The core which is located in SCoBIRC-controlled space on the 4th floor ofthe BBSRB will continue to provide an administrative and organizational framework to support, monitor and coordinate the usage of each of the research cores and related activities and achieve increased collaboration among investigators. Ongoing scheduling of the research cores is done and monitored via our existing OfficeTracker system. Administrative functions will also include financial oversight (including maintenance contracts), and core facility staff management. In addition, the core will continue to maintain a secure server to store and archive scientific data from each of the cores and and individual investigators. The core will also continue to maintain and further develop the existing Spinal Cord Injury-Related Gene Database, or SCIgenes database which is accessible via the internet(httD:// The goal of the database is to serve the spinal cord injury research community by compiling information at a single site about genes and gene products relevant to spinal cord injury such that gene sequence can be linked with protein function so that data mining algorithms will be able to determine patterns in the gene products affected by spinal cord injury. These patterns help predict relationships between proteins and therefore biochemical pathways affected by spinal cord injury.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Center Core Grants (P30)
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National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
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University of Kentucky
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Yonutas, Heather M; Pandya, Jignesh D; Sullivan, Patrick G (2015) Changes in mitochondrial bioenergetics in the brain versus spinal cord become more apparent with age. J Bioenerg Biomembr 47:149-54
Carlson, Shaun W; Madathil, Sindhu K; Sama, Diana M et al. (2014) Conditional overexpression of insulin-like growth factor-1 enhances hippocampal neurogenesis and restores immature neuron dendritic processes after traumatic brain injury. J Neuropathol Exp Neurol 73:734-46
Bolton, Amanda N; Saatman, Kathryn E (2014) Regional neurodegeneration and gliosis are amplified by mild traumatic brain injury repeated at 24-hour intervals. J Neuropathol Exp Neurol 73:933-47
Pandya, Jignesh D; Readnower, Ryan D; Patel, Samir P et al. (2014) N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI. Exp Neurol 257:106-13
Miller, Darren M; Wang, Juan A; Buchanan, Ashley K et al. (2014) Temporal and spatial dynamics of nrf2-antioxidant response elements mediated gene targets in cortex and hippocampus after controlled cortical impact traumatic brain injury in mice. J Neurotrauma 31:1194-201
Srodulski, Sarah; Sharma, Savita; Bachstetter, Adam B et al. (2014) Neuroinflammation and neurologic deficits in diabetes linked to brain accumulation of amylin. Mol Neurodegener 9:30
Singh, Ranjana; Brewer, M Kathryn; Mashburn, Charles B et al. (2014) Calpain 5 is highly expressed in the central nervous system (CNS), carries dual nuclear localization signals, and is associated with nuclear promyelocytic leukemia protein bodies. J Biol Chem 289:19383-94
Yu, C G; Singh, R; Crowdus, C et al. (2014) Fenbendazole improves pathological and functional recovery following traumatic spinal cord injury. Neuroscience 256:163-9
Patel, Samir P; Sullivan, Patrick G; Pandya, Jignesh D et al. (2014) N-acetylcysteine amide preserves mitochondrial bioenergetics and improves functional recovery following spinal trauma. Exp Neurol 257:95-105
Miller, Darren M; Singh, Indrapal N; Wang, Juan A et al. (2013) Administration of the Nrf2-ARE activators sulforaphane and carnosic acid attenuates 4-hydroxy-2-nonenal-induced mitochondrial dysfunction ex vivo. Free Radic Biol Med 57:1-9

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