- Dulin JN, Karoly E, Wang Y, Strobel H, Grill RJ. (2013) Licofelone modulates neuroinflammation and attenuates mechanical hypersensitivity in the chronic phase of spinal cord injury. J of Neurosci, 33(2):652-664.
- Dulin JN, Moore ML, Grill RJ Jr. (2013) The dual COX/5-LOX inhibitor licofelone attenuates P-glycoprotein-mediated drug resistance in the injured spinal cord. J of Neurotrauma, 30:211-226.
- Masel BE, Bell RS, Brossart S, Grill RJ, Hayes RL, Levin HS, Rasband MN, Ritzel DV, Wade CE, and DeWitt DS. (2012) Galveston Brain Injury Conference 2010: clinical and experimental aspects of blast injury. J Neurotrauma, 29:2143.
- Navarro JC, Pillai S, Cherian L, Garcia R, Grill RJ, and Robertson CS. (2012) Histopathological and behavioral effects of immediate and delayed hemorrhagic shock after mild traumatic brain injury in rats. J Neurotrauma, 29:322.
- Peng Z, Ban K, Grill R, Park PY, Costantini TW, Lin W, and Kozar RA. (2012) Syndecan-1 plays a novel role in enteral glutamine’s gut protective effects of the post ischemic gut. Shock, 38:57.
- Robertson C, Cherian L, Mahek S, Garcia R, Cruz-Navarro J, Grill RJ, Cerami-Hand C, and Tian TS. (2012) Neuroprotection with an Erythropoietin mimetic peptide (pHBSP) in a model of mild traumatic brain injury complicated by hemorrhagic shock. J Neurotrauma, 29:1156.
- Robertson CS, Garcia R, Gaddam SS, Grill RJ, Cerami-Hand C, Tian TS, and Hannay HJ. (2012) Treatment of mild traumatic brain injury with an erythropoietin- mimetic peptide. J Neurotrauma. Epublished:September 20.
- Robinson M, Herron A, Goodwin B, Grill RJ. (2012) Suprapubic bladder catheterization of male spinal cord injured Sprague-Dawley rats. J of the Am Assoc of Lab Animal Sci, 51(1):76-82.
- Redell J, Moore A, Grill R, Johnson D, Zhao J, Liu Y, and Dash P. (2012) Analysis of functional pathways altered following mild traumatic brain injury. J of Neurotrauma, Epub, Aug. 23, 2012.
- Bedi SS, Lago MT, Masha LI, Crook RJ, Grill RJ, Walters ET. (2011) Spinal cord injury triggers an intrinsic growth-promoting state in nociceptors. J of Neurotrauma, 29:925-35.
- Dash PK, Clark J, Orsi SA, Zhang M, Zhao J, Grill RJ, Moore A, and Pati S. (2011) Involvement of the glycogen synthase kinase-3 signaling pathway in TBI pathology and neurocognitive outcome. PLoS One, 6:e24648.
- McManus MM, Grill RJ. (2011) Longitudinal evaluation of mouse hind limb bone loss after spinal cord injury using novel, in vivo, methodology. J of Visualized Experiments, 7(58):3791/3246.
- Khaing ZZ, Milman BD, Vanscoy JE, Seidlits SK, Grill RJ, Scmidt CE. (2011) High molecular weight hyaluronic acid limits astrocyte activation and scar formation after spinal cord injury. J of Neural Engineering, 8(4):046033.
- Dulin JN, Moore ML, Gates KW, Queen JH, and Grill RJ. (2011) Spinal cord injury causes sustained disruption of the blood-testis barrier in the rat. PlosOne, 6:e16456.
- Pati S, Khakoo AY, Zhao J, Jimenez F, Gerber MH, Harting M, Redell JB, Grill R, Matsuo Y, Guha S, Cox CS, Reitz MS, Holcomb JB, and Dash PK. (2011) Human mesenchymal stem cells inhibit vascular permeability by modulating vascular endothelial cadherin/β-catenin signaling. Stem Cells, 20:89.
- Bedi S, Yang Q, Crook R, Du J, Wu Z, Fishman H, Grill R, Carlton S, and Walters E. (2010) Chronic spontaneous activity generated in the somata of small dorsal root ganglion neurons is associated with pain-related behavior following spinal cord injury. J Neurosci 30(44),14870-82.
- Herrera JJ, Haywood-Watson II RJ, and Grill R. (2010) Acute and chronic deficits in the urinary bladder following spinal contusion injury in the adult rat. J Neurotrauma 27(2):423-31.
Raymond Grill, Ph.D.
UTHSC, Medical School, (713) 500-6132
UT - Curriculum Vitae
Spinal Cord Injury: Acute and Chronic Inflammation
Traumatic injury to the spinal cord initiates a biochemical hurricane that both destroys and alters tissues in such a manner that successful regeneration and repair are stunted, leaving the individual facing a lifetime of paralysis and neurosensory dysfunction. Inflammation is a broadly-used term that describes several of the biochemical processes elicited by spinal trauma. Injury-induced inflammatory mediators play a host of roles including immune activation, cellular protection and cytotoxicity, to name only a few. The role of inflammation has been described as that of a two-edged sword; acting to destroy and remove damaged cells and tissue, but also to initiate reparative healing. It is thought that the timing of inflammatory events determines outcome; for instance, early inflammation is necessary to activate the immune system for clearance of dead cells while late inflammation may drive such processes as glial scarring and neuronal hyperexcitability, leading to chronic neuropathic pain.
Our laboratory is interested in determining the pathological processes that shape outcome following spinal cord injury. While a great deal of scientific interest is focused on ways of preserving damaged spinal tissue in the early time period following injury, we have largely focused on what is referred to as the “chronic” phase of spinal cord injury which in humans can mean months-to-decades and in rodents (our chosen model) months out to a year from insult. It has been this time period that has been so refractory to regeneration and functional improvement. It has been assumed that the inflammatory process is a hallmark of only the acute phase of spinal cord injury. We have recently demonstrated, however, the presence of a profound inflammatory response involving elements of the arachidonic acid signaling pathway in the chronic phase of spinal cord injury. We are currently collaborating with other members of the CRB and the Department of Integrative Biology and Pharmacology to understand: 1) the mechanisms that continue to promote inflammation in the chronic phase of spinal cord injury and 2) the functional ramifications of such chronic inflammation, including both progressive glial hyper-reactivity and vascular dysfunction, and the establishment and maintenance of chronic neuropathic pain.