; per 20 μg/m3). There were additive interactions between air pollutants and the genetic risk. Compared with participants with low genetic risk and low air pollution exposure, those with high air pollution exposure and high genetic risk had the highest risk of lung cancer (PM2.5: HR, 1.71; 95% CI, 1.45-2.02; PM10: HR, 1.77; 95% CI, 1.50-2.10; NO2: HR, 1.77; 95% CI, 1.42-2.22; NOx: HR, 1.67; 95% CI, 1.43-1.95). Conclusions: Long-term exposure to air pollution may increase the risk of lung cancer, especially in those with high genetic risk.

Chronic inflammation has been associated with the development of lung cancer. In this study, we examined the association between C-reactive protein (CRP) and lung cancer in a prospective cohort study and used Mendelian randomization (MR) to clarify the causality. We included 420 977 participants from the UK Biobank (UKB) in the analyses; 1892 thereof were diagnosed with lung cancer during the follow-up. Hazards ratios (HRs) of CRP concentrations were estimated by Cox proportional hazard models and two approaches of MR analysis were performed. Besides, we added CRP concentrations to epidemiological model of lung cancer to evaluate its prediagnostic role through time-dependent receiver operating characteristic curve analysis. Elevated CRP levels were associated with a 22% increased lung cancer risk per 1 SD increase (HR = 1.22, 95% confidence interval [CI] = 1.18-1.26). Positive associations were observed in small cell lung cancer (HR = 1.21, 95% CI = 1.10-1.33), lung adenocarcinoma (HR = 1.17, 95% CI = 1.11-1.23) and lung squamous cell carcinoma (HR = 1.22, 95% CI = 1.14-1.31). No genetical association of circulating CRP levels and lung cancer risk was observed in MR analysis. When added to a risk model of lung cancer, CRP improved the performance of model as long as 8 years among current smokers (basic model: C-statistic = 0.78 [95% CI = 0.75-0.80]; CRP model: C-statistic = 0.79 [95% CI = 0.76-0.81]; Pnonadjusted = .003, Padjusted = .014). Our results did not support the causal association of circulating CRP with lung cancer risk. However, circulating CRP could be a prediagnostic marker of lung cancer as long as 8 years in advance for current smokers.

2,3,7,8-Tetrachlorobenzo-p-dioxin (TCDD) exposure during embryonic gonadal sex determination had been demonstrated to harm the ovarian development. However, its mechanism was unclear and possibly related to epigenetic regulation. In the present study, the pregnant rats were treated with TCDD (100 ng/kg/day or 500 ng/kg/day) or only vehicle and corn oil on the day 8–14 of gestation through the gavage with a stainless-steel feeding needle. The vaginal opening time and estrous cycle of female offspring rats (F1) were monitored twice a day. The ovarian histology, follicle count, real-time PCR, Western Blotting and DNA methylation analysis for Igf2 and H19 were carried out. The results showed that maternal TCDD exposure disrupted estrous cyclicity, resulted in aberrant concentration of serum E2 and FSH, and affected the number of primordial follicles, secondary follicles and corpus luteum. However, TCDD had no effect on the number of primary follicles and atresia follicles. Furthermore, the mRAN expression of imprinted genes Igf2 and H19 was down-regulated, and the IGF2 protein was also down-regulated. TCDD exposure did not alter the mean methylation rate of Igf2 DMR2 and H19 ICR, and only some CpG sites throughout them were hypermethylated in high-dose TCDD rats. In conclusion, maternal exposure of TCDD could affect the ovary development and functions which were possibly associated with down-regulation expression of IGF2 and H19. However, it was not entirely clear whether the impairment of ovary by TCDD was related to the methylation pattern of Igf2 and H19 ICR.

