Imaging review of neurofibromatosis: helpful aspects for early detection

Neurofibromatosis [NF] is divided into two types, NF type 1 and NF type 2. Optic nerve gliomas have a high degree of association with NF type 1. NF 2, less commonly seen, is a complex of cutaneous and deep neural tumors. It is an autosomal dominant familial disorder in which CNS is affected in about 15% of the cases. Bilateral acoustic neuromas are pathognomonic of NF type 2 which may be associated with meningiomas or ependymomas. Typical clinical manifestations of neurofibromatosis are cafe-au-lait spots and multiple cutaneous tumors. There is bone involvement as scoliosis, pseudoarthrosis of long bones, scalloping of vertebral bodies, abnormal rib tubulation and defective ossification of the skull. Extraskeletal manifestations of neurofibromatosis include optic nerve gliomas, pheochromocytoma, aneurysms of cerebral and renal arteries, acoustic neurilemmoma and superficial skin nodular neurofibromas. Here, we intend to present images of several cases of neurofibromatosis with different patterns of body involvement

[Anti-human herpes virus-6 antibodies titer in patients with multiple sclerosis in Markazy Province]

Multiple sclerosis [MS] is a auto-immune disease of central nervous system. The etiology of MS is unknown, but environmental factors such as viruses are involved in the development of MS. In this study, MS patients were assessed for antibodies titers against Human Herpes virus-6 [HHV-6] in Markazi Province. In this case-control study, 31 new cases of MS patients and 60 healthy subjects were selected with similar demographic criteria such as sex, age and location. Antibodies titer [IgM and IgG] against HHV-6 were examined by ELISA and Immunofluorescence methods. Data were analyzed using Logistic regression and Odds ratio. Data indicates that 74.2% of case group and 34.2% of control group were identified as positive for IgM against HHV-6. The difference between the two groups in terms of IgM against HHv-6 was statistically significant [p=0.001]. Incidence of IgM positivity against HHV-6 was increased more than five times in MS patients compared to control group. Also there was a statistically significant difference between case and control groups in IgG titer [p=0.019]. Acute infection of HHV-6 is a risk factor for MS

Effect of Sesame oil on leukocyte infiltration into the brain of C57/BL6 mice with experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis [EAE] is an animal model of multiple sclerosis distinguished by infiltration of leukocytes into the central nervous system. Changes in composition and levels of unsaturated fatty acids, affect the integrity of blood-brain barrier. In this study, we evaluated the effect of Sesame oil on the leukocyte infiltration into the brain of MOG[35-55] induced EAE male C57BL/6 mice. In this experimental study, male C57BL/6 mice were placed in two therapeutic groups [n=10 per group] with age and weight-matched as follow: 1.Sesame oil-treated EAE mice received 4ml/kg/day of Sesame oil given i.p. from day -3 until day +19 after disease induction, 2.Non-treated EAE mice [EAE control] received Phosphate buffer alone with same schedule. EAE was induced by immunization of mice with MOG[35-55] peptide and complete Freund's adjuvant. Leukocytes infiltration into the brain was investigated 20 days after immunization. Data was analyzed using Mann-Whitney U test. The results show that Sesame oil-treated mice had significantly less clinical score of EAE [2.6 +/- 0.4] than non-treated EAE induced mice [4.2 +/- 0.6], [p<0.001]. Also, there was a significant difference at number of the infiltrating cells in brain between Sesame oil-treated [80 +/- 20] and non treated EAE-induced mice [150 +/- 30], [p<0.01]. These results indicate that Sesame oil reduces infiltration of leukocytes into the brain of EAE mice, therefore lessening the histological changes and clinical signs and thus ameliorating the disease

Correlation of two way active avoidance learning with nitric oxide and ferric reduction / antioxidant power in rats

Oxidative stress may play a critical role in neurodegenerative disorders but the relation between oxidative stress and learning ability in normal rats is not investigated, so the aim of this study was to investigate the correlation between oxidative stress and two way active avoidance learning in Wistar rats. This is an experimental research. 14 Wistar rats were assigned for assessed learning ability in shuttle box. One day after shuttle box learning, cerebrospinal fluid [CSF] and blood samples were obtained. Concentration of Nitric Oxide and Ferric reduction/antioxidant power were assessed. Data was analyzed using Pearson correlation test. The results of the present study demonstrate that there are positive correlation between shuttle box learning ability and Ferric reduction/antioxidant power [p<0.001, r =0.66 4] and Nitric Oxide concentration [p<0.001, r = 0.724] in serum, but not hi CSF. The results of this study suggest that high concentration of antioxidant power and Nitric Oxide concentration in blood can improve shuttle box learning in rats

[Effect of vitamin D3 on IFN-T and IL-10 levels in mice with experimental a utoimmune encephalomylitis]

