Gauged Gravity via Spectral Asymptotics of non-Laplace type Operators

We construct invariant differential operators acting on sections of vector bundles of densities over a smooth manifold without using a Riemannian metric. The spectral invariants of such operators are invariant under both the diffeomorphisms and the gauge transformations and can be used to induce a new theory of gravitation. It can be viewed as a matrix generalization of Einstein general relativity that reproduces the standard Einstein theory in the weak deformation limit. Relations with various mathematical constructions such as Finsler geometry and Hodge-de Rham theory are discussed.Comment: Version accepted by J. High Energy Phys. Introduction and Discussion significantly expanded. References added and updated. (41 pages, LaTeX: JHEP3 class, no figures

Thermal and Chemical Equilibration in Relativistic Heavy Ion Collisions

We investigate the thermalization and the chemical equilibration of a parton plasma created from Au+Au collision at LHC and RHIC energies starting from the early moment when the particle momentum distributions in the central region become for the first time isotropic due to longitudinal cooling. Using the relaxation time approximation for the collision terms in the Boltzmann equations for gluons and for quarks and the real collision terms constructed from the simplest QCD interactions, we show that the collision times have the right behaviour for equilibration. The magnitude of the quark (antiquark) collision time remains bigger than the gluon collision time throughout the lifetime of the plasma so that gluons are equilibrating faster than quarks both chemically and kinetically. That is we have a two-stage equilibration scenario as has been pointed out already by Shuryak sometimes ago. Full kinetic equilibration is however slow and chemical equilibration cannot be completed before the onset of the deconfinement phase transition assumed to be at $T_c=200$ MeV. By comparing the collision entropy density rates of the different processes, we show explicitly that inelastic processes, and \emph{not} elastic processes as is commonly assumed, are dominant in the equilibration of the plasma and that gluon branching leads the other processes in entropy generation. We also show that, within perturbative QCD, processes with higher power in \alpha_s need not be less important for the purpose of equilibration than those with lower power. The state of equilibration of the system has also a role to play. We compare our results with those of the parton cascade model.Comment: 17 pages, revtex+psfig style with 14 embedded postscript figures, to appear in Phys. Rev.

Connecting Numerical Relativity and Data Analysis of Gravitational Wave Detectors

Gravitational waves deliver information in exquisite detail about astrophysical phenomena, among them the collision of two black holes, a system completely invisible to the eyes of electromagnetic telescopes. Models that predict gravitational wave signals from likely sources are crucial for the success of this endeavor. Modeling binary black hole sources of gravitational radiation requires solving the Eintein equations of General Relativity using powerful computer hardware and sophisticated numerical algorithms. This proceeding presents where we are in understanding ground-based gravitational waves resulting from the merger of black holes and the implications of these sources for the advent of gravitational-wave astronomy.Comment: Appeared in the Proceedings of 2014 Sant Cugat Forum on Astrophysics. Astrophysics and Space Science Proceedings, ed. C.Sopuerta (Berlin: Springer-Verlag

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