Arterial Tissue

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A.m. Robertson - One of the best experts on this subject based on the ideXlab platform.

  • EMBC - Theory and application of Arterial Tissue in-host remodelling
    Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and, 2015
    Co-Authors: A. Valentin, D. Notaro, P. Zunino, D. Ambrosi, Y. Wang, Robert A. Allen, A.m. Robertson
    Abstract:

    A central therapeutic goal in many applications of modern Biomedicine is the reconstruction of the diseased Arterial sections via robust and viable Tissue equivalents. In-host remodelling is an emerging technology that exploits the remodelling ability of the host to regenerate Tissue. We develop a general theoretical framework of growth and remodeling of Arterial Tissue starting from a synthetic, degradable, acellularized graft and we demonstrate the potential of mechanistic models to guide the development and assisting in the design of Arterial Tissue engineered constructs.

  • Theory and application of Arterial Tissue in-host remodelling
    2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC), 2015
    Co-Authors: A. Valentin, D. Notaro, P. Zunino, R. Allen, D. Ambrosi, Y. Wang, A.m. Robertson
    Abstract:

    A central therapeutic goal in many applications of modern Biomedicine is the reconstruction of the diseased Arterial sections via robust and viable Tissue equivalents. In-host remodelling is an emerging technology that exploits the remodelling ability of the host to regenerate Tissue. We develop a general theoretical framework of growth and remodeling of Arterial Tissue starting from a synthetic, degradable, acellularized graft and we demonstrate the potential of mechanistic models to guide the development and assisting in the design of Arterial Tissue engineered constructs.

  • A Structural Multi-Mechanism Damage Model for Cerebral Arterial Tissue
    Journal of Biomechanical Engineering-transactions of The Asme, 2009
    Co-Authors: Dalong Li, A.m. Robertson
    Abstract:

    Early stage cerebral aneurysms are characterized by the disruption of the internal elastic lamina. The cause of this breakdown is still not understood, but it has been conjectured to be due to fatigue failure and/or by a breakdown in homeostatic mechanisms in the wall arising from some aspect of the local hemodynamics and wall tension. We propose to model this disruption using a structural damage model. It is built on a previously introduced nonlinear, inelastic multi-mechanism model for cerebral arteries (2005, "An Inelastic Multi-Mechanism Constitutive Equation for Cerebral Arterial Tissue, " Biomech. Model. Mechanobiol., 4(4), pp. 235-248), as well as a recent generalization to include the wall anisotropy (2009, "A Structural Multi-Mechanism Constitutive Equation for Cerebral Arterial Tissue, " Int. J. Solids Struct., 46(14-15), pp. 2920-2928). The current model includes subfailure damage of the elastin, represented by changes in the Tissue mechanical properties and unloaded reference length. A structural model is used to characterize the gradual degradation, failure of elastin, and recruitment of anisotropic collagen fibers. The collagen fibers are arranged in two helically oriented families with dispersion in their orientation. Available inelastic experimental data for cerebral arteries are used to evaluate the constitutive model. It is then implemented in a commercial finite element analysis package and validated using analytical solutions with representative values,for cerebral Arterial Tissue.

  • A structural multi-mechanism constitutive equation for cerebral Arterial Tissue
    International Journal of Solids and Structures, 2009
    Co-Authors: Dalong Li, A.m. Robertson
    Abstract:

    Abstract A structural multi-mechanism constitutive equation is developed to describe the nonlinear, anisotropic, inelastic mechanical behavior of cerebral Arterial Tissue. Elastin and collagen fibers are treated as separate components (mechanisms) of the artery. Elastin is responsible for load bearing at low strain levels while the collagen mechanism is recruited for load bearing at higher strain levels. This work builds on an earlier model in which both the elastin and collagen mechanisms are represented by isotropic response functions [Wulandana, R., Robertson, A.M., 2005. An inelastic multi-mechanism constitutive equation for cerebral Arterial Tissue. Biomech. Model. Mechan. 4 (4), 235–248]. Here, the anisotropic material response of the wall is introduced through the collagen mechanism which is composed of helically distributed families of fibers. The orientation of these families is described using either a finite number of fiber orientations or a fiber distribution function. The fiber orientation or dispersion function can be prescribed directly from Arterial histology data, or, taking a phenomenological approach, based on data fitting from bi-axial measurements. The activation of the collagen mechanism is specified using a new fiber strain based activation criterion. The multi-mechanism constitutive equation is applied to the simple case of cylindrical inflation and material constants are determined based on available inelastic experimental data for cerebral arteries. While the proposed model captures all features of this inelastic data, there is a pressing need for further experiments to refine the model.

  • An inelastic multi-mechanism constitutive equation for cerebral Arterial Tissue.
    Biomechanics and Modeling in Mechanobiology, 2005
    Co-Authors: R. Wulandana, A.m. Robertson
    Abstract:

    Intracranial aneurysms (ICA) are abnormal saccular dilations of cerebral arteries, commonly found at apices of Arterial bifurcations and outer walls of curved Arterial segments. Histological evidence suggests the stages in ICA development include the deformation of a segment of Arterial wall into a “bleb” with no identifiable neck region followed by the development of an aneurysm with a clear neck. Afterwards, the aneurysm may undergo further enlargement, possibly with significant biological response including calcification and thrombosis. Past studies of the biomechanics of cerebral aneurysm Tissue have been directed at modeling elastic deformations of pre-existing aneurysms. Taking this approach, the aneurysm wall is treated as a different entity than the Arterial Tissue from which it developed. In the current work, a nonlinear, inelastic, dual-mechanism constitutive equation for cerebral Arterial Tissue is developed. It is the first to model the recruitment of collagen fibers and degradation of the internal elastic lamina, two important characteristics of early stage aneurysm formation.

