Sophia Mavris
BME PhD Proposal Presentation
Date: 2024-01-16
Time: 2:00-4:00 PM
Location / Meeting Link: IBB (Suddath Seminar Room) https://gatech.zoom.us/j/95121414200
Committee Members:
Rudolph L. Gleason, PhD (Advisor); J. Brandon Dixon, PhD; Laura Hansen, PhD; Lakshmi Dasi, PhD; Dhruv Singhal, MD
Title: Mechanical Characterization of Lymphatic Growth and Remodeling
Abstract:
Approximately 1 in 1000 Americans are impacted by secondary lymphedema (SL), a vascular disease characterized by excess fluid accumulation in the extremities due to severe injury or damage to the lymphatic system. Ultimately, this impairment can lead to disruption of proper function and maintenance of the cardiovascular system and of nearly every organ in the body. While SL can manifest from different degrees of lymphatic damage, the leading cause is attributed to the surgical removal of lymph nodes (LNs) paired with radiation or chemotherapy in many breast and gynecological cancer patients. Standard SL treatments have remained the same for decades with no available cure; thus, there exists a pressing need to explore and define the biomechanical behavior and properties of the lymphatic system from healthy to fully diseased states. Creating a better understanding of the way the lymphatic system responds to an altered mechanical environment will allow us to work towards our long-term goal of uncovering better preventive measures and developing novel and patient-specific therapies for those with lymphatic injury at risk for SL progression. Little data is available regarding the quantification of growth and remodeling (G&R) of the lymphatic system within health and disease, which drives our proposal goal to develop both lymphatic-injured (Aim 1) and SL-diseased (Aim 2) models to characterize the lymphatic system’s mechanical behavior and property response in comparison to a healthy state. In Aim 1, we hypothesize that intact lymphatic vessels in the lower limb of our animal model will compensate for the lymphatic injury by changing vessel pumping function (30% increase in packet transport, 60% decrease in packet amplitude, and 30% increase in packet frequency) and by growing in outer diameter (40% increase) but will have no significant change in tissue stiffness. In contrast, in Aim 2 we hypothesize that in a SL-diseased state, the adaptive remodeling response will become impaired, yielding less significant differences in vessel pumping function (10% increase in packet transport, 20% decrease in packet amplitude, and 10% increase in packet frequency) and growth (20% increase), but will increase in tissue stiffness by 60%.