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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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Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes

Josephine M. Forbes, +2 more
- 01 Jun 2008 - 
TL;DR: There is now an increasing body of data to suggest that strategies involving a more targeted antioxidant approach, using agents that penetrate specific cellular compartments, may be the elusive additive therapy required to further optimize renoprotection in diabetes.
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Randomised controlled trial of dual blockade of renin-angiotensin system in patients with hypertension, microalbuminuria, and non-insulin dependent diabetes: the candesartan and lisinopril microalbuminuria (CALM) study

Carl Erik Mogensen, +6 more
- 09 Dec 2000 - 
TL;DR: Cadesartan 16 mg once daily is as effective as lisinopril 20 mgonce daily in reducing blood pressure and microalbuminuria in hypertensive patients with type 2 diabetes and combination treatment is well tolerated and more effective in reducingBlood pressure.
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Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy

Barry M. Brenner, +2 more
- 01 Jan 2002 - 
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Optical biosensors in drug discovery.

Mark E. Cooper
- 01 Jul 2002 - 
TL;DR: Advances in instrumentation and experimental design have led to the increasing application of optical biosensors in many areas of drug discovery, including target identification, ligand fishing, assay development, lead selection, early ADME and manufacturing quality control.
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Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia

Assam El-Osta, +8 more
- 29 Sep 2008 - 
TL;DR: It is shown that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression.