3,043 research outputs found

    Equation of state for β\beta-stable hot nuclear matter

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    We provide an equation of state for hot nuclear matter in β\beta-equilibrium by applying a momentum-dependent effective interaction. We focus on the study of the equation of state of high-density and high-temperature nuclear matter, containing leptons (electrons and muons) under the chemical equilibrium condition in which neutrinos have left the system. The conditions of charge neutrality and equilibrium under β\beta-decay process lead first to the evaluation of proton and lepton fractions and afterwards of internal energy, free energy, pressure and in total to the equation of state of hot nuclear matter. Thermal effects on the properties and equation of state of nuclear matter are assesed and analyzed in the framework of the proposed effective interaction model. Special attention is dedicated to the study of the contribution of the components of β\beta-stable nuclear matter to the entropy per particle, a quantity of great interest for the study of structure and collapse of supernova.Comment: 28 pages, 18 figure

    Worldwide spreading of economic crisis

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    We model the spreading of a crisis by constructing a global economic network and applying the Susceptible-Infected-Recovered (SIR) epidemic model with a variable probability of infection. The probability of infection depends on the strength of economic relations between the pair of countries, and the strength of the target country. It is expected that a crisis which originates in a large country, such as the USA, has the potential to spread globally, like the recent crisis. Surprisingly we show that also countries with much lower GDP, such as Belgium, are able to initiate a global crisis. Using the {\it k}-shell decomposition method to quantify the spreading power (of a node), we obtain a measure of ``centrality'' as a spreader of each country in the economic network. We thus rank the different countries according to the shell they belong to, and find the 12 most central countries. These countries are the most likely to spread a crisis globally. Of these 12 only six are large economies, while the other six are medium/small ones, a result that could not have been otherwise anticipated. Furthermore, we use our model to predict the crisis spreading potential of countries belonging to different shells according to the crisis magnitude.Comment: 13 pages, 4 figures and Supplementary Materia

    Coordination Specification for Distributed Optimal System Design Using the Chi Language

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76202/1/AIAA-2002-5410-847.pd

    Coordination Specification of the Analytical Target Cascading Process using the Chi Language

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76587/1/AIAA-2002-5637-610.pd

    Counting nodal domains on surfaces of revolution

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    We consider eigenfunctions of the Laplace-Beltrami operator on special surfaces of revolution. For this separable system, the nodal domains of the (real) eigenfunctions form a checker-board pattern, and their number νn\nu_n is proportional to the product of the angular and the "surface" quantum numbers. Arranging the wave functions by increasing values of the Laplace-Beltrami spectrum, we obtain the nodal sequence, whose statistical properties we study. In particular we investigate the distribution of the normalized counts νnn\frac{\nu_n}{n} for sequences of eigenfunctions with KnK+ΔKK \le n\le K + \Delta K where K,ΔKNK,\Delta K \in \mathbb{N}. We show that the distribution approaches a limit as K,ΔKK,\Delta K\to\infty (the classical limit), and study the leading corrections in the semi-classical limit. With this information, we derive the central result of this work: the nodal sequence of a mirror-symmetric surface is sufficient to uniquely determine its shape (modulo scaling).Comment: 36 pages, 8 figure

    Pharmacological screening using an FXN-EGFP cellular genomic reporter assay for the therapy of Friedreich ataxia

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    Copyright @ 2013 Li et al. This 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.Friedreich ataxia (FRDA) is an autosomal recessive disorder characterized by neurodegeneration and cardiomyopathy. The presence of a GAA trinucleotide repeat expansion in the first intron of the FXN gene results in the inhibition of gene expression and an insufficiency of the mitochondrial protein frataxin. There is a correlation between expansion length, the amount of residual frataxin and the severity of disease. As the coding sequence is unaltered, pharmacological up-regulation of FXN expression may restore frataxin to therapeutic levels. To facilitate screening of compounds that modulate FXN expression in a physiologically relevant manner, we established a cellular genomic reporter assay consisting of a stable human cell line containing an FXN-EGFP fusion construct, in which the EGFP gene is fused in-frame with the entire normal human FXN gene present on a BAC clone. The cell line was used to establish a fluorometric cellular assay for use in high throughput screening (HTS) procedures. A small chemical library containing FDA-approved compounds and natural extracts was screened and analyzed. Compound hits identified by HTS were further evaluated by flow cytometry in the cellular genomic reporter assay. The effects on FXN mRNA and frataxin protein levels were measured in lymphoblast and fibroblast cell lines derived from individuals with FRDA and in a humanized GAA repeat expansion mouse model of FRDA. Compounds that were established to increase FXN gene expression and frataxin levels included several anti-cancer agents, the iron-chelator deferiprone and the phytoalexin resveratrol.Muscular Dystrophy Association (USA), the National Health and Medical Research Council (Australia), the Friedreich’s Ataxia Research Alliance (USA), the Brockhoff Foundation (Australia), the Friedreich Ataxia Research Association (Australasia), Seek A Miracle (USA) and the Victorian Government’s Operational Infrastructure Support Program

    Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms

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    Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms
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