M
Mark E. Cooper
Researcher at University of Queensland
Publications - 1514
Citations - 141899
Mark E. Cooper is an academic researcher from University of Queensland. The author has contributed to research in topics: Diabetes mellitus & Diabetic nephropathy. The author has an hindex of 158, co-authored 1463 publications receiving 124887 citations. Previous affiliations of Mark E. Cooper include University of Cambridge & University of Adelaide.
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Characterization of binding sites for amylin, calcitonin, and CGRP in primate kidney
TL;DR: Analysis of receptor distributions in Macaca fascicularis kidney by in vitro autoradiography revealed distinct patterns of binding for each peptide, suggesting potential roles for amylin, calcitonin, and CGRP in primate renal function.
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Effects of liver transplantation and resection on lipid parameters: a longitudinal study
TL;DR: The liver has a large reserve and is able to maintain lipoprotein production and removal despite greater than 50% removal, and the major cause of reduced plasma lipid concentrations in the postoperative period relates to other factors such as fasting and handling of the gut during surgery.
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Rat amylin mediates a pressor response in the anaesthetised rat: implications for the association between hypertension and diabetes mellitus
TL;DR: It is concluded that amylin may act centrally to elevate blood pressure in the anaesthetised rat, possibly through activation of the renin angiotensin system.
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Fluorescent macrolide probes – synthesis and use in evaluation of bacterial resistance
M. Rhia L. Stone,Urszula Łapińska,Stefano Pagliara,Muriel Masi,Joanne T. Blanchfield,Mark E. Cooper,Mark A. T. Blaskovich +6 more
TL;DR: The potential of fluorescent macrolide probes to characterise and explore drug uptake and efflux in bacteria is illustrated and the design of improved drugs and a better understanding of bacterial resistance and persistence is developed.
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Genetic Deletion of Cell Division Autoantigen 1 Retards Diabetes-Associated Renal Injury
Zhonglin Chai,Aozhi Dai,Yugang Tu,Jiaze Li,Tieqiao Wu,Yu Wang,Lorna J Hale,Frank Koentgen,Merlin C. Thomas,Merlin C. Thomas,Mark E. Cooper +10 more
TL;DR: Investigation of the genetic deletion of Tspyl2 in C57BL6 and ApoE knockout mice suggests that CDA1 deletion reduces but does not block renal TGF-β signaling, which may be a potential therapeutic target for retarding DN and perhaps, other kidney diseases associated with T GF-β-mediated fibrogenesis.