Exposures to Air Pollutants during Pregnancy and Preterm Delivery

The association between preterm delivery (PTD) and exposure to air pollutants has recently become a major concern. We investigated this relationship in Incheon, Republic of Korea, using spatial and temporal modeling to better infer individual exposures. The birth cohort consisted of 52,113 singleton births in 2001–2002, and data included residential address, gestational age, sex, birth date and order, and parental age and education. We used a geographic information system and kriging methods to construct spatial and temporal exposure models. Associations between exposure and PTD were evaluated using univariate and multivariate log-binomial regressions. Given the gestational age, birth date, and the mother’s residential address, we estimated each mother’s potential exposure to air pollutants during critical periods of the pregnancy. The adjusted risk ratios for PTD in the highest quartiles of the first trimester exposure were 1.26 [95% confidence interval (CI), 1.11–1.44] for carbon monoxide, 1.27 (95% CI, 1.04–1.56) for particulate matter with aerodynamic diameter ≤ 10 μm, 1.24 (95% CI, 1.09–1.41) for nitrogen dioxide, and 1.21 (95% CI, 1.04–1.42) for sulfur dioxide. The relationships between PTD and exposures to CO, NO(2), and SO(2) were dose dependent (p < 0.001, p < 0.02, p < 0.02, respectively). In addition, the results of our study indicated a significant association between air pollution and PTD during the third trimester of pregnancy. In conclusion, our study showed that relatively low concentrations of air pollution under current air quality standards during pregnancy may contribute to an increased risk of PTD. A biologic mechanism through increased prostaglandin levels that are triggered by inflammatory mediators during exposure periods is discussed

Whole Genome Expression Array Profiling Highlights Differences in Mucosal Defense Genes in Barrett's Esophagus and Esophageal Adenocarcinoma

Esophageal adenocarcinoma (EAC) has become a major concern in Western countries due to rapid rises in incidence coupled with very poor survival rates. One of the key risk factors for the development of this cancer is the presence of Barrett's esophagus (BE), which is believed to form in response to repeated gastro-esophageal reflux. In this study we performed comparative, genome-wide expression profiling (using Illumina whole-genome Beadarrays) on total RNA extracted from esophageal biopsy tissues from individuals with EAC, BE (in the absence of EAC) and those with normal squamous epithelium. We combined these data with publically accessible raw data from three similar studies to investigate key gene and ontology differences between these three tissue states. The results support the deduction that BE is a tissue with enhanced glycoprotein synthesis machinery (DPP4, ATP2A3, AGR2) designed to provide strong mucosal defenses aimed at resisting gastro-esophageal reflux. EAC exhibits the enhanced extracellular matrix remodeling (collagens, IGFBP7, PLAU) effects expected in an aggressive form of cancer, as well as evidence of reduced expression of genes associated with mucosal (MUC6, CA2, TFF1) and xenobiotic (AKR1C2, AKR1B10) defenses. When our results are compared to previous whole-genome expression profiling studies keratin, mucin, annexin and trefoil factor gene groups are the most frequently represented differentially expressed gene families. Eleven genes identified here are also represented in at least 3 other profiling studies. We used these genes to discriminate between squamous epithelium, BE and EAC within the two largest cohorts using a support vector machine leave one out cross validation (LOOCV) analysis. While this method was satisfactory for discriminating squamous epithelium and BE, it demonstrates the need for more detailed investigations into profiling changes between BE and EAC

Identification and rejection of pile-up jets at high pseudorapidity with the ATLAS detector

The rejection of forward jets originating from additional proton–proton interactions (pile-up) is crucial for a variety of physics analyses at the LHC, including Standard Model measurements and searches for physics beyond the Standard Model. The identification of such jets is challenging due to the lack of track and vertex information in the pseudorapidity range |η| &gt; 2.5. This paper presents a novel strategy for forward pile-up jet tagging that exploits jet shapes and topological jet correlations in pile-up interactions. Measurements of the per-jet tagging efficiency are presented using a data set of 3.2 fb−1 of proton–proton collisions at a centre-of-mass energy of 13 TeV collected with the ATLAS detector. The fraction of pile-up jets rejected in the range 2.5 &lt; |η| &lt; 4.5 is estimated in simulated events with an average of 22 interactions per bunch-crossing. It increases with jet transverse momentum and, for jets with transverse momentum between 20 and 50 GeV, it ranges between 49% and 67% with an efficiency of 85% for selecting hard-scatter jets. A case study is performed in Higgs boson production via the vector-boson fusion process, showing that these techniques mitigate the background growth due to additional proton–proton interactions, thus enhancing the reach for such signatures

Dataset for human sensitivity to chemicals during development of motor function

The authors reviewed human data related to motor development following exposure to a subset of chemicals thoroughly reviewed in Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profiles and Addenda. The resulting dataset includes the following variables and confounders: chemical name, exposure route, exposure duration and frequency, study design, cohort name and/or geographic location, sex of cohort subjects, NOAEL, and LOAEL. This data summary can help validate motor development outcomes observed in animal exposure studies; it can also aid in determining whether these outcomes and corresponding exposure windows are relevant to humans. Keywords: Windows of sensitivity, Motor function, Developmental effects, Human exposure effects, in utero exposure effect

Toxicological profile for polybrominated biphenyls and polybrominated diphenyl ethers /

"Prepared ... under contract no. 205-1999-00024.""Chemical manager(s)/Author)s): Hana R. Pohl ... [et al.]"--P. ix."September 2004."Includes bibliographical references (p. 487-557) and index.Mode of access: Internet