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Objective: The purpose of this study was to determine the levels of systemic oxidative stress and genotoxicity (DNA damage) in patients with exudative age-related macular degeneration (AMD) and to investigate the possible role of these factors in development of advanced stage wet AMD. Material-Method: The study comprised 26 patients with exudative AMD (68.9±1.9 years of age) and 26 age- and sexmatched (64.8±2.2 years of age) healthy controls (p=0.268, p=0.258, respectively). Serum total antioxidant status (TAS) and total oxidant status (TOS) were measured with a commercial kit. Oxidative stress index (OSI) was calculated. DNA damage was evaluated using comet analysis following lymphocyte isolation from venous blood. Parameters including tail length and tail moment were evaluated for quantitative analysis of DNA damage. Results: The AMD group had lower TAS and higher OSI values than in the control group, while TOS values did not differ between the two groups (p=0.006, p=0.039 and p=0.319, respectively). Furthermore, tail length (p<0.0001) and tail moment (p=0.005) were significantly higher in the AMD group compared to the control group. Conclusions: Although multiple factors play a role in pathogenesis of AMD, increased systemic oxidative stress and DNA damage might be an important risk factor for development of exudative AMD. In addition, investigating these factors in patients with early AMD might be helpful for developing new preventive therapies. [ABSTRACT FROM AUTHOR]

AIM: The in-vivo proliferation capacity of human corneal endothelial cells (HCECs) is limited. Under pathological conditions, endothelial cell loss causes permanent vision loss due to corneal edema. Currently, the only treatment for corneal endothelial insufficiency is corneal transplantation. However, serious problems in supplying corneal donors worldwide lead researchers developing cell-based approaches based on in-vitro propagation of HCECs. In this study, it was aimed to investigate the effects of TGF-β, ITD-1 (TGF-β inhibitor) and SB431542 (TGF-β receptor inhibitor) on proliferation, function and senescence properties of HCECs. METHODS: In this study, control, TGF-β1, ITD-1, SB431542, TGF-β1+ITD-1 and TGF-β1+SB431542 groups were formed using HCEC line. Proliferation abilities were evaluated by BrdU analysis, corneal endothelial cell markers, ZO-1 and COL8A2, by RT-PCR, cell senescence by SA-β-Gal staining and TGF-β1 levels by Elisa method. Cell groups were treated with TGF-β1 (2 ng/ml), ITD-1 (10 μM), SB431542 (10 μM), TGF-β1 (2 ng/ml)+ITD-1 (10 μM), and TGF-β1 (2 ng)/ml)+SB431542 (10 μM) for 24 and 48 hours. For ELISA and RTPCR experiments, 2 ng/ml TGF-β1, 10 μM ITD-1 and 10 μM SB431542 were selected as effective dose and 48 hours as effective time. For cell senescence, cell groups were fixed at the end of the 1st and 7th days and stained with SA-β-Gal. RESULTS: In this study, TGF-β1 reduced HCEC proliferation; ITD-1 and SB431542 increased cell proliferation (p<0.05). ZO-1 and COL8A2 expressions were increased in the SB431542 group (p<0.05). TGF-β and TGF-β inhibitors did not affect senescence at 7th day, while TGF-β receptor inhibitor improved senescence findings in the early period, which disappeared over time. Based on these findings, TGF-β suppresses proliferation, accelerates senescence and decreases expression of endothelial cell markers in HCECs. CONCLUSION: Therefore, ITD-1 and especially SB431542 can prevent/reduce negative effects of TGF-β on HCECs. These results may contribute to development of cell-based therapies in corneal endothelial insufficiency. [ABSTRACT FROM AUTHOR]

