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Institution

University of Aberdeen

EducationAberdeen, 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 & Health care. 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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Journal ArticleDOI
TL;DR: Diets designed to achieve weight loss in obese subjects can significantly alter the species composition of the gut microbiota, but there is no evidence that the proportions of Bacteroidetes and Firmicutes among fecal bacteria have a function in human obesity.
Abstract: It has been proposed that the development of obesity in humans is influenced by the relative proportions of the two major phyla of bacteria (Bacteroidetes and Firmicutes) present in the large intestine. To examine the relationships between body mass index, weight loss and the major bacterial groups detected in fecal samples. Major groups of fecal bacteria were monitored using fluorescent in situ hybridization (FISH) in obese and non-obese subjects under conditions of weight maintenance, and in obese male volunteers undergoing weight loss on two different reduced carbohydrate weight-loss diets given successively for 4 weeks each. We detected no difference between obese and non-obese individuals in the proportion of Bacteroidetes measured in fecal samples, and no significant change in the percentage of Bacteroidetes in feces from obese subjects on weight loss diets. Significant diet-dependent reductions in a group of butyrate-producing Firmicutes were, however, detected in fecal samples from obese subjects on weight loss diets. Diets designed to achieve weight loss in obese subjects can significantly alter the species composition of the gut microbiota, but we find no evidence that the proportions of Bacteroidetes and Firmicutes among fecal bacteria have a function in human obesity.

1,119 citations

Journal ArticleDOI
Helena Furberg1, Yunjung Kim1, Jennifer Dackor1, Eric Boerwinkle2, Nora Franceschini1, Diego Ardissino, Luisa Bernardinelli3, Luisa Bernardinelli4, Pier Mannuccio Mannucci5, Francesco Mauri, Piera Angelica Merlini, Devin Absher, Themistocles L. Assimes6, Stephen P. Fortmann6, Carlos Iribarren7, Joshua W. Knowles6, Thomas Quertermous6, Luigi Ferrucci8, Toshiko Tanaka8, Joshua C. Bis9, Curt D. Furberg10, Talin Haritunians11, Barbara McKnight9, Bruce M. Psaty9, Bruce M. Psaty12, Kent D. Taylor11, Evan L. Thacker9, Peter Almgren13, Leif Groop13, Claes Ladenvall13, Michael Boehnke14, Anne U. Jackson14, Karen L. Mohlke1, Heather M. Stringham14, Jaakko Tuomilehto15, Jaakko Tuomilehto16, Emelia J. Benjamin17, Shih-Jen Hwang8, Daniel Levy17, Sarah R. Preis8, Ramachandran S. Vasan17, Jubao Duan18, Pablo V. Gejman18, Douglas F. Levinson6, Alan R. Sanders18, Jianxin Shi8, Esther H. Lips19, James McKay19, Antonio Agudo, Luigi Barzan, Vladimir Bencko20, Simone Benhamou21, Simone Benhamou22, Xavier Castellsagué, Cristina Canova23, David I. Conway24, Eleonora Fabianova, Lenka Foretova, Vladimir Janout25, Claire M. Healy26, Ivana Holcatova20, Kristina Kjærheim, Pagona Lagiou27, Jolanta Lissowska, Ray Lowry28, Tatiana V. Macfarlane29, Dana Mates, Lorenzo Richiardi30, Peter Rudnai, Neonilia Szeszenia-Dabrowska31, David Zaridze32, Ariana Znaor, Mark Lathrop, Paul Brennan19, Stefania Bandinelli, Timothy M. Frayling33, Jack M. Guralnik8, Yuri Milaneschi, John R. B. Perry33, David Altshuler34, David Altshuler35, Roberto Elosua, S. Kathiresan34, S. Kathiresan35, Gavin Lucas, Olle Melander13, Christopher J. O'Donnell8, Veikko Salomaa16, Stephen M. Schwartz9, Benjamin F. Voight36, Brenda W.J.H. Penninx37, Johannes H. Smit37, Nicole Vogelzangs37, Dorret I. Boomsma37, Eco J. C. de Geus37, Jacqueline M. Vink37, Gonneke Willemsen37, Stephen J. Chanock8, Fangyi Gu34, Susan E. Hankinson34, David J. Hunter34, Albert Hofman38, Henning Tiemeier38, André G. Uitterlinden38, Cornelia M. van Duijn38, Stefan Walter38, Daniel I. Chasman34, Brendan M. Everett34, Guillaume Paré34, Paul M. Ridker34, Ming D. Li39, Hermine H. Maes40, Janet Audrain-McGovern41, Danielle Posthuma37, Laura M. Thornton1, Caryn Lerman41, Jaakko Kaprio16, Jaakko Kaprio15, Jed E. Rose42, John P. A. Ioannidis43, John P. A. Ioannidis44, Peter Kraft34, Danyu Lin1, Patrick F. Sullivan1 
TL;DR: A meta-analyses of several smoking phenotypes within cohorts of the Tobacco and Genetics Consortium found the strongest association was a synonymous 15q25 SNP in the nicotinic receptor gene CHRNA3, and three loci associated with number of cigarettes smoked per day were identified.
Abstract: Consistent but indirect evidence has implicated genetic factors in smoking behavior1,2. We report meta-analyses of several smoking phenotypes within cohorts of the Tobacco and Genetics Consortium (n = 74,053). We also partnered with the European Network of Genetic and Genomic Epidemiology (ENGAGE) and Oxford-GlaxoSmithKline (Ox-GSK) consortia to follow up the 15 most significant regions (n > 140,000). We identified three loci associated with number of cigarettes smoked per day. The strongest association was a synonymous 15q25 SNP in the nicotinic receptor gene CHRNA3 (rs1051730[A], b = 1.03, standard error (s.e.) = 0.053, beta = 2.8 x 10(-73)). Two 10q25 SNPs (rs1329650[G], b = 0.367, s. e. = 0.059, beta = 5.7 x 10(-10); and rs1028936[A], b = 0.446, s. e. = 0.074, beta = 1.3 x 10(-9)) and one 9q13 SNP in EGLN2 (rs3733829[G], b = 0.333, s. e. = 0.058, P = 1.0 x 10(-8)) also exceeded genome-wide significance for cigarettes per day. For smoking initiation, eight SNPs exceeded genome-wide significance, with the strongest association at a nonsynonymous SNP in BDNF on chromosome 11 (rs6265[C], odds ratio (OR) = 1.06, 95% confidence interval (Cl) 1.04-1.08, P = 1.8 x 10(-8)). One SNP located near DBH on chromosome 9 (rs3025343[G], OR = 1.12, 95% Cl 1.08-1.18, P = 3.6 x 10(-8)) was significantly associated with smoking cessation.

