Thomas Van de Ven, MD, PhD, Assistant Professor of Anesthesiology, has been awarded a one-year, $9,036 voucher for his proposal entitled, “Transcriptional Profiling of Sciatic Nerve Samples from Traumatic Amputees.”
The 2015 Spring Core Facility Voucher Program is a joint program with the School of Medicine (SOM), the Duke Translational Research Institute (DTRI) Pilot Program and the Office of the Provost. The SOM departments, institutes and centers oversee a wide range of research core facilities. To enable investigators to access these services for exciting new studies that are not yet externally funded, they offer the 2015 Spring Core Facility Voucher Program. The program offers vouchers in amounts ranging from $500 to $10,000, redeemable for provision of services at School of Medicine core facilities/shared resources.
Dr. Van de Ven will use the funds for RNA sequencing and Data Analysis at two SOM core facilities/shared resources.
Chronic neuropathic pain (NP) frequently occurs following nerve injury. One significant etiology of NP is limb amputation, where more than 50% of patients experience chronic, unremitting pain in the form of phantom or residual limb pain. The pathogenesis of NP in such patients is not well understood, and consequently, the treatment options available to treat NP are greatly limited. In order to better understand the pathological processes that lead to neuropathic pain after nerve injury, it is necessary to comprehensively study injured human nerves. Toward this end, our collaborators at the Walter Reed Army Medical Center have collected injured sciatic nerve segments from veterans who suffered lower limb amputation due to combat trauma. Analysis of these exceedingly precious human samples would provide unprecedented insights into the molecular pathology of peripheral nerve injury, with wide ranging implications for the study of pain and neural regeneration. Specifically, we propose to investigate the gene expression profiles of these injured sciatic nerves, with the aim of uncovering differentially expressed genes and activated molecular pathways that contribute to NP.