Warped Entanglement Entropy

We study the applicability of the covariant holographic entanglement entropy proposal to asymptotically warped AdS$_3$ spacetimes with an SL(2,R) x U(1) isometry. We begin by applying the proposal to locally AdS$_3$ backgrounds which are written as a real-line fibration over AdS$_2$. We then perturb away from this geometry by considering a warping parameter $a=1+\delta$ to get an asymptotically warped AdS$_3$ spacetime and compute the dual entanglement entropy perturbatively in $\delta$. We find that for large separation in the fiber coordinate, the entanglement entropy can be computed to all orders in $\delta$ and takes the universal form appropriate for two-dimensional CFTs. The warping-dependent central charge thus identified exactly agrees with previous calculations in the literature. Performing the same perturbative calculations for the warped BTZ black hole again gives universal two-dimensional CFT answers, with the left-moving and right-moving temperatures appearing appropriately in the result.Comment: 25 pages plus appendices; v2 references added, discussions clarified and equations sharpene

Lifshitz black holes in higher spin gravity

We study asymptotically Lifshitz solutions to three dimensional higher spin gravity in the SL(3,R)xSL(3,R) Chern-Simons formulation. We begin by specifying the most general connections satisfying Lifshitz boundary conditions, and we verify that their algebra of symmetries contains a Lifshitz sub-algebra. We then exhibit connections that can be viewed as higher spin Lifshitz black holes. We show that when suitable holonomy conditions are imposed, these black holes obey sensible thermodynamics and possess a gauge in which the corresponding metric exhibits a regular horizon.Comment: 34 pages, LaTeX, 10 figures, v2: minor edits, 2 new reference

Holographic RG-flows and Boundary CFTs

Solutions of $(d+1)$-dimensional gravity coupled to a scalar field are obtained, which holographically realize interface and boundary CFTs. The solution utilizes a Janus-like $\mathrm{AdS}_d$ slicing ansatz and corresponds to a deformation of the CFT by a spatially-dependent coupling of a relevant operator. The BCFT solutions are singular in the bulk, but physical quantities such as the holographic entanglement entropy can be calculated.Comment: 26 pages, 11 figure

The Metabochip, a Custom Genotyping Array for Genetic Studies of Metabolic, Cardiovascular, and Anthropometric Traits

PMCID: PMC3410907This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization.

The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.