Mapping trends in hemifacial spasm research: bibliometric and visualization-based analyses of the Web of Science Core Collection.

Hemifacial spasm (HFS) is a common cranial nerve disease. In HFS research, we conducted a bibliometric analysis to examine the development and research trends. A retrieval of HFS studies published between 2011 and 2022 was performed from the Web of Science Core Collection in September 2022. Two scientometric tools were used to perform bibliometric and visualization-based analyses: VOSviewer and CiteSpace. Bibliometric analysis of 1461 studies published between 2011 and 2022 was carried out using data from 444 journals, 6021 authors, 1732 institutions, and 76 countries/regions. China, the USA, Japan, and South Korea were four key contributors to this study. Shanghai Jiaotong University was the major institution with the larger number of publications. Li Shiting was the most prolific author. Jannetta PJ was the most co-cited author. World Neurosurgery was the top prolific journal. Journal of Neurosurgery was the top co-cited journal. The top five keywords were hemifacial spasm, microvascular decompression, trigeminal neuralgia, surgery, and neurovascular compression. This study examines the research trends in global scientific research on HFS over the last decade. Researchers interested in learning more about current trends and novel research frontiers in this area can benefit from the study.

Independent association of the Meckel's cave with trigeminal neuralgia and development of a screening tool.

PURPOSE: To 1) investigate the association of the properties of the Meckel's cave (MC) with TN occurrence (i.e., affected vs. unaffected nerves) and whether such association was independent of neurovascular contact (NVC); and 2) develop an objective screening tool for TN. MATERIALS AND METHODS: Two hundred and nineteen trigeminal nerves were included. (The severity of) NVC was identified for individual nerve, and a set of 107 radiomic features were extracted to characterize various properties of each MC. Both procedures were primarily based on magnetic resonance imaging sequences. A radiomic score (Rad-score) was constructed for each MC to integrate the features associated with TN occurrence. Independent t-test and logistic regression were conducted to assess the association and develop the screening tool mentioned above. RESULTS: Twelve features were selected to build the Rad-score, with the Inverse Difference Moment Normalized (IDMN) having the greatest weight. The Rad-score was significantly (p ≤ 0.05) higher in the affected compared to the unaffected nerves, irrespective of NVC. The Rad-score and NVC were incorporated in the regression model/screening tool, which demonstrated an acceptable discriminating ability (C-statistic = 0.84). CONCLUSION: This study has identified a potential association of the properties/features of the MC with TN occurrence, probably involving the demyelination and axonal injury of the trigeminal ganglion within the MC as suggested by the IDMN. Such association may be independent of NVC. This finding may provide new insight into the etiology and/or pathophysiology of TN. The screening tool, which demonstrated an acceptable discriminating ability, may contribute to an improvement in its diagnosis.

[Retracted] MicroRNA­21 promotes migration and invasion of glioma cells via activation of Sox2 and ß­catenin signaling.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that there were several data panels showing the results of Transwell migration and invasion assay experiments in Figs. 1A and 2A that contained overlapping sections of data, such that these data, which were intended to have shown the results from differently performed experiments, appeared to have been derived from a smaller number of original sources. Furthermore, the data panels shown in Fig. 3A for the 'Control/U343' and 'Control/172', and the 'miR­21/ß­catenin' and 'Control/T98', experiments were also found to be unexpectedly similar, given that these were likewise intended to show the results from differently performed experiments. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [Molecular Medicine Reports 15: 187­193, 2017; DOI: 10.3892/mmr.2016.5971].

Identification of Differentially Expressed microRNAs Associated with Ischemic Stroke by Integrated Bioinformatics Approaches.

Ischemic stroke (IS) is one of the leading causes of disability and mortality worldwide. This study aims to find the crucial exosomal miRNAs associated with IS by using bioinformatics methods, reveal potential biomarkers for IS, and investigate the association between the identified biomarker and immune cell pattern in the peripheral blood of IS patients. In this study, 3 up-regulated miRNAs (hsa-miR-15b-5p, hsa-miR-184, and hsa-miR-16-5p) miRNAs in the serum exosomes between IS patients and healthy controls from GEO database (GSE199942) and 25 down-regulated genes of peripheral blood mononuclear cells of IS patients from GSE22255 were obtained with the help of the R software. GO annotation and KEGG pathway enrichment analysis showed that the 25 down-regulated genes were associated with coenzyme metabolic process and were mainly enriched in the N-glycan biosynthesis pathway. Furthermore, we performed the LASSO algorithm to narrow down the above 25 intersected genes, and identified 8 key genes which had a good diagnostic value in discriminating IS patients from the healthy controls analyzed with ROC curve. CIBERSORT algorithm indicated that the abundance of M0 macrophages and resting mast cells was significantly lower than that of the control group. The spearman correlation analysis showed that STT3A was negatively correlated with the proportion of follicular helper T cells, activated NK cells and resting dendritic cells. Finally, GSE117064 showed that has-miR-16-5p was more advantageous for diagnosing stroke. In conclusion, hsa-miR-15b-5p, hsa-miR-184, and hsa-miR-16-5p are identified as specific related exosomal miRNAs for IS patients. These genes may provide new targets for the early identification of IS.

