Menu
Close
Funded Projects

Quantifying Patellar Tendon Loads During Rehabilitation Exercises in Patients with Patellar Tendon Injuries

Awarded in 2024
Postdoctoral Grant
Updated Sep 8, 2025

At a Glance

Patellar tendon injuries are common and can lead to lasting mobility issues. Exercise is the best treatment, but current methods often misjudge actual tendon load, limiting recovery. This project uses new UW—Madison – Shear Wave Tensiometry (SWT) to directly measure tendon load and quantitative ultrasound (qUS) to assess tendon health. It will test how neuromuscular electrical stimulation (NMES) enhances tendon loading and explore links between tendon structure and function. The findings will guide more precise rehabilitation strategies, improving healing and long-term outcomes for people with tendon injuries.

More Funded Projects

research icon: microscope and stethoscope
Postdoctoral Grant

Longitudinal Changes in Gut Microbiome Composition is Associated with Biofluid Markers of Alzheimer’s Disease

Awarded in 2024
Alzheimer’s disease (AD) affects more than 110,000 older adults in Wisconsin and remains without a cure. Emerging evidence suggests the gut microbiome may play a role in AD pathology, but how these changes unfold over time is not well understood. This project will analyze longitudinal fecal samples, fluid biomarkers and cognitive scores from participants in the Wisconsin Registry for Alzheimer’s Prevention (WRAP) and the Alzheimer’s Disease Research Center (ADRC). The study will test whether shifts in gut microbiome composition are linked to amyloid status, cognitive decline and AD biomarkers in plasma and cerebrospinal fluid. Findings are expected to identify specific gut microbes associated with AD progression, laying the groundwork for future therapeutic targets and larger multicenter studies.
research icon: microscope and stethoscope
Postdoctoral Grant

SDH Inhibition Promotes Cardiac Regeneration in Myocardial Infarction by Reprogramming Myofibroblast Metabolism

Awarded in 2024
Cardiovascular disease remains the leading cause of death in the U.S., in part because the adult heart cannot regenerate after myocardial infarction (MI). This project explores how inhibiting succinate dehydrogenase (SDH) in myofibroblasts can reduce fibrosis and promote heart repair. Preliminary studies show SDH inhibition reprograms fibroblast metabolism, limits scar formation and boosts cardiomyocyte regeneration. By uncovering the mechanisms behind this process, the study aims to pave the way for new regenerative therapies to improve outcomes after heart attack.