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Office: JE 376
Phone: (614) 688-0427
Email: rschugart@mbi.osu.edu
Webpage: http://people.mbi.ohio-state.edu/rschugart/
Mentors: Avner Friedman (MBI) and Chandan Sen (Departments of Surgery and Molecular and Cellular Biochemistry, Davis Heart & Lung Research Institute)
Research Area
My research focuses on differential equation modeling and scientific computing for biomedical problems. The research is usually in collaboration with bioscientists, where we try to identify problems in which our work has the potential for impact on the biomedical field. I am currently working on problems in the areas of wound healing, hemodialysis, and cartilage.
Angiogenesis is the formation of blood vessels from existing vasculature. A mathematical model was developed to analyze how to best promote dermal wound angiogenesis with oxygen treatment. The key components of the model are macrophages, growth factors, fibroblasts, extracellular matrix, oxygen, and endothelial cells, which are divided into endothelial cell tips and sprouts. The level of angiogenesis is measured by the density of endothelial cell sprouts. There is agreement between the model simulations regarding a sufficiently hypoxic wound, hyperoxic treatment, and the use of intermittent hyperbaric oxygen therapy, as cited in [1]. This work in is collaboration with Dr. Chandan Sen, Director of the Comprehensive Wound Center at The Ohio State University, and Dr. Avner Friedman.
In order for hemodialysis to be performed for patients with kidney failure, vascular access is obtained by connecting an artery to a vein. The most common cause of vascular access failure is intimal hyperplasia of vascularized smooth muscle cells (VSMCs), characterized by a narrowing or blockage of a blood vessel due to excess VSMCs and extracellular matrix (ECM), at either the venous end of the connection or in the downstream proximal vein. Several studies have not only implicated the enhanced production of cytokines in the occurrence of neointimal hyperplasia, as cited in [2], but also have suggested these cyokines could be potential therapeutic targets. However, no mathematical model has been constructed to account for all of the cellular and molecular interactions related to hemodialysis access failure. A simplified mathematical model was developed with three variables representing the growth factors, cells, and ECM, and numerically solved on a radially, symmetric cross-section. The simulations suggest that decreasing the initial concentration of cytokines delays vascular access dysfunction due to venous neointimal hyperplasia. This work is in collaboration with Drs. Brad Rovin, Chris Valentine, and Anil Agarwal in the Division of Nephrology of The Ohio State University Medical Center, and Drs. Avner Friedman and Paula Grajdeanu.
Osteoarthritis is characterized by the degradation of cartilage in joints. One surgical procedure used to aid in the healing process is to remove the degraded cartilage down into the subchondral bone where an influx of mesenchymal stem cells can enter the defect region. While this surgical procedure helps the healing response of the tissue, the cartilage still does not heal well. A mathematical model has been developed representing the healing response following surgery. The key features captured in the model are the stem-cell differentiation process and the production of cartilage ECM vs. non-cartilage ECM. The model is to be used to study factors that can improve the healing response of cartilage. This work is in collaboration with Dr. Alicia Bertone, Endowed Chair of Equine Clinical Medicine and Surgery for the Department of Veterinary Clinical Sciences at The Ohio State University, and Dr. Avner Friedman.
My dissertation research involved the development of numerical methods and mathematical models to analyze the mechanics of articular cartilage. The research was motivated by the need to quantify the differences between the normal and osteoarthritic mechano-chemical states of cartilage. The first problem involved the development of an accelerated numerical method for the continuous spectrum biphasic (BPVE) model of articular cartilage formation [3]. The second problem involved the formulation and application of triphasic mechano-chemical models to analyze osmotic loading experiments for both the cartilage cell and chondron, which is the term used to describe the cartilage cell combined with the distinct region of ECM that surrounds the cell [4]. This research was directed under the supervision of my dissertation adviser, Dr. Mansoor Haider, in the Department of Mathematics at North Carolina State University, and was in collaboration with Dr. Farshid Guilak, Director of the Orthopaedic Bioengineering Laboratory at the Duke University Medical Center.
[1] R.C. Schugart, A. Friedman, R. Zhao, and C.K. Sen, Wound angiogenesis as a function of tissue oxygen tension - a mathematical model, Proceedings of the National Academy of Sciences (to appear).
[2] P. Budu-Grajdeanu, R.C. Schugart, C. Valentine, A. K. Agarwal, and B.H. Rovin, A mathematical model of venous neointimal hyperplasia, Theoretical Biology and Medical Modelling (to appear).
[3] M.A. Haider and R.C. Schugart, A numerical method for the continuous spectrum biphasic poroviscoelastic model of articular cartilage, Journal of Biomechanics, 39: 177 - 83 (2006).
[4] M.A. Haider, R.C. Schugart, L.A. Setton, and F. Guilak, A mechano-chemical model for the passive swelling response of an isolated chondron under osmotic loading, Biomechanics and Modeling in Mechanobiology, 5: 160 - 71 (2006).
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