Purpose: This study assessed the influence of state laws governing physical education (PE) on weekly PE class attendance among US high school students. Design: Cross-sectional. Setting: 2003 to 2017 US national Youth Risk Behavior Survey (YRBS). Participants: A total of 533 468 high school students. Measures: Data on state laws governing PE came from National Cancer Institute’s Classification of Laws Associated with School Students (CLASS). Eight distinct state PE policies were scored, with higher scores denoting stronger laws. Analysis: Individual-level YRBS data were merged with CLASS data based on students’ residential state and survey year. State fixed-effect negative binomial regressions were performed, adjusting for individual-level characteristics and YRBS survey design. Results: A 1-score increase in state laws governing PE class time, staffing for PE, joint use agreement for physical activity, assessment of health-related fitness, and PE curriculum was associated with an increase in weekly PE attendance by 0.30, 0.28, 0.22, 0.20, and 0.13 days ( P < .001), respectively. In contrast, a 1-score increase in state laws governing moderate-to-vigorous-intensity physical activity time in PE, PE proficiency, and recess time was associated with a reduction in weekly PE attendance by 0.25, 0.15, and 0.09 days ( P < .001), respectively. The effects of most state PE policies on PE class attendance were larger among girls than boys. Conclusion: State PE policies differentially impacted US high school students’ PE class attendance, with larger effects on female students.

Background Epidemiological evidence remains conflicting regarding diet and risk of lung cancer. Objectives We sought to systematically investigate whether dietary factors are associated with the risk of incident lung cancer in the UK Biobank. Methods A total of 416,588 participants (54% women) from the UK Biobank were included in the present study. Based on baseline data from FFQs, 3 main dietary patterns were identified by using principal component analysis. Cox proportional hazards models were used to investigate the association of individual food groups and dietary patterns with lung cancer risk. Results During a median follow-up of 7.13 y, 1782 incident lung cancer cases were documented. The association analysis showed high intake of red meat and processed meat was associated with an increased risk of lung cancer (HRper 50 g/d: 1.36; 95% CI: 1.13, 1.65 for red meat; HRper 25 g/d: 1.30; 95% CI: 1.10, 1.53 for processed meat). However, the consumption of fruits (HRper 100 g/d: 0.90; 95% CI: 0.84, 0.95), vegetables (HRper 100 g/d: 0.89; 95% CI: 0.81, 0.99), breakfast cereals (HRper 50 g/d: 0.81; 95% CI: 0.74, 0.89), and dietary fiber (HRper 5 g/d: 0.76; 95% CI: 0.69, 0.84) was inversely associated with the risk of lung cancer. For the dietary pattern analysis [quartile (Q) comparison], high adherence to the Prudent pattern (HRQ4 compared with Q1: 0.84; 95% CI: 0.73, 0.96) was associated with a lower risk of lung cancer, whereas the Western pattern (HRQ4 compared with Q1: 1.27; 95% CI: 1.11, 1.46) was associated with a higher risk of lung cancer. Conclusions Our study indicated that a diet characterized by high intake of fruits, vegetables, breakfast cereals, and dietary fiber, as well as low intake of red meat and processed meat, was associated with a lower risk of lung cancer.

Cancer site–specific polygenic risk scores (PRS) effectively identify individuals at high risk of individual cancers, but the effectiveness of PRS on overall cancer risk assessment and the extent to which a high genetic risk of overall cancer can be offset by a healthy lifestyle remain unclear. Here, we constructed an incidence-weighted overall cancer polygenic risk score (CPRS) based on 20 cancer site-specific PRSs. Lifestyle was determined according to smoking, alcohol consumption, physical activity, body mass index, and diet. Cox regression by sex was used to analyze associations of genetic and lifestyle factors with cancer incidence using UK Biobank data (N = 442,501). Compared with participants at low genetic risk (bottom quintile of CPRS), those at intermediate (quintiles 2 to 4) or high (top quintile) genetic risk had HRs of 1.27 (95% confidence interval, 1.21–1.34) or 1.91 (1.81–2.02) for overall cancer, respectively, for men, and 1.21 (1.16–1.27) or 1.62 (1.54–1.71), respectively, for women. A joint effect of genetic and lifestyle factors on overall cancer risk was observed, with HRs reaching 2.99 (2.45–3.64) for men and 2.38 (2.05–2.76) for women with high genetic risk and unfavorable lifestyle compared with those with low genetic risk and favorable lifestyle. Among participants at high genetic risk, the standardized 5-year cancer incidence was significantly reduced from 7.23% to 5.51% for men and from 5.77% to 3.69% for women having a favorable lifestyle. In summary, individuals at high genetic risk of overall cancer can be identified by CPRS, and risk can be attenuated by adopting a healthy lifestyle. Significance: A new indicator of cancer polygenic risk score measures genetic risk for overall cancer, which could identify individuals with high cancer risk to facilitate decision-making about lifestyle modifications for personalized prevention.

