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First measurement of the Hubble Constant from a Dark Standard Siren using the Dark Energy Survey Galaxies and the LIGO/Virgo Binary–Black-hole Merger GW170814
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µ* masses: weak-lensing calibration of the dark energy survey year 1 redMaPPer clusters using stellar masses
We present the weak-lensing mass calibration of the stellar-mass-based µ mass proxy for redMaPPer galaxy clusters in the Dark Energy Survey Year 1. For the first time, we are able to perform a calibration of µ at high redshifts, z > 0.33. In a blinded analysis, we use ~6000 clusters split into 12 subsets spanning the ranges 0.1 = z < 0.65 and µ up to ~5.5 × 1013 M, and infer the average masses of these subsets through modelling of their stacked weak-lensing signal. In our model, we account for the following sources of systematic uncertainty: shear measurement and photometric redshift errors, miscentring, cluster-member contamination of the source sample, deviations from the Navarro-Frenk-White halo profile, halo triaxiality, and projection effects. We use the inferred masses to estimate the joint mass-µz scaling relation given by M200c|µ, z = M0(µ5.16 × 1012 M)Fµ ((1 + z)/1.35)Gz. We find M0 = (1.14 ± 0.07) × 1014 M with Fµ= 0.76 ± 0.06 and Gz = -1.14 ± 0.37. We discuss the use of µ as a complementary mass proxy to the well-studied richness ? for: (i) exploring the regimes of low z, ? < 20 and high ?, z ~ 1; and (ii) testing systematics such as projection effects for applications in cluster cosmology
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