25 research outputs found

    Generalized Jacobi identities and ball-box theorem for horizontally regular vector fields

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    We consider a family of vector fields and we assume a horizontal regularity on their derivatives. We discuss the notion of commutator showing that different definitions agree. We apply our results to the proof of a ball-box theorem and Poincar\'e inequality for nonsmooth H\"ormander vector fields.Comment: arXiv admin note: material from arXiv:1106.2410v1, now three separate articles arXiv:1106.2410v2, arXiv:1201.5228, arXiv:1201.520

    Characterization of the water diffusion in GEM foil material

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    Systematic studies on the GEM foil material are performed to measure the moisture diffusion rate and saturation level.These studies are important because the presence of this compound inside the detector’s foil can possibly change its mechanical and electrical properties,and in such a way,the detector performance can be affected.To understand this phenomenon,a model is developed with COMSOL Multiphysicsv.4.3 which described the adsorption and diffusion within the geometry of GEM foil,the concentration profiles and the time required to saturate the foil.The COMSOL model is verified by experimental observations on a GEM foil sample.This note will describe the model and its experimental verification results

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

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    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
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