1,104 citations

Journal ArticleDOI
Aysu Okbay1, Jonathan P. Beauchamp2, Mark Alan Fontana3, James J. Lee4  +293 moreInstitutions (81)
26 May 2016-Nature
TL;DR: In this article, the results of a genome-wide association study (GWAS) for educational attainment were reported, showing that single-nucleotide polymorphisms associated with educational attainment disproportionately occur in genomic regions regulating gene expression in the fetal brain.
Abstract: Educational attainment is strongly influenced by social and other environmental factors, but genetic factors are estimated to account for at least 20% of the variation across individuals. Here we report the results of a genome-wide association study (GWAS) for educational attainment that extends our earlier discovery sample of 101,069 individuals to 293,723 individuals, and a replication study in an independent sample of 111,349 individuals from the UK Biobank. We identify 74 genome-wide significant loci associated with the number of years of schooling completed. Single-nucleotide polymorphisms associated with educational attainment are disproportionately found in genomic regions regulating gene expression in the fetal brain. Candidate genes are preferentially expressed in neural tissue, especially during the prenatal period, and enriched for biological pathways involved in neural development. Our findings demonstrate that, even for a behavioural phenotype that is mostly environmentally determined, a well-powered GWAS identifies replicable associated genetic variants that suggest biologically relevant pathways. Because educational attainment is measured in large numbers of individuals, it will continue to be useful as a proxy phenotype in efforts to characterize the genetic influences of related phenotypes, including cognition and neuropsychiatric diseases.

1,102 citations

Journal ArticleDOI
TL;DR: The 2016 revision of the ARIA guidelines provides both updated and new recommendations about the pharmacologic treatment of AR, addressing the relative merits of using oral H1‐antihistamines, intranasal H1-antihistsamines, IntranasAL corticosteroids, and leukotriene receptor antagonists either alone or in combination.
Abstract: Background Allergic rhinitis (AR) affects 10% to 40% of the population. It reduces quality of life and school and work performance and is a frequent reason for office visits in general practice. Medical costs are large, but avoidable costs associated with lost work productivity are even larger than those incurred by asthma. New evidence has accumulated since the last revision of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines in 2010, prompting its update. Objective We sought to provide a targeted update of the ARIA guidelines. Methods The ARIA guideline panel identified new clinical questions and selected questions requiring an update. We performed systematic reviews of health effects and the evidence about patients' values and preferences and resource requirements (up to June 2016). We followed the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) evidence-to-decision frameworks to develop recommendations. Results The 2016 revision of the ARIA guidelines provides both updated and new recommendations about the pharmacologic treatment of AR. Specifically, it addresses the relative merits of using oral H1-antihistamines, intranasal H1-antihistamines, intranasal corticosteroids, and leukotriene receptor antagonists either alone or in combination. The ARIA guideline panel provides specific recommendations for the choice of treatment and the rationale for the choice and discusses specific considerations that clinicians and patients might want to review to choose the management most appropriate for an individual patient. Conclusions Appropriate treatment of AR might improve patients' quality of life and school and work productivity. ARIA recommendations support patients, their caregivers, and health care providers in choosing the optimal treatment.

1,098 citations

Journal ArticleDOI
Eli A. Stahl1, Eli A. Stahl2, Gerome Breen3, Andreas J. Forstner  +339 moreInstitutions (107)
TL;DR: Genome-wide analysis identifies 30 loci associated with bipolar disorder, allowing for comparisons of shared genes and pathways with other psychiatric disorders, including schizophrenia and depression.
Abstract: Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P < 1 × 10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P < 5 × 10-8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder.

1,090 citations


Authors

Showing all 21424 results

NameH-indexPapersCitations
Paul M. Thompson1832271146736
Feng Zhang1721278181865
Ian J. Deary1661795114161
Peter A. R. Ade1621387138051
David W. Johnson1602714140778
Pete Smith1562464138819
Naveed Sattar1551326116368
John R. Hodges14981282709
Ruth J. F. Loos14264792485
Alan J. Silman14170892864
Michael J. Keating140116976353
David Price138168793535
John D. Scott13562583878
Aarno Palotie12971189975
Rajat Gupta126124072881
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023141
2022362
20212,195
20202,118
20191,846
20181,894