The Heavy Quark Self-Energy in Nonrelativistic Lattice QCD

The heavy quark self-energy in nonrelativistic lattice QCD is calculated to $O(\alpha_s)$ in perturbation theory. An action which includes all spin-independent relativistic corrections to order $v^2$, where $v$ is the typical heavy quark velocity, and all spin-dependent corrections to order $v^4$ is used. The standard Wilson action and an improved multi-plaquette action are used for the gluons. Results for the mass renormalization, wavefunction renormalization, and energy shift are given; tadpole contributions are found to be large. A tadpole improvement scheme in which all link variables are rescaled by a mean-field factor is also studied. The effectiveness of this scheme in offsetting the large tadpole contributions to the heavy quark renormalization parameters is demonstrated.Comment: 28 pages, SLAC-PUB-598

Multiple electromagnetic electron positron pair production in relativistic heavy ion collisions

We calculate the cross sections for the production of one and more electron-positron pairs due to the strong electromagnetic fields in relativistic heavy ion collisions. Using the generating functional of fermions in an external field we derive the N-pair amplitude. Neglecting the antisymmetrisation in the final state we find that the total probability to produce N pairs is a Poisson distribution. We calculate total cross sections for the production of one pair in lowest order and also include higher-order corrections from the Poisson distribution up to third order. Furthermore we calculate cross sections for the production of up to five pairs including corrections from the Poisson distribution.Comment: 13 pages REVTeX, 4 Postscript figures, This and related papers may also be obtained from http://www.phys.washington.edu/~hencken

Rigorous QCD-Potential for the ttˉt\bar{t}-System at Threshold

Recent evidence for the top mass in the region of 160 $GeV$ for the first time provides an opportunity to use the full power of relativistic quantum field theoretical methods, available also for weakly bound systems. Because of the large decay width \G of the top quark individual energy-levels in "toponium" will be unobservable. However, the potential for the $t\bar{t}$ system, based on a systematic expansion in powers of the strong coupling constant \a_s can be rigorously derived from QCD and plays a central role in the threshold region. It is essential that the neglect of nonperturbative (confining) effects is fully justified here for the first time to a large accuracy, also just {\it because} of the large \G. The different contributions to that potential are computed from real level corrections near the bound state poles of the $t\bar{t}$-system which for \G \ne 0 move into the unphysical sheet of the complex energy plane. Thus, in order to obtain the different contributions to that potential we may use the level corrections at that (complex) pole. Within the relevant level shifts we especially emphasize the corrections of order O(\a_s^4 m_t) and numerically comparable ones to that order also from electroweak interactions which may become important as well.Comment: 36 pages (mailer uncorrupted version), TUW-94-1

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

Bound States of Energy Dependent Singular Potentials

We consider attractive power-law potentials depending on energy through their coupling constant. These potentials are proportional to 1/|x| m with m ≥ 1 in the D = 1 dimensional space, to 1/r m with m ≥ 2 in the D = 3 dimensional space. We study the ground state of such potentials. First, we show that all singular attractive potentials with an energy dependent coupling constant are bounded from below, contrarily to the usual case. In D = 1, a bound state of finite energy is found with a kind of universality for the eigenvalue and the eigenfunction, which become independent on m for m > 1. We prove the solution to be unique. A similar situation arises for D = 3 for m > 2, except that, in this case, the solution is not directly comparable to a bound state: the wave function, though square integrable, diverges at the origin