R. E. Powers
Harvard University
12 Papers
128 Citations
R. E. Powers is an academic researcher from Harvard University. The author has contributed to research in topics: Pancreatitis & Acute pancreatitis. The author has an hindex of 9, co-authored 12 publications. Previous affiliations of R. E. Powers include Medical University of South Carolina.
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Papers
Subcellular redistribution of lysosomal enzymes during caerulein-induced pancreatitis
TL;DR: Electron microscopic immunolabeling studies revealed localization of cathepsin D in discrete organelles that, in the samples from animals infused with a supramaximally stimulating dose of caerulein, were larger, more abundant, and more concentrated in the pellet centrifuged at 1,300 g for 15 min than in the controls.
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Role of oxygen-derived free radicals in diet-induced hemorrhagic pancreatitis in mice.
TL;DR: The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis was studied by evaluating the effects of catalase, allopurinol, and dimethylsulfoxide on diet-induced acute hemorrhagic pancreatic necrosis in mice and it was suggested that edema, but not the other features that characterize this model of pancreatitis, may result from generation of oxygen - derived free radicals.
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The role of oxygen-derived free radicals in two models of experimental acute pancreatitis: effects of catalase, superoxide dismutase, dimethylsulfoxide, and allopurinol.
TL;DR: It is suggested that oxygen-derived free radicals may play an important role in the development of pancreatic edema during pancreatitis but that those free radicals do not play anImportant role inThe development of acinar cell injury.
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A Partial Calcium-Free Linker Confers Flexibility to Inner-Ear Protocadherin-15
TL;DR: Simulations predict that the partial Ca2+-free EC3-4 linker exhibits increased flexural flexibility without compromised mechanical strength, providing insight into the dynamics of tip links and other atypical cadherins.
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Inositol trisphosphate production and amylase secretion in mouse pancreatic acini.
TL;DR: The results indicate that the mechanism of stimulus-secretion coupling in mouse pancreatic acini may proceed by a mechanism similar to many other systems, including rat pancreatic Acini, i.e. secretagogue-stimulated generation of IP3 which induces the subsequent release of intracellular Ca2+.
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