A Study on the Recurrence Rate of Trigeminal Neuralgia after MVD and the Related Factors.

The aim of this article is to investigate the related factors affecting the recurrence of microvascular decompression (MVD) after trigeminal neuralgia. We selected 400 cases of patients who met the diagnostic criteria of primary trigeminal neuralgia. The recurrence rate of patients and their statistical data related factors such as age, gender, disease duration, pain branches, vascular compression, patients, and complications (urban and rural), were collected. Of the 400 cases, 36 had recurrence after 2 years. In female group, the recurrence rate was (9.4%) higher than the recurrence rate in male group (8%); no recurrence rate of vascular compression group (40%) was higher than that of vascular compression group recurrence rate (8.6%); the recurrence rate of each branch in pain group from high to low was V 2-3 (13.4%), V 2 (12.5%), V 1 (9.1%), V 3 (7.5%), V 1-2-3 (4.4%), V 1-2 (4.3%), V 1-3 (0%); and the difference was statistically significant ( p < 0.05).Gender of the patient, the presence of vascular pressure, and the branch of pain could significantly affect the postoperative recurrence rate of trigeminal neuralgia in patients treated with simple MVD ( p < 0.05).

Let-7g-5p inhibits epithelial-mesenchymal transition consistent with reduction of glioma stem cell phenotypes by targeting VSIG4 in glioblastoma.

Epithelial-mesenchymal transition (EMT) and stem-like glioma cells display hallmark therapeutic resistance. Understanding of the mechanisms underlying these properties will be vital for the development of effective therapies. In this study, we found that VSIG4 protein is upregulated in glioblastoma. Overexpressing VSIG4 induced EMT and significantly promoted invasion and migration in glioblastoma U-87MG cells. Moreover, we showed that its overexpression promoted formation of glioma stem cell phenotypes in U-87MG cells. P4HB, VAMP8 and Connexin 43 (CX43) can promote temozolomide (TMZ) resistance in human glioma cells. We showed that P4HB, VAMP8 and CX43 protein were upregulated by VSIG4 in U-87MG cells, implying its upregulation might be a cause for temozolomide resistance. We found that let-7g-5p can inhibit VSIG4 protein expression, but it cannot degrade VSIG4 mRNA in U-87MG cells. Contrary to VSIG4, we demonstrated that overexpressing let-7g-5p promoted mesenchymal-epithelial transition (MET) and significantly inhibited invasion and migration consistent with the reduction of glioblastoma stem cell phenotypes in U-87MG cells. Thus, we concluded that let-7g-5p inhibits epithelial-mesenchymal transition (EMT) consistent with reduction of glioma stem cell (GSC) phenotypes by targeting VSIG4 in glioblastoma.