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Larry D. Spears

Researcher at Washington University in St. Louis

Publications -  10
Citations -  526

Larry D. Spears is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Calcium metabolism & Lipogenesis. The author has an hindex of 6, co-authored 10 publications receiving 359 citations. Previous affiliations of Larry D. Spears include Merck & Co..

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Effects of microbiota-directed foods in gnotobiotic animals and undernourished children

TL;DR: Identifying ingredients in complementary foods, consumed during the transition from exclusive milk feeding to a fully weaned state, that increase the representation and expressed beneficial functions of growth-promoting bacterial taxa in the developing microbiota could provide an effective, affordable, culturally acceptable, and sustainable approach to treatment.
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A calcium-dependent protease as a potential therapeutic target for Wolfram syndrome.

TL;DR: It is reported that the pathway leading to calpain activation offers potential drug targets for Wolfram syndrome and substrates for calpain might serve as biomarkers for this syndrome, and that dantrolene can prevent cell death in neural progenitor cells derived fromWolfram syndrome iPS cells.
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Skeletal Muscle Phospholipid Metabolism Regulates Insulin Sensitivity and Contractile Function.

TL;DR: The results suggest that high-fat feeding and obesity induce CEPT1, which remodels the SR to preserve contractile function at the expense of insulin sensitivity, which is inversely correlated with insulin sensitivity in obese humans.
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Targeting Cellular Calcium Homeostasis to Prevent Cytokine-Mediated Beta Cell Death.

TL;DR: In this paper, the authors showed that modulation of cellular calcium homeostasis can mitigate cytokine and ER stress-mediated beta cell death in type 1 diabetes. But, there are no treatments targeting cellular calcium to combat type 1 Diabetes.
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Interleukins and Atherosclerosis: A Dysfunctional Family Grows

TL;DR: It is suggested that IL-1α, a close relative of interleukin-1, is selectively induced by fatty acids independent of the inflammasome to promote vascular inflammation.