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Träfflista för sökning "WFRF:(Dai James Y) "

Sökning: WFRF:(Dai James Y)

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1.
  • Huckins, Laura M., et al. (författare)
  • Gene expression imputation across multiple brain regions provides insights into schizophrenia risk
  • 2019
  • Ingår i: Nature genetics. - 1546-1718. ; 51:4, s. 659-
  • Tidskriftsartikel (refereegranskat)abstract
    • Transcriptomic imputation approaches combine eQTL reference panels with large-scale genotype data in order to test associations between disease and gene expression. These genic associations could elucidate signals in complex genome-wide association study (GWAS) loci and may disentangle the role of different tissues in disease development. We used the largest eQTL reference panel for the dorso-lateral prefrontal cortex (DLPFC) to create a set of gene expression predictors and demonstrate their utility. We applied DLPFC and 12 GTEx-brain predictors to 40,299 schizophrenia cases and 65,264 matched controls for a large transcriptomic imputation study of schizophrenia. We identified 413 genic associations across 13 brain regions. Stepwise conditioning identified 67 non-MHC genes, of which 14 did not fall within previous GWAS loci. We identified 36 significantly enriched pathways, including hexosaminidase-A deficiency, and multiple porphyric disorder pathways. We investigated developmental expression patterns among the 67 non-MHC genes and identified specific groups of pre- and postnatal expression.
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2.
  • Ripke, Stephan, et al. (författare)
  • Biological insights from 108 schizophrenia-associated genetic loci
  • 2014
  • Ingår i: Nature. - 0028-0836. ; 511:7510, s. 421-427
  • Tidskriftsartikel (refereegranskat)abstract
    • Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
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4.
  • Holmes, Michael V., et al. (författare)
  • Association between alcohol and cardiovascular disease : Mendelian randomisation analysis based on individual participant data
  • 2014
  • Ingår i: BMJ-BRIT MED J. - 1756-1833. ; 349, s. g4164
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To use the rs1229984 variant in the alcohol dehydrogenase 1B gene (ADH1B) as an instrument to investigate the causal role of alcohol in cardiovascular disease. Design Mendelian randomisation meta-analysis of 56 epidemiological studies. Participants 261 991 individuals of European descent, including 20 259 coronary heart disease cases and 10 164 stroke events. Data were available on ADH1B rs1229984 variant, alcohol phenotypes, and cardiovascular biomarkers. Main outcome measures Odds ratio for coronary heart disease and stroke associated with the ADH1B variant in all individuals and by categories of alcohol consumption. Results Carriers of the A-allele of ADH1B rs1229984 consumed 17.2% fewer units of alcohol per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of binge drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non-carriers. Rs1229984 A-allele carriers had lower systolic blood pressure (-0.88 (-1.19 to -0.56) mm Hg), interleukin-6 levels (-5.2% (-7.8 to -2.4%)), waist circumference (-0.3 (-0.6 to -0.1) cm), and body mass index (-0.17 (-0.24 to -0.10) kg/m(2)). Rs1229984 A-allele carriers had lower odds of coronary heart disease (odds ratio 0.90 (0.84 to 0.96)). The protective association of the ADH1B rs1229984 A-allele variant remained the same across all categories of alcohol consumption (P= 0.83 for heterogeneity). Although no association of rs1229984 was identified with the combined subtypes of stroke, carriers of the A-allele had lower odds of ischaemic stroke (odds ratio 0.83 (0.72 to 0.95)). Conclusions Individuals with a genetic variant associated with non-drinking and lower alcohol consumption had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant. This suggests that reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health.
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5.
