Julie A. Smith
University of Nottingham
18 Papers
87 Citations
Julie A. Smith is an academic researcher from University of Nottingham. The author has contributed to research in topics: Sulforaphane & Campylobacter jejuni. The author has an hindex of 10, co-authored 18 publications.
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Papers
Glutathione S-transferase M1 polymorphism and metabolism of sulforaphane from standard and high-glucosinolate broccoli
Amy V. Gasper,Ahmed Al-janobi,Julie A. Smith,J.R. Bacon,Paul Fortun,Clare T. Atherton,Moira A. Taylor,Christopher J. Hawkey,David A. Barrett,Richard Mithen +9 more
TL;DR: GSTM1 genotypes have a significant effect on the metabolism of sulforaphane derived from standard or high-glucosinolate broccoli, and it is possible that the difference in metabolism may explain the greater protection that GSTM1-positive persons gain from consuming broccoli.
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Potential role for peroxisome proliferator activated receptor (PPAR) in preventing colon cancer
Lucina M. Jackson,Walter Wahli,Liliane Michalik,Susan A. Watson,T.J. Morris,K Anderton,D R Bell,Julie A. Smith,Christopher J. Hawkey,Andrew J. Bennett +9 more
TL;DR: PPAR may inhibit colorectal tumour progression, possibly via inhibition of proliferation, and may be an important therapeutic target.
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Intestinal trehalase activity in a UK population: establishing a normal range and the effect of disease
TL;DR: The normal range and very low incidence of isolated enzyme deficiency is comparable with that described in populations from the USA and mainland Europe and there should be no concern over the introduction of trehalose-containing dried foods.
Iron Uptake by Isolated Human Enterocyte Suspensions in Vitro is Dependent on Body Iron Stores and Inhibited by Other Metal Cations
TL;DR: The uptake of 59Fe ascorbate by suspensions of human enterocytes prepared from endoscopically derived duodenal biopsies was studied and it is suggested that these cells will be useful in the study of iron uptake in humans.
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Intestinal disaccharidase deficiency without villous atrophy may represent early celiac disease.
TL;DR: The aim was to determine if generalized disaccharidase deficiency without villous atrophy represented latent celiac disease.
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