| Affiliations: | |
| Project Leader: | Michael E. DeBakey Institute Undergraduate Research Program |
| Faculty Mentor: | Juzar Hussain Juzar94@tamu.edu Biomedical Sciences |
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Meeting Times:
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Stewart, Randolph |
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Team Size:
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Fall 2016: Monday & Wednesday 12:30-4:30 |
| Open Spots: | 0 |
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Special Opportunities:
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2 (Team Full) |
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Team Needs:
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Description:
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The ductus arteriosus (DA) is a muscular artery connecting the aorta to the pulmonary artery in fetuses. It normally regresses shortly after birth, but fails to close in some individuals, causing a multitude of issues ranging from pulmonary hypertension to heart failure. Although it is unknown why the DA spontaneously regresses or becomes patent (i.e., PDA), clinical investigators have identified the existence of a critical radius governing its behavior. In general, if the DA is larger than 1 mm, patients will be treated pharmacologically with Indomethacin. If it remains patent, it will be closed surgically. Three challenges remain for clinical research: 1) reducing the risk factors for PDA, 2) increasing the efficacy of Indomethacin, 3) developing patient-specific criteria for surgery. All three challenges cannot be met without first identifying the primary mechanism of spontaneous regression. There is, however, a fundamental property of adapting vessels that has been previously identified using mathematical modeling. Assuming that arteries primarily adapt to changes in endothelial shear stress leads to the prediction of two equilibrium radii. The larger of the two is always stable, and resists regression. The smaller equilibrium radius is always unstable, and constriction below this critical radius causes vessels to remodel and regress. The purpose of this project is therefore to develop a mathematical model to test the hypothesis that the patency and spontaneous regression of the DA is a manifestation of adaptation to shear stress leading to both stable and unstable equilibrium radii. |