Institution
University of Aberdeen
Education•Aberdeen, United Kingdom•
About: University of Aberdeen is a education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 21174 authors who have published 49962 publications receiving 2105479 citations. The organization is also known as: Aberdeen University.
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Mahidol University1, University of Newcastle2, University of Leicester3, John Hunter Hospital4, Waikato Hospital5, QIMR Berghofer Medical Research Institute6, Queen's University7, University of Washington8, The Chinese University of Hong Kong9, University of Aberdeen10, deCODE genetics11, Tel Aviv University12
TL;DR: Haplotype analysis suggests that there may be an interaction between the two sites, with a lower risk of asthma associated with the Glu27 allele (compared with Gln27), and that this risk is modified by the allele at position 16.
Abstract: A number of studies have investigated two common polymorphisms in the beta(2)-adrenoceptor gene, Arg/Gly16 and Gln/Glu27, in relation to asthma susceptibility. The authors performed a meta-analysis of each polymorphism, as well as haplotype analysis, for adult and pediatric populations separately, using published data, supplemented by additional data requested from the original authors. Individual analysis detected no effect of Arg/Gly16 in adults but did suggest a recessive protective effect of Gly16 for children, with an odds ratio of 0.71 (95% confidence interval (CI): 0.53, 0.96) compared with the other genotypes. Results for Gln/Glu27 in adults seem to indicate that heterozygotes are at decreased risk of asthma than either homozygote (odds ratio = 0.73, 95% CI: 0.62, 0.87), although the studies are heterogeneous; in children, the Glu/Glu genotype has a decreased risk of asthma (odds ratio = 0.60, 95% CI: 0.35, 0.99) compared with the other genotypes. Despite the proximity of these two polymorphic sites, the linkage disequilibrium coefficient of 0.41 was not high (p < 0.001). Haplotype analysis suggests that there may be an interaction between the two sites, with a lower risk of asthma associated with the Glu27 allele (compared with Gln27), and that this risk is modified by the allele at position 16.
328 citations
TL;DR: Evidence for direct and indirect influences that climate change may have on dispersal, some ecological and others evolutionary, is compiled across the fields of dispersal ecology and evolution, species distribution modelling and conservation biology.
Abstract: Dispersal is fundamental in determining biodiversity responses to rapid climate change, but recently acquired ecological and evolutionary knowledge is seldom accounted for in either predictive methods or conservation planning. We emphasise the accumulating evidence for direct and indirect impacts of climate change on dispersal. Additionally, evolutionary theory predicts increases in dispersal at expanding range margins, and this has been observed in a number of species. This multitude of ecological and evolutionary processes is likely to lead to complex responses of dispersal to climate change. As a result, improvement of models of species’ range changes will require greater realism in the representation of dispersal. Placing dispersal at the heart of our thinking will facilitate development of conservation strategies that are resilient to climate change, including landscape management and assisted colonisation.
Synthesis
This article seeks synthesis across the fields of dispersal ecology and evolution, species distribution modelling and conservation biology. Increasing effort focuses on understanding how dispersal influences species' responses to climate change. Importantly, though perhaps not broadly widely-recognised, species' dispersal characteristics are themselves likely to alter during rapid climate change. We compile evidence for direct and indirect influences that climate change may have on dispersal, some ecological and others evolutionary. We emphasise the need for predictive modelling to account for this dispersal realism and highlight the need for conservation to make better use of our existing knowledge related to dispersal.
327 citations
TL;DR: This study replicates the association between alcohol consumption and alcohol metabolizing genes and KLB, and identifies novel gene associations that should be the focus of future studies investigating the neurobiology of alcohol consumption.
Abstract: Alcohol consumption has been linked to over 200 diseases and is responsible for over 5% of the global disease burden. Well-known genetic variants in alcohol metabolizing genes, for example, ALDH2 and ADH1B, are strongly associated with alcohol consumption but have limited impact in European populations where they are found at low frequency. We performed a genome-wide association study (GWAS) of self-reported alcohol consumption in 112 117 individuals in the UK Biobank (UKB) sample of white British individuals. We report significant genome-wide associations at 14 loci. These include single-nucleotide polymorphisms (SNPs) in alcohol metabolizing genes (ADH1B/ADH1C/ADH5) and two loci in KLB, a gene recently associated with alcohol consumption. We also identify SNPs at novel loci including GCKR, CADM2 and FAM69C. Gene-based analyses found significant associations with genes implicated in the neurobiology of substance use (DRD2, PDE4B). GCTA analyses found a significant SNP-based heritability of self-reported alcohol consumption of 13% (se=0.01). Sex-specific analyses found largely overlapping GWAS loci and the genetic correlation (rG) between male and female alcohol consumption was 0.90 (s.e.=0.09, P-value=7.16 × 10-23). Using LD score regression, genetic overlap was found between alcohol consumption and years of schooling (rG=0.18, s.e.=0.03), high-density lipoprotein cholesterol (rG=0.28, s.e.=0.05), smoking (rG=0.40, s.e.=0.06) and various anthropometric traits (for example, overweight, rG=-0.19, s.e.=0.05). This study replicates the association between alcohol consumption and alcohol metabolizing genes and KLB, and identifies novel gene associations that should be the focus of future studies investigating the neurobiology of alcohol consumption.