Darrin Smith - One of the best experts on this subject based on the ideXlab platform.

  • retention of chylomicron remnants by Arterial Tissue importance of an efficient clearance mechanism from plasma
    Atherosclerosis, 1998
    Co-Authors: John C L Mamo, Spencer D Proctor, Darrin Smith
    Abstract:

    Abstract Atherosclerosis is thought to begin with the trapping of cholesterol rich lipoproteins within the intima of Arterial vessels. Thereafter a complex inflammatory cascade involving recruitment and transformation of leukocytes, accumulation of sterols in macrophages and cellular proliferation, can lead to a progressive occlusion in blood flow, or an unstable Arterial lesion prone to prothrombotic events. Primary intervention strategies aimed at reducing atherogenesis are designed to achieve reductions in sterol rich lipoproteins, primarily low density lipoproteins, given the hypothesis that decreased exposure will attenuate the rate of Arterial cholesterol accumulation. Epidemiological evidence has clearly identified a positive relationship between poor dietary (fat) habits and the onset and progression of atherosclerosis. However lipoproteins which mediate the transport of dietary lipid, that is chylomicrons, are not normally considered to be directly involved in atherogenesis, because of their larger size and inability to efficiently penetrate Arterial Tissue. In contrast, this article reviews recent evidence which suggests that once chylomicrons are hydrolysed to their remnant form, the triglyceride depleted chylomicron remnants penetrate Arterial Tissue and moreover, become preferentially trapped within the subendothelial space as concentrated focii. Ongoing studies demonstrate that significant chylomicron remnant accumulation can occur in a number of primary and secondary lipid disorders and in normolipidemic subjects with coronary artery disease. Chylomicron remnant dyslipidemia in conditions prone to premature atherosclerosis is consistent with the putative atherogenicity of these particles and can be explained by increased Arterial exposure to cholesterol rich chylomicron remnants.

John C L Mamo - One of the best experts on this subject based on the ideXlab platform.

  • retention of chylomicron remnants by Arterial Tissue importance of an efficient clearance mechanism from plasma
    Atherosclerosis, 1998
    Co-Authors: John C L Mamo, Spencer D Proctor, Darrin Smith
    Abstract:

    Abstract Atherosclerosis is thought to begin with the trapping of cholesterol rich lipoproteins within the intima of Arterial vessels. Thereafter a complex inflammatory cascade involving recruitment and transformation of leukocytes, accumulation of sterols in macrophages and cellular proliferation, can lead to a progressive occlusion in blood flow, or an unstable Arterial lesion prone to prothrombotic events. Primary intervention strategies aimed at reducing atherogenesis are designed to achieve reductions in sterol rich lipoproteins, primarily low density lipoproteins, given the hypothesis that decreased exposure will attenuate the rate of Arterial cholesterol accumulation. Epidemiological evidence has clearly identified a positive relationship between poor dietary (fat) habits and the onset and progression of atherosclerosis. However lipoproteins which mediate the transport of dietary lipid, that is chylomicrons, are not normally considered to be directly involved in atherogenesis, because of their larger size and inability to efficiently penetrate Arterial Tissue. In contrast, this article reviews recent evidence which suggests that once chylomicrons are hydrolysed to their remnant form, the triglyceride depleted chylomicron remnants penetrate Arterial Tissue and moreover, become preferentially trapped within the subendothelial space as concentrated focii. Ongoing studies demonstrate that significant chylomicron remnant accumulation can occur in a number of primary and secondary lipid disorders and in normolipidemic subjects with coronary artery disease. Chylomicron remnant dyslipidemia in conditions prone to premature atherosclerosis is consistent with the putative atherogenicity of these particles and can be explained by increased Arterial exposure to cholesterol rich chylomicron remnants.

M. D. Walsh - One of the best experts on this subject based on the ideXlab platform.

Yuan Cheng Fung - One of the best experts on this subject based on the ideXlab platform.

  • Tissue Remodeling of Rat Pulmonary Artery in Hypoxic Breathing. I. Changes of Morphology, Zero-Stress State, and Gene Expression
    Annals of Biomedical Engineering, 2001
    Co-Authors: Wei Huang, Yuh-pyng Sher, David Delgado-west, Jonathan T. Wu, Konan Peck, Yuan Cheng Fung
    Abstract:

    The remodeling of the pulmonary Arterial Tissue in response to a step change of the oxygen concentration in the gas in which a rat lives was recorded as function of time and function of O_2 concentration. Three steps of changing from 20.9% to 17.2%, 13.6%, and 10% O_2 were imposed. Earlier work in our laboratory has shown that pulmonary Arterial Tissue remodeling is significant in the first 24 h after a step change of oxygen tension. Hence we made measurements in this period. Furthermore, data were obtained for Tissue remodeling of circumferential and axial lengths of the pulmonary arteries. We recorded the activities of gene expressions in the lung Tissues by microarray, determined the dose response curves of gene expression in the homogenized whole lungs with respect to four levels of O_2 concentration, and obtained the time courses of gene expression in the lung parenchyma in 30 days after a step decrease of O_2 concentration from 20.9% to 10%. We would like to suggest that the correlation of gene expression with physiological function parameters, i.e., time, O_2 tension, blood pressure, opening angle, wall thicknesses, etc., is the way to narrow down the search for specific genes for specific physiological functions. © 2001 Biomedical Engineering Society. PAC01: 8719Uv