Standardisation of the commercial CPUE series for abalone in Zones E and G from 1980 to 2007 using a mixed effects model

The commercial CPUE series is considered during modeling of resource dynamics as an index of population abundance. However, a number of factors other than abundance may influence recorded values. Standardisation is able to take into account some of these effects, thereby producing a more reliable index

Possible Emergence of West Caucasian Bat Virus in Africa

The prevalence of neutralizing antibody against West Caucasian bat virus (WCBV) in Miniopterus bats collected in Kenya ranged from 17% to 26%. Seropositive bats were detected in 4 of 5 locations sampled across the country. These findings provide evidence that WCBV, originally isolated in Europe, may emerge in other continents

Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms

Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms

“Others-in-Law”: Legalism in the Economy of Religious Differences

Religious legalism encompasses a wide range of attitudes that assign religious meaning to legal content or to legal compliance. The phenomenology of religious legalism is assuming a significant role in various contemporary debates about legal pluralism, accommodation of religious minorities, religious freedom, and so forth. This article revises this conception and the commonplace equation of Judaism and legalism. It suggests that we ought to regard both as part of the economy of religious differences by which religious identities are expressed and defined as alternatives. The common ascription of religious legalism to Judaism (and Islam) is criticized here through a historical analysis of the law-religion-identity matrix in three cultural settings: late ancient Judeo-Hellenic, medieval Judeo–Arabic, and post-Reformation Europe

Physics searches at the LHC

With the LHC up and running, the focus of experimental and theoretical high energy physics will soon turn to an interpretation of LHC data in terms of the physics of electroweak symmetry breaking and the TeV scale. We present here a broad review of models for new TeV-scale physics and their LHC signatures. In addition, we discuss possible new physics signatures and describe how they can be linked to specific models of physics beyond the Standard Model. Finally, we illustrate how the LHC era could culminate in a detailed understanding of the underlying principles of TeV-scale physics.Comment: 184 pages, 55 figures, 14 tables, hundreds of references; scientific feedback is welcome and encouraged. v2: text, references and Overview Table added; feedback still welcom

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Towards the european strategy for particle physics: The briefing book

This document was prepared as part of the briefing material for the Workshop of the CERN Council Strategy Group, held in DESY Zeuthen from 2nd to 6th May 2006. It gives an overview of the physics issues and of the technological challenges that will shape the future of the field, and incorporates material presented and discussed during the Symposium on the European Strategy for Particle Physics, held in Orsay from 30th January to 2nd February 2006, reflecting the various opinions of the European community as recorded in written submissions to the Strategy Group and in the discussions at the Symposium

The Data Acquisition and Calibration System for the ATLAS Semiconductor Tracker

The SemiConductor Tracker (SCT) data acquisition (DAQ) system will calibrate, configure, and control the approximately six million front-end channels of the ATLAS silicon strip detector. It will provide a synchronized bunch-crossing clock to the front-end modules, communicate first-level triggers to the front-end chips, and transfer information about hit strips to the ATLAS high-level trigger system. The system has been used extensively for calibration and quality assurance during SCT barrel and endcap assembly and for performance confirmation tests after transport of the barrels and endcaps to CERN. Operating in data-taking mode, the DAQ has recorded nearly twenty million synchronously-triggered events during commissioning tests including almost a million cosmic ray triggered events. In this paper we describe the components of the data acquisition system, discuss its operation in calibration and data-taking modes and present some detector performance results from these tests

Coding Variation in ANGPTL4, LPL, and SVEP1 and the Risk of Coronary Disease.

