Gauge Independence of the Effective Potential Revisited

We apply the formalism of extended BRS symmetry to the investigation of the gauge dependence of the effective potential in a spontaneously symmetry broken gauge theory. This formalism, which includes a set of Grassmann parameters defined as the BRS variations of the gauge-fixing parameters, allows us to derive in a quick and unambiguous way the related Nielsen identities, which express the physical gauge independence, in a class of generalized 't Hooft gauges, of the effective potential. We show in particular that the validity of the Nielsen identities does not require any constraint on the gauge-fixing parameters, to the contrary of some claims found in the literature. We use the method of algebraic renormalization, which leads to results independent of the particular renormalization scheme used.Comment: 13 pages, no figures, Latex, final version published in NP

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Implications of serial measurements of natriuretic peptides in heart failure: insights from BIOSTAT‐CHF

No abstract available

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

Symanzik–Becchi–Rouet–Stora lessons on renormalizable models with broken symmetry: The case of Lorentz violation

In this paper, we revisit the issue intensively studied in recent years on the generation of terms by radiative corrections in models with broken Lorentz symmetry. The algebraic perturbative method of handling the problem of renormalization of the theories with Lorentz symmetry breaking, is used. We hope to make clear the Symanzik's aphorism: “Whether you like it or not, you have to include in the lagrangian all counter terms consistent with locality and power-counting, unless otherwise constrained by Ward identities.”