Fast-Timing measurements in 100zr using labr3(ce) detectors coupled with gammasphere

In order to investigate the evolution of nuclear deformation in the region of the chart of nuclides around mass numbers A ' 110 and A ' 150, an experiment was performed at the Argonne National Laboratory where the gamma-decay radiation emitted from the fission fragments of 252Cf was measured using 51 Gammasphere detectors coupled with 25 LaBr3(Ce) detectors. In this work, a short description of the experimental setup is presented together with some preliminary results from the fast-Timing analysis of the 4+ state of the nucleus 100Zr. A lifetime value of τ = 50(28) ps was obtained using the Generalized Centroid Shift Method. This result agrees with the literature value of τ = 53(4) ps within one standard deviation

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and 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. However, large-scale randomized clinical trials will be essential before any change to clinical practice