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  • By Author: Lubelski, Daniel x
  • By Author: Bydon, Mohamad x
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the non-chondrodystrophic (NCD) or “mongrel” dog that retains its population of notochordal cells (unlike humans) does not develop DDD if at all, until much later in life. Here we demonstrate that NCCM is capable of regenerating the degenerative disc in a pre-clinical animal model of DDD. Materials/Methods: We used a 26-gauge needle and image guidance to develop DDD in a pre-clinical rodent model and characterized the degenerative cascade from healthy through 10-weeks by analyzing the IVD NPs until 6-weeks post injury. Meanwhile we generated notochordal cell

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intervertebral disc (IVD) in animal models induces structural damage and leads to IVD degeneration over time. Prior rodent IVD degeneration models have involved injury to multiple IVDs, which confounds the mechanism of pain generation. This study identifies a behavioral and pain-related sensitivity phenotype after puncture of one lumbar IVD. Materials/Methods: Baseline functional assessments including static weight-bearing, gait analysis, site-specific algesia, and open field testing were done for Sprague-Dawley rats (n=36, 18 weeks old) the day before lumbar IVD

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, with >90% of cells confirmed to have EC identity on flow cytometry (CD45-CD31+). These cells were also significantly enriched for EC-related genes such as Cdh5, Icam2, Nos3 and Pecam1. Microarray results will provide a list of genes that are significantly upregulated or downregulated in BECs after SAH, requiring further validation studies. Conclusion: BBB disruption is greater at 24h than at 48h in an experimental SAH model. This study is the first to provide whole genome expression profiling of freshly-isolated BECs derived from an SAH animal model. Thereby