Multiple sclerosis [MS] is a chronic autoimmune disease with unknown etiology affecting the central nervous system. The pre9alence of MS is highest where environmental supplies of vitamin Dare lowest. Some studies have shown a strong protective effect of vitamin D3 in experimental autoimmune encephalomyelitis [EAE]; a model of MS. However, it is not known whether vitamin D3 has a protective effect in EAE. Vitamin D3 may be inhibit EAE by having an effect on TH1 and TH2 immune responses. To address this question, the effect of vitamin D[3] on cellular immune responses in C57BL/6 mice with experimental autoimmune encephalomyelitis was investigated. Male C57HL/6 mice matched in age and weight were placed in two therapeutic groups [n10 per group] as follows: Vitamin D3-treated EAE mice [5 micro g/kg/every two days of vitamin D3 given i.p from day -3 until day +19 after disease induction]. Non-treated EAE mice [EAE control] received vehicle alone with same schedule. 20 days after immunization, the mononuclear cells [MNCs] of the spleen were isolated from mice and cultured in the presence and absence of MOG35-55 for 96 hours. The supematant of cultured cells was collected and produced cytokines [IL-10 and IFN-gamma] were assayed by ELISA. The results showed that vitamin D3-treated mice had less severe clinical signs and synptoms of EAE [3.2 +/- 0.8] than non-treated EAE induced mice [5.3 +/- 0.44]. [p=0.001]. Also, there was a significant difference regarding the day of onset of disease in the vitamin D3-treated and non treated EAE-induced mice [day 15 +/- 1 and day 11 +/- 1, respectively]. There was no significant difference in IFN-y production between treated and non-treated mice, but the amount of 11-10 production in the D3-treated mice was higher than the non-treated group [p=0.001]. Considering the role of TH1 in the pathogenesis of EAE and MS. it is suggested that vitamin D3 can reduce or delay the onset of EAE by shifting immune responses to TH2 and IL-10 production. Thus, vitamin D3 as an immune modulatory agent is potentially important for treatment of MS

Effect of simvastatin on evolution of experimental autoimmune encephalomyelitis in C57BL/6 mice

Simvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase and widely used as cholesterol-lowering agent. It is a promising candidate for future treatment in multiple sclerosis [MS], as it has been shown to exhibit immunomodulatory and anti-inflammatory effects. This study examined the effect of simvastatin on the evolution of experimental autoimmune encephalomyelitis [EAE], as an animal model for MS. EAE was induced by immunization of 8 week old C57BL/6 mice with MOG35-55 peptide with complete Freunds adjuvant. Therapy with simvastatin [1mg/kg/every day given as oral] was started on day 3 before the immunization until 25 day after immunization Total antioxidant capacity [TAC] was assessed by ferric reducing-antioxidant power [FRAP] method. Nitric oxide [NO] production was also estimated by Griess reaction. The results show that simvastatin-treated mice had significantly less incidence and clinical score of EAE than non-treated [control] EAE induced mice [p=0.001 and p=0.0001, respectively]. Moreover, treated mice displayed a significantly delayed disease onset compared with control mice. Simvastatin significantly increased TAC and level serum uric acid [p=0.001], but had no effect on serum nitrite production. Our results suggest that simvastatin therapy may be effective in the prevention of symptomatic EAE. This resistance to encephalomyelitis may be associated with the inhibition of oxidative stress and the increase of antioxidant capacity

[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

[Comparison of oxidative stress in preeclampsia, normal pregnancy and non-pregnant women]

Preeclampsia is a pregnancy-specific condition characterized by hypertension and proteinuria. Preeclampsia remains a disease of theories as its real etiology has remained elusive. Endothelial cell dysfunction may play a role in the pathobiology of preeclampsia. There is some evidence to suggest that endothelial cell damage result from oxidative stress. The aim of the study was to measure oxidative stress markers in preeclampsia. Total antioxidant capacity [TAC], lipid peroxidation [LPO] and thiol groups was measured in 20 women with preeclampsia, 20 normal pregnant women and 20 nonpregnant women. All three women groups were matched with respect to age, BMI, parity and gestational age. Oxidative stress markers were measured by spectrophotometer methods. Serum concentration of LPO was significantly higher in preeclampsia [17.7 + 3.8 nmol/ml] as compared with nonpregnant women [10.4 + 0.48 nmol/ml, p< 0.0001]. TAC in preeclamptic women was lower than those in normal pregnant and non-pregnant women, but not statistically significantly. There was no significant difference between the mean concentrations of thiol groups in the women groups. Increased levels of LPO products may cause peroxidative damage of vascular endothelium and result in clinical symptoms of preeclampsia. However, further experimental and clinical studies are necessary to clarify the pathogenesis of preeclampsia