ÖZETAmaç: Kronik flor zehirlenmesine florozis denilir. Bu çalışmanın amacı, çocuklardaki florozisin kardiyovasküler sistem üzerine olan etkilerini, QT dispersiyonu (QTd), düzeltilmiş QT dispersiyonu (QTcd), kalp hızı değişkenliği (KHD) ve ekokardiyografi (EKO) bulguları ile incelemektir. Yöntemler: Enine-kesitli bu araştırmada, dental florozisli 35, sağlıklı 26 çocuk çalışmaya alınmıştır. Klinik tanı Dean indeks kullanılarak konulmuştur. Spot idrarda flor seviyesi iyon elektrot metodu ile 0.6 ppm üzerinde ölçülen olgular çalışmaya alınmıştır. Serum elektrolit seviyeleri, tiroit fonksiyon testleri ölçülmüştür. Elektrokardiyografik, ekokardiyografik ve 24-saatlik ambulatuvar Holter monitorizasyonları uygulanmış ve tüm veriler KHD ölç-mek için değerlendirildi, QT ve QTcd aralıkları hesaplanmıştır. Düzeltilmiş QT aralığı Bazzett formülü ile belirlenmiştir. En uzun ve en kısa ölçümler arasındaki fark dispersiyon olarak adlandırılmıştır. Grupların karşılaştırılması Kruskal-Wallis testi ve Pearson korelasyon testi kullanılmıştır. Bulgular: Florozisi bulunan olgularda serbest T4 (ST4) (Kontrol Grup, Grup 2, 1.11 (0.85-1.64) ng/dL, 0.96 (0.85-1.11) ng/dL, sırasıyla, p<0.05) ve kalsiyum seviyelerinde (Kontrol Grup, Grup 1, Grup 2, 9.80, (9.30-10.70) mg/dL, 9.60, (8.90-10.70) mg/dL, 9.50, (8.90-10.10) mg/dL, p<0.05) azalma, serum sodyum değerlerinde artma (Kontrol Grup, Grup 2,(139)(140)(141)(142) ABSTRACTObjective: Chronic fluoride poisoning is called fluorosis. The aim of the study was to investigate effects of fluorosis on cardiovascular system in children by measuring QT dispersion (QTd), corrected QT dispersion (QTcd), heart rate variability (HRV) and echocardiography findings. Methods: Thirty-five children with dental fluorosis and 26 children as control group were included in this cross-sectional study. Dean index was used for the clinical diagnosis. The fluoride levels of subjects measured by ion electrode method in spot urine higher than 0.6 ppm were included in the study. Serum electrolytes and thyroid function tests were analyzed. Electrocardiography (ECG), echocardiography and 24-hour ambulatory Holter monitorizations were applied, and all the data were analyzed for measuring HRV, and calculation of QTd and QTcd intervals. Corrected QT (QTc) intervals were determined with the Bazzett formula. Difference between the longest and shortest intervals was considered as dispersion. Statistical analysis was performed Kruskal-Wallis test and Pearson correlation test. Results: Low free thyroxine hormone (FT4) (Control Group, Group 2 1.11 (0.85-1.64) ng/dL, 0.96 (0.85-1.11) ng/dL, p<0.05), calcium (Control Group, Group 1,2,) mg/dL, p<0.05) and high serum sodium levels (Control Group, Group 2 139 (136-142) mEq/L, 141 (138-148) mEq/L, p<0.01), increased QT (Control Group, Group 2 329.8 (300.0-363.5) msec, 351.8 (318.0-372.0) msec, p<0.05) and QTc intervals (Control Group,) msec, p<0.05) were found in subjects with fluorosis. No significant difference was found with respect to echocardiography and HRV variables. Conclusio...

