Comparing the Effect of Phenytoin Syrup and Triamcinolone Acetonide Ointment on Aphthous Ulcers in Patients with Behcet's Syndrome.

BACKGROUND: Recurrent aphthous stomatitis (RAS) appears to be the most common type of oral ulcers. The lesion is usually self limited but its painful presentation results in some difficulties. Therefore, an efficient therapeutic strategy is required and currently existing therapies seem to be inadequate because of its unclear etiology. Here the therapeutic effect of triamcinolone acetonide ointment as a relatively expensive medication has been compared with phenytoin syrup on aphthous ulcers in patients with Behcet's syndrome. METHODS: Thirty out of 60 our patients with Behcet's syndrome were randomly treated by phenytoin syrup and the remaining were advised to use 0.1% triamcinolone acetonide ointment. After a week, they were visited again to determine the status of aphthous ulcers. RESULT: Positive response in the triamcinolone acetonide group and phenytoin group was 86.7% and 53.3%, respectively. CONCLUSION: The effectiveness of triamcinolone acetonide ointment was more than phenytoin on aphthous ulcers in patients with Behcet's syndrome.

C16 ceramide is crucial for triacylglycerol-induced apoptosis in macrophages.

Triacylglycerol (TG) accumulation caused by adipose triglyceride lipase (ATGL) deficiency or very low-density lipoprotein (VLDL) loading of wild-type (Wt) macrophages results in mitochondrial-mediated apoptosis. This phenotype is correlated to depletion of Ca(2+) from the endoplasmic reticulum (ER), an event known to induce the unfolded protein response (UPR). Here, we show that ER stress in TG-rich macrophages activates the UPR, resulting in increased abundance of the chaperone GRP78/BiP, the induction of pancreatic ER kinase-like ER kinase, phosphorylation and activation of eukaryotic translation initiation factor 2A, the translocation of activating transcription factor (ATF)4 and ATF6 to the nucleus and the induction of the cell death executor CCAAT/enhancer-binding protein homologous protein. C16:0 ceramide concentrations were increased in Atgl-/- and VLDL-loaded Wt macrophages. Overexpression of ceramide synthases was sufficient to induce mitochondrial apoptosis in Wt macrophages. In accordance, inhibition of ceramide synthases in Atgl-/- macrophages by fumonisin B1 (FB1) resulted in specific inhibition of C16:0 ceramide, whereas intracellular TG concentrations remained high. Although the UPR was still activated in Atgl-/- macrophages, FB1 treatment rescued Atgl-/- macrophages from mitochondrial dysfunction and programmed cell death. We conclude that C16:0 ceramide elicits apoptosis in Atgl-/- macrophages by activation of the mitochondrial apoptosis pathway.

TNF-alpha, TNF-beta and IL-4 gene polymorphisms in Iranian patients with multiple sclerosis.

OBJECTIVES: To investigate the association between tumor necrosis factor-alpha (TNF-alpha) G-308A, tumor necrosis factor-beta (TNF-beta) G+252A and interleukin-4 (IL-4) C-590T polymorphisms and susceptibility to multiple sclerosis (MS) development and clinical course of the disease. MATERIALS AND METHODS: Two hundred and seventy patients with MS and 542 sex and ethnic matched controls were enrolled in the present study. An allele-specific oligonucleotide polymerase chain reaction was used to detect the polymorphism at position -308 of the TNF-alpha gene. The genotypes of TNF-beta and IL-4 were determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Allelic and genotypic frequencies for these polymorphisms were similar in patients with MS and population controls or among different types of the disease. CONCLUSION: The results of the present study suggest that the three mentioned functional polymorphisms are not likely to cause susceptibility to MS in the Iranian population.