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    Evaluation of the Association Between Matrix Metalloproteinase 11 and Intervertebral Disc Disease
    (Turkish Neurosurgical Soc, 2016) Aras, Adem Bozkurt; Guven, Mustafa; Balak, Naci; Ayan, Erdogan; Uyar, Suheyla Bozkurt; Elmaci, Ilhan
    AIM: The intervertebral disc starts to degenerate when a human being begins to stand and learn to walk. It is known that many extrinsic, intrinsic and genetic factors play a role in disc degeneration. In this study, we examined whether the matrix metalloproteinase 11 might be associated with intervertebral disc degeneration. MATERIAL and METHODS: Fifty-six patients with lumbar disc herniations who were operated at Gortepe Education and Research Hospital, Neurosurgery Clinic between September 2008 and December 2009 were prospectively reviewed. History and complaints were obtained from the case reports. Neuroradiological evaluation was performed with magnetic resonance imaging. Surgical findings of cases were reported in the operation notes. Microscopic posterior hemipartial laminectomy and discectomy were performed in all cases. Degenerated herniated disc material of all cases extracted during surgery was evaluated with immunohistochemical staining in Marmara University, Institute of Neurological Sciences, Pathology Laboratory. RESULTS: Comparing the immunohistochemical staining of cases who were 50 years or younger and cases who were over 50 years old, statistical significance was determined. CONCLUSION: Matrix metalloproteinase 11 has a role in degenerating intervertebral disc disease, but it is not the only factor. Matrix metalloproteinase 11 might be a genetic factor in young-middle aged patients.
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    The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats1
    (Acta Cirurgica Brasileira, 2014) Cosar, Murat; Kaner, Tuncay; Sahin, Onder; Topaloglu, Naci; Guven, Mustafa; Aras, Adem Bozkurt; Akman, Tarik
    PURPOSE:To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. METHODS: Thirty one Sprague- Dawley rats were used, distributed into group I (sham) n: 7 were used as control. For group II (n: 8), III (n: 8) and IV (n: 8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5 mu g/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5 mu g/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. RESULTS: The MDA and MPO levels increased from group I (control) to group II (I/R) (P < 0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P < 0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). The number of apoptotic neurons increased from group I (control) to group II (I/R) (P < 0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). CONCLUSION: The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.