Gene–smoking interactions play important roles in the development of non-small cell lung cancer (NSCLC). To identify single-nucleotide polymorphisms (SNPs) that modify the association of smoking behavior with NSCLC risk, we conducted a genome-wide gene–smoking interaction study in Chinese populations. The genome-wide interaction analysis between SNPs and smoking status (ever- versus never-smokers) was carried out using genome-wide association studies of NSCLC, which included 13 327 cases and 13 328 controls. Stratified analysis by histological subtypes was also conducted. We used a genome-wide significance threshold of 5 × 10−8 for identifying significant gene–smoking interactions and 1 × 10–6 for identifying suggestive results. Functional annotation was performed to identify potential functional SNPs and target genes. We identified three novel loci with significant or suggestive gene–smoking interaction. For NSCLC, the interaction between rs2746087 (20q11.23) and smoking status reached genome-wide significance threshold [odds ratio (OR) = 0.63, 95% confidence interval (CI): 0.54–0.74, P = 3.31 × 10–8], and the interaction between rs11912498 (22q12.1) and smoking status reached suggestive significance threshold (OR = 0.72, 95% CI: 0.63–0.82, P = 8.10 × 10–7). Stratified analysis by histological subtypes identified suggestive interactions between rs459724 (5q11.2) and smoking status (OR = 0.61, 95% CI: 0.51–0.73, P = 7.55 × 10–8) in the risk of lung squamous cell carcinoma. Functional annotation indicated that both classic and novel biological processes, including nicotine addiction and airway clearance, may modulate the susceptibility to NSCLC. These novel loci provide new insights into the biological mechanisms underlying NSCLC risk. Independent replication in large-scale studies is needed and experimental studies are warranted to functionally validate these associations.

To investigate the characteristics of pulmonary artery distensibility (PAD) in patients with acute pulmonary embolism (APE) and to assess whether a relationship exists between PAD and the disease severity. Clinical and radiological data of 30 APE patients who underwent retrospective electrocardiogram (ECG)-gated computed tomography pulmonary angiography (CTPA) with a definite diagnosis of APE were retrospectively reviewed in the present study, including 15 subjects in severe (SPE) group and 15 subjects in non-severe (NSPE) group. PAD and cardiac function parameters were compared between the two groups, their relationships were investigated, and receiver operating characteristic (ROC) curves were used to determine the sensitivity and specificity of the above parameters for the diagnosis of APE severity. The PAD decreased in the following order: NSPE group (6.065 ± 2.114) × 10−3 (%/mmHg), and SPE group (4.334 ± 1.777) × 10−3 (%/mmHg) (P < 0.05). All the cardiac function parameters except RA/LAdiameter showed statistically significant different values between the two groups (P < 0.05). As APE severity increased, the cardiac morphological measurements of RV/LVdiameter, RV/LVarea, RVEDV/LVEDV and RVESV/LVESV increased. There was a weak to moderate negative correlation between PAD and PAmax, PAmin, PA/AAmin, PA/AAmax, RV/LVdiameter, RV/LVarea (r = −0.393 to −0.625), that is, PAD was inversely correlated with cardiac function parameters. There was a moderate negative correlation between PAD and hemoptysis(r = −0.672). The area under the ROC curve (AUC) of PAD was 0.724, the critical value was 4.137 × 10−3 mm/Hg, and the sensitivity and specificity were 60.0% and 93.3%, respectively. PAmin showed the strongest discriminatory power to identify high-risk patients (AUC = 0.827), with the highest sensitivity of 100%, which was also achieved by RA/LAarea. The PAD obtained by retrospective ECG-gated CTPA could be an indicator to be used in the evaluation of the presence and severity of APE.

