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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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Effects of the combination of an angiotensin II antagonist with an HMG-CoA reductase inhibitor in experimental diabetes.

TL;DR: The combination of an angiotensin antagonist with an HMG-CoA reductase inhibitor confers superiority over monotherapies on renal function, as assessed by prevention of albuminuria and rise in plasma BUN and creatinine.
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Petrography and geochemistry of the Mesoarchean Bikoula banded iron formation in the Ntem complex (Congo craton), Southern Cameroon: Implications for its origin

TL;DR: In this article, the Bikoula BIF is characterized by alternating micro-bands of magnetite, quartz and pyroxene, and positive correlations among Al2O3, TiO2, HFSEs, LILEs and transition metals (V, Cr, Ni, Cu and Zn), suggest that the BIF protolith included a significant amount of clastic material.
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A high sensitivity assay for the inflammatory marker C-Reactive protein employing acoustic biosensing.

TL;DR: Overall, the present study revealed that CRP concentrations in serum that might be expected in both normal and pathological conditions can be detected in a time-efficient, label-free immunoassay with RAP™ detection technology with determined CRp concentrations in close agreement with those determined using a commercially available high sensitivity ELISA.
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Cell- and biomarker-based assays for predicting nephrotoxicity

TL;DR: This review discusses traditional and emerging kidney injury biomarkers that are used for the determination of nephrotoxicity and for evaluation and diagnosis of other kidney diseases and the potential for in vivo biomarkers to predict renal toxicity in high-throughput in vitro screening assays is discussed.
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C5a, but not C5a-des Arg, induces upregulation of heteromer formation between complement C5a receptors C5aR and C5L2

TL;DR: Investigation of receptor localization in transfected HEK293 cells and human monocyte‐derived macrophages suggested that C5aR‐C5L2 can form heteromers in a process enhanced by C5A, but not by C 5a‐des Arg, which may be of benefit in understanding the regulation of C5 a in acute inflammation.