  • Wensley, Frances, et al. (författare)
  • Association between C reactive protein and coronary heart disease : mendelian randomisation analysis based on individual participant data
  • 2011
  • Ingår i: BMJ. British Medical Journal. - BMJ Publishing Group. ; 342, s. d548
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To use genetic variants as unconfounded proxies of C reactive protein concentration to study its causal role in coronary heart disease. Design Mendelian randomisation meta-analysis of individual participant data from 47 epidemiological studies in 15 countries. Participants 194 418 participants, including 46 557 patients with prevalent or incident coronary heart disease. Information was available on four CRP gene tagging single nucleotide polymorphisms (rs3093077, rs1205, rs1130864, rs1800947), concentration of C reactive protein, and levels of other risk factors. Main outcome measures Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals. Results CRP variants were each associated with up to 30% per allele difference in concentration of C reactive protein (P<10(-34)) and were unrelated to other risk factors. Risk ratios for coronary heart disease per additional copy of an allele associated with raised C reactive protein were 0.93 (95% confidence interval 0.87 to 1.00) for rs3093077; 1.00 (0.98 to 1.02) for rs1205; 0.98 (0.96 to 1.00) for rs1130864; and 0.99 (0.94 to 1.03) for rs1800947. In a combined analysis, the risk ratio for coronary heart disease was 1.00 (0.90 to 1.13) per 1 SD higher genetically raised natural log (ln) concentration of C reactive protein. The genetic findings were discordant with the risk ratio observed for coronary heart disease of 1.33 (1.23 to 1.43) per 1 SD higher circulating ln concentration of C reactive protein in prospective studies (P=0.001 for difference). Conclusion Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.
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6.
  • Bagley, Micaela B., et al. (författare)
  • A High Space Density of Luminous Ly alpha Emitters at z similar to 6.5
  • 2017
  • Ingår i: Astrophysical Journal. - 0004-637X. ; 837:1
  • Tidskriftsartikel (refereegranskat)abstract
    • We present the results of a systematic search for Ly alpha emitters (LAEs) at 6 less than or similar to z less than or similar to 7.6 using the HST WFC3 Infrared Spectroscopic Parallel (WISP) Survey. Our total volume over this redshift range is similar to 8 x 10(5) Mpc(3), comparable to many of the narrowband surveys despite their larger area coverage. We find two LAEs at z = 6.38 and 6.44 with line luminosities of L-Lya similar to 4.7 x 10(43) erg s(-1), putting them among the brightest LAEs discovered at these redshifts. Taking advantage of the broad spectral coverage of WISP, we are able to rule out almost all lower-redshift contaminants. The WISP LAEs have a high number density of 7.7 x 10(-6) Mpc (3). We argue that the LAEs reside in megaparsec-scale ionized bubbles that allow the Ly alpha photons to redshift out of resonance before encountering the neutral intergalactic medium. We discuss possible ionizing sources and conclude that the observed LAEs alone are not sufficient to ionize the bubbles.
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7.
  • Neumeyer, Sonja, et al. (författare)
  • Mendelian randomisation study of age at menarche and age at menopause and the risk of colorectal cancer
  • 2018
  • Ingår i: British Journal of Cancer. - NATURE PUBLISHING GROUP. - 0007-0920 .- 1532-1827. ; 118:12, s. 1639-1647
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Substantial evidence supports an association between use of menopausal hormone therapy and decreased colorectal cancer (CRC) risk, indicating a role of exogenous sex hormones in CRC development. However, findings on endogenous oestrogen exposure and CRC are inconsistent.METHODS: We used a Mendelian randomisation approach to test for a causal effect of age at menarche and age at menopause as surrogates for endogenous oestrogen exposure on CRC risk. Weighted genetic risk scores based on 358 single-nucleotide polymorphisms associated with age at menarche and 51 single-nucleotide polymorphisms associated with age at menopause were used to estimate the association with CRC risk using logistic regression in 12,944 women diagnosed with CRC and 10,741 women without CRC from three consortia. Sensitivity analyses were conducted to address pleiotropy and possible confounding by body mass index.RESULTS: Genetic risk scores for age at menarche (odds ratio per year 0.98, 95% confidence interval: 0.95-1.02) and age at menopause (odds ratio 0.98, 95% confidence interval: 0.94-1.01) were not significantly associated with CRC risk. The sensitivity analyses yielded similar results.CONCLUSIONS: Our study does not support a causal relationship between genetic risk scores for age at menarche and age at menopause and CRC risk.
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8.
  • Roy, Sushmita, et al. (författare)
  • Identification of functional elements and regulatory circuits by Drosophila modENCODE.
