The aims of our study were to evaluate the antioxidant defence mechanisms of liver tissue challenged by doxorubucin (DOX) and to compare the possible protective effects of N-acetylcysteine (NAC) (n=10), deferoxamine (DOF) (n=10), DOF+NAC (n= 10) and selenium (n=9) on doxorubicin-induced hepatotoxicity. Fifty-six male rats (Mean weight = 250 ± 50 g) randomly divided into five groups. Animals in study groups were pretreated with a single dose of Dox, which was administered intravenously. Control group (n=7) was treated with intravenous saline injection. Selenium was given intraperitoneally. Blood and urine samples were collected before sacrifice. Liver tissue samples were collected and tissue superoxide dismutase (SOD), glutathione peroxidase (GSH-px), CAT activity, MDA, Zn, iron and copper were determined. DFO decreased lipid peroxidation significantly. DFO and NAC decreased CAT activity significantly. Antioxidant regimes increase SOD activities significantly. DOF and NAC increase GSH-px activities and copper levels significantly. Beneficial effect of selenium seems to result from its stimulation of SOD but not to GSH-px. It has been found that DOF, NAC and selenium have protective effects on Dox-induced hepatocellular damage. DOF+NAC did not result additional benefit.

Introduction and Aim:Many etiological reasons are blamed for enuresis nocturna (EN). The aim of this study was to research prevalence and severity of EN among elementary school-age children and sociodemographic risk factors related to it.Materials and Methods:The study was performed in three elementary schools in Ankara, Turkey between January and May 2011. It was planned to have 2500 students of 6–14 ages in the study. The questionnaire, which consisted of questions, aiming to evaluate the EN condition of participants and their characteristics, were distributed to the parents. It was observed that 2314 participants’ questionnaires (92.56%) were in accordance with evaluation criteria.Statistical Analysis:The relation between EN and the sociodemographic factors was evaluated through Chi-square test and logistic regression analysis.Results:The mean age of 2314 participants was 9.21 ± 2.08. 48.5% (n = 1123) of the students were male and 51.5% (n = 1191) were female. While the general EN prevalence was 9.9% (n = 230); 10.7% (n = 120) for males, as 9.2% (n = 110) for females. Statistical significant difference was determined between the two groups, with EN and without EN, regarding age groups (P < 0.001), education level of parents (P < 0.001, P < 0.001), and the number of sibling (P = 0.002), income level (P < 0.001), and positive family history (P < 0.001). However, logistic regression analysis revealed that there was a significant difference only between EN and age groups (odds ratio [OR] =4.42, P < 0.001), education level of mother (OR = 2.13, P = 0.017) and family history (OR = 0.12, P < 0.001).Conclusions:As a consequence, such factors as age groups, education level of parents, positive family history could be accepted as a risk of concerning EN. It is important to perform a detailed evaluation on population, carrying risk of having EN.

In this study, our aim was to investigate the prevalence of Mediterranean fever (MEFV) gene mutations in patients with ankylosing spondylitis (AS) and assessing their clinical significance. Ninety-five consecutive patients (12 women, 83 men) with active AS were included to the study. All patient's relevant clinical data were recorded at the beginning and patient assessment measures were performed. The frequency of the eight most common MEFV mutations: M694V, V726A, E148Q, M680I, M694I, P369S, F479L, and the R761H were determined. Genetic analysis was carried out by the NanoChip Molecular Genetics Workstation. NSAIDs were given to patients for treatment. The rate of MEFV mutations and their clinical significance were assessed. With regard to the MEFV mutation analysis, 30.5% of AS patients were found to have at least one mutation. The response rate to the NSAIDs (P=0.825) or frequency of patients having active disease (P=0.066) after the treatment, were not found different between the patients those have MEFV mutations and the patients those were non-carriers. Furthermore, no clinical and laboratory difference between MEFV mutation carriers and non-carriers were found. We think that although prevalence of MEFV mutations is significantly high in AS patients without clinical features of familial Mediterranean fever, its influence to the prognosis is less likely. Further investigations are needed to define the impact of MEFV mutations on the disease course of ankylosing spondylitis.

