Nan-Xiang Xiong

Vagoglossopharyngeal Neuralgia Treated by Microvascular Decompression and Glossopharyngeal Rhizotomy: Clinical Results of 21 Cases

Background: Microvascular decompression (MVD) and rhizotomy are all selected for treating vagoglossopharyngeal neuralgia (VGPN). Nonetheless, controversies still exist about their curative effect on VGPN. Here we evaluate the effectiveness of MVD together with rhizotomy of the glossopharyngeal nerve for the treatment of VGPN. Methods: This study was carried out on 21 patients who were diagnosed with VGPN between the years 2005 and 2010. Patients underwent MVD and glossopharyngeal rhizotomy through a retromastoid keyhole approach. Surgical technique, operation results and complications were our particular concern. Results: Eighteen (85.7%) of 21 patients experienced immediate and complete relief of pain after surgery. In the remaining 3 patients (14.3%), the pain faded away within the following week. No patient complained of dysphonia or dysphagia. All 21 patients reported no change in their outcome at follow-up. Conclusions: Intracranial vagoglossopharyngeal nerve MVD with glossopharyngeal rhizotomy is an effective and safe procedure to treat VGPN.

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

ObjectiveNogo-A is an axon regeneration inhibitor, and its function in central nervous system (CNS) is still unknown. The present study is to explore the relationship between the expression of Nogo-A and the malignancy of oligodendroglial tumors in patients.MethodsTumor tissue samples with different malignancy grade were obtained from the hospitals. The samples used for detection had been diagnosed as oligodendroglial tumors (oligodendroglioma or anaplastic oligodendroglioma). The expression of Nogo-A was detected by immunohistochemistry and western-blot analysis. The correlation test between the Nogo-A expression and the morphological changes (the percentages of atypical cells and mitotic cells in the tumors) related to the malignancy of tumor tissues was performed.ResultsThere was significant negative correlation between the Nogo-A expression and the morphological change of tumor tissues according to immunohistochemistry. Western-blot analysis also indicated that the gray value of Nogo-A protein band in the oligodendroglioma group was significantly higher than that in the anaplastic oligodendroglioma group.ConclusionNogo-A expression was negatively correlated with the malignancy grade of oligodendroglial tumors.摘要目的探讨 Nogo-A 蛋白在少突胶质细胞肿瘤中的表达水平与该肿瘤恶性程度之间的关系。方法选取来自临床上经病理检查确诊为少突胶质细胞肿瘤的组织标本, 其中少突胶质细胞瘤 16 例, 间变型少突胶质细胞瘤 10 例。 免疫组织化学染色检测 Nogo-A 的表达, 并与同视野下瘤细胞的核分裂与核异型性比例作相关分析; 另外, 把病理标本按照分级进行蛋白印迹 试验。结果免疫组织化学结果显示, Nogo-A 免疫阳性染色的光密度值与肿瘤细胞核分裂、 核异型比例呈明显的负相关, 对蛋白印迹试验结果进行光密度分析也发现少突胶质细胞瘤中的 Nogo-A 蛋白条带灰度值明显高于间变型少突胶质细胞瘤中的灰度值。结论Nogo-A 蛋白在少突胶质细胞肿瘤中的表达水平与该肿瘤恶性程度呈负相关。

MiR-338-5p suppresses proliferation, migration, invasion, and promote apoptosis of glioblastoma cells by directly targeting EFEMP1

OBJECTIVE We aimed to investigate the effect of miR-338-5p on proliferation, migration and invasion of glioblastoma (GBM) cells by regulating EFEMP1. METHODS The expression of miR-338-5p and EFEMP1 was measured by qRT-PCR and western blot. Transfection was conducted to regulate the expression of miR-338-5p and EFEMP1 in U87 cell lines. Cell proliferation, apoptosis, migration and invasion were evaluated using CCK-8 assay, flow cytometry and Transwell assay respectively. Dual luciferase reporter assay was performed to verify whether miR-338-5p directly targeted EFEMP1. RESULTS MiR-338-5p was significantly down-regulated in human GBM tumor tissues and cells while EFEMP1 was strongly upregulated (P<0.05). Upregulated miR-338-5p was able to suppress cell proliferation, migration, invasion, and promote cell apoptosis in GBM cells (P<0.05). Dual luciferase reporter gene assay determined that miR-338-5p directly targeted EFEMP1 (P<0.05). CONCLUSIONS MiR-338-5p suppressed proliferation, migration and invasion of GBM cells through inhibiting EFEMP1.

