R
Ronald D. Guttmann
Researcher at McGill University
Publications - 118
Citations - 4738
Ronald D. Guttmann is an academic researcher from McGill University. The author has contributed to research in topics: Transplantation & Antigen. The author has an hindex of 35, co-authored 118 publications receiving 4666 citations. Previous affiliations of Ronald D. Guttmann include Yale University & Harvard University.
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Journal ArticleDOI
The Emotional Impact of End-Stage Renal Disease: Importance of Patients' Perceptions of Intrusiveness and Control
Gerald M. Devins,Yitzchak M. Binik,Tom A. Hutchinson,David J. Hollomby,Paul E. Barre,Ronald D. Guttmann +5 more
TL;DR: Patients' perceptions of increased intrusiveness, and their perceptions of limited control over eleven life dimensions, each correlated significantly and uniquely with increased negative and decreased positive mood, suggesting that each of these two factors contributes importantly and independently to patients' distress.
Journal ArticleDOI
Myoblast transfer in duchenne muscular dystrophy
George Karpati,Djordje Ajdukovic,Douglas L. Arnold,Robert B. Gledhill,Ronald D. Guttmann,Paul C. Holland,Penelope A. Koch,Eric A. Shoubridge,Desmond G. Spence,Michel Vanasse,Gordon V. Watters,M. Abrahamowicz,Catherine Duff,Ronald G. Worton +13 more
TL;DR: The overall therapeutic efficiency of the myoblast transfer was poor as judged by the results in maximal voluntary force generation, dystrophin content of the muscle, magnetic resonance imaging of the Muscle, and the lack of donor‐derived DNA and dyStrophin messenger RNA in the injected muscle.
Journal ArticleDOI
The case for allowing kidney sales
J Radcliffe-Richards,A. S. Daar,Ronald D. Guttmann,R Hoffenberg,Ian Kennedy,Margaret Lock,RA Sells,Nicholas L. Tilney +7 more
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Effects of initial ischemia/reperfusion injury on the transplanted kidney.
Journal ArticleDOI
SPONTANEOUS DIABETES MELLITUS SYNDROME IN THE RAT I. Association with the Major Histocompatibility Complex
TL;DR: Data demonstrate (a) MHC linkage with spontaneous diabetes in this rat model; (b) penetrance similar to the human disease; and (c) a possible association of MHC haplotype with pancreatic inflammation as well as insulin content in nondiabetic F2 siblings.