P
Peter Hansell
Researcher at Uppsala University
Publications - 143
Citations - 4727
Peter Hansell is an academic researcher from Uppsala University. The author has contributed to research in topics: Kidney & Renal blood flow. The author has an hindex of 32, co-authored 141 publications receiving 4415 citations. Previous affiliations of Peter Hansell include La Jolla Institute for Allergy and Immunology & Karolinska Institutet.
Papers
More filters
Journal ArticleDOI
Pathophysiology of contrast medium-induced nephropathy.
TL;DR: Many experimental studies provide evidence for a greater perturbation in renal functions by dimeric contrast media in comparison to nonionic monomers as the widely used nonionic low osmolar contrast media.
Journal ArticleDOI
Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension
TL;DR: It is concluded that oxidative stress occurs in kidneys of diabetic rats predominantly in the medullary region and relates to augmented oxygen consumption and impaired oxygen tension in the tissue.
Journal ArticleDOI
L-selectin function is required for beta 2-integrin-mediated neutrophil adhesion at physiological shear rates in vivo.
U H von Andrian,Peter Hansell,J D Chambers,E. M. Berger,I. P. Torres Filho,Eugene C. Butcher,K E Arfors +6 more
TL;DR: It is indicated that primary neutrophil interaction with inflamed EC through the L-selectin is a prerequisite for neutrophils function at physiological shear rates in vivo.
Journal ArticleDOI
Determinants of kidney oxygen consumption and their relationship to tissue oxygen tension in diabetes and hypertension
TL;DR: Good knowledge is gained about major changes in O2 metabolism occurring in diabetic and hypertensive kidneys, however, further efforts are needed to elucidate how these alterations can be prevented or reversed before translation into clinical practice.
Journal ArticleDOI
Activation of Hypoxia-Inducible Factors Prevents Diabetic Nephropathy
Lina Nordquist,Malou Friederich-Persson,Angelica Fasching,Per Liss,Kumi Shoji,Masaomi Nangaku,Peter Hansell,Fredrik Palm +7 more
TL;DR: Activation of HIFs prevents diabetes-induced alteration in kidney oxygen metabolism by normalizing glomerular filtration, which reduces tubular electrolyte load, preventing mitochondrial leak respiration and improving tubular transport efficiency, which could be related to reduced oxidative stress and account for the reduced proteinuria and tubulointerstitial damage.