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Yoshimasa Oyama

Researcher at University of Colorado Denver

Publications -  23
Citations -  230

Yoshimasa Oyama is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: PER2 & Hypoxia-inducible factors. The author has an hindex of 8, co-authored 23 publications receiving 164 citations. Previous affiliations of Yoshimasa Oyama include Anschutz Medical Campus & Oita University.

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Intense light-elicited upregulation of miR-21 facilitates glycolysis and cardioprotection through Per2-dependent mechanisms.

TL;DR: MiR-21 is identified as cardioprotective downstream target of Per2 and intense light therapy is suggested as a potential strategy to enhance miR- 21 activity and subsequent carbohydrate metabolism in humans.
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Circadian MicroRNAs in Cardioprotection.

TL;DR: This review will focus on circadian microRNAs in the context of cardioprotection and will highlight new discoveries, which could lead to novel therapeutic concepts to treat myocardial ischemia.
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Intense Light-Mediated Circadian Cardioprotection via Transcriptional Reprogramming of the Endothelium

TL;DR: It is demonstrated that intense light is cardioprotective via circadian PER2 amplitude enhancement, mimicking hypoxia-elicited adenosine- and HIF1A-metabolic adaptation to myocardial ischemia under normoxic conditions.
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The Circadian PER2 Enhancer Nobiletin Reverses the Deleterious Effects of Midazolam in Myocardial Ischemia and Reperfusion Injury.

TL;DR: Findings highlight PER2 as a cardioprotective mechanism and suggest the PER2 enhancers nobiletin or tangeritin as a preventative therapy for myocardial IR-injury in the perioperative setting where midazolam pretreatment occurs frequently.
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Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice.

TL;DR: It is suggested that uncoupling of peripheral and master clock gene rhythms by reversed feeding exacerbates inflammatory responses and may also increase the levels of inflammatory cytokines, thereby increasing mortality in a mouse sepsis model.