The r-modes in accreting neutron stars with magneto-viscous boundary layers

We explore the dynamics of the r-modes in accreting neutron stars in two ways. First, we explore how dissipation in the magneto-viscous boundary layer (MVBL) at the crust-core interface governs the damping of r-mode perturbations in the fluid interior. Two models are considered: one assuming an ordinary-fluid interior, the other taking the core to consist of superfluid neutrons, type II superconducting protons, and normal electrons. We show, within our approximations, that no solution to the magnetohydrodynamic equations exists in the superfluid model when both the neutron and proton vortices are pinned. However, if just one species of vortex is pinned, we can find solutions. When the neutron vortices are pinned and the proton vortices are unpinned there is much more dissipation than in the ordinary-fluid model, unless the pinning is weak. When the proton vortices are pinned and the neutron vortices are unpinned the dissipation is comparable or slightly less than that for the ordinary-fluid model, even when the pinning is strong. We also find in the superfluid model that relatively weak radial magnetic fields ~ 10^9 G (10^8 K / T)^2 greatly affect the MVBL, though the effects of mutual friction tend to counteract the magnetic effects. Second, we evolve our two models in time, accounting for accretion, and explore how the magnetic field strength, the r-mode saturation amplitude, and the accretion rate affect the cyclic evolution of these stars. If the r-modes control the spin cycles of accreting neutron stars we find that magnetic fields can affect the clustering of the spin frequencies of low mass x-ray binaries (LMXBs) and the fraction of these that are currently emitting gravitational waves.Comment: 19 pages, 8 eps figures, RevTeX; corrected minor typos and added a referenc

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

Click detection in Italian and English

Contains fulltext : 6070.pdf (publisher's version ) (Open Access