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Terho Lehtimäki

Researcher at University of Tampere

Publications -  1375
Citations -  129159

Terho Lehtimäki is an academic researcher from University of Tampere. The author has contributed to research in topics: Population & Genome-wide association study. The author has an hindex of 142, co-authored 1304 publications receiving 106981 citations. Previous affiliations of Terho Lehtimäki include Boston University & National Institutes of Health.

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Meta-analysis of exome array data identifies six novel genetic loci for lung function

Victoria E. Jackson, +122 more
TL;DR: In this article, the authors carried out meta-analyses of exome array data and three lung function measures: forced expiratory volume in one second (FEV 1), forced vital capacity (FVC), and the ratio of FEV 1 to FVC, and identified significant associations with six SNPs: a nonsynonymous variant in RPAP1, which is predicted to be damaging, three intronic SNPs (SEC24C, CASC17 and UQCC1) and two intergenic SNPs near to LY86 and FGF10.
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Factors associated with six-year weight change in young and middle-aged adults in the Young Finns Study.

TL;DR: Socio-economic factors, temperamental and physical characteristics, and some dietary factors are related with weight change in young/middle-aged adults and the weight change occurring in adulthood is also determined by childhood factors, such as high BMI and low family income.
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Synthesis and absorption of cholesterol in Finnish boys by serum non-cholesterol sterols: the cardiovascular risk in Young Finns Study.

TL;DR: Even though cholesterol absorption and synthesis are usually changed in opposite directions, in cases with high absorption the maintenance of homeostasis of cholesterol metabolism can be lost, so that synthesis and absorption of cholesterol are changed independently of each other.
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Talin and vinculin are downregulated in atherosclerotic plaque; Tampere Vascular Study.

TL;DR: The central role of talin and vinculin in cell adhesions suggests that the disintegration of the tissue in atherosclerosis could be partially driven by downregulation of these genes, leading to loosening of cell-ECM interactions and remodeling of the tissues.