Background Chronic respiratory diseases have become a non-negligible cause of death globally. Although smoking and environmental exposures are primary risk factors for chronic respiratory diseases, genetic factors also play an important role in determining individual’s susceptibility to diseases. Here we performed integrated gene-based and pathway analyses to systematically illuminate the heritable characteristics of chronic respiratory diseases. Methods UK (United Kingdom) Biobank is a very large, population-based prospective study with over 500,000 participants, established to allow detailed investigations of the genetic and nongenetic determinants of the diseases. Utilizing the GWAS-summarized data downloaded from UK Biobank, we conducted gene-based analysis to obtain associations of susceptibility genes with asthma, chronic obstructive pulmonary disease (COPD) and pneumonia using FUSION and MAGMA software. Across the identified susceptibility regions, functional annotation integrating multiple functional data sources was performed to explore potential regulatory mechanisms with INQUISIT algorithm. To further detect the biological process involved in the development of chronic respiratory diseases, we undertook pathway enrichment analysis with the R package (clusterProfiler). Results A total of 195 susceptibility genes were identified significantly associated with chronic respiratory diseases (Pbonferroni Conclusions This study implemented an integrated gene-based and pathway strategy to explore the underlying biological mechanisms and our findings may serve as promising targets for future clinical treatments of chronic respiratory diseases.

2,3,7,8-Tetrachlorobenzo-p-dioxin (TCDD) exposure in utero had been shown to affect ovarian development and functions. However, its mechanism remained unknown. In this study, to investigate the effect of maternal exposure to TCDD on ovaries, the pregnant Sprague Dawley (SD) rats were treated with TCDD (100 ng/kg or 500 ng/kg) or only vehicle and corn oil on the day 8–14 of gestation through the gavage with a stainless-steel feeding needle (once a day). The vaginal opening and estrous cycle of female offspring rats (F1) were monitored twice a day. The ovarian histology, follicle counts, real-time PCR, western blotting and DNA methylation analysis about Gdf9 and Bmp15 were carried out in F1 rats. The results showed that exposure to TCDD (especially the dose of 500 ng/kg) in utero on GD8-14 might change the ovary weight, the concentration of E2 and FSH, the estrous cycles and the numbers of primordial and secondary follicles of the offspring rats. In addition, the mRNA and protein expression of GDF9 and BMP15 was down-regulated, while the methylation patterns of Gdf9 and Bmp15 were not affected. In conclusion, maternal exposure to TCDD could affect the ovary development and functions which were possibly associated with down-regulation of mRNA and protein expression of GDF9 and BMP15. However, the down-regulation was not related to the pattern of methylation of Gdf9 and Bmp15.

Evidence on the association between maternal Hb concentration and preterm birth (PTB) risk is inconclusive. This paper aimed to explore whether women with anaemia or high Hb level before pregnancy would be at higher risk of PTB. We conducted a population-based cohort study with 2 722 274 women aged 20–49 years, who participated in National Free Pre-Pregnancy Checkups Project between 2013 and 2015 and delivered a singleton before 2016 in rural China. Logistic models were used to estimate OR and 95 % CI after adjusting for confounding variables. Restricted cubic spline models were applied to evaluate the dose–response relationships. A total of 192 819 (7·08 %) women had preterm deliveries. Compared with women with Hb of 110–149 g/l, the multivariable-adjusted OR for PTB was 1·19 (95 % CI 0·98, 1·44) for women with Hb

