Jason Marvin Chang (Jason C. Marvin)
5th Year PhD Candidate in Biomedical Engineering
NSF GRFP Fellow, Cornell Provost Diversity Fellow, & Cornell Dean’s Scholar
Email: jmc722@cornell.edu
Personal Website: https://www.jasoncmarvin.com/
Twitter: @JasonCMarvin
Curriculum Vitae
Education
M.S. in Biomedical Engineering, Cornell University, 2019
B.S. in Biomedical Engineering, University of Texas at Dallas, 2017
Research
Injured tendons heal by forming fibrotic scar tissue (‘scar-mediated healing’) which results in impaired biomechanical properties and increased risk of re-injury. A major hurdle to the development of tissue engineering approaches and therapeutics for restoring function in injured tendons is that the biological mechanisms underlying tendon healing are unknown. However, the regenerative capacity across multiple tissue types in the Murphy Roths Large (MRL/MpJ) mouse strain has identified it as a promising model to study scarless tendon healing. My research investigates the utility of the MRL/MpJ extracellular matrix (ECM) to promote scarless tendon healing in typically scar-mediated environments.
Personal Biography
Jason (he/they) is originally from Dallas, Texas. Outside of the lab, Jason serves as a Graduate Resident Fellow (GRF) in the West Campus Housing System, a Center for Teaching Innovation (CTI) Graduate Teaching Fellow, and organizer for ComSciCon-ScienceWriters 2019. He also participates in several mentoring and K-12 STEM outreach programs at Cornell. In his free time, Jason enjoys cooking (and eating) new cuisines, playing with dogs, good coffee and discussing current events.
Marguerite Pacheco
3rd Year PhD Student in Biomedical Engineering
Cornell Dean’s Scholar & Sloan UCEM Affiliate
NSF GRFP Fellow
Email: map476@cornell.edu
Education
B.A. in Biochemistry; Engineering, Smith College, 2019
Research
Tendinopathies are debilitating injuries and we have a very poor mechanistic understanding of the pathogenesis and healing of this injury. I research the underlying mechanism of healing with the intent to optimize this function for therapeutic applications.
Personal Biography
Marguerite is from Montclair, NJ and enjoys playing soccer, dancing, and reading in her free time. She is actively involved in the Latinx Graduate Student Coalition, QGrads, and BMES outreach activities such as Girl Scout Engineering Day (GSED) and the Graduate Student School Outreach Program (GRASSHOPR).
Lainie Eisner
2nd Year PhD Student in Biomedical Engineering
Pre-doctoral Fellow, HSS-Cornell T32 Combined Engineering and Orthopaedic Training Program
Email: lee45@cornell.edu
Education
B.S.E. in Biomedical Engineering, University of Michigan, 2020
Research
Healthy tendons experience multi-scale mechanotransduction of stresses and strains from the bulk tissue-scale to the matrix- and cell- scales. However, accumulation of matrix damage and altered cell-matrix interactions may disrupt this process in fatigue injured tendon, driving abberant biological outcomes that are a hallmark of tendinopathy. Therefore, my goal is to quantify tendon’s micro-mechanical environment in our lab’s existing in vivo models of fatigue injury and therapeutic exercise, which will contribute to the development of mechanistically-informed strategies for tendon repair.
Personal Biography
Lainie (she/her) is originally from Livingston, New Jersey, a suburb of New York City. She is the current President of Cornell’s Graduate BMES chapter, having previously served as Community Engagement Co-Chair. She is also a Pre-doctoral Fellow in the Cornell-Hospital for Special Surgery Combined Engineering and Orthopaedics Training Program, an NIH T32-funded training program for trainees in the orthopaedic research field. When not in lab, Lainie enjoys theatre, sports, yoga, cooking and playing guitar.
Ben Johnston
1st Year PhD Student in Biomedical Engineering
Email: bbj9@cornell.edu
Education
B.S. in Biomedical Engineering with minor in Computer Science, Washington University in St. Louis, 2021
Research
The early stages of chronic tendon injury are not well understood. I aim to further outline
the pathway and mechanisms by which fatigue loading and overuse leads to disease initiation and progression.