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Patients with inflammatory bowel disease (IBD) have numerous risk factors for low bone mineral density (BMD). We aimed to study the prevalence of low BMD in IBD and the factors associated with it. BMD was measured by radial quantitative ultrasound, and clinical and biochemical characteristics were compared in prospectively enrolled patients and healthy age and gender-matched controls. Chi-square test, t test for independent samples, analysis of variance (ANOVA), Mann–Whitney U test and Kruskal–Wallis H tests were used as appropriate for univariate analysis to compare the characteristics between patients with and without abnormal BMD. Binary logistic regression analysis was done to determine the factors associated with low BMD in IBD patients. One hundred and six patients (Crohn’s disease [CD] = 35, ulcerative colitis [UC] = 71) and 55 controls were included. Low BMD was equally prevalent in CD, UC and controls (42.9%, 36.6%, 36.4% respectively, p = 0.791). Serum calcium and vitamin D were significantly lower in IBD patients compared to controls (p

To study the clinical and biochemical profiles across the different ranges of impaired fasting glucose (IFG) based on American Diabetes Association (ADA) and World Health Organization (WHO) criteria. A cross-sectional study was conducted on 149 subjects, of which 63 belonged to group 1 (IFG = 100–110 mg/dl) and 86 to group 2 (IFG = 111–125 mg/dl). Basic anthropometric and clinical examinations were done for all subjects. Data was collected from patient by a questionnaire, which included the history of hypertension and diabetes and other comorbidities and complications. Biochemical profiles including Fasting Plasma Glucose (FPG), Oral Glucose Tolerance Test (OGTT), HbA1c, Fasting insulin levels and Fasting Lipid Profile were measured. Assessment of insulin resistance and beta cell function was done by Homeostasis Model Assessment (HOMA). Data were analysed using SPSS software version 15 and p

Appropriate doses of fluoride (F) have therapeutic action against dental caries, but higher levels can cause disturbances in soft and mineralized tissues. Interestingly, the susceptibility to the toxic effects of F is genetically determined. This study evaluated the effects of F on the liver proteome of mice susceptible (A/J) or resistant (129P3/J) to the effects of F. Weanling male A/J (n = 12) and 129P3/J (n = 12) mice were housed in pairs and assigned to two groups given low-F food and drinking water containing 15 or 50 ppm F for 6 weeks. Liver proteome profiles were examined using nano-LC-ESI-MS/MS. Difference in expression among the groups was determined using the PLGS software. Treatment with the lower F concentration provoked more pronounced alterations in fold change in liver proteins in comparison to the treatment with the higher F concentration. Interestingly, most of the proteins with fold change upon treatment with 15 ppm F were increased in the A/J mice compared with their 129P3/J counterparts, suggesting an attempt of the former to fight the deleterious effects of F. However, upon treatment with 50 ppm F, most proteins with fold change were decreased in the A/J mice compared with their 129P3/J counterparts, especially proteins related to oxidative stress and protein folding, which might be related to the higher susceptibility of the A/J animals to the deleterious effects of F. Our findings add light into the mechanisms underlying genetic susceptibility to fluorosis.