Objectives: In this study, we explored the potential impact of disasters on individuals' fruit and vegetable consumption. Methods: Individual-level data (N = 351,229) from the Behavioral Risk Factor Surveillance System (BRFSS) 2011 survey were merged with county-level disaster declaration data from the Federal Emergency Management Agency (FEMA) based on disaster duration, interview month and residential county. Multilevel mixed-effects generalized linear models were conducted to examine the impact of different types of disasters on self-reported daily fruit, 100% pure fruit juice, beans, green vegetables, orange vegetables, other vegetables and overall vegetables consumption frequencies, adjusting for individual covariates. Results: No associations between disasters and daily fruit and overall vegetable consumption frequency were identified at either national or state levels. Only floods were consistently associated with reduced consumption of orange vegetables. Conclusions: This study did not identify an association between natural disasters and daily overall fruit/vegetable consumption frequency at national or state levels, whereas disasters were found to alter the consumption of certain vegetable subgroup (orange vegetables) slightly. Longitudinal studies with validated and detailed measures on diet and disaster are warranted to advance research in this field.

Objectives: Hurricane Katrina was an intense tropical cyclone that made landfall in the United States (US) in August 2005, causing catastrophic damage in several states. This study examined the impact of Hurricane Katrina on mental health status among US adults. Methods: Multilevel regressions based on the difference-in-differences study design were performed on individual-level data (N = 70,267) retrieved from the Behavioral Risk Factor Surveillance System 2004-2006 surveys. Results: Hurricane Katrina was found to be associated with an increase of 0.68 poor mental health days among residents of Katrina-affected states. The negative impact of Hurricane Katrina on mental health status tended to be larger among Louisiana residents, women, young and middle-aged adults, lower income respondents, and those with poor/fair self-rated physical health than among Mississippi residents, men, older adults, higher income respondents, and those with good/excellent self-rated physical health. Conclusion: Hurricane Katrina adversely impacted mental health of residents in Katrina-affected states, and the impact differed across population subgroups. Future studies should investigate other potential risk and protective factors for the mental health consequences of disasters. They should examine long-term impacts on mental health following disasters to better inform population-based mental health interventions for disaster survivors.

Exposure to environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes cleft palate at high rates, but little is known about the underlying biological mechanisms. In the present study, we cultured osteoblasts from human fetal palate mesenchymal cells (hFPMCs) to explore the effects of TCDD on osteogenic differentiation. The results showed that TCDD significantly decreased cell proliferation, alkaline phosphatase (ALP) activity and calcium deposition. RNA analyses and protein detection demonstrated that TCDD downregulated a wide array of pro-osteogenic biomarkers. Further investigation of the underlying molecular mechanisms revealed that exposure to TCDD activated aryl hydrocarbon receptor (AhR) signaling and inhibited BMP-2/TGF-β1/Smad pathway molecules. The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. The cotreatment with TGF-β1 or BMP-2 and TCDD significantly relieved the activation of AhR and rescued the impairment of osteogenesis caused by TCDD. Taken together, our findings indicated that TCDD inhibited the osteogenic differentiation of hFPMCs via crosstalk between AhR and BMP-2/TGF-β1/Smad signaling pathway.

2,3,7,8-Tetrachlorobenze-p-dioxin (TCDD), one of representive Endocrine Disrupting Chemicals (EDCs), has potential adverse effects on human health. Direct exposure to TCDD has been implicated in ovarian follicles development and functions deficits in adulthood. However, it is rarely reported whether indirect exposure to TCDD can cause similar negative impact on F3. The aim of our study was to evaluate the effect of ancestral TCDD exposure on ovarian toxicity in offspring rats (F3), focusing on the Igf2/H19 pathway which was important for follicular development. Pregnant Sprague-Dawley female rats (F0) were given with either vehicle or TCDD (100 or 500 ng/kg BW/day) by gavages during days 8–14 of gestation. Ovarian development and functions of F3 generation was assessed using the ovary coefficient, the vaginal opening time, and regularity of estrous cycle, ovarian pathology, follicles counts and apoptosis of granular cells. The level of E2, FSH and LH in the serum was also detected. Results showed that in the F3 generation 500 ng/kg BW/day TCDD group, ovarian coefficient, LH concentration in serum and number of primary follicles were decreased, and the apoptosis of granular cells was significantly increased. The abnormal rate of estrous cycle and advance rate of vaginal opening time displayed a significantly increase in TCDD-treated groups. RT-PCR analysis showed that the expression level of H19 mRNA in ovary of TCDD treated F3 female rats was increased, compared to the control. Our data showed that ancestral TCDD exposure may impair transgenerational adult ovary development and functions, which may be related to an inhibition of the Igf2/H19 pathway in the ovarian.

