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Kenneth Williams

Researcher at University of Toronto

Publications -  15
Citations -  213

Kenneth Williams is an academic researcher from University of Toronto. The author has contributed to research in topics: Cardiac fibrosis & Fibrosis. The author has an hindex of 5, co-authored 12 publications receiving 87 citations. Previous affiliations of Kenneth Williams include Mount Allison University & University Health Network.

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Human cardiac fibrosis-on-a-chip model recapitulates disease hallmarks and can serve as a platform for drug testing.

TL;DR: A cardiac-fibrosis-on-a-chip model consisting of a microfabricated device with live force measurement capabilities using co-cultured human cardiac fibroblasts and pluripotent stem cell-derived cardiomyocytes is engineered to study human heart failure in vitro.
Posted ContentDOI

Human cardiac fibrosis-on-a-chip model recapitulates disease hallmarks and can serve as a platform for drug screening

TL;DR: A cardiac-fibrosis-on-a-chip model consisting of a microfabricated device with live force measurement capabilities using co-cultured human cardiac fibroblasts and pluripotent stem cell-derived cardiomyocytes is engineered to study human heart failure in vitro.
Journal ArticleDOI

Diel cycling hypoxia enhances hypoxia-tolerance in rainbow trout (Oncorhynchus mykiss): evidence of physiological and metabolic plasticity

TL;DR: Hypoxia tolerance is a plastic trait in fish, and a putatively sensitive species can remodel its physiology and metabolism to effectively cope with diel cycling hypoxia.
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Hospital-Acquired Infections After Cardiac Surgery and Current Physician Practices: A Retrospective Cohort Study

TL;DR: HAIs are commonly treated without being verified and treatment is often not discontinued after negative cultures are received, and the effect of this could contribute to increased selective pressure for antimicrobial resistant bacteria.
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Nanoparticulate-specific effects of silver on teleost cardiac contractility.

TL;DR: The results suggest that nAg, but not Ag+ alone, inhibits force production by the myocardium, that Ag in any form disrupts normal pacing of cardiac contractions, and that these responses are likely not due to cytotoxicity.