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    A comparative histopathological and immunohistochemical study of Survivin and Ki-67 proteins in glial tumours
    (Taylor & Francis Ltd, 2019) Topyalin, Nur; Budak, Metin; Ozbay, Nurver; Yildiz, Mustafa; Kaner, Tuncay; Aydin, Abdullah; Gezen, Ahmet Ferruh
    Survivin is a bifunctional protein which regulates cell division and inhibits apoptosis. Survivin is a member of the inhibitor of apoptosis protein (IAP) family. Expression of survivin has been shown to be responsible for apoptosis and resistance to ionizing radiation. The aim of the present study was to investigate the association between -31 G/C promoter polymorphism, survivin protein and glial tumour grading, and to compare survivin versus Ki-67 as a marker. In this study, DNA was isolated from paraffin-embedded sections of 29 patients diagnosed with glial tumours. Survivin gene promoter -31 G/C polymorphism was investigated using PCR-RFLP. For the analysis, 10 mu m sections were stained with survivin protein and Ki-67 antibody. Immunohistochemical staining was performed. Survivin showed a positive correlation with Ki-67 (r = 0.604; p = 0.001). The tumour grades correlated with survivin; however, the relationship was not statistically significant (r = 0.345; p > 0.05). We found a significant correlation between tumour grades and Ki-67 (r = 0.663; p < 0.01), suggesting that Ki-67 is a more sensitive marker compared to survivin.
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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.