Aim: Thyroidectomy followed by administration of large activities of I-131 is the treatment of choice for differentiated thyroid carcinoma (DTC). Although I-131 was suggested to form chain fractures in DNA of thyroid cells, the effect of RAIT on peripheral blood cell DNA remains controversial. The aim of this study was to determine the effect of RAIT on DNA damage in lymphocytes in patients with DTC. Method: Totally 21 DTC patients were included in our study (mean age 45.09±10.02 years). Of the 21 patients; 6 (%28.6) were treated with a low (30 mCi) RAIT dose, 11 (%52.4) with ablation (100 mCi) dose and 4 (%19) with higher dose (>100 mCi). Venous blood samples were taken from each patient before treatment, 7 days and 6 months after the treatment. DNA damage was assessed using comet assay following lymphocyte isolation from venous whole blood. Seventy-five cells per slide per sample were scored to evaluate DNA damage. Head length, tail length, head intensity, tail intensity, tail moment were evaluated for quantitative analysis of DNA damage. Data were analyzed with the SPSS 24.0 program. Repeated measures analysis of variance was used when parametric test assumptions were provided; and the Friedman test was used when parametric test assumptions were not provided. P<0.05 was considered statistically significant. Results: Tail intensity values were significantly lower after treatment (1st week and 6 months) (18.30±6.48 and 18.06±5.58) compared to before treatment (23.83±9.82) (p=0.002). The head intensity values were statistically significantly higher after treatment (1st week and 6 months) (81.69±6.48 and 81.93±5.58) than before treatment (76.16±9.82) (p=0.002). The tail moment was lower at 6 months following treatment compared to before treatment (5.24±2.51 vs. 8.04±3.86) (p=0.005) (Table 1). Conclusion: The increase in head intensity and decrease in tail intensity and moment followed by treatment have shown that RAIT does not cause significant DNA damage in peripheral blood cells. RAIT may have activated protective effects on lymphocyte DNA by activating repair mechanisms. [ABSTRACT FROM AUTHOR]

Amaç: Diferansiye tiroit kanserinde (DTK) tiroidektomi sonrası radyoaktif I-131 tedavisi (RAİT), kalan rezidü tiroit dokusunun ablasyonu veya tiroit loju içinde ve uzak bölgelerdeki kanser metastazlarını tedavi etmek amacıyla kullanılan bir tedavi şeklidir. Oksidatif stresin DTK patogenezinde önemli olduğu ispatlanmış olmasına rağmen, RAİT'nin DTK'li hastalarda hemoreolojik ve oksidatif stres parametreleri üzerine etkilerini inceleyen bir çalışmaya rastlanmamıştır. Çalışmamız kapsamında, DTK'de RAİT'nin hemoreolojik parametreler (eritrosit deformabilite ve agregasyonu), total oksidan/ antioksidan düzey (TOS/TAS), oksidatif stres indeksi (OSİ) üzerine etkilerinin incelenmesi amaçlanmıştır. Yöntem: Çalışmamıza 15 DTK hastası (ortalama yaş 44,93±3,05 yıl) dahil edilmiştir. Hastalardan RAİT'den hemen önce, 7-10 gün sonra ve 1 ay sonra olmak üzere 3 kez venöz kan örnekleri alınmıştır. Eritrosit agregasyonu ve deformabilitesi bir ektasitometre aracılığıyla, TOS/TAS ticari bir kitle ölçülmüş, OSİ hesaplanmıştır. İstatistiksel analiz için Tekrarlı Ölçümler İçin Varyans Analizi ve Friedman testi kullanılmış, p<0,05 değerler anlamlı kabul edilmiştir. Bulgular: Hastaların 1. haftada elde edilen eritrosit deformabilite değerlerinde 0,53 ve 0,95 Pa kayma kuvvetlerinde bazale göre istatistiksel olarak önemli düzeyde azalma, 1. ayda ise 1,69 ve 3,00 Pa'da 1. haftaya göre artış saptanmıştır (p=0,024, p=0,017, p=0,009, p=0,046, sırasıyla). Hastaların eritrosit agregasyon değerleri, TOS, TAS ve OSİ parametrelerinde istatistiksel olarak önemli düzeyde değişiklik saptanmamıştır. Sonuç: Çalışmamız, DTK'li hastalarda tiroidektomi sonrası uygulanan RAİT'den 1 hafta sonra eritrosit deformabilitesinin azaldığını böylece RAİT'nin dolaşım üzerinde olumsuz etkilere yol açabileceğini ancak 1 ay sonrasında ise deformabilite değerlerinin bazal değerlere yaklaşarak düzelme sağladığını göstermektedir. Verilerimiz doğrultusunda DTK'li hastaların özellikle RAİT'yi izleyen ilk 1 hafta boyunca kardiyovasküler açıdan yakından takip edilmelerinin uygun bir yaklaşım olabileceği ileri sürülebilir. [ABSTRACT FROM AUTHOR]