Big bounce from spin and torsion

The Einstein-Cartan-Sciama-Kibble theory of gravity naturally extends general relativity to account for the intrinsic spin of matter. Spacetime torsion, generated by spin of Dirac fields, induces gravitational repulsion in fermionic matter at extremely high densities and prevents the formation of singularities. Accordingly, the big bang is replaced by a bounce that occurred when the energy density $\epsilon\propto gT^4$ was on the order of $n^2/m_\textrm{Pl}^2$ (in natural units), where $n\propto gT^3$ is the fermion number density and $g$ is the number of thermal degrees of freedom. If the early Universe contained only the known standard-model particles ($g\approx 100$), then the energy density at the big bounce was about 15 times larger than the Planck energy. The minimum scale factor of the Universe (at the bounce) was about $10^{32}$ times smaller than its present value, giving \approx 50 \mum. If more fermions existed in the early Universe, then the spin-torsion coupling causes a bounce at a lower energy and larger scale factor. Recent observations of high-energy photons from gamma-ray bursts indicate that spacetime may behave classically even at scales below the Planck length, supporting the classical spin-torsion mechanism of the big bounce. Such a classical bounce prevents the matter in the contracting Universe from reaching the conditions at which a quantum bounce could possibly occur.Comment: 6 pages; published versio

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