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Leverage of genetic variants proxying smoking intensity to explore the broad health consequences of smoking.

作者信息

Gill Dipender

机构信息

Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.

Centre for Pharmacology and Therapeutics, Department of Medicine, Hammersmith Campus, Imperial College London, London, United Kingdom.

出版信息

EClinicalMedicine. 2020 Aug 15;26:100498. doi: 10.1016/j.eclinm.2020.100498. eCollection 2020 Sep.

Abstract
摘要

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本文引用的文献

1
Mendelian randomization case-control PheWAS in UK Biobank shows evidence of causality for smoking intensity in 28 distinct clinical conditions.
EClinicalMedicine. 2020 Jul 31;26:100488. doi: 10.1016/j.eclinm.2020.100488. eCollection 2020 Sep.
2
Genetic predisposition to smoking in relation to 14 cardiovascular diseases.
Eur Heart J. 2020 Sep 14;41(35):3304-3310. doi: 10.1093/eurheartj/ehaa193.
3
How humans can contribute to Mendelian randomization analyses.
Int J Epidemiol. 2019 Jun 1;48(3):661-664. doi: 10.1093/ije/dyz152.
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Associations of genetically determined iron status across the phenome: A mendelian randomization study.
PLoS Med. 2019 Jun 20;16(6):e1002833. doi: 10.1371/journal.pmed.1002833. eCollection 2019 Jun.
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The UK Biobank resource with deep phenotyping and genomic data.
Nature. 2018 Oct;562(7726):203-209. doi: 10.1038/s41586-018-0579-z. Epub 2018 Oct 10.
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Triangulation in aetiological epidemiology.
Int J Epidemiol. 2016 Dec 1;45(6):1866-1886. doi: 10.1093/ije/dyw314.
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PheWAS: demonstrating the feasibility of a phenome-wide scan to discover gene-disease associations.
Bioinformatics. 2010 May 1;26(9):1205-10. doi: 10.1093/bioinformatics/btq126. Epub 2010 Mar 24.

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