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Keith Morris

Researcher at RMIT University

Publications -  14
Citations -  262

Keith Morris is an academic researcher from RMIT University. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Oxidative stress. The author has an hindex of 8, co-authored 14 publications receiving 217 citations. Previous affiliations of Keith Morris include University of Wales & Cardiff University.

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Journal ArticleDOI

Exercise-associated generation of PPARγ ligands activates PPARγ signaling events and upregulates genes related to lipid metabolism

TL;DR: It is suggested that parallel exercise-induced benefits may occur in monocytes, as monocyte PPARγ activation has been linked to beneficial antidiabetic effects and may constitute an additional rationale for prescribing exercise to type 2 diabetes patients.
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The Ability of Exercise-Associated Oxidative Stress to Trigger Redox-Sensitive Signalling Responses.

TL;DR: The responses of muscle and non-muscle cells to exercise-associated redox-sensitive signalling effects will be reviewed, and the consequences of such responses in the context of management of chronic inflammatory conditions, and also their implications for the design of exercise training programmes.
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Moderate-intensity exercise alters markers of alternative activation in circulating monocytes in females: a putative role for PPARγ

TL;DR: Exercise participation suppressed M1 markers and induced M2 markers in monocytes, potentially via PPARγ-triggered signalling, and these effects may contribute (perhaps via priming of monocytes for differentiation into M2 tissue-macrophages) to improved systemic insulin sensitivity in exercising participants.
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Outcomes following PCI in patients with previous CABG: a multi centre experience.

TL;DR: PCI significantly improved angina in these patients with low overall rates of TVR, however TVR rate was significantly higher in patients undergoing graft PCI than those undergoing native vessel PCI.
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The contributions of oxidative stress, oxidised lipoproteins and AMPK towards exercise-associated PPARγ signalling within human monocytic cells

TL;DR: Exercise-associated PPARγ signalling effects appear, at least in monocytes, to be mediated by increased generation ofPPARγ ligands via oxidation of lipoproteins (following exercise-associated transient increases in oxidative stress), rather than via [ROS]cyto-mediated AMPK activation.