Numerical study of pattern formation following a convective instability in non-Boussinesq fluids

We present a numerical study of a model of pattern formation following a convective instability in a non-Boussinesq fluid. It is shown that many of the features observed in convection experiments conducted on $CO_{2}$ gas can be reproduced by using a generalized two-dimensional Swift-Hohenberg equation. The formation of hexagonal patterns, rolls and spirals is studied, as well as the transitions and competition among them. We also study nucleation and growth of hexagonal patterns and find that the front velocity in this two dimensional model is consistent with the prediction of marginal stability theory for one dimensional fronts.Comment: 9 pages, report FSU-SCRI-92-6

Mean flows and the onset of chaos in large-cell convection

Numerical simulations of two-dimensional model equations show that a coupling between amplitude and vertical-vorticity fields allows chaotic flows near the onset of Rayleigh-Bénard convection in large-aspect-ratio domains. In cylindrical cells, mean flows arising from this coupling lead to a chaotic nucleation of dislocations that is remarkably similar to recent observations in convection experiments

Enhancer connectome in primary human cells identifies target genes of disease-associated DNA elements

The challenge of linking intergenic mutations to target genes has limited molecular understanding of human diseases. Here we show that H3K27ac HiChIP generates high-resolution contact maps of active enhancers and target genes in rare primary human T cell subtypes and coronary artery smooth muscle cells. Differentiation of naive T cells into T helper 17 cells or regulatory T cells creates subtype-specific enhancer-promoter interactions, specifically at regions of shared DNA accessibility. These data provide a principled means of assigning molecular functions to autoimmune and cardiovascular disease risk variants, linking hundreds of noncoding variants to putative gene targets. Target genes identified with HiChIP are further supported by CRISPR interference and activation at linked enhancers, by the presence of expression quantitative trait loci, and by allele-specific enhancer loops in patient-derived primary cells. The majority of disease-associated enhancers contact genes beyond the nearest gene in the linear genome, leading to a fourfold increase in the number of potential target genes for autoimmune and cardiovascular diseases