Joint effect of physical activity and sedentary behavior with the female urinary incontinence: an analysis of NHANES 2011-2016.

INTRODUCTION: Our study aimed to assess the independent and joint effects of leisure-time physical activity and sedentary behavior with urinary incontinence (UI). METHODS: Data were obtained from the National Health and Nutrition Examination Survey 2011-2016. The primary endpoint was the risk of different subtypes of UI, including stress UI, urgency UI, and mixed UI. The primary exposures were leisure-time physical activity and sedentary behavior. Sedentary behavior was assessed by screen time. Weighted univariate and multivariate logistic regression models were used to observe the independent and joint relationship of leisure-time physical activity and sedentary behavior with UI risk (including stress UI, urgency UI, and mixed UI). RESULTS: In total, 6,927 female participants were included in this analysis. 3,377 females did not have UI, 1,534 had stress UI, 836 had urgency UI, and 1,180 had mixed UI. Screen time with ≥5h/day was associated with increased odds of urgency UI [odds ratio (OR) =1.31, 95% confidence intervals (CI): 1.06-1.61], which indicated the relationship of sedentary behavior and urgency UI. Engaging in leisure-time physical activity with of ≥750 metabolic equivalent (MET)·min/week was found to be significantly associated with reduced likelihood of mixed UI (OR=0.68, 95%CI: 0.55-0.85). Additionally, the interaction term of leisure-time physical activity<750 MET· min/week and screen time≥5h/day was observed to be linked with increased odds of urgency and mixed UI. CONCLUSION: Participants experiencing a lower level of leisure-time physical activity and a higher level of sedentary behavior together might enhance the urgency and mixed UI risk.

A co-twin control study of in utero exposure to poly- and perfluoroalkyl substances and associations with neonatal thyroid-stimulating hormone.

Research quantifying associations between early-life exposure to poly- and perfluoroalkyl substances (PFAS) and neonatal thyroid hormone levels is limited and reports inconsistent results. This study aimed to examine the associations of in utero PFAS exposure with neonatal thyroid-stimulating hormone (TSH), and to verify whether genetic and familial factors contribute to these associations. Within Wuhan Twin Birth Cohort study, we included 148 mother-twin pairs recruited between March 2016 and January 2018. Maternal plasma PFAS concentrations were measured at three different trimesters and averaged. Additionally, we measured cord plasma PFAS concentrations for twin newborns and retrieved their TSH levels from the medical system. Multivariable linear regression, generalized estimation equation, and linear mixed models were used to examine the covariate-adjusted associations. For maternal PFAS analyses, a 2-fold increment of average maternal perfluorooctanoic acid (PFOA) and perfluorodecanoic acid (PFDA) concentrations was linked with a 15% (95% CI: 2.5%, 28%) and 14% (95% CI: 2.4%, 28%) increase in neonatal TSH, respectively. For twin newborns discordant for PFAS exposure, a 2-fold increment of cord plasma PFOA, PFDA, perfluoroundecanoic acid (PFUdA), and perfluorohexanesulfonic acid (PFHxS) concentrations was related to a 7.1% (95% CI: 0.31%, 14%), 12% (95% CI: 4.8%, 20%), 7.5% (95% CI: 0.30%, 15%), and 8.5% (95% CI: 3.0%, 14%) increase in TSH among twins as individuals, respectively. Although these associations were mainly observed between twin pairs, certain PFAS exposure might have an independent association with increased TSH. Our present study suggests that higher maternal and cord plasma PFAS concentrations are associated with increased neonatal TSH, and genetic and familial factors contribute to these associations.

Maternal paraben exposure and intra-pair thyroid-stimulating hormone difference in twin neonates.

Thyroid hormones are essential for fetal growth and neurodevelopment. The recent frequent use of parabens has raised concerns about their endocrine-disrupting potential. However, the effects of maternal paraben exposure on neonatal thyroid hormone levels are still largely unknown. In our study, a co-twin control design was employed to analyze the relationships between maternal paraben exposure and neonatal thyroid-stimulating hormone (TSH) difference. We collected information from 252 mother-twin pairs from a twin birth cohort in Wuhan, China. Concentrations of six parabens were measured in maternal urine samples collected at < 16, 16-28, and > 28 weeks of gestation. Data of neonatal TSH levels were retrieved from medical records. Multiple informant models were applied to explore the time-specific relationships between paraben exposure and intra-twin TSH difference and to determine the susceptible window of exposure. We found that maternal urinary methyl paraben (MeP) during early pregnancy was positively associated with intra-twin TSH difference (%change = 5.96 %; 95 % confidant interval (CI): 0.04 %, 12.2 %). However, no significant differences were observed for exposure to ethyl paraben (EtP) and propyl paraben (PrP), and the associations between parabens and intra-twin TSH difference did not differ materially across pregnancy. Further, a stratified analysis based on twin zygosity and chorionicity and sex types indicated that the positive association between early pregnancy MeP exposure and intra-twin TSH difference was significant in monochorionic diamniotic (MCDA) twins of female-female fetuses and dichorionic diamniotic (DCDA) twins of opposite-sex. The prospective twin study provides first evidence that MeP exposure in early pregnancy was associated with an increased TSH difference in twin neonates, especially in female fetuses.

