New vegetation type map of India prepared using satellite remote sensing: Comparison with global vegetation maps and utilities

International audienceA seamless vegetation type map of India (scale 1: 50,000) prepared using medium-resolution IRS LISS-III images is presented. The map was created using an on-screen visual interpretation technique and has an accuracy of 90%, as assessed using 15,565 ground control points. India has hitherto been using potential vegetation/forest type map prepared by Champion and Seth in 1968. We characterized and mapped further the vegetation type distribution in the country in terms of occurrence and distribution, area occupancy, percentage of protected area (PA) covered by each vegetation type, range of elevation, mean annual temperature and precipitation over the past 100 years. A remote sensing-amenable hierarchical classification scheme that accommodates natural and semi-natural systems was conceptualized, and the natural vegetation was classified into forests, scrub/shrub lands and grasslands on the basis of extent of vegetation cover. We discuss the distribution and potential utility of the vegetation type map in a broad range of ecological, climatic and conservation applications from global, national and local perspectives. We used 15,565 ground control points to assess the accuracy of products available globally (i.e., GlobCover, Holdridge’s life zone map and potential natural vegetation (PNV) maps). Hence we recommend that the map prepared herein be used widely. This vegetation type map is the most comprehensive one developed for India so far. It was prepared using 23.5 m seasonal satellite remote sensing data, field samples and information relating to the biogeography, climate and soil. The digital map is now available through a web portal (http://bis.iirs.gov.in)

Measurement of dijet azimuthal decorrelation in pp collisions at √s=8TeV

A measurement of the decorrelation of azimuthal angles between the two jets with the largest transverse momenta is presented for seven regions of leading jet transverse momentum up to 2.2TeV. The analysis is based on the proton-proton collision data collected with the CMS experiment at a centre-of-mass energy of 8TeV corresponding to an integrated luminosity of 19.7fb-1. The dijet azimuthal decorrelation is caused by the radiation of additional jets and probes the dynamics of multijet production. The results are compared to fixed-order predictions of perturbative quantum chromodynamics (QCD), and to simulations using Monte Carlo event generators that include parton showers, hadronization, and multiparton interactions. Event generators with only two outgoing high transverse momentum partons fail to describe the measurement, even when supplemented with next-to-leading-order QCD corrections and parton showers. Much better agreement is achieved when at least three outgoing partons are complemented through either next-to-leading-order predictions or parton showers. This observation emphasizes the need to improve predictions for multijet production. © 2016, CERN for the benefit of the CMS collaboration

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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