Exosomal microRNA-23b-3p from bone marrow mesenchymal stem cells maintains T helper/Treg balance by downregulating the PI3k/Akt/NF-κB signaling pathway in intracranial aneurysm.

Bone marrow mesenchymal stem cells (BMSCs) are involved in cancer initiation and metastasis, and sometimes mediate cell communication by releasing exosomes and delivering microRNAs (miRNAs). The study aims to investigate the effects of exosomal hsa-miR-23b-3p derived from human BMSCs on intracranial aneurysm (IA). Firstly, human BMSCs-derived exosomes were extracted by ultra-high speed centrifugation. After clinical specimen collection, imbalance of T helper (Th) 17/Treg was found in patients with IA. Then, basilar artery aneurysm models were established and BMSCs-derived exosomes were isolated and identified. The results showed that BMSCs-derived exosomes improved pathological remodeling of IA wall, upregulated the contractile phenotype and inhibited the secretory phenotype of smooth muscle cells and reduced the number of Th17 cells to maintain the balance of Th17/Treg. In addition, human BMSCs-derived exosomes inhibited the activation of the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt)/nuclear factor-kappa B (NF-κB) signaling pathway and maintained Th17/Treg balance, which in turn interfered with aneurysm formation. Finally, the targeting relationship between hsa-miR-23b-3p and KLF5 was confirmed. We further noted that BMSCs-derived exosomal hsa-miR-23b-3p inhibited IA formation by targeting KLF5 through suppression of the PI3k/Akt/NF-κB signaling pathway. All in all, our study concluded that BMSCs-derived exosomal hsa-miR-23b-3p could maintain Th17/Treg balance by targeting KLF5 through suppression of the PI3k/Akt/NF-κB signaling pathway, thus inhibit IA formation.

Gambogic Acid Affects Ribosomal Occurrence in Glioma Cells by Downregulating the Phosphoinositide Kinase-3/Protein Kinase B/Mammalian Target of Rapamycin Signaling Pathway.

Gambogic acid (GA) is a natural compound with a polyprenylated xanthone structure that has antiinflammatory, antioxidant, and neuroprotective properties and acts as a chemopreventive agent. GA exhibits anti-tumor, antimicrobial, and anti-proliferative effects on cancer cells. In the current study, the effect of GA on phosphoinositide kinase-3 (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway was examined in human U251 glioma cells. Cell viability and apoptosis were evaluated by MTT and Annexin V/PI Double Staining. The expressions of P38, AKT, and mTOR were evaluated by western blot and qRT-PCR, respectively. MagBeads Total RNA Extraction Kit was used to isolate cell tissue RNA. GA decreased the phosphorylation of P38, AKT, and mTOR. Inhibitors of PI3K (LY294002) enhanced the phosphorylation of P38, AKT, and mTOR. GA reduced the phosphorylation of ribosomal protein precursors (Pre) and upstream binding factor (UBF), and insulin-like growth factor I (IGF-1) further enhanced the cell proliferation and expression of Pre and UBF. These results suggested that downregulation of PI3K/AKT/mTOR signaling pathway may be an important mediator in GA-affected ribosomal occurrence in glioma cells.

Preoperative Imaging and Microscopic Navigation During Surgery Can Avoid Unnecessarily Opening the Mastoid Air Cells Through Craniotomy Using the Retrosigmoid Approach.

OBJECTIVE: To analyze treatment of microvascular decompression using the retrosigmoid approach (RA) in primary trigeminal neuralgia and hemifacial spasm using preoperative images combined with intraoperative microscopic navigation to avoid unnecessarily opening the mastoid air cells (MACs). METHODS: Ten patients with primary trigeminal neuralgia and 20 patients with hemifacial spasm (test group) were treated using RA for microvascular decompression. Preoperative head magnetic resonance angiography and temporal bone computed tomography were performed and the images registered using SPM12 and fused with MRIcron to determine the relationship between MACs and sigmoid sinuses. An O-arm was used for navigation, and the transverse sigmoid sinus was projected under a microscope to guide RA. A control group comprised 139 patients who had the same surgical procedure as the test group but without image processing or intraoperative navigation. RESULTS: The relationship between MACs and the ipsilateral sigmoid sinus was classified as follows: I, MACs did not exceed the lateral edge of the ipsilateral sigmoid sinus (10/60); II, MACs exceeded the ipsilateral lateral edge of the sigmoid sinus but did not exceed the medial edge (42/60); and III, MACs exceeded the medial edge of the ipsilateral sigmoid sinus (8/60). Test and control groups showed significant differences in the incidences of opening MACs (P = 0.003). There was no cerebrospinal fluid leakage or scalp and intracranial infection at follow-up. CONCLUSIONS: Image processing and intraoperative microscopic navigation can avoid unnecessarily opening MACs and might reduce postoperative cerebrospinal leakage and scalp infection after RA craniotomy.

miR-135a-5p and miR-124-3p Inhibit Malignancy of Glioblastoma by Downregulation of Syndecan Binding Protein.

