1. This study compared the effect of dietary supplementation with organic or inorganic selenium (Se) sources plus control amounts or large amounts of vitamin E (alpha-tocopherol acetate) in broilers raised at control (20 to 24 degrees C) or low (14.5 to 16.8 degrees C) temperatures after 2 weeks of age. 2. The following dietary treatments were used from one day old. Diet 1, the control diet, comprised a commercial diet containing 0.15 mg/kg inorganic Se and 50 mg vitamin E/kg feed. Diet 2 was the same as diet 1, supplemented with 0.15 mg/kg inorganic Se. Diet 3 was the same as diet 2 but was supplemented with 200 mg/kg vitamin E. Diet 4 was the same as diet 1, but inorganic Se was replaced with 0.30 mg/kg organic Se. Diet 5 was the same as diet 4, supplemented with 200 mg/kg vitamin E. 3. Low temperature reduced the growth rate of broilers; however, at 6 weeks, there were no differences in the body weights of birds fed on organic Se supplemented diets housed at low or control temperature. The feed conversion ratio was significantly affected by low temperature but not by diet. The heterophil/lymphocyte ratio was higher in chicks after one week in the cold, indicating mild stress. Blood triiodothyronine levels were significantly higher in birds after 1 and 4 weeks in the cold but thyroxin was not affected. 4. Organic Se supplementation increased relative lung weight at the control temperature, which might lead to greater respiratory capacity. Relative spleen weight significantly decreased in broilers fed diets supplemented with inorganic Se under cold conditions, a possible indication of chronic oxidative stress. 5. At the low temperature, supplementation with organic Se alone, or with inorganic Se and vitamin E increased glutathione peroxidase (GSHPx) activity and glutathione (GSH) concentration in the liver of broilers, which may indicate increased activity of birds' antioxidant defence against suboptimal environments.

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Hypermethylated genomic DNA is a common feature in tumoral tissues, although the prevalence of this modification remains poorly understood. We aimed to determine the frequency of five tumor suppressor (TS) genes in prostate cancer and the correlation between promoter hypermethylation of these genes and low and high grade of prostate carcinomas. A total of 30 prostate tumor specimens were investigated for promoter methylation status of TS hypermethylated in cancer 1 (HIC1), death-associated protein kinase 1 (DAPK1), secreted frizzled-related protein 2 (SFRP2), cyclin-dependent kinase inhibitor 2A (p16), and O-6-methylguanine-DNA methyltransferase (MGMT) genes by using bisulfite modifying method. A high frequency of promoter hypermethylation was found in HIC1 (70.9%), SFRP2 (58.3%), and DAPK1 (33.3%) genes in tumor samples that were examined. The current data show high frequency of hypermethylation changes in HIC1, SFRP2, and DAPK1 genes in prostate carcinomas of high Gleason Score (GS).

The standardized uptake value (SUV) has gained recognition in recent years as a semiquantitative evaluation parameter in positron emission tomography (PET) studies. However, there is as yet no consensus on the way in which this index should be determined. One of the confusing factors is the normalisation procedure. Among the proposed anthropometric parameters for normalisation is lean body mass (LBM); LBM has been determined by using a predictive equation in most if not all of the studies. In the present study, we assessed the degree of agreement of various LBM predictive equations with a reference method. Secondly, we evaluated the impact of predicted LBM values on a hypothetical value of 2.5 SUV, normalised to LBM (SUV(LBM)), by using various equations. The study population consisted of 153 women, aged 32.3+/-11.8 years (mean+/-SD), with a height of 1.61+/-0.06 m, a weight of 71.1+/-17.5 kg, a body surface area of 1.77+/-0.22 m(2) and a body mass index of 27.6+/-6.9 kg/m(2). LBM (44.2+/-6.6 kg) was measured by a dual-energy X-ray absorptiometry (DEXA) method. A total of nine equations from the literature were evaluated, four of them from recent PET studies. Although there was significant correlation between predicted and measured LBM values, 95% limits of agreement determined by the Bland and Altman method showed a wide range of variation in predicted LBM values as compared with DEXA, no matter which predictive equation was used. Moreover, only one predictive equation was not statistically different in the comparison of means (DEXA and predicted LBM values). It was also shown that the predictive equations used in this study yield a wide range of SUV(LBM) values from 1.78 to 5.16 (29% less or 107% more) for an SUV of 2.5. In conclusion, this study suggests that estimation of LBM by use of a predictive equation may cause substantial error for an individual, and that if LBM is chosen for the SUV normalisation procedure, it should be measured, not predicted.

The multidrug resistance gene-1 (MDR1, adenosine triphosphate-binding cassette transporter: ABCB1, P-glycoprotein) encodes membrane proteins that play a crucial role in protecting cells from xenobiotics, chemicals, and drugs. The TT genotype of 3435 codon in exon 26 of MDR1 gene causes overexpression of gene activity and effluxes many chemically diverse compounds across the plasma membrane. We studied the association between C3435T polymorphisms (single nucleotide polymorphism) of MDR1 gene and colchicine-resistant familial Mediterranean fever (FMF) patients. Total genomic DNA samples from 52 FMF patients of colchicine unresponsiveness were used for FMF (MEFV) and MDR1 genes profile analyses. Target genes were genotyped by multiplex PCR-based reverse-hybridization Strip Assay method. The preliminary current results showed increased T allele frequency (0.596) in colchicine unresponsiveness of FMF patients. The distributions of the CC, CT, and TT genotypes in colchicine nonresponder FMF patients were 17%, 46%, and 37%, respectively. Our results indicate that C3435T polymorphism in exon 26 of MDR1 gene is associated with colchicine resistance in nonresponder FMF patients during the common therapy protocol.