433 research outputs found

    The Sloan Digital Sky Survey: The Cosmic Spectrum and Star-Formation History

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    We present a determination of the `Cosmic Optical Spectrum' of the Universe, i.e. the ensemble emission from galaxies, as determined from the red-selected Sloan Digital Sky Survey main galaxy sample and compare with previous results of the blue-selected 2dF Galaxy Redshift Survey. Broadly we find good agreement in both the spectrum and the derived star-formation histories. If we use a power-law star-formation history model where star-formation rate (1+z)β\propto (1+z)^\beta out to z=1, then we find that β\beta of 2 to 3 is still the most likely model and there is no evidence for current surveys missing large amounts of star formation at high redshift. In particular `Fossil Cosmology' of the local universe gives measures of star-formation history which are consistent with direct observations at high redshift. Using the photometry of SDSS we are able to derive the cosmic spectrum in absolute units (i.e.WA˚ W \AA^{-1}Mpc Mpc^{-3})at25A˚resolutionandfindgoodagreementwithpublishedbroadbandluminositydensities.ForaSalpeterIMFthebestfitstellarmass/lightratiois3.77.5) at 2--5\AA resolution and find good agreement with published broad-band luminosity densities. For a Salpeter IMF the best fit stellar mass/light ratio is 3.7--7.5 \Msun/\Lsunintherband(correspondingto in the r-band (corresponding to \omstars h = 0.00250.0055)andfromboththestellaremissionhistoryandtheH--0.0055) and from both the stellar emission history and the H\alphaluminositydensityindependentlywefindacosmologicalstarformationrateof0.030.04h luminosity density independently we find a cosmological star-formation rate of 0.03--0.04 h \Msunyr yr^{-1}Mpc Mpc^{-3}$ today.Comment: 17 pages, 11 figures, ApJ in press (April 10th 2003

    A Powerful Statistical Framework for Generalization Testing in GWAS, with Application to the HCHS/SOL

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    In GWAS, “generalization” is the replication of genotype-phenotype association in a population with different ancestry than the population in which it was first identified. The standard for reporting findings from a GWAS requires a two-stage design, in which discovered associations are replicated in an independent follow-up study. Current practices for declaring generalizations rely on testing associations while controlling the Family Wise Error Rate (FWER) in the discovery study, then separately controlling error measures in the follow-up study. While this approach limits false generalizations, we show that it does not guarantee control over the FWER or False Discovery Rate (FDR) of the generalization null hypotheses. In addition, it fails to leverage the two-stage design to increase power for detecting generalized associations. We develop a formal statistical framework for quantifying the evidence of generalization that accounts for the (in)consistency between the directions of associations in the discovery and follow-up studies. We develop the directional generalization FWER (FWERg) and FDR (FDRg) controlling r-values, which are used to declare associations as generalized. This framework extends to generalization testing when applied to a published list of SNP-trait associations. We show that our framework accommodates various SNP selection rules for generalization testing based on p-values in the discovery study, and still control FWERg or FDRg. A key finding is that it is often beneficial to use a more lenient p-value threshold then the genome-wide significance threshold. For instance, in a GWAS of Total Cholesterol (TC) in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), when testing all SNPs with p-values\u3c 5 × 10−8 (15 genomic regions) for generalization in a large GWAS of whites, we generalized SNPs from 15 regions. But when testing all SNPs with p-values\u3c 6.6×10−5 (89 regions), we generalized SNPs from 27 regions

    Drug-gene interactions of antihypertensive medications and risk of incident cardiovascular disease: a pharmacogenomics study from the CHARGE consortium

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    Background Hypertension is a major risk factor for a spectrum of cardiovascular diseases (CVD), including myocardial infarction, sudden death, and stroke. In the US, over 65 million people have high blood pressure and a large proportion of these individuals are prescribed antihypertensive medications. Although large long-term clinical trials conducted in the last several decades have identified a number of effective antihypertensive treatments that reduce the risk of future clinical complications, responses to therapy and protection from cardiovascular events vary among individuals. Methods Using a genome-wide association study among 21,267 participants with pharmaceutically treated hypertension, we explored the hypothesis that genetic variants might influence or modify the effectiveness of common antihypertensive therapies on the risk of major cardiovascular outcomes. The classes of drug treatments included angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, each study performed array-based genome-wide genotyping, imputed to HapMap Phase II reference panels, and used additive genetic models in proportional hazards or logistic regression models to evaluate drug-gene interactions for each of four therapeutic drug classes. We used meta-analysis to combine study-specific interaction estimates for approximately 2 million single nucleotide polymorphisms (SNPs) in a discovery analysis among 15,375 European Ancestry participants (3,527 CVD cases) with targeted follow-up in a case-only study of 1,751 European Ancestry GenHAT participants as well as among 4,141 African-Americans (1,267 CVD cases). Results Although drug-SNP interactions were biologically plausible, exposures and outcomes were well measured, and power was sufficient to detect modest interactions, we did not identify any statistically significant interactions from the four antihypertensive therapy meta-analyses (Pinteraction > 5.0×10−8). Similarly, findings were null for meta-analyses restricted to 66 SNPs with significant main effects on coronary artery disease or blood pressure from large published genome-wide association studies (Pinteraction ≥ 0.01). Our results suggest that there are no major pharmacogenetic influences of common SNPs on the relationship between blood pressure medications and the risk of incident CVD

