147 research outputs found

    The Blackbody Radiation Spectrum Follows from Zero-Point Radiation and the Structure of Relativistic Spacetime in Classical Physics

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    The analysis of this article is entirely within classical physics. Any attempt to describe nature within classical physics requires the presence of Lorentz-invariant classical electromagnetic zero-point radiation so as to account for the Casimir forces between parallel conducting plates at low temperatures. Furthermore, conformal symmetry carries solutions of Maxwell's equations into solutions. In an inertial frame, conformal symmetry leaves zero-point radiation invariant and does not connect it to non-zero-temperature; time-dilating conformal transformations carry the Lorentz-invariant zero-point radiation spectrum into zero-point radiation and carry the thermal radiation spectrum at non-zero temperature into thermal radiation at a different non-zero-temperature. However, in a non-inertial frame, a time-dilating conformal transformation carries classical zero-point radiation into thermal radiation at a finite non-zero-temperature. By taking the no-acceleration limit, one can obtain the Planck radiation spectrum for blackbody radiation in an inertial frame from the thermal radiation spectrum in an accelerating frame. Here this connection between zero-point radiation and thermal radiation is illustrated for a scalar radiation field in a Rindler frame undergoing relativistic uniform proper acceleration through flat spacetime in two spacetime dimensions. The analysis indicates that the Planck radiation spectrum for thermal radiation follows from zero-point radiation and the structure of relativistic spacetime in classical physics.Comment: 21 page

    On slip pulses at a sheared frictional viscoelastic/ non deformable interface

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    We study the possibility for a semi-infinite block of linear viscoelastic material, in homogeneous frictional contact with a non-deformable one, to slide under shear via a periodic set of ``self-healing pulses'', i.e. a set of drifting slip regions separated by stick ones. We show that, contrary to existing experimental indications, such a mode of frictional sliding is impossible for an interface obeying a simple local Coulomb law of solid friction. We then discuss possible physical improvements of the friction model which might open the possibility of such dynamics, among which slip weakening of the friction coefficient, and stress the interest of developing systematic experimental investigations of this question.Comment: 23 pages, 3 figures. submitted to PR

    Variable geometries of connection: Urban digital divides and the uses of Information Technology

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    This paper proposes a new way of conceptualising urban ‘digital divides’. It focuses on the ways in which Information and Communication Technologies (ICTs) unevenly affect the pace of life within the urban environment. Based on a detailed case study of how ICT s are being used in an affluent and a marginalised neighbourhood in Newcastle-upon-Tyne, the paper suggests that urban digital divides need to be understood as more than uneven patterns of access. They emerge in this work as more than the presence or absence of specific technological artefacts. Rather, it is argued that different styles and speeds of technologically mediated life now work to define urban socio-spatial inequalities. The paper distinguishes between two such key styles and speeds. First, the paper argues that affluent and professional groups now use new media technologies pervasively and continuously as the ‘background’ infrastructure to sustain privileged and intensely distanciated, but time-stressed, lifestyles. Second, more marginalised neighbourhoods tend to be characterised by instrumental and episodic ICT usage patterns which are often collectively organised through strong neighbourhood ties. For the former, mediated networks help orchestrate neighbourhood ties; for the latter it is those neighbourhood ties that enable online access

    Predicting stroke through genetic risk functions: the CHARGE Risk Score Project.

