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.
Papers
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Journal Article
Potential influence of lipids in diabetic nephropathy: insights from experimental data and clinical studies.
Fabrice Bonnet,Mark E. Cooper +1 more
TL;DR: It remains controversial whether apolipoprotein E gene polymorphism is an important factor in the development of diabetic nephropathy, and larger prospective studies are required to better ascertain the role of lipids in the progression of diabetes nephrophropathy.
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Physicochemical characterization of airborne particulate matter at a mainline underground railway station.
Matthew Loxham,Mark E. Cooper,Miriam E. Gerlofs-Nijland,Flemming R. Cassee,Donna E. Davies,Martin R. Palmer,Damon A. H. Teagle +6 more
TL;DR: It is suggested that the potential health effects of exposure to the ultrafine fraction of underground PM warrant further investigation as a consequence of its greater surface area/volume ratio and high metal content.
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Blockade of the Renin-Angiotensin and Endothelin Systems on Progressive Renal Injury
Zemin Cao,Mark E. Cooper,Leonard L. Wu,Alison J. Cox,Karin Jandeleit-Dahm,Darren J. Kelly,Richard E. Gilbert +6 more
TL;DR: The findings suggest that the RAS but not the endothelin system is a major mediator of progressive renal injury after renal mass reduction and that the combination of an AT1 receptor antagonist with an ACE inhibitor may have advantages over the single agent of RAS blocker treatment.
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Gene-to-phenotype models and complex trait genetics
TL;DR: A gene-to-phenotype (G→P) modelling framework for quantitative genetics that explicitly deals with the context-dependent gene effects that are attributed to genes functioning within networks, i.e. epistasis, gene × environment interactions, and pleiotropy is developed.
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Evolving concepts in advanced glycation, diabetic nephropathy, and diabetic vascular disease
TL;DR: It is postulate that the chemical pathways leading to advanced glycation endproduct formation and the renin angiotensin systems may interact through the generation of free radicals, induced both by glucose and ang Elliotensin II.