This study investigated the changes in event-related potential (ERP) waveforms under different central visual field conditions using a three-stimulus oddball paradigm. Circular checkerboards were presented in the center of a computer screen with a visual angle of 5°, 10°, 20°, or 30°, which were regarded as target stimuli. The ERP waveforms were analyzed separately for different stimulus conditions. Participants responded more slowly and had lower accuracy for the 30° visual field level than the other three visual field levels. The ERP results revealed that the amplitudes of target P2 gradually increased from the 5° to 20° visual field conditions, while they decreased abruptly in the 30° visual field condition. Regional effects showed that the amplitudes of target P2 were larger from the occipital electrodes than that from the temporal sites. Besides the negative-going deflection of target N2 and visual mismatch negativity (vMMN) components having an increasing tendency with expansion of the visual field, there was also a trend that the amplitudes of target P3 were decreased and the peak latencies were prolonged with increasing visual field ranges. In addition, the latencies of the difference P3 had a similar trend to the latencies of the target P3, and all the differences were more obvious at the 30° visual field level. The study demonstrated that middle-late components of ERPs can reflect changes in the visual field to some extent.

As a common birth defect, Cleft palate can be caused by the disturbance during the developmental process of the palatal shelves. The 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) is a well-known environmental teratogenic agent for cleft palate and Aryl hydrocarbon receptor (AhR) pathway can be activated by dioxins. Oct4 as a pluripotent stem cell transcription factor is also involved in the process of embryonic development. The AHR and retinoid receptors have cross-talk at CYP1A1 (cytochrome P450, family 1, subfamily A, polypeptide 1) promoter. There are also bidirectional talk between AhR and Oct4. In this study, we used C57/BL6 N mice and TCDD (64 μg/Kg body weight) to establish a model of fetal cleft palate to observe the effects of dioxin on fetal mesenchymal proliferation and apoptosis, and explore the role of Oct4 in inducing cleft palate. The results showed that dioxin inhibited mesenchymal proliferation and promoted apoptosis. In addition, dioxin inhibited Oct4 expression, and preliminary data suggest that hypermethylation of the Oct4 promoter may be a putative mechanism, suggesting that TCDD might induce cleft palate by inhibiting the proliferation of palatal mesenchymal cells mediated by Oct4.

Objective We assessed the relationship between county-level prevalence of adult obesity and voting behaviors in the 2016 US presidential election. Methods Spatial autoregressive regression was performed to examine county-level obesity rate in relation to the vote margin for the Republican Party presidential candidate, defined as the percentage difference in votes received by the Republican presidential candidate and those received by the Democratic presidential candidate, adjusting for county sociodemographics and state fixed effects. Results A quadratic association was found between county-level obesity rate and the vote margin for the Republican Party presidential candidate-the margin increased when obesity rate increased from 11.8% to 34.1%, but after reaching its peak of 36.1%, it started to decrease when obesity rate further increased to 47.9%. Conclusion Typically, health disparity has been considered as a political outcome, whereas its impact on political behavior is rarely examined. Our findings indicate obesity disparities may not only be influenced by political decisions but also affect political behavior. Future studies should elucidate the pathway linking obesity to voting behavior and track the long-term trend of this relationship.

