Kimberly R. Byrnes, Ph.D.

Kimberly R. Byrnes, Ph.D.

Kimberly Byrnes

Name: Kimberly R. Byrnes, Ph.D.

Department of Primary Appointment: Anatomy, Physiology & Genetics
Position: USU Faculty
Title: Associate Professor

Email: kimberly.byrnes@usuhs.edu (link sends e-mail)
Office Phone: (301) 295-3217
Lab Phone: 301-295-9372
Room: Room C2115

Profile

  • Ph.D., Uniformed Services University of the Health Sciences, 2003

 

Traumatic Brain and Spinal Cord Injury: Post-Injury Inflammation and Metabolic Changes

 

The research in Dr. Byrnes' laboratory focuses on the mechanisms of inflammation following traumatic brain and spinal cord injury using animal modeling, non-invasive imaging, behavioral assessments and a variety of therapeutic approaches.  There are two major lines of investigation currently ongoing in the lab:

 

1.      The role of NADPH oxidase in recovery after spinal cord injury.  Spinal cord injury (SCI) results in both acute and chronic inflammation.  This inflammation includes activation of microglia, invasion of macrophages and activation of the NADPH oxidase (NOX) enzyme.  We have previously shown that NOX, particularly the NOX2 and 4 isoforms, are up-regulated after central nervous system (CNS) injury in a number of cells, including microglia and macrophages.  This enzyme is responsible for producing reactive oxygen species, and contributes to oxidative stress that can lead to further inflammation, neuronal damage and impairment of recovery.  The lab is now investigating the mechanism behind NOX activation, the effects of inhibition of the NOX enzyme, and the role of NOX in aging with SCI, using both animal and cell culture models, as well as behavioral, histological, magnetic resonance imaging, and biochemical outcomes. 

 

2.      The role of glucose uptake in outcome after brain and spinal cord injury.  Previously, we have shown that a single mild traumatic brain injury (mTBI) results in a transient reduction in brain glucose uptake as measured by [18F]fluorodeoxyglucose (FDG) with positron emission tomography (PET).  This transient reduction in uptake is maximally depressed at 24 hours post-injury with a return to baseline level by 16 days.  Glucose uptake impairments have been correlated with impairments in motor function, cognitive function and glial activation.  The lab is now investigating the correlation of glucose uptake alterations with outcome after a repeated mTBI model and after spinal cord injury.  In addition, the lab is investigating novel therapeutic approaches to improve glucose uptake and alter recovery after injury.

 

Pubmed Link (http://www.ncbi.nlm.nih.gov/pubmed?term=Byrnes%20KR[Author])