Formation of a galaxy with a central black hole in the Lemaitre-Tolman model

We construct two models of the formation a galaxy with a central black hole, starting from a small initial fluctuation at recombination. This is an application of previously developed methods to find a Lemaitre-Tolman model that evolves from a given initial density or velocity profile to a given final density profile. We show that the black hole itself could be either a collapsed object, or a non-vacuum generalisation of a full Schwarzschild-Kruskal-Szekeres wormhole. Particular attention is paid to the black hole's apparent and event horizons.Comment: REVTeX, 22 pages including 11 figures (25 figure files). Replacement has minor changes in response to the referee, and editorial corrections. To appear in PR

Photon-photon absorption above a molecular cloud torus in blazars

Gamma rays have been observed from two blazars at TeV energies. One of these, Markarian 421, has been observed also at GeV energies and has roughly equal luminosity per decade at GeV and TeV energies. Photon-photon pair production on the infrared background radiation is expected to prevent observation above about 1 TeV. However, the infrared background is not well known and it may be possible to observe the nearest blazars up to energies somewhat below about 100 TeV where absorption on the cosmic microwave background will give a sharp cut-off. Blazars are commonly believed to correspond to low power radio galaxies, seen down along a relativistic jet; as such they are all expected to have the nuclear activity encircled by a dusty molecular torus, which subtends an angle of 90 degrees or more in width as seen from the central source. Photon-photon pair production can also take place on the infrared radiation produced at the AGN by this molecular torus and surrounding outer disk. We calculate the optical depth for escaping gamma-rays produced near the central black hole and at various points along the jet axis for the case of blazars where the radiation is observed in a direction closely aligned with the jet. We find that the TeV emission site must be well above the top of the torus. For example, if the torus has an inner radius of 0.1 pc and an outer radius of 0.2 pc, then the emission site in Mrk 421 would have be at least 0.25 pc above the upper surface of the torus, and if Mrk 421 is observed above 50 TeV in the future, the emission site would have to be at least 0.5 pc above the upper surface. This has important implications for models of gamma-ray emission in active galactic nuclei.Comment: 18 pages, 6 figures, accepted for publication in Astroparticle Physics. Revised version contains 2 additional figures and more detailed discussio

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

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

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