Continuity of the Maximum-Entropy Inference

We study the inverse problem of inferring the state of a finite-level quantum system from expected values of a fixed set of observables, by maximizing a continuous ranking function. We have proved earlier that the maximum-entropy inference can be a discontinuous map from the convex set of expected values to the convex set of states because the image contains states of reduced support, while this map restricts to a smooth parametrization of a Gibbsian family of fully supported states. Here we prove for arbitrary ranking functions that the inference is continuous up to boundary points. This follows from a continuity condition in terms of the openness of the restricted linear map from states to their expected values. The openness condition shows also that ranking functions with a discontinuous inference are typical. Moreover it shows that the inference is continuous in the restriction to any polytope which implies that a discontinuity belongs to the quantum domain of non-commutative observables and that a geodesic closure of a Gibbsian family equals the set of maximum-entropy states. We discuss eight descriptions of the set of maximum-entropy states with proofs of accuracy and an analysis of deviations.Comment: 34 pages, 1 figur

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