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Kevin D. Burns

Researcher at Ottawa Hospital Research Institute

Publications -  140
Citations -  4884

Kevin D. Burns is an academic researcher from Ottawa Hospital Research Institute. The author has contributed to research in topics: Kidney disease & Kidney. The author has an hindex of 34, co-authored 130 publications receiving 4285 citations. Previous affiliations of Kevin D. Burns include University of Ottawa & Ottawa Hospital.

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Hypertension Canada's 2016 Canadian Hypertension Education Program Guidelines for Blood Pressure Measurement, Diagnosis, Assessment of Risk, Prevention, and Treatment of Hypertension

Alexander A. Leung, +77 more
TL;DR: In the diagnosis and assessment of hypertension, automated office blood pressure, taken without patient-health provider interaction, is now recommended as the preferred method of measuring in-office blood pressure as mentioned in this paper.
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Human endothelial colony-forming cells protect against acute kidney injury: role of exosomes.

TL;DR: Protective effects of human cord blood-derived ECFCs in experimental AKI are indicated and it is suggested that ECFC-derived exosomes may mediate the protective response via inhibition of endothelial cell apoptosis.
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Transfer of microRNA-486-5p from human endothelial colony forming cell-derived exosomes reduces ischemic kidney injury.

TL;DR: In mice with ischemic kidney injury, infusion of ECFC exosomes induced potent functional and histologic protection, associated with increased kidney miR-486-5p levels, decreased PTEN, and activation of Akt.
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The 2008 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 2 – therapy

TL;DR: The evidence-based recommendations for the prevention and management of hypertension in adults for 2009 are updated and treatment thresholds and targets should be predicated on by the patient's global atherosclerotic risk, target organ damage and comorbid conditions.
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Nitric oxide stimulates guanylate cyclase and regulates sodium transport in rabbit proximal tubule

TL;DR: It is concluded that NO is an important autocrine or paracrine factor directly regulating Na+ transport in the proximal tubule and is at least partly mediated by generation of cGMP.