Endoscopic microvascular decompression versus microscopic microvascular decompression for trigeminal neuralgia: A systematic review and meta-analysis.

BACKGROUND: To compare the efficacy and safety of full endoscopic or endoscope-assisted microvascular decompression (E-MVD) and microscopic microvascular decompression (M-MVD) for primary trigeminal neuralgia (TN). METHODS: We systematically searched the online database, including PubMed, Embase and Cochrane Library. The search terms used included, but were not limited to, "Trigeminal Neuralgia", "Microvascular Decompression Surgery" and "Endoscope". Postoperative facial pain relief and postoperative complications were considered for meta-analysis. All the outcomes were calculated as odds ratios (ORs) with 95% confidence intervals using R language. RESULTS: A total of three studies involving 442 (E-MVD [218] versus M-MVD [224]) patients were included for analysis in our study. Postoperative facial pain relief (very much improved or much improved) was no difference between the two groups (OR, 0.95;95% CI, 0.57-1.58; I2 = 0%; p = 0.83). In addition, the occurrence of some postoperative complications was not statistically different between the two groups, including CSFleak (OR, 1.35;95% CI, 0.16-11.13; I2 = 0%; p = 0.94), facial paralysis (OR, 0.26;95% CI, 0.03-2.54; I2 = 0%; p = 0.67), hearing loss (OR, 0.87;95% CI, 0.30-2.55; I2 = 32%; p = 0.22), facial numbness (OR, 1.03;95% CI, 0.56-1.87; I2 = 62%; p = 0.10). CONCLUSIONS: Both endoscopic microvascular decompression and microscopic microvascular decompression for trigeminal neuralgia appear to provide patients with equivalent facial pain relief outcomes. Complication rates were also similar between the groups.

Proteomics identifies differentially expressed proteins in glioblastoma U87 cells treated with hederagenin.

OBJECTIVE: We investigated differentially expressed proteins (DEPs) in human glioblastoma U87 cells after treatment with hederagenin as a therapeutic screening mechanism and provided a theoretical basis for hederagenin in treating glioblastoma. METHODS: The Cell Counting Kit 8 assay was used to analyze the inhibitory effect of hederagenin on the proliferation of U87 cells. Protein was identified by tandem mass tags and LC-MS/MS analysis techniques. Annotation of DEPs, Gene Ontology enrichment and function, and Kyoto Encyclopedia of Genes and Genomes pathways and domains were all examined by bioinformatics. According to the TMT results, hub protein was selected from DEPs for WB verification. RESULTS: Protein quantitative analysis found 6522 proteins in total. Compared with the control group, 43 DEPs (P < 0.05) were involved in the highly enriched signaling pathway in the hederagenin group, among which 20 proteins were upregulated, and 23 proteins were downregulated. These different proteins are mainly involved in the longness regulating pathway-WORM, the hedgehog signaling pathway, Staphylococcus aureus infection, complement, coagulation cascades, and mineral absorption. KIF7 and ATAD2B expression were significantly down-regulated and PHEX and TIMM9 expression were significantly upregulated, according to WB analysis, supporting the TMT findings. CONCLUSION: Hederagenin inhibition of GBM U87 cells may be related to KIF7, which is mainly involved in the hedgehog signaling pathway. Our findings lay a foundation for additional study of the therapeutic mechanism of hederagenin.

Screening seven hub genes associated with prognosis and immune infiltration in glioblastoma.

Glioblastoma (GBM) is the most common and deadly primary brain tumor in adults. Diagnostic and therapeutic challenges have been raised because of poor prognosis. Gene expression profiles of GBM and normal brain tissue samples from GSE68848, GSE16011, GSE7696, and The Cancer Genome Atlas (TCGA) were downloaded. We identified differentially expressed genes (DEGs) by differential expression analysis and obtained 3,800 intersected DEGs from all datasets. Enrichment analysis revealed that the intersected DEGs were involved in the MAPK and cAMP signaling pathways. We identified seven different modules and 2,856 module genes based on the co-expression analysis. Module genes were used to perform Cox and Kaplan-Meier analysis in TCGA to obtain 91 prognosis-related genes. Subsequently, we constructed a random survival forest model and a multivariate Cox model to identify seven hub genes (KDELR2, DLEU1, PTPRN, SRBD1, CRNDE, HPCAL1, and POLR1E). The seven hub genes were subjected to the risk score and survival analyses. Among these, CRNDE may be a key gene in GBM. A network of prognosis-related genes and the top three differentially expressed microRNAs with the largest fold-change was constructed. Moreover, we found a high infiltration of plasmacytoid dendritic cells and T helper 17 cells in GBM. In conclusion, the seven hub genes were speculated to be potential prognostic biomarkers for guiding immunotherapy and may have significant implications for the diagnosis and treatment of GBM.

Transdifferentiation-Induced Neural Stem Cells Promote Recovery of Middle Cerebral Artery Stroke Rats.

