160 research outputs found

    Palaeotectonic setting of the south-eastern Kédougou-Kéniéba Inlier, West Africa: new insights from igneous trace element geochemistry and U-Pb zircon ages

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    New U-Pb zircon ages and geochemistry from the eastern Kédougou-Kéniéba Inlier are presented and integrated with published data to generate a revised tectonic framework for the westernmost Birimian terranes. The Falémé Volcanic Belt and Kofi Series are highly prospective, hosting several multi-million ounce gold deposits and a significant iron ore resource, but remain under-researched. It is therefore important to constrain the fundamental geological setting. The igneous rocks of the eastern Kédougou-Kéniéba Inlier are dominantly of high-K calc-alkaline affinity, with fractionated REE patterns and negative Nb-Ta anomalies. The plutonic rocks in the Falémé Belt are dioritic to granodioritic in composition, with moderately fractionated REE patterns and metaluminous A/CNK signatures. Felsic, peraluminous granite stocks, dykes and plutons with fractionated REE patterns and negative Eu, Ti and P anomalies intruded both the Falémé Belt and Kofi Series. Albitisation masks the affinity of some units, although use of the Th-Co diagram shows that prior to albitisation, all igneous units belonged to the high-K calc-alkaline series. New U-Pb age data for the Boboti and Balangouma plutons indicate crystallisation at 2088.5 ± 8.5 Ma and at 2112 ± 13 Ma, respectively. Inherited zircons in the Boboti pluton indicate magmatic activity in the Falémé Belt at 2218 ± 83 Ma coincided with the oldest dated units in the Mako Belt to the West. Systematic changes in Dy/Yb, Sm/La, Nb/Zr, Rb concentration, Eu-anomaly and ɛNdt over ∼200 Ma reveal that the tectonic setting in the KKI evolved from a volcanic island arc environment to an active continental margin. Crustal thickening, as a result of a shift to collisional tectonic setting, combined with magmatic differentiation, led to the generation of peraluminous, granitic melts with a significant crustal component. A small suite of more basic intrusive and extrusive rocks on the eastern margin of the Dialé-Daléma basin are highly metaluminous and display limited LILE enrichment, with normalised HREE values close to unity. The Daléma igneous rocks may have formed in an extensional back arc, related to the arc system

    Letter from S. Austin Allibone, Philadelphia, Pennsylvania, to James William Kimball, Boston, Massachusetts : autograph manuscript signed, 1868 October 6

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    The letter is about religious tracts.https://repository.wellesley.edu/autographletters/1032/thumbnail.jp

    Letter from S. Austin Allibone, Philadelphia, Pennsylvania, to James Thomas Fields, Boston, Massachusetts : autograph manuscript signed, 1957 March 5

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    https://repository.wellesley.edu/autographletters/1030/thumbnail.jp

    Letter from S. Austin Allibone, New York, New York, to Robert Ellis Thompson: autograph manuscript signed, 1882 March 20

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    https://repository.wellesley.edu/autographletters/1031/thumbnail.jp

    Stable C, O, and S isotope record of magmatic-hydrothermal interactions between the Falémé Fe Skarn and the Loulo Au Systems in Western Mali

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    Abstract The Gara, Yalea, and Gounkoto Au deposits of the >17 Moz Loulo mining district, largely hosted by the Kofi series metasediments, are located several kilometers to the east of the 650-Mt Fe skarn deposits in the adjacent Falémé batholith. The Au deposits are interpreted to have formed through phase separation of an aqueous-carbonic fluid, which locally mixed with a hypersaline brine of metaevaporite origin. Recognition of an intrusive relationship between the Falémé batholith and Kofi series opens the possibility that the Fe skarns and Au deposits are part of the same mineral system. In this paper, we combine new δ13C, δ18O, and δ34S data from the Karakaene Ndi skarn, Au occurrences along the western margin of the Kofi series, and zircons within plutonic rocks of the Falémé batholith. We combine these with existing data from the Loulo Au deposits to model the contribution of magmatic volatiles to Au mineralization. C and O isotope compositions of auriferous carbonate-quartz-sulfide veins from the Loulo Au deposits have wide ranges (δ13C: –21.7 to –4.5‰ and δ18O: 11.8 to 23.2‰), whereas values from carbonate veins in Kofi series Au prospects close to the Falémé batholith and the Karakaene Ndi Fe skarn deposit have more restricted ranges (δ13C: –16.8 to –3.7‰, δ18O: 11.4 to 17.2‰, and δ13C: –3.0 ± 1‰, δ18O: 12.6 ± 1‰, respectively). Kofi series dolostones have generally higher isotopic values (δ13C: –3.1 to 1.3‰ and δ18O: 19.1 to 23.3‰). Pyrite from Kofi series Au prospects adjacent to the Falémé batholith have a wide range of δ34S values (–4.6 to 14.2‰), similar to pyrite from the Karakaene Ndi skarn (2.8 to 11.9‰), whereas δ34S values of pyrite and arsenopyrite from the Loulo deposits are consistently >6‰. Comparison of the C and O isotope data with water-rock reaction models indicates the Loulo Au deposits formed primarily through unmixing of an aqueous carbonic fluid derived from the devolatilization of sedimentary rocks with an organic carbon component. Isotopic data are permissive of the hypersaline brine that enhanced this phase separation including components derived from both Kofi series evaporite horizons interlayered with the dolostones and a magmatic-hydrothermal brine. This magmatic-hydrothermal component is particularly apparent in O, C, and S isotope data from the Gara deposit and Au prospects immediately adjacent to the Falémé batholith

    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 hospitalization2–4 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

    Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity

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    The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)

    Genetic mechanisms of critical illness in Covid-19.

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    Host-mediated lung inflammation is present,1 and drives mortality,2 in critical illness caused by Covid-19. Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development.3 Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study(GWAS) in 2244 critically ill Covid-19 patients from 208 UK intensive care units (ICUs). We identify and replicate novel genome-wide significant associations, on chr12q24.13 (rs10735079, p=1.65 [Formula: see text] 10-8) in a gene cluster encoding antiviral restriction enzyme activators (OAS1, OAS2, OAS3), on chr19p13.2 (rs2109069, p=2.3 [Formula: see text] 10-12) near the gene encoding tyrosine kinase 2 (TYK2), on chr19p13.3 (rs2109069, p=3.98 [Formula: see text] 10-12) within the gene encoding dipeptidyl peptidase 9 (DPP9), and on chr21q22.1 (rs2236757, p=4.99 [Formula: see text] 10-8) in the interferon receptor gene IFNAR2. We identify potential targets for repurposing of licensed medications: using Mendelian randomisation we found evidence in support of a causal link from low expression of IFNAR2, and high expression of TYK2, to life-threatening disease; transcriptome-wide association in lung tissue revealed that high expression of the monocyte/macrophage chemotactic receptor CCR2 is associated with severe Covid-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms, and mediators of inflammatory organ damage in Covid-19. Both mechanisms may be amenable to targeted treatment with existing drugs. Large-scale randomised clinical trials will be essential before any change to clinical practice
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