  • 2010
  • Ingår i: Science (New York, N.Y.). - 1095-9203. ; 330:6012, s. 1787-1797
  • Tidskriftsartikel (refereegranskat)abstract
    • To gain insight into how genomic information is translated into cellular and developmental programs, the Drosophila model organism Encyclopedia of DNA Elements (modENCODE) project is comprehensively mapping transcripts, histone modifications, chromosomal proteins, transcription factors, replication proteins and intermediates, and nucleosome properties across a developmental time course and in multiple cell lines. We have generated more than 700 data sets and discovered protein-coding, noncoding, RNA regulatory, replication, and chromatin elements, more than tripling the annotated portion of the Drosophila genome. Correlated activity patterns of these elements reveal a functional regulatory network, which predicts putative new functions for genes, reveals stage- and tissue-specific regulators, and enables gene-expression prediction. Our results provide a foundation for directed experimental and computational studies in Drosophila and related species and also a model for systematic data integration toward comprehensive genomic and functional annotation.
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9.
  • Wang, Xiaoliang, et al. (författare)
  • Mendelian randomization analysis of C-reactive protein on colorectal cancer risk
  • 2019
  • Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 48:3, s. 767-780
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Chronic inflammation is a risk factor for colorectal cancer (CRC). Circulating C-reactive protein (CRP) is also moderately associated with CRC risk. However, observational studies are susceptible to unmeasured confounding or reverse causality. Using genetic risk variants as instrumental variables, we investigated the causal relationship between genetically elevated CRP concentration and CRC risk, using a Mendelian randomization approach.Methods: Individual-level data from 30 480 CRC cases and 22 844 controls from 33 participating studies in three international consortia were used: the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colorectal Transdisciplinary Study (CORECT) and the Colon Cancer Family Registry (CCFR). As instrumental variables, we included 19 single nucleotide polymorphisms (SNPs) previously associated with CRP concentration. The SNP-CRC associations were estimated using a logistic regression model adjusted for age, sex, principal components and genotyping phases. An inverse-variance weighted method was applied to estimate the causal effect of CRP on CRC risk.Results: Among the 19 CRP-associated SNPs, rs1260326 and rs6734238 were significantly associated with CRC risk (P = 7.5 × 10-4, and P = 0.003, respectively). A genetically predicted one-unit increase in the log-transformed CRP concentrations (mg/l) was not associated with increased risk of CRC [odds ratio (OR) = 1.04; 95% confidence interval (CI): 0.97, 1.12; P = 0.256). No evidence of association was observed in subgroup analyses stratified by other risk factors.Conclusions: In spite of adequate statistical power to detect moderate association, we found genetically elevated CRP concentration was not associated with increased risk of CRC among individuals of European ancestry. Our findings suggested that circulating CRP is unlikely to be a causal factor in CRC development.
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10.
  • Wang, Zheng, et al. (författare)
  • Future perspectives and challenges of fungal systematics in the age of big data
  • 2016
  • Ingår i: Biology of Microfungi. - Switzerland : Springer International Publishing. - 978-3-319-29135-2 ; s. 25-46
  • Bokkapitel (refereegranskat)abstract
    • Mycological research, especially research on fungal evolution and ecology, requires a robust and detailed fungal classification and phylogeny to facilitate efficient and informative communication among mycologists as well as for comparative biology relevant to the larger bioscience community. The field of fungal systematics has undergone numerous revisions recently, from early morphological classifications to an integrative taxonomy that is increasingly reliant on molecular phylogeny. These revisions have taken place at a range of taxonomic ranks, fueled by advances surmounting two major challenges, namely, adequate and balanced sampling of genetic markers and taxa and reinterpretation of phylogenetic informativeness of numerous morphological and ecological characters. The Assembling the Fungal Tree of Life (AFTOL) projects reflected a corresponding surge of collaborative effort in fungal molecular phylogeny using PCR and Sanger sequencing. Here we review recent progress in fungal systematics after AFTOL, in the post-Sanger age, and discuss the future fungal systematics that is emerging as a result of the extraordinary volume of data being gathered by high-throughput sequencing. We examine how environmental DNA surveys, sequence-based classification, and phylogenomics and phylotranscriptomics can impact fungal systematics and point out that sequenced fungal genomes could significantly improve multi-marker phylogenetic inference at a range of levels of fungal systematics by facilitating application of phylogenetically informative experimental design. We argue that it is time to integrate fungal systematics, genome-enabled mycology, and other dimensions of fungal research within the framework of evolutionary biology.
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