Dispersion of Ordered Stripe Phases in the Cuprates

A phase separation model is presented for the stripe phase of the cuprates, which allows the doping dependence of the photoemission spectra to be calculated. The idealized limit of a well-ordered array of magnetic and charged stripes is analyzed, including effects of long-range Coulomb repulsion. Remarkably, down to the limit of two-cell wide stripes, the dispersion can be interpreted as essentially a superposition of the two end-phase dispersions, with superposed minigaps associated with the lattice periodicity. The largest minigap falls near the Fermi level; it can be enhanced by proximity to a (bulk) Van Hove singularity. The calculated spectra are dominated by two features -- this charge stripe minigap plus the magnetic stripe Hubbard gap. There is a strong correlation between these two features and the experimental photoemission results of a two-peak dispersion in La$_{2-x}$Sr$_x$CuO$_4$, and the peak-dip-hump spectra in Bi$_2$Sr$_2$CaCu$_2$O$_{8+\delta}$. The differences are suggestive of the role of increasing stripe fluctuations. The 1/8 anomaly is associated with a quantum critical point, here expressed as a percolation-like crossover. A model is proposed for the limiting minority magnetic phase as an isolated two-leg ladder.Comment: 24 pages, 26 PS figure

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

On the design of optimization strategies based on global response surface approximation models

Striking the correct balance between global exploration of search spaces and local exploitation of promising basins of attraction is one of the principal concerns in the design of global optimization algorithms. This is true in the case of techniques based on global response surface approximation models as well. After constructing such a model using some initial database of designs it is far from obvious how to select further points to examine so that the appropriate mix of exploration and exploitation is achieved. In this paper we propose a selection criterion based on the expected improvement measure, which allows relatively precise control of the scope of the search. We investigate its behavior through a set of artificial test functions and two structural optimization problems. We also look at another aspect of setting up search heuristics of this type: the choice of the size of the database that the initial approximation is built upon