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Steffan D. Bos

Researcher at Oslo University Hospital

Publications -  60
Citations -  3378

Steffan D. Bos is an academic researcher from Oslo University Hospital. The author has contributed to research in topics: Multiple sclerosis & Genome-wide association study. The author has an hindex of 27, co-authored 55 publications receiving 2948 citations. Previous affiliations of Steffan D. Bos include Leiden University Medical Center & Loyola University Medical Center.

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Identification of new susceptibility loci for osteoarthritis (arcOGEN): A genome-wide association study

TL;DR: One of the signals close to genome-wide significance was within the FTO gene, which is involved in regulation of bodyweight—a strong risk factor for osteoarthritis.
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Incidence of gastrointestinal stromal tumours is underestimated: results of a nation-wide study.

TL;DR: The reported incidence of GIST and GIST-like tumours before and after the routine availability of the specific diagnostic marker CD117 antigen was investigated and it was indicated that almost 50% of the GIST was considered to be at high-risk for malignant behaviour according to the consensus criteria.
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Identification of DIO2 as a new susceptibility locus for symptomatic osteoarthritis

TL;DR: A genome-wide linkage scan and combined linkage association analysis indicated a new susceptibility gene (DIO2) conferring risk to osteoarthritis, which converts intracellular pro-hormone-3,3',5,5'-tetraiodothyronine (T4) into the active thyroid hormone 3,3,5-triiodothyrone (T3) thereby regulating intrace cellular levels of active T3 in target tissues such as the growth plate.
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A meta-analysis of thyroid-related traits reveals novel loci and gender-specific differences in the regulation of thyroid function

Eleonora Porcu, +93 more
- 07 Feb 2013 - 
TL;DR: A large meta-analysis of genome-wide association studies for serum levels of the highly heritable thyroid function markers TSH and FT4 improves the current knowledge of the regulation of hypothalamic-pituitary-thyroid axis function and the consequences of genetic variation for hypo- or hyperthyroidism.