On the derived category of a regular toric scheme

Let X be a quasi-compact scheme, equipped with an open covering by affine schemes. A quasi-coherent sheaf on X gives rise, by taking sections over the covering sets, to a diagram of modules over the various coordinate rings. The resulting "twisted" diagram of modules satisfies a certain gluing condition, stating that the data is compatible with restriction to smaller open sets. In case X is a regular toric scheme over an arbitrary commutative ring, we prove that the unbounded derived category D(X) of quasi-coherent sheaves on X can be obtained from a category of twisted diagrams which do not necessarily satisfy any gluing condition by inverting maps which induce homology isomorphisms on hyper-derived inverse limits. Moreover, we given an explicit construction of a finite set of weak generators for the derived category. For example, if X is projective n-space then D(X) is generated by n+1 successive twists of the structure sheaf; the present paper gives a new homotopy-theoretic proof of this classical result. The approach taken uses the language of model categories, and the machinery of Bousfield-Hirschhorn colocalisation. The first step is to characterise colocal objects; these turn out to be homotopy sheaves in the sense that chain complexes over different open sets agree on intersections up to quasi-isomorphism only. In a second step it is shown that the homotopy category of homotopy sheaves is the derived category of X.Comment: 35 pages; diagrams need post script viewer or PDF v2: removed "completeness" assumption, changed titl

Homotopy Theoretic Models of Type Theory

We introduce the notion of a logical model category which is a Quillen model category satisfying some additional conditions. Those conditions provide enough expressive power that one can soundly interpret dependent products and sums in it. On the other hand, those conditions are easy to check and provide a wide class of models some of which are listed in the paper.Comment: Corrected version of the published articl

A model structure for coloured operads in symmetric spectra

We describe a model structure for coloured operads with values in the category of symmetric spectra (with the positive model structure), in which fibrations and weak equivalences are defined at the level of the underlying collections. This allows us to treat R-module spectra (where R is a cofibrant ring spectrum) as algebras over a cofibrant spectrum-valued operad with R as its first term. Using this model structure, we give suficient conditions for homotopical localizations in the category of symmetric spectra to preserve module structures.Comment: 16 page

The stack of Yang-Mills fields on Lorentzian manifolds

We provide an abstract definition and an explicit construction of the stack of non-Abelian Yang-Mills fields on globally hyperbolic Lorentzian manifolds. We also formulate a stacky version of the Yang-Mills Cauchy problem and show that its well-posedness is equivalent to a whole family of parametrized PDE problems. Our work is based on the homotopy theoretical approach to stacks proposed in [S. Hollander, Israel J. Math. 163, 93-124 (2008)], which we shall extend by further constructions that are relevant for our purposes. In particular, we will clarify the concretification of mapping stacks to classifying stacks such as BGcon

Relative Artin motives and the reductive Borel-Serre compactification of a locally symmetric variety

We introduce the notion of Artin motives and cohomological motives over a scheme X. Given a cohomological motive M over X, we consider the universal Artin motive mapping to M and denote it ω0X(M). We use this to define a motive

Blood Leukocyte DNA Methylation Predicts Risk of Future Myocardial Infarction and Coronary Heart Disease

BACKGROUND: DNA methylation is implicated in coronary heart disease (CHD), but current evidence is based on small, cross-sectional studies. We examined blood DNA methylation in relation to incident CHD across multiple prospective cohorts. METHODS: Nine population-based cohorts from the United States and Europe profiled epigenome-wide blood leukocyte DNA methylation using the Illumina Infinium 450k microarray, and prospectively ascertained CHD events including coronary insufficiency/unstable angina, recognized myocardial infarction, coronary revascularization, and coronary death. Cohorts conducted race-specific analyses adjusted for age, sex, smoking, education, body mass index, blood cell type proportions, and technical variables. We conducted fixed-effect meta-analyses across cohorts. RESULTS: Among 11 461 individuals (mean age 64 years, 67% women, 35% African American) free of CHD at baseline, 1895 developed CHD during a mean follow-up of 11.2 years. Methylation levels at 52 CpG (cytosine-phosphate-guanine) sites were associated with incident CHD or myocardial infarction (false discovery rate<0.05). These CpGs map to genes with key roles in calcium regulation (ATP2B2, CASR, GUCA1B, HPCAL1), and genes identified in genome- and epigenome-wide studies of serum calcium (CASR), serum calcium-related risk of CHD (CASR), coronary artery calcified plaque (PTPRN2), and kidney function (CDH23, HPCAL1), among others. Mendelian randomization analyses supported a causal effect of DNA methylation on incident CHD; these CpGs map to active regulatory regions proximal to long non-coding RNA transcripts. CONCLUSION: Methylation of blood-derived DNA is associated with risk of future CHD across diverse populations and may serve as an informative tool for gaining further insight on the development of CHD

The Influence of Age and Sex on Genetic Associations with Adult Body Size and Shape : A Large-Scale Genome-Wide Interaction Study

Genome-wide association studies (GWAS) have identified more than 100 genetic variants contributing to BMI, a measure of body size, or waist-to-hip ratio (adjusted for BMI, WHRadjBMI), a measure of body shape. Body size and shape change as people grow older and these changes differ substantially between men and women. To systematically screen for age-and/or sex-specific effects of genetic variants on BMI and WHRadjBMI, we performed meta-analyses of 114 studies (up to 320,485 individuals of European descent) with genome-wide chip and/or Metabochip data by the Genetic Investigation of Anthropometric Traits (GIANT) Consortium. Each study tested the association of up to similar to 2.8M SNPs with BMI and WHRadjBMI in four strata (men 50y, women 50y) and summary statistics were combined in stratum-specific meta-analyses. We then screened for variants that showed age-specific effects (G x AGE), sex-specific effects (G x SEX) or age-specific effects that differed between men and women (G x AGE x SEX). For BMI, we identified 15 loci (11 previously established for main effects, four novel) that showed significant (FDR= 50y). No sex-dependent effects were identified for BMI. For WHRadjBMI, we identified 44 loci (27 previously established for main effects, 17 novel) with sex-specific effects, of which 28 showed larger effects in women than in men, five showed larger effects in men than in women, and 11 showed opposite effects between sexes. No age-dependent effects were identified for WHRadjBMI. This is the first genome-wide interaction meta-analysis to report convincing evidence of age-dependent genetic effects on BMI. In addition, we confirm the sex-specificity of genetic effects on WHRadjBMI. These results may providefurther insights into the biology that underlies weight change with age or the sexually dimorphism of body shape.Peer reviewe