Background: Microalbuminuria (MA) is common in hypertensive population and is a marker for endothelial dysfunction and a predictor of increased cardiovascular risk. A great body of data shows the importance of MA as a strong predictor of renal and cardiovascular disease (CVD) risk in hypertensive population. Aim: In this study, we aimed to compare the antialbuminuric effects of an angiotensin II receptor antagonist, valsartan, with a calcium channel blocker, amlodipine, in newly diagnosed hypertensive patients. Material and methods: Totally, 20 patients were recruited into the study. Patients were randomized to one of the following intervention protocols: An (a) angiotensin II receptor blocker (valsartan, 80-320 mg/day) or (b) calcium channel blocker (amlodipine, 5-10 mg/day), for 12 weeks immediately after baseline measurements. Ten patients were randomized into valsartan group and 10 patients into the amlodipine group. Twenty-four-hour urinary albumin excretion (UAE) levels of the patient groups were measured before treatment and on the 12th week. Results: Patients of the two groups were matched for age and body mass index. In the amlodipine group, baseline urine microalbumin levels were higher compared to valsartan group, although the difference was not statistically significant (p ¼ 0.082). At the 12th week, there was a significant decrease in urine microalbumin levels in the amlodipine group, but no significant change was observed in the valsartan group. Conclusion: Amlodipine seems to be superior to valsartan in decreasing UAE. To reduce cardiovascular risks, endothelial dysfunction, and microinflammation, these factors are taken into consideration while prescribing antihypertensive drugs in hypertensive patients.

Although reproducibility of ABI values was found satisfactory, up to 12% of participants displayed more than 0.15 alternations between measurements, either on the same day or more than a week apart.

The results of all measurement methods were close to each other. The most sensitive and specific method was home measurement when compared with ambulatory measurement. But both office and pharmacy measurements had also high sensitivity and specificity.

Recent evidence shows that leptin may contribute to elevated blood pressure (BP) and interact with the renin-angiotensin-aldosterone and cellular immune systems. Altered T-cell activities and changes in T-cell subset ratios have also been reported in hypertension. However, little is known about the effects of AT1-receptor antagonism on T-cell activities and plasma leptin concentrations in primary hypertension. We have, therefore, investigated the relationship between leptin and T-cell activities and the effect of an AT1-receptor antagonist, losartan, in primary hypertension. Twenty recently-diagnosed and untreated young adults (11 males and 9 females, age; 39.9±7.6 years, range 23—49 years, BMI; 27.6±3.7 kg/m2) and 20 normotensive healthy, age-, sex- and BMI-matched controls were studied. The [3H]-thymidine uptakes of cultured lymphocytes were determined, both spontaneously and after stimulation with phytohaemagglutinin. The tests were performed before and after three months of treatment with losartan. The results indicate that the blastogenic responses of T-cells to phytohaemagglutinin are significantly higher in the patient group compared with controls (p=0.02). After normalisation of BP, T-cell responses were significantly reduced and were lower than in the controls (p=0.01). Pretreatment plasma leptin levels were significantly higher in hypertensives than in controls (p=0.01). However, losartan treatment had no significant effect on leptin concentrations; moreover, no correlation between leptin levels and T-cell activity was found. Our data show that plasma leptin levels and T-cell activity are markedly enhanced in untreated essential hypertension and that the alteration of T-cell activity is not related to plasma leptin levels. Antihypertensive treatment with losartan decreases T-cell activities but does not influence plasma leptin levels. We conclude that leptin levels are not affected by AT1-receptor blockade and are not related to T-cell activity.

Since the effect of smoking on plasma leptin has been divergent in clinical trials, which might have occurred due to selection of heterogeneous study populations, we investigated whether there is such an association in a group of healthy, non-obese, young male adults.A total of 54 smokers (mean age: 21.18±1.62; body mass index (BMI): 19.60±0.85) and 26 non-smokers (mean age 21.69±3.0; BMI: 21.59±1.39) with similar daily physical activities and diet and without any documented disease were enrolled, and their plasma leptin levels were determined for the comparison between the two groups.The mean BMI and plasma leptin of smokers were significantly lower than in non-smokers. Plasma leptin in the smokers group correlated inversely with BMI and the amount of daily smoking. Below BMI 20 kg/m2 and between 20.0 and 20.9 kg/m2 the plasma leptin levels in smokers were significantly lower when compared to non-smokers.Plasma leptin is decreased in healthy, young non-obese male smokers independently of the amount of body fat. High amount of smoking is associated with lower serum leptin as well.