3 research outputs found

    Identification of the Jπ = 1− state in 218Ra populated via α decay of 222Th

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    The α decay of 222Th populating the low-lying J π = 3− state, and also a proposed 1− state, in 218Ra has been observed. The observations suggest an excitation energy of 853 keV for the 1− state, which is 60 keV above the 3− state. The hindrance factors of these α decays give a possible boundary to the region of ground-state octupole deformation in the light-actinide nuclei. The relative positions of the J π = 1− and 3− states suggest they are produced by an octupole-vibrational mechanism, as opposed to α clustering or rotations of a reflection-asymmetric octupole-deformed shape.peerReviewe

    Genetic architecture of human plasma lipidome and its link to cardiovascular disease

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    Abstract Understanding genetic architecture of plasma lipidome could provide better insights into lipid metabolism and its link to cardiovascular diseases (CVDs). Here, we perform genome-wide association analyses of 141 lipid species (n = 2,181 individuals), followed by phenome-wide scans with 25 CVD related phenotypes (n = 511,700 individuals). We identify 35 lipid-species-associated loci (P <5 ×10−8), 10 of which associate with CVD risk including five new loci-COL5A1, GLTPD2, SPTLC3, MBOAT7 and GALNT16 (false discovery rate<0.05). We identify loci for lipid species that are shown to predict CVD e.g., SPTLC3 for CER(d18:1/24:1). We show that lipoprotein lipase (LPL) may more efficiently hydrolyze medium length triacylglycerides (TAGs) than others. Polyunsaturated lipids have highest heritability and genetic correlations, suggesting considerable genetic regulation at fatty acids levels. We find low genetic correlations between traditional lipids and lipid species. Our results show that lipidomic profiles capture information beyond traditional lipids and identify genetic variants modifying lipid levels and risk of CVD

    Genetic architecture of human plasma lipidome and its link to cardiovascular disease

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