From crystal to amorphopus: a novel route towards unjamming in soft disk packings

It is presented a numerical study on the unjamming packing fraction of bi- and polydisperse disk packings, which are generated through compression of a monodisperse crystal. In bidisperse systems, a fraction f_+ = 40% up to 80% of the total number of particles have their radii increased by \Delta R, while the rest has their radii decreased by the same amount. Polydisperse packings are prepared by changing all particle radii according to a uniform distribution in the range [-\Delta R,\Delta R]. The results indicate that the critical packing fraction is never larger than the value for the initial monodisperse crystal, \phi = \pi/12, and that the lowest value achieved is approximately the one for random close packing. These results are seen as a consequence of the interplay between the increase in small-small particle contacts and the local crystalline order provided by the large-large particle contacts.Comment: two columns, 14 pages, 12 figures, accepted for publication in Eur. Phys. J.

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

Civilian soldiers in Staffordshire 1793-1823

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