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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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Role of hyperlipidemia in progressive renal disease: focus on diabetic nephropathy

TL;DR: Atorvastatin therapy was associated with a modest reduction in proteinuria and glomerulosclerosis without influencing lipid levels or renal function in STNx rats, and appears to confer renoprotection via effects on prosclerotic cytokines such as TGF-beta and macrophage accumulation, independent of their lipid-lowering properties.
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Management of patients with diabetes and CKD: conclusions from a “Kidney Disease: Improving Global Outcomes” (KDIGO) Controversies Conference

TL;DR: The current state of knowledge regarding optimal glycemic control, current antidiabetic agents and their safety, and new therapies being developed to improve kidney function and cardiovascular outcomes for this vulnerable population of people with diabetes are assessed.
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Transpiration Response of Maize Hybrids to Atmospheric Vapour Pressure Deficit

TL;DR: Transpiration rate was examined of 35 single-cross hybrids to determine whether hybrids can be identified that express limited transpiration under high vapour pressure deficit (VPD) conditions, indicating that expression of the trait was consistent.
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Modulation of nephrin in the diabetic kidney: association with systemic hypertension and increasing albuminuria.

TL;DR: Reduction in renal nephrin gene and protein expression is closely associated with the development of albuminuria, as observed in an experimental model of diabetes and hypertension.
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Osteopontin expression in progressive renal injury in remnant kidney: Role of angiotensin II

TL;DR: An up-regulation of OPN expression may play a role in progressive renal injury following subtotal nephrectomy in rats and may be one of the mechanisms by which Ang II blockade attenuated renal injury after renal ablation.