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Ronald G. Tompkins

Researcher at Harvard University

Publications -  531
Citations -  44641

Ronald G. Tompkins is an academic researcher from Harvard University. The author has contributed to research in topics: Burn injury & Poison control. The author has an hindex of 93, co-authored 526 publications receiving 41859 citations. Previous affiliations of Ronald G. Tompkins include University of Toronto & Tulane University.

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Adipocyte apoptosis after burn injury is associated with altered fat metabolism

TL;DR: Epididymal adipose tissue showed increased apoptosis manifested by the positive TUNEL staining and increased DNA fragmentation by enzyme-linked immunoassay at day 3 and 7 after burn injury, correlated with decrease in DNA content and tissue weight in the epidydimis.
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Detecting differential protein expression in large-scale population proteomics

TL;DR: A Significance Analysis for Large-scale Proteomics Studies (SALPS) that handles missing peptide intensity values caused by the two mechanisms mentioned above, and has a robust performance in both simulated data and proteomics data from a large clinical study.
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An ALPHA7 Nicotinic Acetylcholine Receptor Agonist (GTS-21) Promotes C2C12 Myonuclear Accretion in Association with Release of Interleukin-6 (IL-6) and Improves Survival in Burned Mice.

TL;DR: The in vitro findings suggest that GTS-21-induced IL-6 release from muscle is mediated via &agr;7AChRs upstream of Stat-3 and -5 pathways and is associated with myonuclear accretion, possibly via MyoD and Pax7 expression.
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Thermal injury-induced changes in the rat intestine brush border cytoskeleton.

TL;DR: It is suggested that disruption of the brush border cytoskeleton may, in part, be responsible for the loss of intestinal barrier function after thermal injury in animal models.
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Role of Protein Farnesylation in Burn-Induced Metabolic Derangements and Insulin Resistance in Mouse Skeletal Muscle

TL;DR: It is demonstrated that burn increased FTase expression and protein farnesylation along with insulin resistance, metabolic alterations and inflammatory response in mouse skeletal muscle, all of which were prevented by FTI-277 treatment.