Modeling the observed tropospheric BrO background: Importance of multiphase chemistry and implications for ozone, OH, and mercury

Aircraft and satellite observations indicate the presence of ppt (ppt ≡ pmol/mol) levels of BrO in the free troposphere with important implications for the tropospheric budgets of ozone, OH, and mercury. We can reproduce these observations with the GEOS-Chem global tropospheric chemistry model by including a broader consideration of multiphase halogen (Br–Cl) chemistry than has been done in the past. Important reactions for regenerating BrO from its non-radical reservoirs include HOBr+Br−/Cl− in both aerosols and clouds, and oxidation of Br− by ClNO3 and ozone. Most tropospheric BrO in the model is in the free troposphere, consistent with observations, and originates mainly from the photolysis and oxidation of ocean-emitted CHBr3. Stratospheric input is also important in the upper troposphere. Including production of gas phase inorganic bromine from debromination of acidified sea salt aerosol increases free tropospheric Bry by about 30 %. We find HOBr to be the dominant gas-phase reservoir of inorganic bromine. Halogen (Br-Cl) radical chemistry as implemented here in GEOS-Chem drives 14 % and 11 % decreases in the global burdens of tropospheric ozone and OH, respectively, a 16 % increase in the atmospheric lifetime of methane, and an atmospheric lifetime of 6 months for elemental mercury. The dominant mechanism for the Br-Cl driven tropospheric ozone decrease is oxidation of NOx by formation and hydrolysis of BrNO3 and ClNO3

Modeling risk for severe adverse outcomes using angiogenic factor measurements in women with suspected preterm preeclampsia

Introduction: Preeclampsia (PE) is a pregnancy-specific syndrome associated with adverse maternal and fetal outcomes. Patient-specific risks based on angiogenic factors might better categorize those who might have a severe adverse outcome. Methods: Women evaluated for suspected PE at a tertiary hospital (2009–2012) had pregnancy outcomes categorized as ‘referent’ or ‘severe’, based solely on maternal/fetal findings. Outcomes that may have been influenced by a PE diagnosis were considered ‘unclassified’. Soluble fms-like tyrosine kinase (sFlt1) and placental growth factor (PlGF) were subjected to bivariate discriminant modeling, allowing patient-specific risks to be assigned for severe outcomes. Results: Three hundred twenty-eight singleton pregnancies presented at ≤34.0 weeks' gestation. sFlt1 and PlGF levels were adjusted for gestational age. Risks above 5 : 1 (10-fold over background) occurred in 77% of severe (95% CI 66 to 87%) and 0.7% of referent (95% CI <0.1 to 3.8%) outcomes. Positive likelihood ratios for the modeling and validation datasets were 19 (95% CI 6.2–58) and 15 (95% CI 5.8–40) fold, respectively. Conclusions: This validated model assigns patient-specific risks of any severe outcome among women attending PE triage. In practice, women with high risks would receive close surveillance with the added potential for reducing unnecessary preterm deliveries among remaining women. © 2015 The Authors. Prenatal Diagnosis published by John Wiley & Sons Ltd

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts