Although the incidence of CL showed a sharp decline from 1997 to 2000 in Sanliurfa, this does not mean that the disease is on its way to eradication.

Soil transmitted helminth (STH) infection are endemic in developing countries

The pathophysiologic mechanisms leading to acute ischemic renal failure are not completely understood. Melatonin, a compound with well-known antioxidant properties, reduces IR-induced renal injury. The purpose of the present study was to investigate the changes in levels of tumor necrosis factor (TNF)-alpha, IL-beta, and IL-6 in postischemic reperfused renal tissue, and to determine whether the protective effect of melatonin is related the modulation of the production of these inflammatory molecules. Male Wistar albino rats were unilaterally nephrectomized and subjected to 1 hr of renal pedicle occlusion followed by 2 hr or 24 hr of reperfusion. Melatonin (10 mg/kg, i.p.) or vehicle was administrated at 10 min prior to ischemia. After 24 hr of the reperfusion, following decapitation, kidney samples were taken both for histologic examination and for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, total antioxidant capacity (TAC), total oxidative stress (TOS), creatinine, and blood urea nitrogen (BUN). These were measured in serum samples. TNF-alpha, IL-beta, and IL-6 were measured in kidney samples after 2 hr of reperfusion. IR caused a significant increase in renal MDA, MPO, TOS, creatinine, and BUN while decrease TAC without any change in TNF-alpha, IL-beta, and IL-6 levels. Melatonin treatment reduced the biochemical indices without any change in the cytokine levels and ameliorated histopathologic alterations induced by IR. The protective effect of melatonin on IR-induced renal injury is related to its antioxidant properties but not to proinflammatory cytokines.

Animal studies have demonstrated lower levels of 1,25(OH)2D3 in a type 2 diabetes model compared with controls (1). Alterations in circulating vitamin D3 metabolites, such as decreased 1␣-hydroxylase activity and enhanced renal 25-hydroxylase activity, have been found in both experimental and human diabetes. These alterations in vitamin D metabolism may be associated with the deranged mineral homeostasis and skeletal morphology observed in rats and people with chronic insulin deficiency (2). Experimentally, vitamin D deficiency progressively reduces insulin secretion, and this reduction soon becomes irreversible (3). It was also shown that insulin deficiency may be associated with lower vitamin D-binding protein and 1,25(OH)2D3 serum levels in rats. These decreases are somewhat dependent on androgen concentration, but they are counteracted by estrogens (4).Several studies have demonstrated abnormalities in calcium, phosphate, and vitamin D metabolism in diabetic patients. In particular, Pietschmann et al. (5) evaluated 25(OH)D levels in type 1 and type 2 diabetic patients and found no difference in 25(OH)D levels between type 1 diabetic patients and control subjects, whereas 25(OH)D levels were significantly decreased in type 2 diabetic patients (5).We conducted an observational study in 799 ambulatory postmenopausal Italian women in order to assess the prevalence of hypovitaminosis D and dietary calcium insufficiency. In all patients, the levels of 25(OH)D3 (obtained by radioimmunoassay method with double antibody provided by DiaSorin), calcium intake (obtained by a questionnaire filled in by a general practitioner), and several Activity Daily Living (ADL) criteria were assessed. The samples were collected in February and March 2000.We identified 66 type 2 diabetic patients based on medical history. Female patients and control subjects were comparable for age and years since menopause, but BMI was significantly higher in diabetic patients. The ADL score was significantly worse in diabetic patients than in control subjects (P Ͻ 0.01). The 25(OH)D levels (means Ϯ SD) were significantly lower in diabetic patients than in control subjects (11 Ϯ 9.8 vs. 9 Ϯ 11.3 ng/ml, P Ͻ 0.008), and the prevalence of 25(OH) deficiency (Ͻ5 ng/ml) was significantly higher in diabetic patients than in control subjects (39 vs. 25%). Dietary calcium intake was significantly lower in diabetic patients than in control subjects (792.9 Ϯ 400.9 vs. 679 Ϯ 316.9 mg/day, P Ͻ 0.020). The significance of these findings remains unclear. The general recommendation for overweight diabetic patients to lower fat dairy product consumption may explain the lower calcium intake. We have no data that might explain the higher prevalence of hypovitaminosis D among diabetic patients. We believe our results will lead to additional studies on the hypothetical circular relationship among diabetes, vitamin D repletion, and calcium intake and absorption. We believe this relationship leads to both a worsening of diabetes and an increased risk of fractures (6), d...