Three Dimensional MHD Wave Propagation and Conversion to Alfven Waves near the Solar Surface. I. Direct Numerical Solution

The efficacy of fast/slow MHD mode conversion in the surface layers of sunspots has been demonstrated over recent years using a number of modelling techniques, including ray theory, perturbation theory, differential eigensystem analysis, and direct numerical simulation. These show that significant energy may be transferred between the fast and slow modes in the neighbourhood of the equipartition layer where the Alfven and sound speeds coincide. However, most of the models so far have been two dimensional. In three dimensions the Alfven wave may couple to the magneto-acoustic waves with important implications for energy loss from helioseismic modes and for oscillations in the atmosphere above the spot. In this paper, we carry out a numerical ``scattering experiment'', placing an acoustic driver 4 Mm below the solar surface and monitoring the acoustic and Alfvenic wave energy flux high in an isothermal atmosphere placed above it. These calculations indeed show that energy conversion to upward travelling Alfven waves can be substantial, in many cases exceeding loss to slow (acoustic) waves. Typically, at penumbral magnetic field strengths, the strongest Alfven fluxes are produced when the field is inclined 30-40 degrees from the vertical, with the vertical plane of wave propagation offset from the vertical plane containing field lines by some 60-80 degrees.Comment: Accepted for the HELAS II/ SOHO 19/ GONG 2007 Topical Issue of Solar Physic

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