327 citations
University of New South Wales1, University of California, Los Angeles2, Max Planck Society3, Queen's University4, University of Guelph5, University of Innsbruck6, University of Arizona7, VU University Amsterdam8, National University of Cordoba9, Royal Botanic Gardens10, Centre national de la recherche scientifique11, Austral University of Chile12, ETH Zurich13, Goethe University Frankfurt14, University of Oldenburg15, Tohoku University16, Macquarie University17, University of Life Sciences in Lublin18, Moscow State University19, Kyoto University20, Spanish National Research Council21, Universidade Federal do Rio Grande do Sul22, Hokkaido University23, Syracuse University24, Empresa Brasileira de Pesquisa Agropecuária25, University of Amsterdam26, University of Aberdeen27, Michigan State University28, University of Wisconsin–Eau Claire29, University of Tartu30
TL;DR: This work quantified the strength of the relationships between temperature and precipitation and 21 plant traits from 447,961 species-site combinations worldwide and used meta-analysis to provide an overall answer to the question.
Abstract: Question: Are plant traits more closely correlated with mean annual temperature, or with mean annual precipitation? Location: Global. Methods: We quantified the strength of the relationships between temperature and precipitation and 21 plant traits from 447,961 species-site combinations worldwide. We used meta-analysis to provide an overall answer to our question.
327 citations
TL;DR: Subjects are at substantial increased odds of developing CWP if they display features of somatization, health-seeking behaviour and poor sleep, and Psychosocial distress has a strong aetiological influence on CWP.
Abstract: Objective Chronic widespread pain (CWP) is strongly associated with psychosocial distress both in a clinical setting and in the community The aim of this study was to determine the contribution of measures of psychosocial distress, health-seeking behaviour, sleep problems and traumatic life events to the development of new cases of CWP in the community Methods In a population-based prospective study, 3171 adults aged 25-65 yrs free of CWP were followed-up 15 months later to identify those with new CWP Baseline data were available on their scores from a number of psychological scales including Illness Attitude Scales (IAS), Somatic Symptom Checklist (SSC), Hospital Anxiety & Depression Scale, Sleep Problems Scale, and Life Events Inventory Results 324 subjects [10%, 95% confidence interval (CI) 92, 113] developed new CWP at follow-up After adjustment for age and sex, three factors independently predicted the development of CWP: scoring three or more on the SSC [odds ratio (OR) 18, 95% CI 11, 31], scoring eight or more on the Illness Behaviour subscale of the IAS (OR 33, 95% CI 23, 48), and nine or more on the Sleep Problem Scale (OR 27, 95% CI 16, 32) Subjects exposed to all three factors were at 12 times the odds of new CWP than those with low scores on all scales Conclusion Subjects are at substantial increased odds of developing CWP if they display features of somatization, health-seeking behaviour and poor sleep Psychosocial distress has a strong aetiological influence on CWP
326 citations
Authors
Showing all 21424 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul M. Thompson | 183 | 2271 | 146736 |
Feng Zhang | 172 | 1278 | 181865 |
Ian J. Deary | 166 | 1795 | 114161 |
Peter A. R. Ade | 162 | 1387 | 138051 |
David W. Johnson | 160 | 2714 | 140778 |
Pete Smith | 156 | 2464 | 138819 |
Naveed Sattar | 155 | 1326 | 116368 |
John R. Hodges | 149 | 812 | 82709 |
Ruth J. F. Loos | 142 | 647 | 92485 |
Alan J. Silman | 141 | 708 | 92864 |
Michael J. Keating | 140 | 1169 | 76353 |
David Price | 138 | 1687 | 93535 |
John D. Scott | 135 | 625 | 83878 |
Aarno Palotie | 129 | 711 | 89975 |
Rajat Gupta | 126 | 1240 | 72881 |