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Patricia Zadnik, Rachel Sarabia-Estrada, Mari L. Groves, Camilo Molina, Christopher Jackson, Edward McCarthy, Ziya L. Gokaslan, Ali Bydon, Jean-Paul Wolinsky, Timothy F. Witham and Daniel M. Sciubba

palliative, merely slowing the progression of impairment and relieving pain, and patient outcome is dependent on the preintervention level of functioning. 26 , 27 Animal models are needed to study what governs metastatic progression and to investigate novel interventions in a preclinical environment. A variety of animal models have emerged in the study of spinal metastasis, in which techniques ranging from intracardiac injection to orthotopic human bone implants to direct intraosseous injections have been used. 7 , 12 , 18 , 19 , 25 , 30 , 32 , 34 In our group, we have

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Camilo A. Molina, Rachel Sarabia-Estrada, Ziya L. Gokaslan, Timothy F. Witham, Ali Bydon, Jean-Paul Wolinsky and Daniel M. Sciubba

of rhBMPs. Conclusions In an animal model of metastatic spine disease utilizing an intravertebral implantation of rat breast adenocarcinoma, the local administration of rhBMP-2 (15 μg, 10 μl of 1.5-mg/ml solution) resulted in a neurological and survival advantage in comparison with animals that did not receive the same treatment. Although results are specific to the model utilized, this is the first preclinical study demonstrating that the local administration of rhBMP-2 on a tumor bed may actually decrease tumor growth, suggesting that patients undergoing

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Matthew J. McGirt, Beril Gok, Starane Shepherd, Joseph Noggle, Giannina L. Garcés Ambrossi, Ali Bydon and Ziya L. Gokaslan

compression and ischemic injury from MESCC. Hyperglycemia has been shown to potentiate ischemic damage after CNS injury by quenching important vasodilators, potentiating lactate accumulation, worsening tissue acidosis, and increasing free radical–induced reperfusion injury. 11 , 14 , 18 , 26 , 31 Furthermore, studies of ischemic SCI have suggested that induced hypoglycemia attenuates ischemic SCI. 35 , 37 However, the effect of hyperglycemia on spinal cord compression remains unknown. In the present study, we use an established animal model of metastatic spinal tumors

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Donald Seyfried, Yuxia Han, Dunyue LU, Jieli Chen, Ali Bydon and Michael Chopp

of differentiating into various cerebral cell types, including neurons. 4, 15 Analysis of experiments in ischemic and TBI reveals that cells in this region participate in the recovery process. 2, 3, 15 Data from studies of the mechanisms of cellular injury following ICH both clinically and in animal models implicate a traumatic or mechanical component, an ischemic component, and direct toxic effects of the blood clot. Given the proximity of clinically observed ICH to the patient's ventricular system, the natural process of recovery from one or all three of the

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Scott L. Parker, Anubhav G. Amin, S. Harrison Farber, Matthew J. McGirt, Daniel M. Sciubba, Jean-Paul Wolinsky, Ali Bydon, Ziya L. Gokaslan and Timothy F. Witham

misidentification of approximately one-half of all medial breaches. With a specificity of 99.9%, however, any stimulation below this threshold must be immediately evaluated, because it most likely represents a misplaced screw. Because of its poor sensitivity, even at high thresholds, EMG monitoring should not be used as a screening tool to detect potential breaches. There is a growing body of evidence on the role of intraoperative EMG monitoring in determining lumbar pedicle screw malpositioning. Using an animal model, Lenke and cowokers 12 established normative stimulation

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lung cancer. Surgical intervention is often required to stabilize the spine, and these procedures can have significant morbidity that could be avoided with prevention or containment of the metastases by therapeutics. To date, this condition has not been replicated in a pre-clinical animal model, which would greatly aid the study of potential interventions. Methods Twenty-seven athymic rats underwent transperitoneal exposure and injection of 50,000 luciferase-labeled A549 lung cancer cells into the L5 vertebral body. At 4 weeks post-implantation, in vivo

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010

, Canada) 8 2010 113 2 A420 A420 This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose. 2010 Introduction: Our previous studies on a mouse model showed that endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) uncoupling plays a role in vasospasm after subarachnoid hemorrhage (SAH). Simvastatin may decrease vasospasm in both patients and an animal model of SAH. This study investigated the link between the beneficial effect of simvastatin with eNOS/NO uncoupling

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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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, 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

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extracellular water content of brain for improved MR imaging. Preclinical safety testing in a large brain, animal model is now complete, and a clinical trial is being designed to assess the feasibility in patients with movement disorders. J Neurosurg Journal of Neurosurgery JNS 0022-3085 1933-0693 American Association of Neurological Surgeons 2015.6.JNS.AANS2014ABSTRACTS Philip L. Gildenberg Resident Award 639. Brain Computer Interface Technology for Patients Suffering Disorder of Consciousness Robert Prueckl , (Schiedlberg