[Prevalence of fungal and fungal like superficial infections in patients who refered to skin clinic of Arak university of medical science]

There are wide-ranging types of fungal infection and dependent on the site of involvement it is divided into five groups; superficial, cutaneous, mucocutaneous, subcutaneous and visceral infections. In humans cutaneous infection includes skin hair and nail disease. This study was done on 148 patients suspected to fungal infection. Samples were studied by direct smear and culture in S, SC and SCC culture media. From 148 patients referred to Medical laboratory, 90 patients had cutaneous infection [60.8%] among which 11 were infected with Tinea versicolor [12.23%], 4 with Candidiasis [4.44%], 73 with dermatophytosis [81.11%] and finally 2 patients with Demodecosis [2.22%]. In this study, dermatophytosis was the most prevalent infection and Tinea corporis had the most incidence among fungal infections. T. verocosome, a zoophyllic fungus, was the main culprit

[Effect of vitamin E on the inhibition of experimental autoimmune encephalomyelitis in C57BL/6 mouse]

Free radical-mediated per-oxidation of biological molecules, such as lipids, is implicated in the pathogenesis of multiple sclerosis and it's animal model experimental allergic encephalomyelitis [EAE]. Low concentration of antioxidant vitamin E has been observed in serum of multiple sclerosis. However, it is not known whether vitamin E has protective effect in EAE. Vitamin E may inhibit EAE by effect on the level of uric acid and Nitric Oxide [NO] production. In this experimental study some male C57BL/6 mice were placed in two therapeutic groups [n=8 per group] with age and weight-matched as follow: 1] Vitamin E-treated EAE mice [10mg/kg/every two days of vitamin E given i.P from day-3 until day + 19 after disease induction, 2] Non-treated EAE mice [EAE control] received vehicle alone with same schedule. In addition, 5 age and weight-matched male C57BL/6 mice served as normal [non-EAE] controls. Clinical score of disease, uric acid and NO levels of the groups were analysed. Results showed that vitamin E-treated mice had significantly less clinical score of EAE [4 +/- 0.8] than non-treated EAE induced mice [5.3 +/- 0.44], [p< 0.01]. Also, there was difference at the onset day of the disease between vitamin E-treated and non-treated EAE-induced mice [day 13 +/- 1 and day 11 +/- 1, respectively], although was not significant. Concentration of uric acid in vitamin E treated mice were significantly lower than EAE control [p< 0.001]. There was no difference at the level of NO between the groups. Vitamin E had no effect on NO level, but decreased serum uric acid level. It suggests that vitamin E can reduce or delay the onset of EAE by increasing uric acid consumption

[Effect of sesame oil on the development of experimental autoimmune encephalomyelitis in C57BL/6 mice]

Experimental autoimmune encephalomyelitis [EAE] is a inflammatory demyelinating autoimmune disease of the CNS that servers as an animal model for multiple sclerosis [MS]. Seame oil effect was evaluated in the treatment of EAE in C57BL/6 mice. Seame oil shows profound anti-inflammatory activity and has been traditionally used to treat inflammatory disorders. EAE was induced by immunization of 8 week old mice with MOG[35-55] with complete freunds adjuvant. Therapy with sesame oil was started on day 2 before the immunization. total antioixdant capacity [TAC] was assessed by ferric reducing-antioxidant power [FRAP] method. nitric oxide [NO] producation was also estimated by Griess reaction. After daily intraperitoneal dosage the seame oil significantly reduced the clinical symptoms in c57BL/6 mice with EAE [p< 0.01]. Also, treated mice displayed a significantly delayed disease onset compared with control mice. seame oil significantly increased TAC [p< 0.05], but had no effect on serum nitrie production. Our results suggest for the first time that seame oil therapy may be effective in the prevention of symptomatic EAE. this resistance to encephalomyelities may be associated with inhibition of oxidative stress