Macromolecular transport in heart valves and blood vessel walls.
Item
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Title
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Macromolecular transport in heart valves and blood vessel walls.
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Identifier
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AAI3232035
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identifier
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3232035
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Creator
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Zeng, Zhongqing.
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Contributor
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Adviser: David S. Rumschitzki
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Date
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2006
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Language
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English
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Publisher
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City University of New York.
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Subject
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Engineering, Chemical | Engineering, Biomedical
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Abstract
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In vivo experiments with horseradish peroxidase (HRP) show that macromolecular transport in heart valves depends not only on the direction normal but also parallel to the endothelium, that advection, as well as molecular diffusion, plays an important mass transfer role, and that there is a very thin, sparse subendothelial layer. Based on this hypothesis, a new, two-dimensional convection-diffusion model is proposed for macromolecular transport in heart valves. By allowing for different numbers of isolated macromolecular endothelial leaks and different section positions relative to the leak(s), the model plausibly explains the large variations in size and magnitude in transvalvular LDL profiles (Tompkins et al., Circ Res, 1989) from squirrel monkeys with a single parameter set. The model accurately predicts the growth of localized HRP leakage spots in rats using this same parameter set. The nucleation-polymerization model hierarchy for liposome formation proposed originally for the arterial intima is applied in heart valves. Using parameters determined from artery, the model predicts size distributions in excellent agreement with experiments.;There are large differences in the hydraulic conductivity, void space available for macromolecules and normal transmural pressure among the aorta, pulmonary artery (PA), and inferior vena cava (IVC). Despite these differences the growth of HRP spots with tracer circulation time was similar in shape as well as in magnitude between the aorta and the PA, and the latter was markedly smaller in size but had a greater fractional growth rate than the IVC. A two-dimensional convection-diffusion model is developed for the PA, which shows that the overall transmural water flow and the rates of HRP spot growth are remarkably similar between the PA and the aorta. The liposome model indicates vital differences in liposome growth that may be relevant to understanding why these vessels have very different susceptibilities to atherosclerosis. The IVC model, similar to but differing in important ways from the aorta, explains its HRP spot growth.;Using separation of scales, one obtains asymptotic, thin intima solutions for the transport model. Numerical solutions agree with the asymptotic model far from the leak but disagree (since scale separation breaks down) in the immediate leak vicinity.
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
