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Arterial Tissue

The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform

A.m. Robertson – 1st expert 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.

Darrin Smith – 2nd expert 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 – 3rd expert 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.