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Leishmaniasis is widespread in many countries, including Turkey. We present the clinical characteristics and the retrospective analysis of 22 children with visceral leishmaniasis, identified between 1995-2008. The mean age at presentation was 3.3±1.96 years (range 0-8). All patients had splenomegaly. Fever was found in 19 (86.3%) cases. Anemia, thrombocytopenia, and leukopenia was observed in all, 19 (86.3%), and 13 (61%) cases respectively. Diagnosis of visceral leishmaniasis was made with the identification of amastigotes in giemsa-stained bone-marrow aspirate smears. Initial treatment consisted of meglumine antimoniate in 19 (86.3%) patients and liposomal amphotericin B in 3 (13.7%) patients. Three children who did not respond to meglumine antimoniate were cured with liposomal amphotericin B. The findings highlight liposomal amphotericin B as an effective therapy for visceral leishmaniasis in children. Early detection and appropriate management of complications may reduce morbidity and mortality in childhood visceral leishmaniasis. [ABSTRACT FROM AUTHOR]

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 (p < 0.001). 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 = 0.018, p = 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.

Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role in the pathogenesis of FMF. We investigated gene polymorphisms of the antioxidative enzymes, glutathione peroxidase (GPX) and paraoxonase (PON) in FMF patients, and possible associations with FMF pathogenesis. Sixty FMF patients during an attack-free period and 51 healthy children as the control group were included in our study. PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms were assayed. Blood urea nitrogen, creatinine and serum lipid profile were also measured. PON1 Q/R192 genotype distribution was 52% QQ, 46% QR and 2% RR in the FMF group and 45% QQ, 45% QR and 10% RR in the control group (P>0.05). GPX1 Pro197Leu genotype distribution was 28% PP, 57% PL, 15% LL in the FMF group and 18% PP, 53% PL, 29% LL in the control group (P>0.05). Blood urea nitrogen, serum creatinine, lipid levels, and the distribution of PON1 Q/R192 and GPX1 Pro197Leu genotypes were similar in the two groups. We conclude that the PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms are not important risk factors in the development of FMF. However, larger studies are warranted to validate these conclusions.

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.

Objective: 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, 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) 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, Group I2 390.6 (309.0-418.5) msec, 366.8 (318.2-468.5) msec, p<0.05) were found in subjects with fluorosis. No significant difference was found with respect to echocardiography and HRV variables., Conclusion: Endemic fluorosis is a risk factor for decrease in calcium and FT4 levels, increase in sodium levels and QT prolongation. These findings might be related with some cardiovascular system dysfunctions such as arrhythmias or syncope. Subjects with fluorosis should be monitored in terms of long QT and QTc intervals.