Neurosurgery
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Epidermal growth factor (EGF) and fibroblast growth factor-2 (FGF-2) play a critical role in neurogenesis. In the present study, we evaluated the additive effect of administering these two factors on post-ischemic progenitor cell proliferation, survival, and phenotypic maturation in the hippocampal dentate gyrus (DG) and the subventricular zone (SVZ) in the adult rat brain after transient middle cerebral artery occlusion. ⋯ Specific growth factor infusion enhances post-ischemic progenitor cell proliferation by 5 days of reperfusion and neuronal maturation by 21 days of reperfusion in both the DG and SVZ in the adult rat brain.
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Radiosurgery is used to destroy a predetermined target within the brain, with minimal radiation injury to the surrounding tissue. We hereby present our in vivo model to study the effects of single-session, high-dose radiation on the cerebral vessels that are targeted with radiosurgery using the Leksell Gamma Knife. ⋯ The experiment was able to establish in vivo increased leukocyte adhesion to the cerebral vascular endothelial cells in response to radiation injury and elaborate the time frame within which the leukocyte adhesion response increases, reaches a peak and then starts decreasing.
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Nitric oxide (NO) and oxygen free radicals are implicated in the pathophysiology of traumatic brain injury (TBI). Peroxynitrite formation from NO and superoxide contributes to secondary neuronal injury but the neuroprotective effects of nitric oxide synthase (NOS)-inhibitors have been contradictory. This study was undertaken to examine whether PTtic administration of the (NOS)-inhibitor N-nitro-l-arginine methyl ester (L-NAME), and a combination of L-NAME and the nitrone radical scavenger 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN) favorable affects neuronal injury in a model of TBI. ⋯ NO from NOS contributes to secondary neuronal injury in this TBI-model. PTtic treatment does not inhibit early beneficial NO-related effects. L-NAME and S-PBN limit peroxynitrite formation, promoting neuronal survival. The combination of L-NAME and S-PBN was neuroprotective; surprisingly no additive effects were found on nitrotyrosine formation, apoptosis or neuronal survival.
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Malignant gliomas are prominent targets for cancer gene therapy approaches because of their poor prognosis despite all available therapies. Endothelial cells (ECs) are considered attractive vehicles for cell-based gene therapy because of their tropism to the tumor vasculature. In this study, we investigated the potential of ECs to incorporate into glioma vessels after intra-arterial or local application to establish whether ECs can be used as cellular vectors for gene therapy in gliomas. ⋯ Cell-based therapy approaches to brain tumor treatment using BECs as cellular vectors might be hampered by the rapid downregulation of transgene expression and by the fact that these cells do not home specifically to tumor vessels after intra-arterial injection. Nevertheless, locoregional administration of BECs might be an interesting approach for delivering molecules to brain tumors when short-term expression of transgene in the perivascular space is desirable.
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Delayed repair of peripheral nerve injuries often results in poor motor functional recovery. This may be a result of the deterioration or loss of endoneurial pathways in the distal nerve stump before motor axons can regenerate into the stump. ⋯ We conclude that even 2 months of denervation of the distal nerve pathway is deleterious to regeneration and that protection of the pathway improves subsequent reinnervation and regeneration. Moreover, if the desired regeneration is motor, protection of the distal nerve pathway by a motor nerve conditions is better than a sensory nerve.