Magnetic anomalies in the spin chain system, Sr3_3Cu1−x_{1-x}Znx_xIrO6_6

We report the results of ac and dc magnetization (M) and heat-capacity (C) measurements on the solid solution, Sr$_3$Cu$_{1-x}$Zn$_x$IrO$_6$. While the Zn end member is known to form in a rhombohedral pseudo one-dimensional K$_4$CdCl$_6$ structure with an antiferromagnetic ordering temperature of (T$_N$ =) 19 K, the Cu end member has been reported to form in a monoclinically distorted form with a Curie temperature of (T$_C$ =) 19 K. The magnetism of the Zn compound is found to be robust to synthetic conditions and is broadly consistent with the behavior known in the literature. However, we find a lower magnetic ordering temperature (T$_o$) for our Cu compound (~ 13 K), thereby suggesting that T$_o$ is sensitive to synthetic conditions. The Cu sample appears to be in a spin-glass-like state at low temperatures, judged by a frequency dependence of ac magnetic susceptibility and a broadening of the C anomaly at the onset of magnetic ordering, in sharp contrast to earlier proposals. Small applications of magnetic field, however, drive this system to ferromagnetism as inferred from the M data. Small substitutions for Cu/Zn (x = 0.75 or 0.25) significantly depress magnetic ordering; in other words, T$_o$ varies non-monotonically with x (T$_o$ ~ 6, 3 and 4 K for x = 0.25, 0.5, and 0.67 respectively). The plot of inverse susceptibility versus temperature is non-linear in the paramagnetic state as if correlations within (or among) the magnetic chains continuously vary with temperature. The results establishComment: 7 pages, 7 figures, Revte

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