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Charles E. Alpers

Researcher at University of Washington

Publications -  418
Citations -  35650

Charles E. Alpers is an academic researcher from University of Washington. The author has contributed to research in topics: Renal pathology & Glomerulonephritis. The author has an hindex of 89, co-authored 409 publications receiving 32440 citations. Previous affiliations of Charles E. Alpers include New York Medical College & University of Washington Medical Center.

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Journal Article

Participation of glomerular endothelial cells in the capillary repair of glomerulonephritis.

TL;DR: Evidence is provided for glomerular capillary repair (angiogenesis) in the adult injured glomerulus, and glomeruli are capable of healing microaneurysms, and the mechanism involves basic fibroblast growth factor- and VPF/VEGF-mediated endothelial proliferative responses.
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Wiskott-Aldrich syndrome protein is required for regulatory T cell homeostasis

TL;DR: Wiskott-Aldrich syndrome protein (WASp) Tregs exhibited a marked selective advantage in vivo in a WAS patient with a spontaneous revertant mutation, indicating that altered Treg fitness likely explains the autoimmune features in human WAS.
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Carotid plaque morphology and clinical events

TL;DR: In patients with highly stenoticCarotid lesions who are undergoing carotid endarterectomy, gross plaque composition is similar regardless of preoperative symptom status, and it is unlikely that differences in the volume of intraplaque hemorrhage, lipid core, necrotic core, or calcification in atheroscleroticcarotid plaques explain their embolic history.
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Human renal cortical interstitial cells with some features of smooth muscle cells participate in tubulointerstitial and crescentic glomerular injury.

TL;DR: It is demonstrated that a population of interstitial cells with some muscle-like features can be identified in normal kidneys, including fibroblasts and not capillary endothelial cells or leukocytes.
Journal Article

Tubulointerstitial disease in glomerulonephritis. Potential role of osteopontin (uropontin).

TL;DR: It is demonstrated that osteopontin messenger RNA and protein levels are up-regulated in a proportion of proximal and distal tubules in three experimental models of glomerulonephritis, suggesting that osteobontin may be important for macrophage accumulation at specific sites in diseased tissue and may have a role in the pathogenesis of the tubulointerstitial injury that accompanies glomeral disease.