Abstract polymer models with general pair interactions

A convergence criterion of cluster expansion is presented in the case of an abstract polymer system with general pair interactions (i.e. not necessarily hard core or repulsive). As a concrete example, the low temperature disordered phase of the BEG model with infinite range interactions, decaying polynomially as $1/r^{d+\lambda}$ with $\lambda>0$, is studied.Comment: 19 pages. Corrected statement for the stability condition (2.3) and modified section 3.1 of the proof of theorem 1 consistently with (2.3). Added a reference and modified a sentence at the end of sec. 2.

A note on cluster expansions, tree graph identities, extra 1/ N ! factors!!!

We draw attention to a new tree graph identity which substantially improves on the usual tree graph method of proving convergence of cluster expansions in statistical mechanics and quantum field theory. We can control expansions that could not be controlled before.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43217/1/11005_2004_Article_BF00420041.pd

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

Universality of the Hall Conductivity in Interacting Electron Systems

We prove the quantization of the Hall conductivity for general weakly interacting gapped fermionic systems on two-dimensional periodic lattices. The proof is based on fermionic cluster expansion techniques combined with lattice Ward identities, and on a reconstruction theorem that allows us to compute the Kubo conductivity as the analytic continuation of its imaginary time counterpart