If searched for the ebook Cardiovascular Solid Mechanics: Cells, Tissues, and Organs by Jay D. Humphrey in pdf format, then you've come to the faithful website. We presented the full edition of this ebook in PDF, doc, DjVu, ePub, txt forms. You can read Cardiovascular Solid Mechanics: Cells, Tissues, and Organs online or load. In addition, on our website you can read instructions and diverse art books online, either downloading them as well. We wish draw note what our website not store the eBook itself, but we grant ref to the site wherever you may download either read online. So that if want to downloading by Jay D. Humphrey pdf Cardiovascular Solid Mechanics: Cells, Tissues, and Organs, then you've come to the loyal site. We own Cardiovascular Solid Mechanics: Cells, Tissues, and Organs PDF, DjVu, txt, doc, ePub forms. We will be pleased if you get back us again. a rule-of-mixtures model for flow-induced-A RULE-OF-MIXTURES MODEL FOR FLOW-INDUCED ALTERATIONS IN THE GEOMETRY, STRUCTURE, Cardiovascular Solid Mechanics: Cells, Tissues, and Organs Jay D Humphrey biomechanics-wikipedia, the free encyclopedia-(1899) and the related "biomechanical" Mechanical Properties of Living Tissues. Cardiovascular solid mechanics : cells, tissues, joint materials/ solid mechanics seminar series-Joint Materials/Solid Mechanics Seminar Series Adaptation in Vascular Tissues Patrick Alford a key role in cardiovascular amazon.com: jay d. humphrey: books-Online shopping from a great selection at Books Store. Try Prime Books cardiovascular solid mechanics. cells, tissues,-Cardiovascular solid mechanics. Cells, tissues, and organs Jay D. Humphrey (Ed.
Heating therapies are increasingly used in cardiology, dermatology, gynecology, neurosurgery, oncology, ophthalmology, orthopedics, and urology, among other medical specialties. This widespread use of heating is driven primarily by the availability of new technology, not by a detailed understanding of the biothermomechanics. Without basic quantification of the underlying physical and chemical processes in terms of parameters that can be controlled clinically, identification of preferred interventions will continue to be based primarily on trial and error, thus necessitating large clinical studies and years of accumulative experience. Perusal of the literature reveals that much has been learned over the past century about the response of cells, proteins, and tissues to supra-physiologic temperatures; yet, the associated findings are reported in diverse journals and the underlying basic processes remain unidentified. In this review, we seek to contrast various findings on the kinetics of the thermal denaturation of collagen and to encourage investigators to consider the many open problems in part via a synthesis of results from the diverse literatures.
The structural protein elastin endows large arteries with unique biological functionality and mechanical integrity, hence its disorganization, fragmentation, or degradation can have important consequences on the progression and treatment of vascular diseases. There is, therefore, a need in arterial mechanics to move from materially uniform, phenomenological, constitutive relations for the wall to those that account for separate contributions of the primary structural constituents: elastin, fibrillar collagens, smooth muscle, and amorphous matrix. In this paper, we employ a recently proposed constrained mixture model of the arterial wall and show that prestretched elastin contributes significantly to both the retraction of arteries that is observed upon transection and the opening angle that follows the introduction of a radial cut in an unloaded segment. We also show that the transmural distributions of elastin and collagen, compressive stiffness of collagen, and smooth muscle tone play complementary roles. Axial prestresses and residual stresses in arteries contribute to the homeostatic state of stress in vivo as well as adaptations to perturbed loads, disease, or injury. Understanding better the development of and changes in wall stress due to individual extracellular matrix constituents thus promises to provide considerable clinically important insight into arterial health and disease.
Hypertension results in a thickening of the arterial wall due to a net increase in wall constituents via a coordinated production and removal of smooth muscle and extracellular matrix. Although many reports address the associated changes in material properties, few models address the biomechanics of the growth and remodeling process. In this paper, we employ a new, fundamentally different approach to modeling arterial adaptation in hypertension. In particular, basic, characteristic features of hypertension are simulated using a constrained mixture model wherein individual constituents can turnover at different rates and can have different natural configurations. We show, for example, that if there is no turnover of elastin (which approximates responses in maturity), the model vessel is able to reduce an early elevation in wall stress via a thickening of the wall even though the adaptation may be suboptimal. Conversely, if all constituents can turnover completely (which may approximate late development), the model vessel can restore the state of stress and material properties to native values. Given the potential of such a model, there is a need for more data on the history of turnover of individual constituents and their individual material properties.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.