25 research outputs found

    Stripes in cuprate superconductors: Excitations and dynamic dichotomy

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    We present a short account of the present experimental situation of stripes in cuprates followed by a review of our present understanding of their ground state and excited state properties. Collective modes, the dynamical structure factor, and the optical conductivity of stripes are computed using the time-dependent Gutzwiller approximation applied to realistic one band and three band Hubbard models, and are found to be in excellent agreement with experiment. On the other hand, experiments like angle-resolved photoemission and scanning tunneling microscopy show the coexistence of stripes at high energies with Fermi liquid quasiparticles at low energies. We show that a phenomenological model going beyond mean-field can reconcile this dynamic dichotomy.Comment: 20 pages, 14 figures. Review paper for a Special Issue of Physica C on "Stripes and Electronic Liquid Crystals in Strongly Correlated Systems

    De novo mutations in histone modifying genes in congenital heart disease

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    Congenital heart disease (CHD) is the most frequent birth defect, affecting 0.8% of live births1. Many cases occur sporadically and impair reproductive fitness, suggesting a role for de novo mutations. By analysis of exome sequencing of parent-offspring trios, we compared the incidence of de novo mutations in 362 severe CHD cases and 264 controls. CHD cases showed a significant excess of protein-altering de novo mutations in genes expressed in the developing heart, with an odds ratio of 7.5 for damaging mutations. Similar odds ratios were seen across major classes of severe CHD. We found a marked excess of de novo mutations in genes involved in production, removal or reading of H3K4 methylation (H3K4me), or ubiquitination of H2BK120, which is required for H3K4 methylation2–4. There were also two de novo mutations in SMAD2; SMAD2 signaling in the embryonic left-right organizer induces demethylation of H3K27me5. H3K4me and H3K27me mark `poised' promoters and enhancers that regulate expression of key developmental genes6. These findings implicate de novo point mutations in several hundred genes that collectively contribute to ~10% of severe CHD
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