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Wesley L. Harris. Tekleab, Yonatan Massachusetts Institute of Technology. Dept. of Aeronautics and Astronautics. Massachusetts Institute of Technology. Department of Aeronautics and Astronautics 2011-11-18T20:59:07Z 2011-11-18T20:59:07Z 2011 2011 http://hdl.handle.net/1721.1/67195 758673438 Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 2011. Cataloged from PDF version of thesis. Includes bibliographical references (p. 143-144). Sickle cell disease is a genetic disorder that alters red blood cells such that their hemoglobin cannot effectively bind and release oxygen. This causes issues that affect how the cell operates in the smallest vessels of the body. In the past, computational models have been used to study the microcirculation to gain a better understanding of blood disorders such as sickle cell disease. A fast, time efficient computational model has been developed to analyze perturbations in the microcirculation caused by sickle cell disease. The model uses a finite difference, Crank-Nicholson scheme for the flow and oxygen computation, while using the level set computational method to advect the red blood cell membrane on a staggered grid. A number of initial and boundary conditions were tested in the model. The simulation data shows several important parameters to be significant in the perturbation of the blood flow and oxygen concentration profiles. Specifically, the Hill coefficient, arterial oxygen partial pressure, oxygen partial pressure at 50% hemoglobin saturation, and cell membrane stiffness are significant factors. by Yonatan Tekleab. S.M. 144 p. eng Massachusetts Institute of Technology M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission. http://dspace.mit.edu/handle/1721.1/7582 Aeronautics and Astronautics. A perturbation model for normal and sickle cell blood microcirculation Thesis application/pdf Publication unknown unknown <Publication xmlns="https://www.openaire.eu/cerif-profile/1.1/" id="ff8057fa-cf13-4e74-8e0c-5aca0785f552"> <Type xmlns="https://www.openaire.eu/cerif-profile/vocab/COAR_Publication_Types">http://purl.org/coar/resource_type/c_1843</Type> <Language>eng</Language> <Title>A perturbation model for normal and sickle cell blood microcirculation</Title> <PublishedIn> <Publication> </Publication> </PublishedIn> <PublicationDate>2011</PublicationDate> <Authors> <Author> <DisplayName>Tekleab, Yonatan</DisplayName> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> </Authors> <Editors> </Editors> <Publishers> <Publisher> <DisplayName>Massachusetts Institute of Technology</DisplayName> <OrgUnit /> </Publisher> </Publishers> <License>http://dspace.mit.edu/handle/1721.1/7582</License> <Keyword>Aeronautics and Astronautics.</Keyword> <Abstract>Sickle cell disease is a genetic disorder that alters red blood cells such that their hemoglobin cannot effectively bind and release oxygen. This causes issues that affect how the cell operates in the smallest vessels of the body. In the past, computational models have been used to study the microcirculation to gain a better understanding of blood disorders such as sickle cell disease. A fast, time efficient computational model has been developed to analyze perturbations in the microcirculation caused by sickle cell disease. The model uses a finite difference, Crank-Nicholson scheme for the flow and oxygen computation, while using the level set computational method to advect the red blood cell membrane on a staggered grid. A number of initial and boundary conditions were tested in the model. The simulation data shows several important parameters to be significant in the perturbation of the blood flow and oxygen concentration profiles. Specifically, the Hill coefficient, arterial oxygen partial pressure, oxygen partial pressure at 50% hemoglobin saturation, and cell membrane stiffness are significant factors.</Abstract> <Access xmlns="http://purl.org/coar/access_right" > </Access> </Publication>