| 1. |
- Pacaud, F., et al.
(författare)
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The XXL Survey: XXV. Cosmological analysis of the C1 cluster number counts
- 2018
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 620
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Forskningsöversikt (refereegranskat)abstract
- Context. We present an estimation of cosmological parameters with clusters of galaxies. Aims. We constrain the Ωm, σ8, and w parameters from a stand-alone sample of X-ray clusters detected in the 50 deg2 XMM-XXL survey with a well-defined selection function. Methods. We analyse the redshift distribution of a sample comprising 178 high signal-to-noise ratio clusters out to a redshift of unity. The cluster sample scaling relations are determined in a self-consistent manner. Results. In a lambda cold dark matter (ΛCDM) model, the cosmology favoured by the XXL clusters compares well with results derived from the Planck Sunyaev-Zel'dovich clusters for a totally different sample (mass/redshift range, selection biases, and scaling relations). However, with this preliminary sample and current mass calibration uncertainty, we find no inconsistency with the Planck CMB cosmology. If we relax the w parameter, the Planck CMB uncertainties increase by a factor of ~10 and become comparable with those from XXL clusters. Combining the two probes allows us to put constraints on Ωm = 0.316 ± 0.060, σ8 = 0.814 ± 0.054, and w = -1.02 ± 0.20. Conclusions. This first self-consistent cosmological analysis of a sample of serendipitous XMM clusters already provides interesting insights into the constraining power of the XXL survey. Subsequent analysis will use a larger sample extending to lower confidence detections and include additional observable information, potentially improving posterior uncertainties by roughly a factor of 3.
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| 2. |
- Saunders, Charlie N., et al.
(författare)
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Lack of association between modifiable exposures and glioma risk : a Mendelian randomization analysis
- 2020
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Ingår i: Neuro-Oncology. - : OXFORD UNIV PRESS INC. - 1522-8517 .- 1523-5866. ; 22:2, s. 207-215
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Forskningsöversikt (refereegranskat)abstract
- Background. The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (MR) framework to examine if lifestyle, cardiometabolic, and inflammatory factors influence the risk of glioma. This methodology reduces bias from confounding and is not affected by reverse causation. Methods. We identified genetic instruments for 37 potentially modifiable risk factors and evaluated their association with glioma risk using data from a genome-wide association study of 12488 glioma patients and 18169 controls. We used the estimated odds ratio of glioma associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures: Lifestyle and dietary factors-height, plasma insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A; Cardiometabolic factors-birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; and Inflammatory factors- C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E. Results. After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, P-Corrected > 0.05). Conclusions. This study did not provide evidence supporting any of the 37 factors examined as having a significant influence on glioma risk.
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