Induced neural stem cells (iNSCs) can be directly transdifferentiated from somatic cells. One potential clinical application of the iNSCs is for nerve regeneration. However, it is unknown whether iNSCs function in disease models. We produced transdifferentiated iNSCs by conditional overexpressing Oct4, Sox2, Klf4, c-Mycin mouse embryonic fibroblasts. They expanded readily in vitro and expressed NSC mRNA profile and protein markers. These iNSCs differentiated into mature astrocytes, neurons and oligodendrocytes in vitro. Importantly, they reduced lesion size, promoted the recovery of motor and sensory function as well as metabolism status in middle cerebral artery stroke rats. These iNSCs secreted nerve growth factors, which was associated with observed protection of neurons from apoptosis. Furthermore, iNSCs migrated to and passed through the lesion in the cerebral cortex, where Tuj1+ neurons were detected. These findings have revealed the function of transdifferentiated iNSCs in vivo, and thus provide experimental evidence to support the development of personalized regenerative therapy for CNS diseases by using genetically engineered autologous somatic cells.

Transplanted hUCB-MSCs migrated to the damaged area by SDF-1/CXCR4 signaling to promote functional recovery after traumatic brain injury in rats.

Transplanted human umbilical cord mesenchymal stem cells (hUC-MSCs) have exhibited considerable therapeutic potential for traumatic brain injury (TBI). However, how hUC-MSCs migrating to the injury region and the mechanism of hUC-MSCs promoting functional recovery after TBI are still unclear. In this study, we investigated whether stromal cell-derived factor-1 (SDF-1) was involved in the hUC-MSCs migration and the possible mechanisms that might be involved in the beneficial effect on functional recovery. In vitro experiments demonstrated that SDF-1 induces a concentration-dependent migration of hUC-MSCs. Furthermore, pre-treatment with the CXCR4-specific antagonist AMD3100 significantly prevented the migration of hUC-MSCs in vitro. We found that the expression of SDF-1 increased significantly around the damaged area. Transplanted hUC-MSCs were localized to regions where SDF-1 was highly expressed. Additionally, our results showed that hUC-MSCs-treated animals showed significantly improved functional recovery compared with controls. In hUC-MSCs-transplanted group, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were decreased and BrdU-positive cells were significantly increased compared with control group, more of BrdU-positive cells co-localized with GFAP. These suggest that SDF-1 plays an important role in the migration of hUC-MSCs to the damaged area and hUC-MSCs are beneficial for functional recovery after TBI.

Transplanted iNSCs migrate through SDF-1/CXCR4 signaling to promote neural recovery in a rat model of spinal cord injury.

The ability of transplanted induced neural stem cells (iNSCs) to promote functional recovery after spinal cord injury and the mechanism by which iNSCs migrate to injured areas are poorly understood. Stromal cell-derived factor-1 (SDF-1) is a cytokine, whereas CXCR4 is its cognate receptor. The aim of this study was to determine whether SDF-1 regulates the migration of iNSCs and to explore the potential mechanism by which iNSCs promotes functional recovery. In-vitro experiments demonstrated that SDF-1 induces a concentration-dependent migration of iNSCs. Pretreatment with the CXCR4-specific antagonist AMD3100 significantly prevented the migration of iNSCs. We found that the expression of SDF-1 increased significantly in spinal cord lesions and was mainly associated with neurons and astrocytes. We also demonstrated that transplanted green fluorescent protein-labeled iNSCs were localized to regions where SDF-1 was highly expressed. In addition, iNSC-treated animals showed significantly improved functional recovery as assessed by BBB at 7 days after injection compared with controls. iNSCs also increased cell proliferation, enhanced vascularity, and reduced apoptosis. These results suggest that upregulated SDF-1 plays an important role in the migration of iNSCs to the injured region and that iNSCs are beneficial for functional recovery after spinal cord injury.

Ligand-mediated endocytosis of nanoparticles in neural stem cells: implications for cellular magnetic resonance imaging.

Neural stem cells (NSCs) have great prospects in therapy for neurological disorders. However, the correlation between improved function and stem cell transplantation has not been fully elucidated. A non-invasive method for stem cell tracking is crucial for clinical studies. In the present study, NSCs were infected with lentiviral vectors, and the expression of transferrin receptor (TfR) in neural stem cells after lentivirus transfection (TfR-NSC) was confirmed by western blot analysis. TfR-NSCs were incubated with 1.8 nM ultra-small super-paramagnetic iron oxide nanoparticles (USPIOs) or transferrin (Tf)-conjugate of USPIO nanoparticles (Tf-USPIOs). Tf-USPIO enhanced the cellular iron content in TfR-NSCs 80 ± 18 % compared to USPIOs. These results demonstrated that TfR overexpressed in neural stem cells specifically internalized Tf-USPIOs. Furthermore, the results indicate that TfR reporter imaging may be a valuable way to evaluate the efficacy of neural stem cell treatment.