13 research outputs found

    The New Look pMSSM with Neutralino and Gravitino LSPs

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    The pMSSM provides a broad perspective on SUSY phenomenology. In this paper we generate two new, very large, sets of pMSSM models with sparticle masses extending up to 4 TeV, where the lightest supersymmetric particle (LSP) is either a neutralino or gravitino. The existence of a gravitino LSP necessitates a detailed study of its cosmological effects and we find that Big Bang Nucleosynthesis places strong constraints on this scenario. Both sets are subjected to a global set of theoretical, observational and experimental constraints resulting in a sample of \sim 225k viable models for each LSP type. The characteristics of these two model sets are briefly compared. We confront the neutralino LSP model set with searches for SUSY at the 7 TeV LHC using both the missing (MET) and non-missing ET ATLAS analyses. In the MET case, we employ Monte Carlo estimates of the ratios of the SM backgrounds at 7 and 8 TeV to rescale the 7 TeV data-driven ATLAS backgrounds to 8 TeV. This allows us to determine the pMSSM parameter space coverage for this collision energy. We find that an integrated luminosity of \sim 5-20 fb^{-1} at 8 TeV would yield a substantial increase in this coverage compared to that at 7 TeV and can probe roughly half of the model set. If the pMSSM is not discovered during the 8 TeV run, then our model set will be essentially void of gluinos and lightest first and second generation squarks that are \lesssim 700-800 GeV, which is much less than the analogous mSUGRA bound. Finally, we demonstrate that non-MET SUSY searches continue to play an important role in exploring the pMSSM parameter space. These two pMSSM model sets can be used as the basis for investigations for years to come.Comment: 54 pages, 22 figures; typos fixed, references adde

    Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies

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    Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [rg], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (rgs = −0.19 to −0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors. © 2020 Society for the Study of Addictio

    Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa

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    Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness1, affecting 0.9–4% of women and 0.3% of men2–4, with twin-based heritability estimates of 50–60%5. Mortality rates are higher than those in other psychiatric disorders6, and outcomes are unacceptably poor7. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)8,9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes. © 2019, The Author(s), under exclusive licence to Springer Nature America, Inc

    Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa.

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    Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness <sup>1</sup> , affecting 0.9-4% of women and 0.3% of men <sup>2-4</sup> , with twin-based heritability estimates of 50-60% <sup>5</sup> . Mortality rates are higher than those in other psychiatric disorders <sup>6</sup> , and outcomes are unacceptably poor <sup>7</sup> . Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI) <sup>8,9</sup> and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes

    Social Work Practice With Homeless Persons: State of the Art

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