Approximate solution of the Duffin-Kemmer-Petiau equation for a vector Yukawa potential with arbitrary total angular momenta

The usual approximation scheme is used to study the solution of the Duffin-Kemmer-Petiau (DKP) equation for a vector Yukawa potential in the framework of the parametric Nikiforov-Uvarov (NU) method. The approximate energy eigenvalue equation and the corresponding wave function spinor components are calculated for arbitrary total angular momentum in closed form. Further, the approximate energy equation and wave function spinor components are also given for case. A set of parameter values is used to obtain the numerical values for the energy states with various values of quantum levelsComment: 17 pages; Communications in Theoretical Physics (2012). arXiv admin note: substantial text overlap with arXiv:1205.0938, and with arXiv:quant-ph/0410159 by other author

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

Exome-wide association study reveals novel psoriasis susceptibility locus at<em> TNFSF15</em> and rare protective alleles in genes contributing to type I IFN signalling.

Psoriasis is a common inflammatory skin disorder for which multiple genetic susceptibility loci have been identified, but few resolved to specific functional variants. In this study we sought to identify common and rare psoriasis-associated gene-centric variation. Using exome arrays we genotyped four independent cohorts, totalling 11,861 psoriasis cases and 28,610 controls, aggregating the dataset through statistical meta-analysis. Single variant analysis detected a previously unreported risk locus at TNFSF15 (rs6478108; p = 1.50&thinsp;&times;&thinsp;10-8, OR&thinsp;=&thinsp;1.10), and association of common protein-altering variants at 11 loci previously implicated in psoriasis susceptibility. We validate previous reports of protective low-frequency protein-altering variants within IFIH1 (encoding an innate antiviral receptor) and TYK2 (encoding a Janus kinase), in each case establishing a further series of protective rare variants (minor allele frequency &lt; 0.01) via gene-wide aggregation testing (IFIH1: pburden = 2.53&thinsp;&times;&thinsp;10-7, OR&thinsp;=&thinsp;0.707; TYK2: pburden = 6.17&thinsp;&times;&thinsp;10-4, OR&thinsp;=&thinsp;0.744). Both genes play significant roles in type I interferon (IFN) production and signalling. Several of the protective rare and low-frequency variants in IFIH1 and TYK2 disrupt conserved protein domains, highlighting potential mechanisms through which their effect may be exerted