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Project description Traumatic spinal cord injury (SCI) is characterized by a primary mechanical insult, followed by widespread, coordinated changes in gene expression. These may be associated with pathogenic auto-destructive events such as hemorrhage, metabolic failure, inflammatory/immune activation, loss of ionic homeostasis, lipid degradation, production of free radicals, and neurotransmitter and growth factor imbalances. These changes may contribute to neuronal and oligodendroglial cell death, astrocyte proliferation (scarring) and demyelination. Alternatively, reactive expression changes that are neuroprotective and/or promote recovery (regeneration/plasticity) may also be induced. In addition, not all mechanisms following SCI are well known. The NINDS recently supported the creation of a large database of quality-controlled Affymetrix profiles of spinal cord tissue taken from 1 hour to 6 months after mild, moderate or severe thoracic SCI (T9) in the rat. Spinal cord samples were also profiled from 30 minutes to 28 days after moderate thoracic injury (T9) in the mouse. Sampled regions included areas above (rostral), at (epicenter) and below (caudal) the site of impact. The goal of this project is provide a large scale analysis of expression events after SCI. To promote the utility of the project, we developed an information visualization tool, named "SpinalCordLink." SpinalCordLink also integrates "biological pathways" from WikiPathways.org. We used a new data processing framework to integrate relevant pathway information into the analysis process. Support This work was supported by NIH NINDS-01 (NS-1-2339) and by NIH NCMRR/NINDS 5R24 HD 050846 (Integrated Molecular Core for Rehabilitation Medicine). SpinalCordLink Participants
Availability SpinalCordLink is a Java application built on Piccolo toolkit.
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