BACKGROUND: The discovery of low-frequency coding variants affecting the risk of coronary artery disease has facilitated the identification of therapeutic targets. METHODS: Through DNA genotyping, we tested 54,003 coding-sequence variants covering 13,715 human genes in up to 72,868 patients with coronary artery disease and 120,770 controls who did not have coronary artery disease. Through DNA sequencing, we studied the effects of loss-of-function mutations in selected genes. RESULTS: We confirmed previously observed significant associations between coronary artery disease and low-frequency missense variants in the genes LPA and PCSK9. We also found significant associations between coronary artery disease and low-frequency missense variants in the genes SVEP1 (p.D2702G; minor-allele frequency, 3.60%; odds ratio for disease, 1.14; P=4.2×10(-10)) and ANGPTL4 (p.E40K; minor-allele frequency, 2.01%; odds ratio, 0.86; P=4.0×10(-8)), which encodes angiopoietin-like 4. Through sequencing of ANGPTL4, we identified 9 carriers of loss-of-function mutations among 6924 patients with myocardial infarction, as compared with 19 carriers among 6834 controls (odds ratio, 0.47; P=0.04); carriers of ANGPTL4 loss-of-function alleles had triglyceride levels that were 35% lower than the levels among persons who did not carry a loss-of-function allele (P=0.003). ANGPTL4 inhibits lipoprotein lipase; we therefore searched for mutations in LPL and identified a loss-of-function variant that was associated with an increased risk of coronary artery disease (p.D36N; minor-allele frequency, 1.9%; odds ratio, 1.13; P=2.0×10(-4)) and a gain-of-function variant that was associated with protection from coronary artery disease (p.S447*; minor-allele frequency, 9.9%; odds ratio, 0.94; P=2.5×10(-7)). CONCLUSIONS: We found that carriers of loss-of-function mutations in ANGPTL4 had triglyceride levels that were lower than those among noncarriers; these mutations were also associated with protection from coronary artery disease. (Funded by the National Institutes of Health and others.).Supported by a career development award from the National Heart, Lung, and Blood Institute, National Institutes of Health (NIH) (K08HL114642 to Dr. Stitziel) and by the Foundation for Barnes–Jewish Hospital. Dr. Peloso is supported by the National Heart, Lung, and Blood Institute of the NIH (award number K01HL125751). Dr. Kathiresan is supported by a Research Scholar award from the Massachusetts General Hospital, the Donovan Family Foundation, grants from the NIH (R01HL107816 and R01HL127564), a grant from Fondation Leducq, and an investigator-initiated grant from Merck. Dr. Merlini was supported by a grant from the Italian Ministry of Health (RFPS-2007-3-644382). Drs. Ardissino and Marziliano were supported by Regione Emilia Romagna Area 1 Grants. Drs. Farrall and Watkins acknowledge the support of the Wellcome Trust core award (090532/Z/09/Z), the British Heart Foundation (BHF) Centre of Research Excellence. Dr. Schick is supported in part by a grant from the National Cancer Institute (R25CA094880). Dr. Goel acknowledges EU FP7 & Wellcome Trust Institutional strategic support fund. Dr. Deloukas’s work forms part of the research themes contributing to the translational research portfolio of Barts Cardiovascular Biomedical Research Unit, which is supported and funded by the National Institute for Health Research (NIHR). Drs. Webb and Samani are funded by the British Heart Foundation, and Dr. Samani is an NIHR Senior Investigator. Dr. Masca was supported by the NIHR Leicester Cardiovascular Biomedical Research Unit (BRU), and this work forms part of the portfolio of research supported by the BRU. Dr. Won was supported by a postdoctoral award from the American Heart Association (15POST23280019). Dr. McCarthy is a Wellcome Trust Senior Investigator (098381) and an NIHR Senior Investigator. Dr. Danesh is a British Heart Foundation Professor, European Research Council Senior Investigator, and NIHR Senior Investigator. Drs. Erdmann, Webb, Samani, and Schunkert are supported by the FP7 European Union project CVgenes@ target (261123) and the Fondation Leducq (CADgenomics, 12CVD02). Drs. Erdmann and Schunkert are also supported by the German Federal Ministry of Education and Research e:Med program (e:AtheroSysMed and sysINFLAME), and Deutsche Forschungsgemeinschaft cluster of excellence “Inflammation at Interfaces” and SFB 1123. Dr. Kessler received a DZHK Rotation Grant. The analysis was funded, in part, by a Programme Grant from the BHF (RG/14/5/30893 to Dr. Deloukas). Additional funding is listed in the Supplementary Appendix.This is the author accepted manuscript. The final version is available from the Massachusetts Medical Society via http://dx.doi.org/10.1056/NEJMoa150765