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Barbara A. Thornhill

Researcher at University of Virginia

Publications -  56
Citations -  3202

Barbara A. Thornhill is an academic researcher from University of Virginia. The author has contributed to research in topics: Kidney & Obstructive Nephropathy. The author has an hindex of 27, co-authored 56 publications receiving 2940 citations. Previous affiliations of Barbara A. Thornhill include University of South Florida & University of Iowa.

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Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy

TL;DR: The UUO model is likely to reveal useful biomarkers of progression of renal disease, as well as new therapies, which are desperately needed to allow intervention before the establishment of irreversible renal injury.
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Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy.

TL;DR: The cellular and molecular events responsible for obstructive injury to the developing kidney have been elucidated from animal models and revealed nephron loss through cellular phenotypic transition and cell death, leading to the formation of atubular glomeruli and tubular atrophy.
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Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice

TL;DR: It is demonstrated conclusively that angiotensin regulates at least 50% of the renal interstitial fibrotic response in obstructive nephropathy, an effect independent of systemic hemodynamic changes.
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Recovery following relief of unilateral ureteral obstruction in the neonatal rat.

TL;DR: The relief of obstruction in the neonatal rat attenuates, but does not reverse, renal vascular, glomerular, tubular, and interstitial injury resulting from five days of UUO, which is likely to lead to deterioration of renal function later in life.
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Ureteral obstruction in neonatal mice elicits segment-specific tubular cell responses leading to nephron loss.

TL;DR: Following UUO, the co-localization of hypoxia with cellular proliferation, necrosis, and TBM thickening of the PT is consistent with ischemic injury resulting from vasoconstriction, and Nephron loss in the obstructed developing kidney likely results from complex, segment-specific cellular responses.