Stoichiometry deviation in amorphous zirconium dioxide

Amorphous zirconia (a-ZrO(2)) has been simulated using a synergistic combination of state-of-the-art methods: employing reverse Monte-Carlo, molecular dynamics and density functional theory together. This combination has enabled the complex chemistry of the amorphous system to be efficiently investigated. Notably, the a-ZrO(2) system was observed to accommodate excess oxygen readily – through the formation of neutral peroxide (O(2)(2−)) defects – a result that has implications not only in the a-ZrO(2) system, but also in other systems employing network formers, intermediates and modifiers. The structure of the a-ZrO(2) system was also determined to have edge-sharing characteristics similar to structures reported in the amorphous TeO(2) system and other chalcogenide-containing glasses

Identification of significant E0E0 strength in the 22+→21+2^+_2 \rightarrow 2^+_1 transitions of 58,60,62^{58, 60, 62}Ni

The $E0$ transition strength in the $2^+_2 \rightarrow 2^+_1$ transitions of $^{58,60,62}$Ni have been determined for the first time following a series of measurements at the Australian National University (ANU) and the University of Kentucky (UK). The CAESAR Compton-suppressed HPGe array and the Super-e solenoid at ANU were used to measure the $\delta(E2/M1)$ mixing ratio and internal conversion coefficient of each transition following inelastic proton scattering. Level half-lives, $\delta(E2/M1)$ mixing ratios and $\gamma$-ray branching ratios were measured at UK following inelastic neutron scattering. The new spectroscopic information was used to determine the $E0$ strengths. These are the first $2^+ \rightarrow 2^+$ $E0$ transition strengths measured in nuclei with spherical ground states and the $E0$ component is found to be unexpectedly large; in fact, these are amongst the largest $E0$ transition strengths in medium and heavy nuclei reported to date

Identification of Significant \u3cem\u3eE\u3c/em\u3e0 Strength in the 2\u3csub\u3e2\u3c/sub\u3e\u3csup\u3e+\u3c/sup\u3e → 2\u3csub\u3e1\u3c/sub\u3e\u3csup\u3e+\u3c/sup\u3e Transitions of \u3csup\u3e58,60,62\u3c/sup\u3eNi

The E0 transition strength in the 22+ → 21+ transitions of 58,60,62Ni have been determined for the first time following a series of measurements at the Australian National University (ANU) and the University of Kentucky (UK). The CAESAR Compton-suppressed HPGe array and the Super-e solenoid at ANU were used to measure the δ(E2/M1) mixing ratio and internal conversion coefficient of each transition following inelastic proton scattering. Level half-lives, δ(E2/M1) mixing ratios and γ-ray branching ratios were measured at UK following inelastic neutron scattering. The new spectroscopic information was used to determine the E0 strengths. These are the first 2+ → 2+ E0 transition strengths measured in nuclei with spherical ground states and the E0 component is found to be unexpectedly large; in fact, these are amongst the largest E0 transition strengths in medium and heavy nuclei reported to date

E0 transition strength in stable Ni isotopes

Excited states in 58,60,62Ni were populated via inelastic proton scattering at the Australian National University as well as via inelastic neutron scattering at the University of Kentucky Accelerator Laboratory. The Super-e electron spectrometer and the CAESAR Compton-suppressed HPGe array were used in complementary experiments to measure conversion coefficients and δ(E2/M1) mixing ratios, respectively, for a number of 2+→2+ transitions. The data obtained were combined with lifetimes and branching ratios to determine E0,M1, and E2 transition strengths between 2+ states. The E0 transition strengths between 0+ states were measured using internal conversion electron spectroscopy and compare well to previous results from internal pair formation spectroscopy. The E0transition strengths between the lowest-lying 2+ states were found to be consistently large for the isotopes studied

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 hospitalization2–4 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

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