83 research outputs found
Light Propagation and Large-Scale Inhomogeneities
We consider the effect on the propagation of light of inhomogeneities with
sizes of order 10 Mpc or larger. The Universe is approximated through a
variation of the Swiss-cheese model. The spherical inhomogeneities are
void-like, with central underdensities surrounded by compensating overdense
shells. We study the propagation of light in this background, assuming that the
source and the observer occupy random positions, so that each beam travels
through several inhomogeneities at random angles. The distribution of
luminosity distances for sources with the same redshift is asymmetric, with a
peak at a value larger than the average one. The width of the distribution and
the location of the maximum increase with increasing redshift and length scale
of the inhomogeneities. We compute the induced dispersion and bias on
cosmological parameters derived from the supernova data. They are too small to
explain the perceived acceleration without dark energy, even when the length
scale of the inhomogeneities is comparable to the horizon distance. Moreover,
the dispersion and bias induced by gravitational lensing at the scales of
galaxies or clusters of galaxies are larger by at least an order of magnitude.Comment: 27 pages, 9 figures, revised version to appear in JCAP, analytical
estimate included, typos correcte
Correspondence between kinematical backreaction and scalar field cosmologies - the `morphon field'
Spatially averaged inhomogeneous cosmologies in classical general relativity
can be written in the form of effective Friedmann equations with sources that
include backreaction terms. In this paper we propose to describe these
backreaction terms with the help of a homogeneous scalar field evolving in a
potential; we call it the `morphon field'. This new field links classical
inhomogeneous cosmologies to scalar field cosmologies, allowing to reinterpret,
e.g., quintessence scenarios by routing the physical origin of the scalar field
source to inhomogeneities in the Universe. We investigate a one-parameter
family of scaling solutions to the backreaction problem. Subcases of these
solutions (all without an assumed cosmological constant) include
scale-dependent models with Friedmannian kinematics that can mimic the presence
of a cosmological constant or a time-dependent cosmological term. We explicitly
reconstruct the scalar field potential for the scaling solutions, and discuss
those cases that provide a solution to the Dark Energy and coincidence
problems. In this approach, Dark Energy emerges from morphon fields, a
mechanism that can be understood through the proposed correspondence: the
averaged cosmology is characterized by a weak decay (quintessence) or growth
(phantom quintessence) of kinematical fluctuations, fed by `curvature energy'
that is stored in the averaged 3-Ricci curvature. We find that the late-time
trajectories of those models approach attractors that lie in the future of a
state that is predicted by observational constraints.Comment: 36 pages and 6 Figures, matches published version in Class.Quant.Gra
The Effect of Large-Scale Inhomogeneities on the Luminosity Distance
We study the form of the luminosity distance as a function of redshift in the
presence of large scale inhomogeneities, with sizes of order 10 Mpc or larger.
We approximate the Universe through the Swiss-cheese model, with each spherical
region described by the Tolman-Bondi metric. We study the propagation of light
beams in this background, assuming that the locations of the source and the
observer are random. We derive the optical equations for the evolution of the
beam area and shear. Through their integration we determine the configurations
that can lead to an increase of the luminosity distance relative to the
homogeneous cosmology. We find that this can be achieved if the Universe is
composed of spherical void-like regions, with matter concentrated near their
surface. For inhomogeneities consistent with the observed large scale
structure, the relative increase of the luminosity distance is of the order of
a few percent at redshifts near 1, and falls short of explaining the
substantial increase required by the supernova data. On the other hand, the
effect we describe is important for the correct determination of the energy
content of the Universe from observations.Comment: 27 pages, 5 figures Revised version. References added. Conclusions
clarifie
Accelerated expansion from structure formation
We discuss the physics of backreaction-driven accelerated expansion. Using
the exact equations for the behaviour of averages in dust universes, we explain
how large-scale smoothness does not imply that the effect of inhomogeneity and
anisotropy on the expansion rate is small. We demonstrate with an analytical
toy model how gravitational collapse can lead to acceleration. We find that the
conjecture of the accelerated expansion being due to structure formation is in
agreement with the general observational picture of structures in the universe,
and more quantitative work is needed to make a detailed comparison.Comment: 44 pages, 1 figure. Expanded treatment of topics from the Gravity
Research Foundation contest essay astro-ph/0605632. v2: Added references,
clarified wordings. v3: Published version. Minor changes and corrections,
added a referenc
The Fourteenth Data Release of the Sloan Digital Sky Survey: First Spectroscopic Data from the Extended Baryon Oscillation Spectroscopic Survey and from the Second Phase of the Apache Point Observatory Galactic Evolution Experiment
The fourth generation of the Sloan Digital Sky Survey (SDSS-IV) has been in operation since 2014 July. This paper describes the second data release from this phase, and the 14th from SDSS overall (making this Data Release Fourteen or DR14). This release makes the data taken by SDSS-IV in its first two years of operation (2014–2016 July) public. Like all previous SDSS releases, DR14 is cumulative, including the most recent reductions and calibrations of all data taken by SDSS since the first phase began operations in 2000. New in DR14 is the first public release of data from the extended Baryon Oscillation Spectroscopic Survey; the first data from the second phase of the Apache Point Observatory (APO) Galactic Evolution Experiment (APOGEE-2), including stellar parameter estimates from an innovative data-driven machine-learning algorithm known as "The Cannon"; and almost twice as many data cubes from the Mapping Nearby Galaxies at APO (MaNGA) survey as were in the previous release (N = 2812 in total). This paper describes the location and format of the publicly available data from the SDSS-IV surveys. We provide references to the important technical papers describing how these data have been taken (both targeting and observation details) and processed for scientific use. The SDSS web site (www.sdss.org) has been updated for this release and provides links to data downloads, as well as tutorials and examples of data use. SDSS-IV is planning to continue to collect astronomical data until 2020 and will be followed by SDSS-V
Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis.
BACKGROUND: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. RESULTS: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3-5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. CONCLUSIONS: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk
Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis
Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk
Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis
Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe
Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis
Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD
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