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Objective To study the influencing factors of recurrence of trigeminal neuralgia after microvascular decompression and its microsurgical management.Methods Twenty one patients with recurrent trigeminal neuralgia after microvascular decompression (MVD),admitted to our hospital from 2006 to 2011,were treated by microsurgical operations assisted by neuroendoscope.MVD was performed again in 17 patients,arachnoid membranes reflaxation in 2,partial rhizotomy (PR) in 1,and both MVD and PR in 1.Results All patients were followed up for about 28.5 months (mean duration).The total effective rate during the follow-up period was 95.2％.Facial numbness was found in 2 patients and light facial paralysis in 1.Conclusion Many factors were responsible for the recurrence of trigeminal neuralgia after MVD; and vascular compression is still the main cause; MVD should be the first choice; curative effect and safety would be improved by the assistance ofneuroendoscope.
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MicroRNA (miR)-125b has been shown to play a potential role in the development of glioma stem cells. However, the relationship between miRNA and glioma stem cells is still elusive. This study was designed to elucidate this potential relationship. We established a highly invasive glioma stem cell and progenitor (GSCP) cell line SU3. SU3 cell suspensions were injected into nude mice brains in situ, and the invasiveness of graft tumors was analyzed using hematoxylin and eosin staining as well as immunohistochemistry. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of miR-125b in SU3 and other cells. In vitro, SU3 cells expressed CD133 and nestin as well as differentiation markers glial fibrillary acidic protein (GFAP) and β-tubulin III, which were consistent with the characteristics of glioma stem cells. Scratch assays indicated that the migration ability of SU3 cells was stronger than that of U251 stem cells (U251s). In vivo, SU3 cells invaded into each part of the mouse brain from the caudate nucleus in a diffuse pattern and highly expressed invasive and proliferative cell markers matrix metalloprotease 2 (MMP2), MMP9, and Ki-67. Real-time PCR results revealed that the levels of miR-125b and MMP9 were significantly higher in SU3 and SU2, also a highly invasive GSCP cell line we established before, than in U251s. High expression of miR-125b both in newly established GSCPs, SU3, and long-term cultured GSCPs, SU2 suggests that miR-125b exhibits oncogene-like behavior. This behavior should be considered in further studies of miR-125b in cancer stem cells. Furthermore, MMP9, which plays a role in cancer stem cell invasion, may be a target gene of miR-125b.