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Andrew Collins

Researcher at University of Oslo

Publications -  733
Citations -  44066

Andrew Collins is an academic researcher from University of Oslo. The author has contributed to research in topics: Comet assay & DNA damage. The author has an hindex of 100, co-authored 684 publications receiving 40634 citations. Previous affiliations of Andrew Collins include Norwegian University of Life Sciences & Pontifical Xavierian University.

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UV-sensitive rodent mutant cell lines of complementation groups 6 and 8 differ phenotypically from their human counterparts.

TL;DR: It is found that rodent UV‐sensitive mutant cell lines of complementation groups 6 and 8 have wild‐type capacity for DNA repair as indicated by incision, cyclobutane pyrimidine dimer, and (6‐4) photoproduct removal, and ERCC6, the product of the gene defective in CS‐B and group 6 mutants, is implicated in the regulation of repair of actively transcribed genes in Cockaynesyndrome.
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Does haplotype diversity predict power for association mapping of disease susceptibility

TL;DR: St retention of haplotype diversity in simulations that do not mirror genomic allele frequencies has no relevance to power for association mapping and favours a multi-stage design in which both models and density change adaptively.
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Seasonal changes in markers of oxidative damage to lipids and DNA; correlations with seasonal variation in diet.

TL;DR: High winter MDA levels are seen in those individuals with relatively low folic acid; they never occur in subjects with high plasma folic Acid, implying that folic acids might directly protect against lipid oxidation.
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A comparative performance test of standard, medium- and high-throughput comet assays.

TL;DR: The potential problem of anomalous comets seen at the border of the gel, the so-called 'edge effects', has been addressed and a reliable, high throughput comet assay has applications in genotoxicity testing as well as ecogenotoxicology and human biomonitoring.
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Nutritional supplementation with antioxidants decreases chromosomal damage in humans.

TL;DR: The hypothesis that antioxidants decrease genetic damage is supported, as well as the ferric reducing ability of plasma (a measure of total plasma antioxidant status) and the concentration of malondialdehyde as an indicator of oxidative stress.