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Natural course of HTLV-1 proviral DNA levels in carriers during pregnancy.

Related Articles Natural course of HTLV-1 proviral DNA levels in carriers during pregnancy. J Infect Dis. 2018 Jan 16;: Authors: Fuchi N, Miura K, Tsukiyama T, Sasaki D, Ishihara K, Tsuruda K, Hasegawa H, Miura S, Yanagihara K, Masuzaki H Abstract The measurement of human T-cell leukemia virus type 1 (HTLV-1) proviral DNA levels using polymerase chain reaction has been beneficial for confirming HTLV-1 infection during pregnancy. However, the influence of pregnancy on HTLV-1 infection and proviral DNA levels among pregnant women with HTLV-1 has not been clarified. We prospectively gathered blood samples from 36 pregnant women who were previously diagnosed as HTLV-1 carriers and sequentially measured their proviral DNA levels. The HTLV-1 proviral DNA levels remained in a plateau during pregnancy but were elevated after delivery. Moreover, flow-cytometric and serological analyses revealed that the regulatory T-cell population and soluble interleukin-2 receptor levels were similarly elevated after birth in comparison with control pregnant women. This study is the first to provide data on the sequential changes in the HTLV-1 proviral DNA levels during and after pregnancy. These findings will guide the establishment of a better program to prevent HTLV-1 mother-to-child transmission. PMID: 29346571 [PubMed - as supplied by publisher]

Prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances and childhood atopic dermatitis: a prospective birth cohort study.

Related Articles Prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances and childhood atopic dermatitis: a prospective birth cohort study. Environ Health. 2018 Jan 17;17(1):8 Authors: Chen Q, Huang R, Hua L, Guo Y, Huang L, Zhao Y, Wang X, Zhang J Abstract BACKGROUND: Perfluoroalkyl and polyfluoroalkyl substances (PFASs) have been reported to suppress immune function. However, previous studies on prenatal exposure to PFASs and allergic disorders in offspring provided inconsistent results. We aimed to examine the association between prenatal exposure to PFASs and childhood atopic dermatitis (AD) in offspring up to 24 months of age. METHODS: A prospective birth cohort study involving 1056 pregnant women was conducted in two hospitals in Shanghai from 2012 to 2015. Prenatal information was collected by an interview with the women and from medical records. Fetal umbilical cord blood was collected at birth. Cord blood plasma PFASs were measured. Children were followed at 6, 12 and 24 months and information on the development of AD was recorded. AD was diagnosed by 2 dermatologists independently based on the questionnaires. Multiple logistic regression was used to compute odds ratio (OR) and corresponding 95% confidence interval (CI) for the association between AD and each PFASs, adjusting for potential confounders. RESULTS: A total of 687 children completed a 2-year follow-up visit and had PFASs measurement. AD was diagnosed in 173 (25.2%) children during the first 24 months. In female children, a log-unit increase in perfluorooctanoic acid (PFOA) was associated with a 2.1-fold increase in AD risk (AOR 2.07, 95% CI 1.13-3.80) after adjusting for potential confounders. The corresponding risk was 2.22 (1.07-4.58) for perfluorononanoic acid (PFNA). The highest PFOA quartile was significantly associated with AD (2.52, 1.12-5.68) compared with the lowest quartile. The highest quartile of PFNA, perfluorodecanoic acid (PFDA) and perfluorohexane sulfonic acid (PFHxS) were associated with AD with AOR (95% CI) being 2.14 (0.97-4.74), 2.14 (1.00-4.57), and 2.30 (1.03-5.15), respectively. Additionally, the second quartile of perfluorododecanoic acid (PFDoA) was associated with a 3.2-fold increase in AD risk (3.24, 1.44-7.27). However, no significant associations were found in male children. CONCLUSIONS: Prenatal exposure to PFOA, PFDA, PFDoA and PFHxS significantly increased the risk of childhood AD in female children during the first 24 months of life. In addition, the associations between AD with prenatal exposure to PFNA were close to statistical significance. PMID: 29343261 [PubMed - in process]

Does artificial light-at-night exposure contribute to the worldwide obesity pandemic?

Related Articles Does artificial light-at-night exposure contribute to the worldwide obesity pandemic? Int J Obes (Lond). 2016 05;40(5):815-23 Authors: Rybnikova NA, Haim A, Portnov BA Abstract BACKGROUND: Worldwide overweight and obesity rates are on the rise, with about 1 900 billion adults being defined as overweight and about 600 million adults being defined as obese by the World Health Organization (WHO). Increasing exposure to artificial light-at-night (ALAN) may influence body mass, by suppression of melatonin production and disruption of daily rhythms, resulting in physiological or behavioral changes in the human body, and may thus become a driving force behind worldwide overweight and obesity pandemic. METHODS: We analyzed most recent satellite images of night time illumination, available from the US Defense Meteorological Satellite Program (DMSP), combining them with country-level data on female and male overweight and obesity prevalence rates, reported by the WHO. The study aims to identify and measure the strength of association between ALAN and country-wide overweight and obesity rates, controlling for per capita GDP, level of urbanization, birth rate, food consumption and regional differences. RESULTS: ALAN emerged as a statistically significant and positive predictor of overweight and obesity (t>1.97; P<0.05), helping to explain, together with other factors, about 70% of the observed variation of overweight and obesity prevalence rates among females and males in more than 80 countries worldwide. Regional differences in the strength of association between ALAN and excessive body mass are also noted. CONCLUSIONS: This study is the first population-level study that confirms the results of laboratory research and cohort studies in which ALAN was found to be a contributing factor to excessive body mass in humans. PMID: 26795746 [PubMed - indexed for MEDLINE]