| Name: | Joe E. Springer |
| Position Type: | Chair |
| Appointment Start Date: | 07/01/04 |
| Appointment End Date: | 06/30/09 |
| Area of Specialty: | Work with COX2 inhibitors in slowing injury to cells, ID markers in cell indicating area of injury |
| Summary Vita: | Dr. Springer was appointed to the Cardinal Hill Rehabilitation Endowed Chair for Neuro-rehabilitation in July, 2004. He currently has active research in COX-2 Pathophysiology in Spinal Cord Injury, COX-2 Induction in Traumatic Spinal Cord Injury, & Apoptosis in Traumatic Spinal Cord Injury. Funding support is from NIH and KSCHIRT. He is the Vice-Chair for Research in the Department of Physicial Medicine& Rehabilitation, where he has been active in recruiting for the endowed professorship in Spinal Cord Injury and Head Injury. He maintains an active teaching schedule & Serves as post-doctorial advisor. He serves on several professional boards, grant review committees and editorial boards. He has over 175 articles, abstracts and book chapters, many as the first author. |
| Highest Degree: | Ph.D. |
| Professional Affiliations: | Cardinal Hill Research Committee; NSD-A Study section: New Jersey Commission on Spinal Cord Injury Research Review Board; Ad Hoc Grant Reviewer - NSF, VA, Wellcom Trust, New Zealand Neurological Foundation & Medical Research Council of Canada; Editorial Board Member - Journal of Neurochemistry, Journal of Neurotrauma; College of Medicine Faculty Appointments, Appeals, Promotions, & Tenure; Chair & Organizer for 2005 Advances in Neurorehabilitative Research; Executive Committee, Advisory Board and Associate Member Spianl Cord & Brain Injur Research Center; President-elect - Bluegrass Chapter of the Society for Neuroscience; & Advisory Board for the Kentucky Neuroscience Orthopedic Research Institute. |
| Primary Research Focus: | CNS trauma especially spinal cord injury. |
| Key Contributions: | Work with COX2 inhibitors in slowing injury to cells, ID markers in cell indicating area of injury, Treatment strategies In CNS trauma, Recovery of funtion following CNS damage. |
| Publications: | Treatment with the cyclosporine derivative NIM811 improves mitochondrial function and reduces oxidative damage following spinal cord contusion Journal of Neurotrauma The mitochondrial uncoupling agent 2, 4-dinitrophenol improves mitochondrial function, attenuates oxidative damage and increases white matter sparing in the contused spinal cord. Journal of Neurotrauma Time course of caspase-3 activation following traumatic spinal cord injury Journal of Histochemistry and Cytochemistry XIAP overexpresson prevents cell death in an immortalized oligodendroglial cell death? Cellular and Molecular Neurobiology Targeting mitochondrial uncoupling as a possible therapeutic intervention following traumatic brain injury Journal of Neuroscience Research Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death Journal of Neuroscience Research Post-treatment with the cyclosporine derivative NIM811 reduces cytochrome c release and cell death, and increases white matter sparing following spinal cord injury Journal of Neurotrauma The Biology of Caspases In Central Nervous System Trauma: A Potential Therapeutic Target Handbook of Neurochemistry and Molecular Neurobiology Effects of spinal cord contusion on gait and parameters of locomotor function in adult rats Journal of Neurotraum |