Resonance Superfluidity: Renormalization of Resonance Scattering Theory

We derive a theory of superfluidity for a dilute Fermi gas that is valid when scattering resonances are present. The treatment of a resonance in many-body atomic physics requires a novel mean-field approach starting from an unconventional microscopic Hamiltonian. The mean-field equations incorporate the microscopic scattering physics, and the solutions to these equations reproduce the energy-dependent scattering properties. This theory describes the high-$T_c$ behavior of the system, and predicts a value of $T_c$ which is a significant fraction of the Fermi temperature. It is shown that this novel mean-field approach does not break down for typical experimental circumstances, even at detunings close to resonance. As an example of the application of our theory we investigate the feasibility for achieving superfluidity in an ultracold gas of fermionic $^6$Li.Comment: 15 pages, 10 figure

Early collective expansion: Relativistic hydrodynamics and the transport properties of QCD matter

Relativistic hydrodynamics for ideal and viscous fluids is discussed as a tool to describe relativistic heavy-ion collisions and to extract transport properties of the quark-gluon plasma from experimentally measured hadron momentum spectra.Comment: Review article, 54 pages, 25 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

Hypokalaemic paresis, hypertension, alkalosis and adrenal-dependent hyperadrenocorticism in a dog

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed