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    The use of methylprednisolone, vitamin E and their combination in acute spinal cord injury: An experimental study
    (Turkish Neurosurgical Society, 2006) İş, Merih; Ulu, Mustafa Onur; Tanriverdi, Taner; Yıldız, Hakan; Akyüz, Fevzullah; Aksoy, Aylin; Gezen, Ferruh
    Objective: The effects of methyprednisolone (MP) and Vitamin E (Vit E) combination treatment was investigated in an experimental spinal cord injury model in rats. Method: Thirty-one rats were randomly divided into the five following groups: control group, MP group, Vit E group, MP+Vit E group and sham operated group. A spinal cord injury was produced in the rats by using a compression injury model at the T8 vertebra level for 10 minutes. MP was injected as a 30 mg/kg IV bolus, 1 hour after the injury, followed by an infusion of 5.4mg/kg for 23 hours. Vit E was administered as a 30 mg/kg IV bolus at the posttraumatic 1st, 7th, 13th and 19th hours. The sham group underwent laminectomy without spinal cord compression and did not receive medication. The animals were sacrificed at the posttraumatic 48th hour and histopathological examination was performed in a blinded fashion for the following criteria: hemorrhage, necrosis, edema, microcyst, microglia proliferation and PMNL infiltration. Results: The pathology evaluation of the groups revealed that the MP+Vit E combination treatment impeded the progress of edema/microcyst formation, microglia proliferation, and necrosis. Conclusion: Vit E, when combined with MP for spinal cord injury treatment, augments the effect of MP probably due to its antioxidant effects.
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    Yings and yangs of acute ethanol intoxication in experimental traumatic brain injury
    (Lippincott Williams & Wilkins, 2005) İş, Merih; Tanrıverdi, Taner; Akyüz, Fevzullah; Ulu, Mustafa Onur; Üstündağ, Nil; Gezen, Ferruh; Yavuz, Özlem
    Although the deleterious effects of acute alcohol intoxication on traumatic brain injury (TBI) are well known, neuroprotective features of lower doses of ethanol (EtOH) before head trauma have been reported during recent years. Inhibition of N-methyl-D-aspartate receptor (NMDA)-mediated excitotoxicity by lower doses of EtOH has been believed to be responsible for this protection. The aim of this study was to show the neuroprotective effects of low and moderate doses of EtOH and to compare their efficacy in each group. Acute EtOH intoxication at low and moderate doses was induced 40 minutes before trauma. Severe TBI was administered in Sprague-Dawley rats using an impact acceleration model. At 24 hours after trauma, all the rats were decapitated and hippocampi were evaluated under light microscopy. According to our results, red neuron formation and vacuolar degeneration in the CA1 and CA3 sectors of the hippocampi were less prominent in the lowdose and moderate-dose EtOH plus trauma groups than in the trauma only group. In addition, edema formation was less prominent in the EtOH plus trauma group. When comparing the low-dose EtOH Plus trauma and moderate-dose EtOH Plus trauma groups, an almost normal appearance of the hippocampus was noted in the moderate-dose EtOH plus trauma group. EtOH may have a neuroprotective effect when administered at a lower dose, particularly a moderate dose, and this protection may be a result of the inhibition of NMDA receptor-mediated excitotoxicity.