Metamorphosis and Taxonomy of Andreev Bound States

We analyze the spatial and energy dependence of the local density of states in a SNS junction. We model our system as a one-dimensional tight-binding chain which we solve exactly by numerical diagonalization. We calculate the dependence of the Andreev bound states on position, phase difference, gate voltage, and coupling with the superconducting leads. Our results confirm the physics predicted by certain analytical approximations, but reveal a much richer set of phenomena beyond the grasp of these approximations, such as the metamorphosis of the discrete states of the normal link (the normal bound states) into Andreev bound states as the leads become superconducting.Comment: 23 pages, 15 figure

The power of popular publicity: new social media and the affective dynamics of the sport racism scandal

Sociologists have tended to take insufficient account of the importance of emotions to the social power of the institution of media, particularly as altered by the emergence of social media in the current media ecology. This paper compensates for this neglect by means of a brief illustrative case study of the effect of social media on the public reception of the 2011 Sepp Blatter racism scandal and of other ‘race-related’ scandals in the UK. In proposing media scandals’ wider sociological significance regarding the dynamic, multi-accented relationships between emotions and power, it analyses how England’s prevailing climate of ‘postcolonial guilt’ was reinforced and conveyed through social media networks

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