Gamma Knife Radiosurgery for Glossopharyngeal Neuralgia by Targeting the Medial Cisternal Segment of the Glossopharyngeal Nerve: Report of 3 Cases.

Gamma knife surgery (GKS) is now used as a treatment option for glossopharyngeal neuralgia (GPN). Most authors have selected the distal part of the nerve as the gamma knife target. Here we report on 3 patients with medically intractable GPN who were treated with GKS. All 3 patients had a single shot with a 4-mm collimator which was used to deliver 80 Gy to the 100% isodose line. The GKS targets were the medial cisternal segments of the glossopharyngeal nerve. Patients were investigated prospectively, treated, and then assessed periodically with respect to pain relief and neurological function. Three patients felt pain reduced at 2, 7, and 11 days, respectively. None of them have suffered recurrent pain since becoming pain free. The follow-up after radiosurgery was 25 months, 22 months, and 20 months, respectively. This preliminary experience provides encouraging evidence that choosing the medial cisternal segment of the glossopharyngeal nerve as the target is also an option for the treatment of GPN with stereotactic radiosurgery and is consistent with previous reports. Additional follow-ups and a larger number of patients are needed to demonstrate the long-term safety and effectiveness for this indication.

Overexpression of Tau Rescues Nogo-66-Induced Neurite Outgrowth Inhibition In Vitro

Nogo-66 plays a central role in the myelin-mediated inhibition of neurite outgrowth. Tau is a microtubule-associated protein involved in microtubule assembly and stabilization. It remains unverified whether tau interacts directly with growth factor receptors, or engages in cross-talk with regeneration inhibitors like Nogo-66. Here, we report that plasmid overexpression of tau significantly elevated the protein levels of total tau, phosphorylated tau, and microtubule-affinity regulating kinase (MARK). Nogo-66 transiently elevated the total tau protein level and persistently reduced the level of p-S262 tau (tau phosphorylated at serine 262), whereas it had little influence on the level of p-T205 tau (tau phosphorylated at threonine 205). Nogo-66 significantly decreased the protein level of MARK. Hymenialdisine, an inhibitor of MARK, significantly reduced the level of p-S262 tau. Overexpression of tau rescued the Nogo-66-induced inhibition of neurite outgrowth in neuroblastoma 2a (N2a) cells and primary cortical neurons. However, concomitant inhibition of MARK abolished the rescue of neurite outgrowth by tau in N2a cells. We conclude that dephosphorylation of tau at S262 is able to regulate Nogo-66 signaling, and that overexpression of tau can rescue the Nogo-66-induced inhibition of neurite outgrowth in vitro.

Current status and potential challenges of mesenchymal stem cell-based therapy for malignant gliomas

Glioma, which accounts for more than 30% of primary central nervous system tumours, is characterised by symptoms such as headaches, epilepsy, and blurred vision. Glioblastoma multiforme is the most aggressive, malignant, and lethal brain tumour in adults. Even with progressive combination treatment with surgery, radiotherapy, and chemotherapy, the prognosis for glioma patients is still extremely poor. Compared with the poor outcome and slowly developing technologies for surgery and radiotherapy, the application of targeted chemotherapy with a new mechanism has become a research focus in this field.Moreover, targeted therapy is promising for most solid tumours. The tumour-tropic ability of stem cells, including neural stem cells and mesenchymal stem cells, provides an alternative therapeutic approach. Thus, mesenchymal stem cell-based therapy is based on a tumour-selective capacity and has been thought to be an effective anti-tumour option over the past decades. An increasing number of basic studies on mesenchymal stem cell-based therapy for gliomas has yielded complex outcomes.In this review, we summarise the biological characteristics of human mesenchymal stem cells, and the current status and potential challenges of mesenchymal stem cell-based therapy in patients with malignant gliomas.