Residential greenness and air pollution concerning excessive gestational weight gain during pregnancy: A cross-sectional study in Wuhan, China.

BACKGROUND: Previous studies have indicated that exposure to residential greenness may benefit the health status of pregnant women, and air pollution may exert a mediating effect. Gestational weight gain (GWG) is an important indicator of pregnant women and fetuses' health and nutrition status. However, evidence concerning the impact of residential greenness on excessive gestational weight gain (EGWG) is scarce, and to what extent air pollution in urban settings mediates this relationship remains unclear. OBJECTIVE: This study aims to explore the association of residential greenness with EGWG, consider the mediating effect of air pollution, and estimate the combined impact of residential greenness and air pollution exposures on EGWG. METHOD: This population-based cross-sectional study involved 51,507 pregnant women with individual-level data on residential addresses in the Wuhan Maternal and Child Health Management Information System. Two spectral indexes, the normalized difference vegetation index (NDVI) and soil-adjusted vegetation index (SAVI), were used to proxy residential greenness. The air pollution data included six indicators (PM2.5, PM10, SO2, CO, NO2, O3) and used the Ordinary Kriging interpolation method to estimate overall pregnancy exposure to air pollutants. Generalized linear mixed regression models were utilized to explore the relationship between residential greenness and EGWG. Restricted cubic spline (RCS) models were developed to examine the dose-response relationships. Mediation analyses explored the potential mediating role of air pollution in the residential greenness-EGWG associations. Finally, the weighted-quantile-sum (WQS) regression model was used to investigate the association between residential greenness-air pollutants co-exposure and EGWG. RESULT: Among all participants, 26,442 had EGWG. In the adjusted model, the negative association was found significant for NDVI100-m, NDVI200-m, and NDVI500-m with EGWG. For example, each IQR increase in NDVI100-m was associated with 2.8% (95% CI: 0.6-5.0) lower odds for EGWG. The result of WQS regression showed that, when considering the six air pollutants and NDVI-100m together, both positive and negative WQS indices were significantly associated with EGWG, PM10, PM2.5, with SO2 having significant weights in the positive effect direction and CO, O3, NO2, and NDVI100-m having a negative effect. Our results also suggested that SO2, NO2, PM10, PM2.5, and CO significantly mediated the association between NDVI-100m and EGWG, and our estimates were generally robust in the sensitivity analysis. CONCLUSION: Exposure to a higher level of residential greenness is associated with a reduced risk of EGWG, in which air pollution may exert a mediating effect. Pregnant women might benefit more in gaining healthy gestational weight when greenness levels increase from low to medium than from medium to high. Given the current cross-sectional study design, large-sale prospective cohort studies are needed to confirm our findings further.

Prenatal Genetic Diagnosis in Three Fetuses With Left Heart Hypoplasia (LHH) From Three Unrelated Families.

Background: Congenital heart defects (CHDs) are the most common birth defects, and left heart hypoplasia (LHH) is a severe form of CHD and responsible for more than 20% cardiac deaths during the first week of life, however, its genetic causes remain largely elusive. Methods: Three families with fetal LHH were recruited. Genomic DNA from amniotic fluid or peripheral blood, and trio whole exome sequencing (trio-WES) and copy number variation sequencing (CNV-seq) were performed. Results: All the three couples had no family history, and mid-gestation ultrasound revealed LHH and other variable cardiovascular defects in the fetuses. Trio-WES revealed de novo pathogenic variations in KMT2D (p.Gly3465Aspfs*37) (NM_003482) and WDFY3 (p.Ser117Xfs*) (NM_014991), and CNV-seq identified a deletion of 150 kb encompassing NOTCH1. KMT2D and NOTCH1 previously have been reported to be associated with CHDs, however, WDFY3 is reported for the first time to be possibly related to CHD in human. Conclusion: Our study suggested that genetic component is an important risk factor for the development of LHH, and next generation sequencing is a powerful tool for genetic diagnosis in fetuses with CHDs and genetic counseling, however, more studies and data are need to establish the correlation of fetal phenotypes and genotypes.