US Cosmic Visions: New Ideas in Dark Matter 2017: Community Report

This white paper summarizes the workshop "U.S. Cosmic Visions: New Ideas in Dark Matter" held at University of Maryland on March 23-25, 2017

Search for the Standard Model Higgs boson decay to μ+μ− with the ATLAS detector

A search is reported for Higgs boson decay to μ+μ−μ+μ− using data with an integrated luminosity of 24.8 fb−124.8 fb−¹ collected with the ATLAS detector in pp collisions at √s=7 and 8 TeV at the CERN Large Hadron Collider. The observed dimuon invariant mass distribution is consistent with the Standard Model background-only hypothesis in the 120–150 GeV search range. For a Higgs boson with a mass of 125.5 GeV, the observed (expected) upper limit at the 95% confidence level is 7.0 (7.2) times the Standard Model expectation. This corresponds to an upper limit on the branching ratio BR(H→μ+μ−)of 1.5×10−31.5×10−3

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Effect of anakinra on mortality in patients with COVID-19: a systematic review and patient-level meta-analysis

International audienc