Browsing by Author "Turan, V"

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    Effect of Nicotine on RANKL and OPG and Bone Mineral Density
    Mizrak, S; Turan, V; Inan, S; Uysal, A; Yilmaz, C; Ercan, G
    Aim: The signaling pathway OPG/RANK/RANKL is a key in maintaining the balance between the activity of osteoblasts and osteoclasts in order to prevent bone loss. In this study, our aim was to assess the effects of long-term nicotine exposure on plasma RANKL and OPG levels, tissue RANKL and OPG immunoreactivities, and bone mineral density (BMD) scores in rats. Materials and Methods: Thirty-six Swiss Albino rats weighing 70 +/- 10 g were divided into three groups. While the controls (n = 12) were only given normal drinking water, for low-dose nicotine (LDN) group (n = 12) 0.4 mg/kg/day; for high-dose nicotine (HDN) group (n = 12), 6.0 mg/kg/day nicotine was added to drinkingwater for a year. At the end of 12th month, BMD scores were measured using an Xray absorptiometry and bone turnover was assessed by measuring plasma RANKL and OPG levels and RANKL and OPG immunoreactivities in tail vertebrae of the rats. Results: There was no statistically significant difference in BMD scores of lumbar spine and femoral regions of the nicotine groups in comparison to controls. Plasma OPG levels were found to be significantly higher in HDN group, in comparison to the controls and LDN groups (p = .001) unlike plasma RANKL levels. Tissue RANKL and OPG immunoreactivities decreased significantly in the LDN and HDN groups (p < .001, p < .01, respectively). Conclusions: The results of this study show that nicotine is not primarily responsible for the decrease in BMD frequently seen in smokers. Measuring plasma RANKL and OPG levels did not reflect tissue immunoreactivities.
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    Lymphovascular space invasion and cervical stromal invasion are independent risk factors for nodal metastasis in endometrioid endometrial cancer
    Solmaz, U; Mat, E; Dereli, M; Turan, V; Gungorduk, K; Hasdemir, P; Tosun, G; Dogan, A; Ozdemir, A; Adiyeke, M; Sanci, M
    AimsThe purpose of this study was to investigate the potential roles of pathological variables in the prediction of nodal metastasis in women with endometrioid endometrial cancer (EC). Materials and MethodsWomen who underwent surgery for endometrioid EC between 1995 and 2012 were retrospectively reviewed. Those who underwent prior neoadjuvant chemotherapy or radiotherapy and inadequate lymphadenectomy as well as those with nonendometrioid histology, synchronous cancers, International Federation of Gynecology and Obstetrics stage IV disease, gross uterine serosal and/or gross adnexal involvement were excluded. Lymph node dissemination was defined as occurring in the following circumstances: (i) when nodal metastasis with pelvic and/or para-aortic (P/PA) lymph node dissection (LND) was performed or (ii) when there was recurrence in the P/PA lymph nodes after a negative LND or when LND was not performed. Univariate and multivariate logistic regression models were used to identify the pathological predictors of lymphatic dissemination. ResultsA total of 827 women with endometrioid EC were assessed; 516 (62.4%) of whom underwent P/PA LND and 205 (24.8%) underwent P LND. Sixty-seven (13%) women in the P/PA LND group and 5 (2.4%) in the P LND group had positive lymph nodes. Multivariate analysis confirmed cervical stromal invasion (OR 4.04, 95% CI 2.02-8.07 (P<0.001)) and lymphovascular space invasion (LVSI) (OR 110.18, 95% CI 38.43-315.87 (P<0.001)) as independent predictors of lymphatic dissemination. ConclusionCervical stromal invasion and LVSI are highly associated with LN metastasis. These markers may serve as a surrogate for nodal metastasis.