Pathogenic variants in genes that cause dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM) convey high risks for the development of heart failure through unknown mechanisms. Using single-nucleus RNA sequencing, we characterized the transcriptome of 880,000 nuclei from 18 control and 61 failing, nonischemic human hearts with pathogenic variants in DCM and ACM genes or idiopathic disease. We performed genotype-stratified analyses of the ventricular cell lineages and transcriptional states. The resultant DCM and ACM ventricular cell atlas demonstrated distinct right and left ventricular responses, highlighting genotype-associated pathways, intercellular interactions, and differential gene expression at single-cell resolution. Together, these data illuminate both shared and distinct cellular and molecular architectures of human heart failure and suggest candidate therapeutic targets.

We calculate the decay width and the τ -lepton energy distribution as well as relevant moments for inclusiveB → X c τν τ process including power corrections up to order Λ 3 QCD /m 3 b and QCD corrections to the partonic level. We compare the result with the sum of the standard-model predictions of the branching fractions of the exclusive semileptonic B → (D, D * , D * * )τν τ decays as well as with the relevant experimental data. Our prediction is in agreement with the LEP measurement and is consistent with the standard-model calculation of the exclusive modes. We discuss the impact from physics beyond the Standard Model.

We re-investigate the effects of the 1/mc corrections on the spectrum of the lowest orbitally excited D-meson states. We argue that one should expect the 1/mc corrections to induce a significant mixing between the two lowest lying 1 + states. We discuss the implications of this mixing and compute its effect on the semileptonic decays B → D * * ν and the strong D * * decays.