New constraints on elemental and Pb and Nd isotope compositions of South American and Southern African aerosol sources to the South Atlantic Ocean

Improving the geochemical database available for characterising potential natural and anthropogenic aerosol sources from South America and Southern Africa is a critical precondition for studies aimed at understanding trace metal controls on the marine biogeochemical cycles of the South Atlantic Ocean. We here present new elemental and isotopic data for a wide range of sample types from South America and Southern Africa that are potentially important aerosol sources. This includes road dust from Buenos Aires and lichen samples from Johannesburg, soil dust from Patagonia, volcanic ash from the Andean volcanic belt, and aerosol samples from São Paulo. All samples were investigated for major (Al, Ca, Fe, Mg, Na, K, Mn) and trace element (Cd, Co, Cr, Cu, Ni, Pb, REE, Sc, Th, Y, V, Zn) concentrations and Nd and Pb isotopic compositions. We show that diagrams of 208Pb/207Pb vs. εNd, 208Pb/207Pb vs. Pb/Al, 1/[Pb], Zn/Al, Cd/Al, Cu/Al, and εNd vs. Pb/Al, and 1/[Nd] are best suited to separate South American and South African source regions as well as natural and anthropogenic sources. A subset of samples from Patagonia and the Andes was additionally subjected to separation of a fine (<5 μm) fraction and compared to the composition of the bulk sample. We show that differences in the geochemical signature of bulk samples between individual regions and source types are significantly larger than between grain sizes. Jointly, these findings present an important step forward towards a quantitative assessment of aeolian trace metal inputs to the South Atlantic Ocean

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

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

peer reviewe

Assessment of physical weathering in bedrock areas at the Trinity Peninsula, Antarctica: Towards a classification of the current weathering grade in polar areas

International audienceThe Antarctic Peninsula is one of the world's most rapidly warming regions; over the last hundred years, glaciers have retreated, exposing new rocky areas to physical weathering. In its northernmost part, the Trinity Peninsula, physical weathering processes on exposed bedrock between west and east coasts may not be at the same weathering stage as surface temperature conditions are assumed historically different. Thus, we examined rock outcrops in ice-free coasts, assessed surface temperature conditions, rock fracturing degree from rock samples, and analyzed the local context for permafrost occurrence. The survey through Trinity Peninsula covered a transect over three ice-free locations between Cape Legoupil and Düse Bay (63°30'S). Our findings support that ice-free-bedrock surfaces at both coasts of the Trinity Peninsula are at an early weathering stage under equivalent air temperature and wind speed conditions over the last decades. Temperature analysis indicated that if surface temperatures sustain its 2015-2016 magnitude, the permafrost distribution will likely become sporadic. Findings indicate that the physical weathering rates should have been significantly slower or have remained ice-covered much longer than in other areas of the Antarctic Peninsula. Nevertheless, a sustained surface warming will elicit higher physical weathering rates beyond the initial stage attested

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