Institution
University of Western Australia
Education•Perth, Western Australia, Australia•
About: University of Western Australia is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 29613 authors who have published 87405 publications receiving 3064466 citations. The organization is also known as: UWA & University of WA.
Topics: Population, Poison control, Galaxy, Context (language use), Medicine
Papers published on a yearly basis
Papers
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Momoko Horikoshi1, Robin N Beaumont2, Felix R. Day3, Nicole M. Warrington4 +182 more•Institutions (55)
TL;DR: In this paper, the authors performed a meta-analysis of birth weight in 153,781 individuals, identifying 60 loci where fetal genotype was associated with birth weight (P < 5.5×10−8).
Abstract: Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease1. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10−8). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure (Rg = −0.22, P = 5.5 × 10−13), T2D (Rg = −0.27, P = 1.1 × 10−6) and coronary artery disease (Rg = −0.30, P = 6.5 × 10−9). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions (P = 1.9 × 10−4). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.
370 citations
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TL;DR: It is shown that activation of PAR2, which co-localizes immunohistochemically with trypsin(ogen) in airway epithelium, causes the relaxation of airway preparations from mouse, rat, guinea-pig and humans by the release of a cyclooxygenase product from the epithelia.
Abstract: The protection of cells in the upper intestine against digestion by pancreatic trypsin depends on the prostanoid prostaglandin E2 (PGE2) and is mediated by protease-activated receptors in the epithelium. As the airway epithelium is morphologically similar and also expresses one of these receptors, PAR2, and is a major source of PGE2, we reasoned that bronchial epithelial PAR2 might also participate in prostanoid-dependent cytoprotection in the airways. Here we show that activation of PAR2, which co-localizes immunohistochemically with trypsin(ogen) in airway epithelium, causes the relaxation of airway preparations from mouse, rat, guinea-pig and humans by the release of a cyclooxygenase product from the epithelium. This physiological protective response in isolated airways also occurred in anaesthetized rats, where activation of PAR2 caused a marked and prolonged inhibition of bronchoconstriction. After desensitization of PAR2, the response to trypsin recovered rapidly by mechanisms dependent on de novo synthesis and trafficking of proteins. Our results indicate that trypsin released from the epithelium can initiate powerful bronchoprotection in the airways by activation of epithelial PAR2.
370 citations
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TL;DR: The results support the immunocompetence-handicap hypothesis for male faces in that masculine traits signalled health during adolescence, but suggest that any health-related evolutionary benefits obtained from preferences for attractive facial traits may be weak.
Abstract: Evolutionary psychologists suggest that a preference for sexually dimorphic traits in human faces is an adaptation for mate choice, because such traits reflect health during development. For male faces, this claim rests on the immunocompetence-handicap hypothesis, which states that the increased testosterone levels needed to develop large masculine traits stress the immune system. We examined whether masculine traits in adolescent male faces are associated with health during development, and also whether feminine traits in adolescent female faces signal health. Feminine traits are attractive, but it is less clear whether they should signal health. Rated masculinity in adolescent male faces correlated modestly with actual health, and was perceived as healthy, but not as attractive. Rated femininity in adolescent female faces did not correlate with actual health, although it was perceived as healthy and attractive. These results support the immunocompetence-handicap hypothesis for male faces in that masculine traits signalled health during adolescence. However, they suggest that any health-related evolutionary benefits obtained from preferences for attractive facial traits may be weak.
370 citations
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National Institute on Drug Abuse1, Université de Montréal2, Duke University3, Icahn School of Medicine at Mount Sinai4, University of Montpellier5, Karolinska Institutet6, University of Toronto7, Columbia University8, University of Würzburg9, Indiana University10, University of Glasgow11, University of Western Australia12, Medical University of Graz13, University of Barcelona14
TL;DR: This commentary considers research questions underlying the proposed nomenclature, with recommendations for receptor heteromer identification in native tissues and their use as targets for drug development.
Abstract: Receptor heteromers constitute a new area of research that is reshaping our thinking about biochemistry, cell biology, pharmacology and drug discovery. In this commentary, we recommend clear definitions that should facilitate both information exchange and research on this growing class of transmembrane signal transduction units and their complex properties. We also consider research questions underlying the proposed nomenclature, with recommendations for receptor heteromer identification in native tissues and their use as targets for drug development.
370 citations
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TL;DR: In this article, the structural properties of a family of GARCH processes are investigated, and necessary and sufficient conditions for the existence of the moments are derived, where α∈(0, 1] and δ>0.
369 citations
Authors
Showing all 29972 results
Name | H-index | Papers | Citations |
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Nicholas G. Martin | 192 | 1770 | 161952 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Steven N. Blair | 165 | 879 | 132929 |
David W. Bates | 159 | 1239 | 116698 |
Mark E. Cooper | 158 | 1463 | 124887 |
David Cameron | 154 | 1586 | 126067 |
Stephen T. Holgate | 142 | 870 | 82345 |
Jeremy K. Nicholson | 141 | 773 | 80275 |
Xin Chen | 139 | 1008 | 113088 |
Graeme J. Hankey | 137 | 844 | 143373 |
David Stuart | 136 | 1665 | 103759 |
Joachim Heinrich | 136 | 1309 | 76887 |
Carlos M. Duarte | 132 | 1173 | 86672 |
David Smith | 129 | 2184 | 100917 |