524 research outputs found

    The geometry of sound rays in a wind

    Full text link
    We survey the close relationship between sound and light rays and geometry. In the case where the medium is at rest, the geometry is the classical geometry of Riemann. In the case where the medium is moving, the more general geometry known as Finsler geometry is needed. We develop these geometries ab initio, with examples, and in particular show how sound rays in a stratified atmosphere with a wind can be mapped to a problem of circles and straight lines.Comment: Popular review article to appear in Contemporary Physic

    Traffic Noise and the Hyperbolic Plane

    Full text link
    We consider the problem of sound propagation in a wind. We note that the rays, as in the absence of a wind, are given by Fermat's principle and show how to map them to the trajectories of a charged particle moving in a magnetic field on a curved space. For the specific case of sound propagating in a stratified atmosphere with a small wind speed we show that the corresponding particle moves in a constant magnetic field on the hyperbolic plane. In this way we give a simple `straightedge and compass' method to estimate the intensity of sound upwind and downwind. We construct Mach envelopes for moving sources. Finally, we relate the problem to that of finding null geodesics in a squashed anti-de Sitter spacetime and discuss the SO(3,1)×RSO(3,1)\times \mathbb{R} symmetry of the problem from this point of view.Comment: Typos correcte

    Circulating microRNA changes in patients with impaired glucose regulation

    Get PDF
    © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. We analysed if levels of four miRNAs would change after a lifestyle intervention involving dietary and exercises in prediabetes. MiRNAs previously shown to be associated with diabetes (Let-7a, Let-7e, miR-144 and miR-92a) were extracted from serum pre- and post-intervention. mRNA was extracted from fat-tissue for gene expression analyses. The intervention resulted in increased Let-7a and miR-92a. We found correlations between miRNAs and clinical variables (triglycerides, cholesterol, insulin, weight and BMI). We also found correlations between miRNAs and target genes, revealing a link between miR-92a and IGF system. A lifestyle intervention resulted in marked changes in miRNAs. The association of miRNAs with insulin and the IGF system (both receptors and binding proteins) may represent a mechanism of regulating IGFs metabolic actions

    Retailing in the United Kingdom - a synopsis

    Get PDF
    This paper illustrates the structure of, and trends in, the retail market of the United Kingdom (UK). This industry analysis describes the retail environment compared to continental Europe and considers the regulatory issues which have helped form this retail environment. By using secondary data we describe concentration and consolidation tendencies and explain specific features of the UK retail market. Major trends are identified and discussed, concluding with an outlook on future developments

    Expansion and further delineation of the SETD5 phenotype leading to global developmental delay, variable dysmorphic features, and reduced penetrance

    Get PDF
    Diagnostic exome sequencing (DES) has aided delineation of the phenotypic spectrum of rare genetic etiologies of intellectual disability (ID). A SET domain containing 5 gene (SETD5) phenotype of ID and dysmorphic features has been previously described in relation to patients with 3p25.3 deletions and in a few individuals with de novo sequence alterations. Herein, we present additional patients with pathogenic SETD5 sequence alterations. The majority of patients in this cohort and previously reported have developmental delay, behavioral/psychiatric issues, and variable hand and skeletal abnormalities. We also present an apparently unaffected carrier mother of an affected individual and a carrier mother with normal intelligence and affected twin sons. We suggest that the phenotype of SETD5 is more complex and variable than previously presented. Therefore, many features and presentations need to be considered when evaluating a patient for SETD5 alterations through DES

    Gene and environmental risk factors: interplay between CNR1 genetic variants cannabis use, childhood trauma and psychosis [abstract only]

    Get PDF
    Background: Cannabis use and childhood trauma have been proposed as environmental risk factors for psychosis and its known that gene-environment (G×E) interactions increase the risk of psychosis [1]. In particular, a recent finding suggests a link between genetic variants in the cannabinoid receptor type 1 (CNR1) gene, which encodes CB1 receptors and is expressed widely in the central and peripheral systems, and cannabis playing a role in the multifactorial pathogenesis of psychosis [2]. However, how the genetic variants interact with lifetime cannabis use and other environmental risk factors, such as childhood trauma, underlying psychosis remains challenging. Objective: To investigate whether there are associations of gene and environmental factors with psychosis, as well as G×E interactions in the relationship between lifetime cannabis use, childhood trauma, and single nucleotide variants (SNVs) of CNR1 and psychosis in a Brazilian sample. Methods: In a population-based case-control study nested in an incident study (STREAM, Brazil) [3], part of the WP2 EU-GEI consortium, 143 first-episode psychosis patients (FEPp) and 286 community-based controls of both sexes, aged between 16 and 64 years, were included over a period of three years. Thirteen SNVs of CNR1 gene (rs806380, rs806379, rs1049353, rs6454674, rs1535255, rs2023239, rs12720071, rs6928499, rs806374, rs7766029, rs806378, rs10485170, rs9450898), were genotyped from peripheral blood DNA using a custom Illumina HumanCoreExome-24 BeadChip genotyping arrays (GWAS Cardiff chip). Environmental adversities were evaluated using the Cannabis Experience and the Childhood Trauma Questionnaires. Data were analysed using a binary logistic regression model (Adj OR, 95% CI), including a binary outcome (community-based controls and FEPp), adjusted by sex, age, skin colour, years of education and tobacco smoking. Genotype frequencies were analysed under the dominant model (homozygous ancestral x heterozygous + homozygous variant). The significance level was set at α≀0.05. Results: Lifetime cannabis use and childhood trauma increased the risk for psychosis (OR=3.7; 2.6-6.195% CI, p<0.001; OR=3.0; 1.9-4.7 95% CI, p<0.001, respectively). We also showed that the presence of CNR1 rs12720071-T-allele moderated the association between lifetime cannabis use and psychosis (OR=6.0; 2.0-17.5 95% CI; p=0.001). Moreover, the combination of CNR1 rs12720071-T-allele carriers with childhood trauma also suggests a change in the risk of psychosis (OR=3.6; 1.4-9.0 95% CI; p=0.006). No significant associations between the environmental factors and other SNVs were found. Conclusions: We demonstrated a significant interaction between CNR1 rs12720071 SNV and two important environmental risk factors in their association with psychosis. T allele carriers of CNR1 rs12720071 had a higher risk of psychosis when lifetime cannabis use or childhood trauma were present. Our results suggest a G×E interaction involving the CNR1 gene, trauma and cannabis in psychosis. We will explore the associations between genetic and epigenetic markers of the CNR1 gene with environmental factors in larger and longer follow-up cohorts to better understand the mechanisms of endocannabinoid system dysfunction in the etiology of psychosis
    • 

    corecore