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Träfflista för sökning "(WFRF:(Goel G)) srt2:(2020-2024)"

Search: (WFRF:(Goel G)) > (2020-2024)

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  • Avigo, R., et al. (author)
  • Low-lying electric dipole gamma-continuum for the unstable Fe-62,64 nuclei : Strength evolution with neutron number
  • 2020
  • In: Physics Letters B. - : ELSEVIER. - 0370-2693 .- 1873-2445. ; 811
  • Journal article (peer-reviewed)abstract
    • The gamma-ray emission from the nuclei Fe-62,Fe-64 following Coulomb excitation at bombarding energy of 400-440 AMeV was measured with special focus on E1 transitions in the energy region 4-8 MeV. The unstable neutron-rich nuclei Fe-62,Fe-64 were produced at the FAIR-GSI laboratories and selected with the FRS spectrometer. The gamma decay was detected with AGATA. From the measured gamma-ray spectra the summed E1 strength is extracted and compared to microscopic quasi-particle phonon model calculations. The trend of the E1 strength with increasing neutron number is found to be fairly well reproduced with calculations that assume a rather complex structure of the 1(-) states (three-phonon states) inducing a strong fragmentation of the E1 nuclear response below the neutron binding energy.
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  • Aragam, KG, et al. (author)
  • Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants
  • 2022
  • In: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 54:12, s. 1803-1815
  • Journal article (peer-reviewed)abstract
    • The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD.
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  • Result 11-20 of 37

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