Hypertension and related oxidative stress are involved in the pathogenesis of any renal diseases. Angiotensin-converting enzyme inhibitors have multi-directional renoprotective effects. In this study, we aimed to investigate whether lisinopril treatment has any biochemical alterations on renal tissue in L-NAME (Nε-nitro-L-arginine methyl ester) induced hypertension model. Twenty-eight Sprague-Dawley rats were included in this study and divided into four equal groups (n = 7): control group, L-NAME treated group (75 mg/kg/day), L-NAME plus lisinopril treated group and only lisinopril treated group (10 mg/kg/day). L-NAME and lisinopril were continued for 6 weeks. Systolic blood pressures were measured by using tail cuff method. In biochemical analysis, malondialdehyde (MDA, an index of lipid peroxidation) levels, the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in renal tissues were used as markers of oxidative stress-induced renal impairment. Microalbumin and N-acetyl-β-D-glucosaminidase (NAG) in urine were determined as markers of renal tubular damage related to hypertension. Chronic L-NAME administration resulted in a significant depletion of serum nitric oxide (NO). When compared with control group, serum creatinine, microalbumin, urine NAG, renal tissue MDA level, and CAT activities were significantly high, while renal tissue SOD and GSH-Px activities low in L-NAME group. In the L-NAME plus lisinopril treated group, serum creatinine, microalbumin and urine NAG, renal MDA level and CAT activity decreased, whereas SOD, GSH-Px activities in renal tissue and serum NO levels were increased. Thus, lisinopril treatment reversed these effects. There were not any significant difference between L-NAME plus lisinopril treated group and control group concerning serum creatinine, renal tissue MDA level and SOD, GSH-Px, CAT activities. These results suggest that lisinopril could diminish biochemical alterations in L: -NAME induced hypertensive renal damage that occurs by oxidative stress.

Purpose The aim of the present study was to investigate oxidative stress and apoptosis in kidney tissues of male Wistar rats that pre-and postnatally exposed to wireless electromagnetic field (EMF) with an internet frequency of 2.45 GHz for a long time. Methods The study was conducted in three groups of rats which were pre-natal, post-natal. and sham exposed groups. Oxidative stress markers and histological evaluation of kidney tissues were studied. Results Renal tissue malondialdehyde (MDA) and total oxidant (TOS) levels of pre-natal group were high and total antioxidant (TAS) and superoxide dismutase (SOD) levels were low. Spot urine NAG/ creatinine ratio was significantly higher in pre-and post-natal groups (p50.001). Tubular injury was detected in most of the specimens in post-natal groups. Immunohistochemical analysis showed low-intensity staining with Bax in cortex, high-intensity staining with Bcl-2 in cortical and medullar areas of pre-natal group (p values, 0.000, 0.002, 0.000, respectively) when compared with sham group. Bcl2/Bax staining intensity ratios of medullar and cortical area was higher in pre-natal group than sham group (p ¼ 0.018, p ¼ 0.011). Conclusion Based on this study, it is thought that chronic pre-and post-natal period exposure to wireless internet frequency of EMF may cause chronic kidney damages; staying away from EMF source in especially pregnancy and early childhood period may reduce negative effects of exposure on kidney.ARTICLE HISTORY

Thalassemia major patients have increased risk for thromboembolic complications because of the chronic hypercoagulable state. The question arising from this is whether thromboembolic complications are the result of genetic polymorphisms of prothrombotic factors. Here, we studied factor V 1691 G-A (FVL), factor II polymorphism (G20210A), methyltetrahydrofolate reductase mutation (MTHFR, C677T), and endothelial cell protein C receptor (EPCR) deletion polymorphism and their relationship with thromboembolic complications. We found significant decrements of protein C and protein S and a slight increased prevalence of congenital thrombophilic mutations when compared with controls. Although 5 of the patients had high soluble EPCR (sEPCR) levels, no significant change was found in sEPCR values between patients and controls.

An 11-year-old girl was referred to the authors' hospital with a complaint of growth retardation. Physical examination revealed splenomegaly. Laboratory examination revealed increased sedimentation rate. Her imaging studies showed a splenic mass. Splenectomy was performed and histopathological examination revealed sclerosing angiomatoid nodular transformation (SANT) of the spleen. The disease rarely affects children but it could cause growth retardation and increased sedimentation rate, mimicking the chronic inflammatory diseases.