Gamma Knife Radiosurgery of the Superior Laryngeal Neuralgia: A Report of 3 Cases

BACKGROUND Superior laryngeal neuralgia (SLN) is a relatively rare disorder that is characterized by neck pain. There are only a few reported cases and treatment options for SLN to date. In this study, we report 3 patients with SLN who were treated with Gamma Knife radiosurgery (GKRS) at the time of diagnosis. CASE DESCRIPTION For all 3 patients, GKRS was administered using a 4-mm collimator to deliver a single shot of 80 Gy of radiation (100% isodose line). The target was set at the jugular foramen where the vagus and glossopharyngeal nerves emerge from the skull. Follow-up assessments were performed at 32, 31, and 30 months after GKRS. The 3 patients described pain relief at 3 months, 2 days, and 6 weeks. None of the patients developed neurologic deficits during the follow-up period. CONCLUSIONS This preliminary report provides encouraging evidence that GKRS represents an effective, safe, and relatively durable noninvasive treatment option for patients with SLN.

Dehydrocavidine attenuates d-galactose induced learning and memory impairment in rats

OBJECTIVE Dehydrocavidine (DEH) is the major component of a plant corydalis saxicola Bunting, which is used to treat the patients with hepatic disorders, there is still no report about the effect of DEH on the brain disorder. In this study, the effect and mechanism of DEH on d-galactose (d-gala) induced learning and memory impairment in rats was investigated. METHODS A learning and memory impairment rat model was employed by chronic intraperitoneal injection of d-gala and intragastric administration of DEH, then Morris water maze test was used to investigate the effect of DEH on learning and memory impairment, Golgi stain and biochemical methods, real time PCR were used to investigate underlying mechanism. RESULTS Intraperitoneal injection of d-gala could induced severe learning and memory impairment in rats, intragastric administration of DEH could effectively attenuates these deficits. Golgi staining showed DEH supplementary could restored the density of spines to 5.7±1.16 spines per 10μm in the DEH+d-gala group (p<0.05). DEH supplementary administration reversed the lipid peroxides and restored the enzymes activities to reduce oxidative damage (p<0.05). DEH supplementary administration could reduced the production of NO and PGE2 and the mRNA expression of iNOS and COX-2 (p<0.05). CONCLUSIONS DEH could attenuates d-gala induced learning and memory impairment in rats by enhancing synaptic plasticity, reducing oxidative damage and limiting the neuroinflammation.

CD90 determined two subpopulations of glioma-associated mesenchymal stem cells with different roles in tumour progression

Human glioma-associated mesenchymal stem cells (gbMSCs) are the stromal cell components that contribute to the tumourigenesis of malignant gliomas. Recent studies have shown that gbMSCs consist of two distinct subpopulations (CD90+ and CD90− gbMSCs). However, the different roles in glioma progression have not been expounded. In this study, we found that the different roles of gbMSCs in glioma progression were associated with CD90 expression. CD90high gbMSCs significantly drove glioma progression mainly by increasing proliferation, migration and adhesion, where as CD90low gbMSCs contributed to glioma progression chiefly through the transition to pericytes and stimulation of vascular formation via vascular endothelial cells. Furthermore, discrepancies in long non-coding RNAs and mRNAs expression were verified in these two gbMSC subpopulations, and the potential underlying molecular mechanism was discussed. Our data confirm for the first time that CD90high and CD90low gbMSCs play different roles in human glioma progression. These results provide new insights into the possible future use of strategies targeting gbMSC subpopulations in glioma patients.

Severe remote cerebellar hemorrhage with intracerebral hemorrhage after burr-hole evacuation for chronic subdural hematoma

Since remote cerebellar hemorrhage, with intracerebral hemorrhage after supratentorial neurosurgery, is rare, its pathophysiology remains elusive.Here, we report a 64-year-old man who had severe bilateral symmetric remote cerebellar hemorrhage with frontal lobe hemorrhage following burr-hole evacuation for supratentorial chronic subdural hematoma.Computed tomography venography showed undeveloped left internal jugular vein and sigmoid sinus.He received 3 weeks of conservative treatment and fully recovered.Overdrainage of cerebrospinal fluid and head rotation with undeveloped internal jugular vein may have resulted in this complication.This case is the first case in the literature with this event sequence and has some significance for revealing the mechanism of remote cerebellar hemorrhage occurrence after other supratentorial surgeries.