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      Data-driven Modeling of Hemodynamics and its Role on Thrombus Size and Shape in Aortic Dissections

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          Abstract

          Aortic dissection is a pathology that manifests due to microstructural defects in the aortic wall. Blood enters the damaged wall through an intimal tear, thereby creating a so-called false lumen and exposing the blood to thrombogenic intramural constituents such as collagen. The natural history of this acute vascular injury thus depends, in part, on thrombus formation, maturation, and possible healing within the false lumen. A key question is: Why do some false lumens thrombose completely while others thrombose partially or little at all? An ability to predict the location and extent of thrombus in subjects with dissection could contribute significantly to clinical decision-making, including interventional design. We develop, for the first time, a data-driven particle-continuum model for thrombus formation in a murine model of aortic dissection. In the proposed model, we simulate a final-value problem in lieu of the original initial-value problem with significantly fewer particles that may grow in size upon activation, thus representing the local concentration of blood-borne species. Numerical results confirm that geometry and local hemodynamics play significant roles in the acute progression of thrombus. Despite geometrical differences between murine and human dissections, mouse models can provide considerable insight and have gained popularity owing to their reproducibility. Our results for three classes of geometrically different false lumens show that thrombus forms and extends to a greater extent in regions with lower bulk shear rates. Dense thrombi are less likely to form in high-shear zones and in the presence of strong vortices. The present data-driven study suggests that the proposed model is robust and can be employed to assess thrombus formation in human aortic dissections.

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          Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice.

          Increased plasma concentrations of angiotension II (Ang II) have been implicated in atherogenesis. To examine this relationship directly, we infused Ang II or vehicle for 1 month via osmotic minipumps into mature apoE(-/-) mice. These doses of Ang II did not alter arterial blood pressure, body weight, serum cholesterol concentrations, or distribution of lipoprotein cholesterol. However, Ang II infusions promoted an increased severity of aortic atherosclerotic lesions. These Ang II-induced lesions were predominantly lipid-laden macrophages and lymphocytes; moreover, Ang II promoted a marked increase in the number of macrophages present in the adventitial tissue underlying lesions. Unexpectedly, pronounced abdominal aortic aneurysms were present in apoE(-/-) mice infused with Ang II. Sequential sectioning of aneurysmal abdominal aorta revealed two major characteristics: an intact artery that is surrounded by a large remodeled adventitia, and a medial break with pronounced dilation and more modestly remodeled adventitial tissue. Although no atherosclerotic lesions were visible at the medial break point, the presence of hyperlipidemia was required because infusions of Ang II into apoE(+/+) mice failed to generate aneurysms. These results demonstrate that increased plasma concentrations of Ang II have profound and rapid effects on vascular pathology when combined with hyperlipidemia, in the absence of hemodynamic influences.
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            A CONSTRAINED MIXTURE MODEL FOR GROWTH AND REMODELING OF SOFT TISSUES

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              Analysis of the Casson and Carreau-Yasuda non-Newtonian blood models in steady and oscillatory flows using the lattice Boltzmann method

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                Author and article information

                Contributors
                alireza_yazdani@brown.edu
                george_karniadakis@brown.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                6 February 2018
                6 February 2018
                2018
                : 8
                : 2515
                Affiliations
                [1 ]ISNI 0000 0004 1936 9094, GRID grid.40263.33, Division of Applied Mathematics, , Brown University, ; Providence, RI 02912 USA
                [2 ]ISNI 0000000419368710, GRID grid.47100.32, Department of Biomedical Engineering, , Yale University, ; New Haven, CT 06520 USA
                [3 ]ISNI 0000 0000 9003 8934, GRID grid.261128.e, Argonne National Laboratory, , Argonne, IL 60439; Northern Illinois University, ; DeKalb, IL 60115 USA
                Article
                20603
                10.1038/s41598-018-20603-x
                5802786
                29410467
                a325b612-8c54-4e04-a040-34ddd5249d03
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 8 September 2017
                : 22 January 2018
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