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Larry W. Oberley

Researcher at University of Iowa

Publications -  229
Citations -  24150

Larry W. Oberley is an academic researcher from University of Iowa. The author has contributed to research in topics: Superoxide dismutase & Superoxide. The author has an hindex of 82, co-authored 229 publications receiving 23354 citations. Previous affiliations of Larry W. Oberley include Roy J. and Lucille A. Carver College of Medicine & Wabash College.

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Selected contribution: Differential expression of stress-related genes with aging and hyperthermia.

TL;DR: The findings support the postulate that transcriptional changes in response to a physiological challenge such as hyperthermia contribute to the loss of stress tolerance in older organisms.
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Evidence for oxidative stress in NSAID-induced colitis in IL10-/- mice.

TL;DR: Results strongly indicate the presence of oxidative stress in the inflammatory bowel disease in NSAID-treated IL10(-/-) mice and suggests a role for oxidative Stress in the pathophysiology of this model ofinflammatory bowel disease.
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Phospholipid hydroperoxide glutathione peroxidase induces a delay in G1 of the cell cycle.

TL;DR: Results from bromodeoxyuridine pulse-chase experiments and flow cytometry indicate that PhGPx induced a delay in MCF-7 proliferation that was primarily due to a slower progression from G1 to S, and support the hypothesis that Ph GPx plays a regulatory role in the progression of MCF to S possibly by regulating the steady-state levels of PLOOH.
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Immunolocalization of manganese superoxide dismutase in normal and transgenic mice expressing the human enzyme

TL;DR: The results indicate that these transgenic mice overexpress MnSOD in their mitochondria, and that this occurs selectively in at least some mesenchymal tissues.

Molecular Biology of Thermoregulation Selected Contribution: Differential expression of stress-related genes with aging and hyperthermia

TL;DR: Zhang et al. as discussed by the authors found that aging results in altered gene expression in response to heat stress that is indicative of decreased stress protein transcription and increased expression of oxidative stress-related genes.