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Robert J. Levy

Researcher at Children's Hospital of Philadelphia

Publications -  320
Citations -  18481

Robert J. Levy is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Calcification & Gene delivery. The author has an hindex of 68, co-authored 309 publications receiving 17589 citations. Previous affiliations of Robert J. Levy include University of Pennsylvania & University of Nebraska Medical Center.

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Gastrointestinal uptake of biodegradable microparticles: effect of particle size.

TL;DR: There is a microparticle size dependent exclusion phenomena in the gastrointestinal mucosal tissue with 100 nm size particles showing significantly greater tissue uptake, which has important implications in designing of nanoparticle-based oral drug delivery systems, such as an oral vaccine system.
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The mechanism of uptake of biodegradable microparticles in Caco-2 cells is size dependent.

TL;DR: Caco-2 cells are used as an in vitro model for gastrointestinal uptake, and therefore the results obtained in these studies could be of significant importance in optimizing the microparticle-based oral drug delivery systems.
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Calcification of tissue heart valve substitutes: progress toward understanding and prevention.

TL;DR: Current concepts in the pathophysiology of tissue valve calcification are summarized, including emerging concepts of endogenous regulation, progress toward prevention of calcification, and issues related to calcification of the aortic wall of stentless bioprosthetic valves.
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Polymer degradation and in vitro release of a model protein from poly(D,L-lactide-co-glycolide) nano- and microparticles.

TL;DR: The polymer degradation rates in vitro were not substantially different for different size particles despite a 10- and 100-fold greater surface area to volume ratio for 0.1 microm size nanoparticles as compared to 1 and 10microm size microparticles, respectively.
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Tissue heart valves: Current challenges and future research perspectives

TL;DR: Tissue valve mineralization has complex host, implant, and mechanical determinants and degradation mechanisms are largely rationalized on the basis of the changes to natural valves when they are fabricated into a tissue valve, and the subsequent interactions with the physiologic environment that are induced following implantation.