Twist-2 Heavy Flavor Contributions to the Structure Function g2(x,Q2)g_2(x,Q^2)

The twist--2 heavy flavor contributions to the polarized structure function $g_2(x,Q^2)$ are calculated. We show that this part of $g_2(x,Q^2)$ is related to the heavy flavor contribution to $g_1(x,Q^2)$ by the Wandzura--Wilczek relation to all orders in the strong coupling constant. Numerical results are presented.Comment: 17 pages LATEX, 1 style files, 4 figure

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

Mental time travel, somatic markers and “myopia for the future”

The original publication can be found at www.springerlink.comPatients with damage to the ventromedial prefrontal cortex (VMPFC) are often described as having impaired ability for planning and decision making despite retaining intact capacities for explicit reasoning. The somatic marker hypothesis is that the VMPFC associates implicitly represented affective information with explicit representations of actions or outcomes. Consequently, when the VMPFC is damaged explicit reasoning is no longer scaffolded by affective information, leading to characteristic deficits. These deficits are exemplified in performance on the Iowa Gambling Task (IGT) in which subjects with VMPFC perform significantly worse than neurotypicals in a task which requires them learn from rewarding and punishing experience to make decisions. The somatic marker theory adopts a canonical theory of emotion, in which emotions function as part of a valencing system, to explain the role of affective processes. The first part of the paper argues against this canonical account. The second part provides a different account of the role of the role of the VMPFC in decision-making which does not depend on the canonical account of emotion. Together the first and second parts of the paper provide the basis for a different interpretation of results on the Iowa Gambling Task (IGT). In fact the IGT may be probing a deficit in what has been called mental time travel: the ability to access and use information from previous experience and imaginatively rehearse future experiences as part of the process of deliberation.Philip Gerran