An H-alpha survey aiming at the detection of extraplanar diffuse ionized gas in halos of edge-on spiral galaxies II. The H-alpha survey atlas and catalog

In this second paper on the investigation of extraplanar diffuse ionized gas in nearby edge-on spiral galaxies we present the actual results of the individual galaxies of our H-alpha imaging survey. A grand total of 74 galaxies have been studied, including the 9 galaxies of a recently studied sub-sample (Rossa & Dettmar 2000). 40.5% of all studied galaxies reveal extraplanar diffuse ionized gas, whereas in 59.5% of the survey galaxies no extraplanar diffuse ionized gas could be detected. The average distances of this extended emission above the galactic midplane range from 1-2 kpc, while individual filaments in a few galaxies reach distances of up to |z| ~ 6 kpc. In several cases a pervasive layer of ionized gas was detected, similar to the Reynolds layer in our Milky Way, while other galaxies reveal only extended emission locally. The morphology of the diffuse ionized gas is discussed for each galaxy and is compared with observations of other important ISM constituents in the context of the disk-halo connection, in those cases where published results were available. Furthermore, we present the distribution of extraplanar dust in these galaxies, based on an analysis of the unsharp-masked R-band images. The results are compared with the distribution of the diffuse ionized gas.Comment: LaTeX, 21 pages, 7 figures, accepted for publication in A&A, figs. 22-54 are only available in electronic form and figs. 2-11 + 17-20 are also available at http://www.astro.rub.de/jrossa/ha-surve

Perturbation theory and the two-level approximation:A corollary and critique

This analysis addresses the use of a two-level approximation to simplify expressions derived from perturbation theory. It is shown that the limitations of validity for the emergent results are more stringent than is commonly understood, being equivalent in effect to the adoption of a more extensive approximation - one that significantly undermines the perturbative origin of those expressions. Effectively truncating the completeness relation, a series of interconnected operator relations comes into play, some with physically untenable consequences. A new theorem on the expectation values of operator functions highlights additional constraints upon any molecule modelled as a two-level system. © 2010 Elsevier B.V. All rights reserved

Astrophysical magnetic fields and nonlinear dynamo theory

The current understanding of astrophysical magnetic fields is reviewed, focusing on their generation and maintenance by turbulence. In the astrophysical context this generation is usually explained by a self-excited dynamo, which involves flows that can amplify a weak 'seed' magnetic field exponentially fast. Particular emphasis is placed on the nonlinear saturation of the dynamo. Analytic and numerical results are discussed both for small scale dynamos, which are completely isotropic, and for large scale dynamos, where some form of parity breaking is crucial. Central to the discussion of large scale dynamos is the so-called alpha effect which explains the generation of a mean field if the turbulence lacks mirror symmetry, i.e. if the flow has kinetic helicity. Large scale dynamos produce small scale helical fields as a waste product that quench the large scale dynamo and hence the alpha effect. With this in mind, the microscopic theory of the alpha effect is revisited in full detail and recent results for the loss of helical magnetic fields are reviewed.Comment: 285 pages, 72 figures, accepted by Phys. Re

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

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 hospitalization2–4 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

A first update on mapping the human genetic architecture of COVID-19

peer reviewe

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