Retrocerebellar arachnoid cyst resulting in syringomyelia in a patient without tonsillar herniation: successful surgical treatment with reconstruction of CSF flow in the foramen magnum region.

A retrocerebellar arachnoid cyst causing syringomyelia is extremely rare without tonsillar herniation. The authors present a 44-year-old woman with symptoms of foramen magnum compression and syringomyelia. Magnetic resonance imaging demonstrated a large retrocerebellar arachnoid cyst with a large cervicothoracic syrinx but no signs of tonsillar herniation or hydrocephalus. The patient underwent a foramen magnum decompression with C1 laminectomy, microsurgical fenestration of the cyst, and duraplasty. After successful reconstruction of CSF flow, the patient experienced a relief of symptoms and a significant reduction of the syrinx. The intraoperative findings support the theory of a piston mechanism in the development of syringomyelia. Additional arachnoidal adhesions may also obstruct the CSF flow around the craniocervical junction. We recommend the surgical treatment should consist of an adequate decompression of the foramen magnum, wide microsurgical arachnoidal debridement, and duraplasty with autologous grafts sutured in a watertight way.

STI571 protects neuronal cells from neurotoxic prion protein fragment-induced apoptosis.

Prion diseases are neurodegenerative disorders caused by the accumulation of misfolded prion proteins [scrapie form of PrP (PrP(Sc))]. PrP(Sc) accumulation in the brain causes neurotoxicity by inducing mitochondrial-apoptotic pathways. Neurodegeneration can be prevented by imatinib mesylate (Gleevec or STI571) that regulates c-Abl tyrosine kinases, which elicit protective effects in neurodegenerative disease models. However, the protective effect of STI571 against prion disease remains unknown. In the present study, the effect of STI571 on prion peptide-induced neuronal death was investigated. Results showed that STI571 rescued neurons from PrP106-126-induced neurotoxicity by preventing mitochondrial dysfunction. STI571-inhibited c-Abl tyrosine kinases prevented PrP106-126-induced reduction in mitochondrial potential, Bax translocation to the mitochondria and cytochrome c release. The protective effect of STI571 against mitochondrial dysfunction was related to the activation of BIM expression. This study is the first to demonstrate the protective effect of STI571 against prion-mediated neurotoxicity. Our results suggested that imatinib mesylate treatment may be a novel therapeutic strategy to treat prion-mediated neurotoxicity.

[Effect of probiotics on Newcastle Disease Virus].

OBJECTIVE: We studied the antiviral activity of probiotics and possible mechanism thereof. METHODS: With hemagglutination in vitro and 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) of chicken embryo fibroblast (CEF), the hemagglutination titers and virus inhibition rate were respectively determined to evaluate the impact of probiotics on Newcastle Disease Virus (NDV). RESULTS: Five probiotics and their metabolites could reduce the viral titer of NDV, but the two pathogenic bacteria and their metabolites could not. These results indicated that probiotics may destruct the structure of NDV directly and this effect was strain-specific. Probiotics could inhibit the replication rate of NDV significantly in a dose-dependent manner (P<0.01). The inhibitory rate increased when the cells were pre-treated with probiotics, which indicated that the probiotics might block NDV adsorbing to the cells. The fact that addition of probiotics and NDV at the same time reduced the cytopathic effect (CPE) of cells suggested that probiotics could destruct the viral structure directly; the lower inhibitory rate of viral replication when cells infected with NDV before addition of probiotics to the cells suggested that the probiotics worked hardly after the cells were infected. CONCLUSION: Probiotics can not only destruct the virus, but also block the virus infection of the cells and inhibit the viral proliferation in the cells.