    The First Hour of Extra-galactic Data of the Sloan Digital Sky Survey Spectroscopic Commissioning: The Coma Cluster

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    On 26 May 1999, one of the Sloan Digital Sky Survey (SDSS) fiber-fed spectrographs saw astronomical first light. This was followed by the first spectroscopic commissioning run during the dark period of June 1999. We present here the first hour of extra-galactic spectroscopy taken during these early commissioning stages: an observation of the Coma cluster of galaxies. Our data samples the Southern part of this cluster, out to a radius of 1.5degrees and thus fully covers the NGC 4839 group. We outline in this paper the main characteristics of the SDSS spectroscopic systems and provide redshifts and spectral classifications for 196 Coma galaxies, of which 45 redshifts are new. For the 151 galaxies in common with the literature, we find excellent agreement between our redshift determinations and the published values. As part of our analysis, we have investigated four different spectral classification algorithms: spectral line strengths, a principal component decomposition, a wavelet analysis and the fitting of spectral synthesis models to the data. We find that a significant fraction (25%) of our observed Coma galaxies show signs of recent star-formation activity and that the velocity dispersion of these active galaxies (emission-line and post-starburst galaxies) is 30% larger than the absorption-line galaxies. We also find no active galaxies within the central (projected) 200 h-1 Kpc of the cluster. The spatial distribution of our Coma active galaxies is consistent with that found at higher redshift for the CNOC1 cluster survey. Beyond the core region, the fraction of bright active galaxies appears to rise slowly out to the virial radius and are randomly distributed within the cluster with no apparent correlation with the potential merger of the NGC 4839 group. [ABRIDGED]Comment: Accepted in AJ, 65 pages, 20 figures, 5 table

    Separated Response Function Ratios in Exclusive, Forward pi^{+/-} Electroproduction

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    The study of exclusive π±\pi^{\pm} electroproduction on the nucleon, including separation of the various structure functions, is of interest for a number of reasons. The ratio RL=σLπ/σLπ+R_L=\sigma_L^{\pi^-}/\sigma_L^{\pi^+} is sensitive to isoscalar contamination to the dominant isovector pion exchange amplitude, which is the basis for the determination of the charged pion form factor from electroproduction data. A change in the value of RT=σTπ/σTπ+R_T=\sigma_T^{\pi^-}/\sigma_T^{\pi^+} from unity at small t-t, to 1/4 at large t-t, would suggest a transition from coupling to a (virtual) pion to coupling to individual quarks. Furthermore, the mentioned ratios may show an earlier approach to pQCD than the individual cross sections. We have performed the first complete separation of the four unpolarized electromagnetic structure functions above the dominant resonances in forward, exclusive π±\pi^{\pm} electroproduction on the deuteron at central Q2Q^2 values of 0.6, 1.0, 1.6 GeV2^2 at WW=1.95 GeV, and Q2=2.45Q^2=2.45 GeV2^2 at WW=2.22 GeV. Here, we present the LL and TT cross sections, with emphasis on RLR_L and RTR_T, and compare them with theoretical calculations. Results for the separated ratio RLR_L indicate dominance of the pion-pole diagram at low t-t, while results for RTR_T are consistent with a transition between pion knockout and quark knockout mechanisms.Comment: 6 pages, 3 figure

    Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae

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    Although the association between cigarette smoking and atherosclerosis is well established, the mechanisms by which smoking initiates vascular disease remain poorly understood. As heritable differences in DNA repair ability can influence the effect of environmental exposures such as cigarette smoke, we evaluated how 36 DNA repair variants from five genes (XRCC1, APEX1, hOgg1, XPD, and XRCC3) modified the association between ever-smoking and two atherosclerosis outcomes in Atherosclerosis Risk in Communities (ARIC) Study participants: intimal-medial thickness (IMT) and incident coronary heart disease (CHD). The incident CHD analysis was conducted using all cases 1987-1998 (N=1,086) and a random sample (N=1,065) selected from the entire ARIC cohort at baseline (cohort random sample, CRS). Incidence rate ratios were estimated by piecewise constant models and departures from additivity were measured with interaction contrast ratios. When priors for genetic and environmental effects were added to the first-stage model, tagSNPs rs3213282 (XRCC1), rs50871 (XPD), and rs3212024 (XRCC3) were associated with an increase in the estimated effect of ever-smoking on incident CHD while tagSNPs rs1799782 (XRCC1) and rs861531 (XRCC3) were associated with a decrease. We also evaluated the association between DNA repair variants, cigarette smoking, and baseline mean IMT using linear regression models in ARIC participants selected into the CRS. When priors for genetic and environmental effects were added to the first-stage linear regression model, tagSNPs rs3213282 (XRCC1), rs3213245 (XRCC1), rs3212024 (XRCC3), and rs3136814 (APEX1) were associated with increases in the estimated effect of ever-smoking on baseline mean IMT while tagSNPs rs3136817 (APEX1) and rs1799794 (XRCC3) were associated with decreases. Few population-based studies examining the relationship between DNA repair variants, cigarette smoking and atherosclerosis have been published. Our results can stimulate inquiries into potential mechanisms linking cigarette smoke exposure and atherosclerotic diseases and help bridge the gap between observed trends and CHD biology. Future studies in different populations will undoubtedly be required to validate our results and improve our understanding of the complex relationships between DNA repair variants, cigarette smoking, and atherothrombotic disease

    Charged pion form factor between Q^2=0.60 and 2.45 GeV^2. II. Determination of, and results for, the pion form factor

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    The charged pion form factor, Fpi(Q^2), is an important quantity which can be used to advance our knowledge of hadronic structure. However, the extraction of Fpi from data requires a model of the 1H(e,e'pi+)n reaction, and thus is inherently model dependent. Therefore, a detailed description of the extraction of the charged pion form factor from electroproduction data obtained recently at Jefferson Lab is presented, with particular focus given to the dominant uncertainties in this procedure. Results for Fpi are presented for Q^2=0.60-2.45 GeV^2. Above Q^2=1.5 GeV^2, the Fpi values are systematically below the monopole parameterization that describes the low Q^2 data used to determine the pion charge radius. The pion form factor can be calculated in a wide variety of theoretical approaches, and the experimental results are compared to a number of calculations. This comparison is helpful in understanding the role of soft versus hard contributions to hadronic structure in the intermediate Q^2 regime.Comment: 18 pages, 11 figure

    Measurements of electron-proton elastic cross sections for 0.4<Q2<5.5(GeV/c)20.4 < Q^2 < 5.5 (GeV/c)^2

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    We report on precision measurements of the elastic cross section for electron-proton scattering performed in Hall C at Jefferson Lab. The measurements were made at 28 unique kinematic settings covering a range in momentum transfer of 0.4 << Q2Q^2 << 5.5 (GeV/c)2(\rm GeV/c)^2. These measurements represent a significant contribution to the world's cross section data set in the Q2Q^2 range where a large discrepancy currently exists between the ratio of electric to magnetic proton form factors extracted from previous cross section measurements and that recently measured via polarization transfer in Hall A at Jefferson Lab.Comment: 17 pages, 18 figures; text added, some figures replace

    Colors of 2625 Quasars at 0<z<5 Measured in the Sloan Digital Sky Survey Photometric System

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    We present an empirical investigation of the colors of quasars in the Sloan Digital Sky Survey (SDSS) photometric system. The sample studied includes 2625 quasars with SDSS photometry. The quasars are distributed in a 2.5 degree wide stripe centered on the Celestial Equator covering 529\sim529 square degrees. Positions and SDSS magnitudes are given for the 898 quasars known prior to SDSS spectroscopic commissioning. New SDSS quasars represent an increase of over 200% in the number of known quasars in this area of the sky. The ensemble average of the observed colors of quasars in the SDSS passbands are well represented by a power-law continuum with αν=0.5\alpha_{\nu} = -0.5 (fνναf_{\nu} \propto \nu^{\alpha}). However, the contributions of the 3000A˚3000 {\rm \AA} bump and other strong emission lines have a significant effect upon the colors. The color-redshift relation exhibits considerable structure, which may be of use in determining photometric redshifts for quasars. The range of colors can be accounted for by a range in the optical spectral index with a distribution αν=0.5±0.65\alpha_{\nu}=-0.5\pm0.65 (95% confidence), but there is a red tail in the distribution. This tail may be a sign of internal reddening. Finally, we show that there is a continuum of properties between quasars and Seyfert galaxies and we test the validity of the traditional division between the two classes of AGN.Comment: 66 pages, 15 figures (3 color), accepted by A
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