The Chiral Magnetic Effect and Axial Anomalies

We give an elementary derivation of the chiral magnetic effect based on a strong magnetic field lowest-Landau-level projection in conjunction with the well-known axial anomalies in two- and four-dimensional space-time. The argument is general, based on a Schur decomposition of the Dirac operator. In the dimensionally reduced theory, the chiral magnetic effect is directly related to the relativistic form of the Peierls instability, leading to a spiral form of the condensate, the chiral magnetic spiral. We then discuss the competition between spin projection, due to a strong magnetic field, and chirality projection, due to an instanton, for light fermions in QCD and QED. The resulting asymmetric distortion of the zero modes and near-zero modes is another aspect of the chiral magnetic effect.Comment: 33 pages, 5 figures, to appear in Lect. Notes Phys. "Strongly interacting matter in magnetic fields" (Springer), edited by D. Kharzeev, K. Landsteiner, A. Schmitt, H.-U. Ye

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

The value of experience in legal competence

Preprint of a paper by Avrom Sherr, Woolf Professor of Legal Education, Institute of Advanced Legal Studies, University of Londo