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    BACKGROUND AND PURPOSE: Beyond the Framingham Stroke Risk Score, prediction of future stroke may improve with a genetic risk score (GRS) based on single-nucleotide polymorphisms associated with stroke and its risk factors. METHODS: The study includes 4 population-based cohorts with 2047 first incident strokes from 22,720 initially stroke-free European origin participants aged ≥55 years, who were followed for up to 20 years. GRSs were constructed with 324 single-nucleotide polymorphisms implicated in stroke and 9 risk factors. The association of the GRS to first incident stroke was tested using Cox regression; the GRS predictive properties were assessed with area under the curve statistics comparing the GRS with age and sex, Framingham Stroke Risk Score models, and reclassification statistics. These analyses were performed per cohort and in a meta-analysis of pooled data. Replication was sought in a case-control study of ischemic stroke. RESULTS: In the meta-analysis, adding the GRS to the Framingham Stroke Risk Score, age and sex model resulted in a significant improvement in discrimination (all stroke: Δjoint area under the curve=0.016, P=2.3×10(-6); ischemic stroke: Δjoint area under the curve=0.021, P=3.7×10(-7)), although the overall area under the curve remained low. In all the studies, there was a highly significantly improved net reclassification index (P<10(-4)). CONCLUSIONS: The single-nucleotide polymorphisms associated with stroke and its risk factors result only in a small improvement in prediction of future stroke compared with the classical epidemiological risk factors for stroke

    Hadronic contributions to (g2)(g-2) of the leptons and to the effective fine structure constant α(MZ2)\alpha(M_Z^2)

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    The hadronic contributions to the anomalous magnetic moments of the leptons and to the effective fine structure constant at the Z-mass are reevaluated using all presently available e+ee^+ e^- data.Comment: 36 pages, 11 Postscript figures, available at ftp://129.129.40.58/pub/preprints/vapogm2.ps.g

    Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels.

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    Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P<10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P<5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health

    Improving Genetic Prediction by Leveraging Genetic Correlations Among Human Diseases and Traits

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    Genomic prediction has the potential to contribute to precision medicine. However, to date, the utility of such predictors is limited due to low accuracy for most traits. Here theory and simulation study are used to demonstrate that widespread pleiotropy among phenotypes can be utilised to improve genomic risk prediction. We show how a genetic predictor can be created as a weighted index that combines published genome-wide association study (GWAS) summary statistics across many different traits. We apply this framework to predict risk of schizophrenia and bipolar disorder in the Psychiatric Genomics consortium data, finding substantial heterogeneity in prediction accuracy increases across cohorts. For six additional phenotypes in the UK Biobank data, we find increases in prediction accuracy ranging from 0.7 for height to 47 for type 2 diabetes, when using a multi-trait predictor that combines published summary statistics from multiple traits, as compared to a predictor based only on one trait. © 2018 The Author(s)

    Serum magnesium and calcium levels in relation to ischemic stroke : Mendelian randomization study

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    ObjectiveTo determine whether serum magnesium and calcium concentrations are causally associated with ischemic stroke or any of its subtypes using the mendelian randomization approach.MethodsAnalyses were conducted using summary statistics data for 13 single-nucleotide polymorphisms robustly associated with serum magnesium (n = 6) or serum calcium (n = 7) concentrations. The corresponding data for ischemic stroke were obtained from the MEGASTROKE consortium (34,217 cases and 404,630 noncases).ResultsIn standard mendelian randomization analysis, the odds ratios for each 0.1 mmol/L (about 1 SD) increase in genetically predicted serum magnesium concentrations were 0.78 (95% confidence interval [CI] 0.69-0.89; p = 1.3 7 10-4) for all ischemic stroke, 0.63 (95% CI 0.50-0.80; p = 1.6 7 10-4) for cardioembolic stroke, and 0.60 (95% CI 0.44-0.82; p = 0.001) for large artery stroke; there was no association with small vessel stroke (odds ratio 0.90, 95% CI 0.67-1.20; p = 0.46). Only the association with cardioembolic stroke was robust in sensitivity analyses. There was no association of genetically predicted serum calcium concentrations with all ischemic stroke (per 0.5 mg/dL [about 1 SD] increase in serum calcium: odds ratio 1.03, 95% CI 0.88-1.21) or with any subtype.ConclusionsThis study found that genetically higher serum magnesium concentrations are associated with a reduced risk of cardioembolic stroke but found no significant association of genetically higher serum calcium concentrations with any ischemic stroke subtype
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