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Martha Campbell-Thompson

Researcher at University of Florida

Publications -  174
Citations -  10090

Martha Campbell-Thompson is an academic researcher from University of Florida. The author has contributed to research in topics: Type 1 diabetes & Pancreas. The author has an hindex of 54, co-authored 160 publications receiving 8861 citations. Previous affiliations of Martha Campbell-Thompson include American College of Veterinary Surgeons & Core Laboratories.

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Heme oxygenase-1 modulates early inflammatory responses: evidence from the heme oxygenase-1-deficient mouse.

TL;DR: In this article, the authors examined the differences in immune phenotype between HO-1 knockout (HO-1−/−) and wild-type (HME oxygenase-1+/+) mice.
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Expression of estrogen receptor (ER) subtypes and ERbeta isoforms in colon cancer.

TL;DR: Data show that ERbeta is the predominant ER subtype in the human colon and that decreased levels of ER beta1 and ERbeta2 mRNA are associated with colonic tumorigenesis in females, which suggests that activation of ERbeta-mediated processes in the superficial colonic epithelium may have a role in the preventive effects observed for female gender and ERT usage.
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Marked Expansion of Exocrine and Endocrine Pancreas With Incretin Therapy in Humans With Increased Exocrine Pancreas Dysplasia and the Potential for Glucagon-Producing Neuroendocrine Tumors

TL;DR: In conclusion, incretin therapy in humans resulted in a marked expansion of the exocrine and endocrine pancreatic compartments, the former being accompanied by increased proliferation and dysplasia and the latter by α-cell hyperplasia with the potential for evolution into neuroendocrine tumors.
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Nanodroplet processing platform for deep and quantitative proteome profiling of 10-100 mammalian cells.

TL;DR: A robotically controlled chip-based nanodroplet processing platform is established and its ability to profile the proteome from 10–100 mammalian cells is demonstrated, illustrating the application of nanoPOTS for spatially resolved proteome measurements from clinical tissues.
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Diabetic endothelial nitric oxide synthase knockout mice develop advanced diabetic nephropathy

TL;DR: Inhibition of eNO predisposes mice to classic diabetic nephropathy, likely due to VEGF-NO uncoupling with excessive endothelial cell proliferation coupled with altered autoregulation consequent to the development of preglomerular arteriolar disease.