Objective In this study, we assessed the impact of state laws governing competitive foods/beverages sold in schools on childhood overweight/obesity among children aged 10-17 years with and without special healthcare needs (SHCN). Methods Individual-level data from 2007-2008, 2011-2012, and 2016 National Survey of Children's Health (N = 108,009) were merged to data on state codified laws regulating competitive foods/beverages sold in schools based on children's residential state and survey year. State random-effect logistic regressions were performed to estimate the odds of childhood overweight/obesity in relation to the presence and strength of competitive food/beverage laws, adjusting for child/family characteristics and state soda sales tax. Results No association between state laws governing competitive foods/beverages sold in schools and childhood overweight/obesity was identified among children with and without SHCN. In addition, no impact of state soda sales tax on childhood overweight/obesity was found among children with SHCN. Conclusions No protective effect of state laws governing competitive foods/beverages sold in schools against obesity risk among children with SHCN was revealed. This study has design and measurement limitations. Future research should replicate findings of this study and assess school district competitive food/beverage policies in relation to adiposity among this highly vulnerable child population.

As the prevalence of coronary computed tomographic angiography (CCTA), it is meaningful that CCTA can provide not only the structural details of artery, but also functional information of vessel elasticity. Our aim was to explore the elasticity characteristics of ascending aorta (AA), descending aorta (DA), main pulmonary artery (MPA), left pulmonary artery (LPA), right pulmonary artery (RPA), and their relationship between each other using 640 slice-volume computed tomography (CT). Furthermore, this study will also observe their relations with age. A total of 42 subjects that were free of cardiovascular disease, high blood pressure, diabetes, and hyperlipidemia underwent CCTA on 640 slice-volume CT and were enrolled in this study. The subjects were divided into 2 groups: Group 1, age .05). The elasticity characteristics of AA, DA, MPA, LPA, and RPA could be well shown by 640 slice-volume CT. The elasticity relativity was observed and was different between AA and DA, AA and MPA, LPA and MPA, LPA and RPA. An obvious age-related decrease in vascular elasticity was found in AA, DA, MPA, and LPA, which should be taken into consideration in clinical trials and treatments for the elasticity-related cardiovascular diseases.

This study investigated the subjective visual acuity by recording ERPs elicited by task-irrelevant visual changes. Optotypes stimuli were presented in the center of the visual field at three threshold levels (supra-threshold, threshold and sub-threshold) while participants were listening to stories. The results showed that neither vMMN nor P3a component was elicited by optotypes stimuli on the sub-threshold condition, whereas, vMMN was elicited under supra-threshold and threshold conditions, with no significant differences between those vMMN amplitudes of two conditions. The P3a amplitude was larger for supra-threshold condition than that for threshold condition. These data demonstrated that the emergence of vMMN could only reflect the automatic detection of orientation-changes in the supra-threshold and threshold conditions compared to the sub-threshold condition, whereas the P3a amplitude could reflect the difference in processing of supra-threshold and threshold stimuli.

Racial differences have been reported in hemoglobin (Hb). However, distributions of Hb and anemia rate in ethnic minorities were rarely reported. We aimed to observe whether there are ethnic differences in Hb distributions and prevalence of anemia. The data included 480,699 women 20 to 49 years’ old from 10 ethnic minorities in China in 2014. Analyses of variance were used to examine the differences of Hb distribution among the 10 ethnic groups, as well as the differences in Hb level between different ages, education levels, occupations, and non- or ethnic enclaves in each ethnic group. χ2-test was adopted to analyze the differences in anemia rate among the 10 ethnic groups and between different ages and nonethnic or ethnic enclaves in each ethnic group. The ethnic differences of the Hb distribution and anemia prevalence were observed in the 10 ethnic groups. The lowest mean Hb concentration was shown in Chuang (126.8 g/L), and the highest mean Hb concentration was in Tibetan (138.5 g/L). According to the World Health Organization criteria to define anemia, the highest prevalence was in Tibetan (46.9%) after the adjustment of Hb concentration for altitude, and the lowest prevalence was in Yi (10.6%). Furthermore, there were differences on mean Hb concentration or anemia rate in participants between ethnic enclaves and non-ethnic enclaves in most ethnic groups. The ethnic differences of the Hb distribution and anemia prevalence were observed in the 10 ethnic groups, which might be associated with geographic conditions, genetic background, and eating habits.