Due to its high invasiveness, glioblastoma is difficult to treat by surgery, radiotherapy, chemotherapy or any combination therapy. Syndecan binding protein (SDCBP), a widely distributed intracellular scaffold protein, has an important role in both physiological and pathological process. In the current work, we have identified target sequences for miR-135a-5p and miR-124-3p in the 3'-untranslated region of the SDCBP mRNA. Therefore, we have investigated the relationship between SDCBP, miR-135a-5p and miR-124-3p in glioblastoma multiforme cells T98G and U87 in vitro and in vivo. Dual luciferase activity assay documented that SDCBP is, in fact, the target of miR-135a-5p, miR-124-3. Western blot, qRT-PCR, proliferation, migration, and invasion assays have demonstrated that of silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p significantly interferes with the malignant properties of glioblastoma cells. In vivo studies have shown that silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p result in a marked decrease of tumor size and prolong life of tumor-bearing mice. A therapy combining the three treatments inhibits synergistically subcutaneous tumor growth in nude mice. In conclusion, proliferation, migration and invasion of glioblastoma can be inhibited by targeted regulation of SDCBP through upregulation of miR-135a-5p and miR-124-3p.

MicroRNA­21 promotes migration and invasion of glioma cells via activation of Sox2 and ß­catenin signaling.

The expression of microRNA 21 (miR-21) has been reported to be upregulated in various types of cancer, including malignant gliomas. However, its functions and mechanisms in glioma remain to be fully elucidated. The present study established miRNA­21 overexpression and knockdown cell lines using SRY­box 2 (Sox2) small interfering RNA (siRNA) to knockdown expression and Sox2 cDNA was cloned into pcDNA 3.1 mammalian expression vector for ectopic expression. BIO and XAV­939 were used for ß­catenin signaling activation and knockdown, respectively. Transwell chambers were used to assay the capacity of cells to migrate. The present study determined that increased expression of miR­21 significantly promoted the migration and invasion of glioma cells, which was accompanied by an upregulated expression of the Sox2 protein. Sox2 overexpression also promoted glioma cell migration and invasion, whereas Sox2 siRNA markedly reduced the miR­21­enhanced migration and invasion of glioma cells, indicating Sox2 may act as a crucial mediator of miR­21 function. Furthermore, miR­21 also upregulated the protein expression level of ß­catenin, whereas anti­miR­21 and Sox2 knockdown significantly reduced ß­catenin expression. BIO, a ß­catenin specific agonist, enhanced migration and invasion of glioma cells. XAV­939, an inhibitor of ß­catenin signaling, markedly inhibited the migration and invasion of glioma cells, suggesting that ß­catenin may be associated with miR­21­ and Sox2­induced invasion of glioma cells. Notably, BIO restored the migration and invasion potential of glioma cells, which were inhibited by Sox2 siRNA and anti­miR­21. These findings indicated that ß­catenin may be an important downstream mediator of miR­21 and Sox2. Therefore, the present study identified the miR­21/Sox2/ß­catenin signaling pathway, which may regulate the migration and invasion of human glioma cells.

Social isolation produces anxiety-like behaviors and changes PSD-95 levels in the forebrain.

Isolation rearing induces profound behavioral and neurochemical abnormalities in rodents. However there have been many controversies with its anxiogenic-like effects using models like elevated-plus maze. In the current study we aimed to address this by using one novelty-based anxiety paradigm that has been largely overlooked in previous isolation rearing studies. We found that eight-week isolation rearing produced potent anxiogenic-like effects in novelty-induced hypophagia test in mice. We also demonstrated PSD-95 levels were elevated in the hippocampus and amygdala and reduced in the frontal cortex after social isolation. This study provides further behavioral and neurochemical evidence to support that isolation rearing can produce anxiogenic-like effects in rodents.

Autophagy inhibition promotes gambogic acid-induced suppression of growth and apoptosis in glioblastoma cells.

OBJECTIVE: To investigate the effects of gambogic acid (GA) on the growth of human malignant glioma cells. METHODS: U251MG and U87MG human glioma cell lines were treated with GA and growth and proliferation were investigated by MTT and colony formation assays. Cell apoptosis was analyzed by annexin V FITC/PI flow cytometry, mitochondrial membrane potential assays and DAPI nuclear staining. Monodansylcadaverine (MDC) staining and GFP-LC3 localisation were used to detect autophagy. Western blotting was used to investigate the molecular changes that occurred in the course of GA treatment. RESULTS: GA treatment significantly suppressed cell proliferation and colony formation, induced apoptosis in U251 and U87MG glioblastoma cells in a time- and dose-dependent manner. GA treatment also lead to the accumulation of monodansylcadaverine (MDC) in autophagic vacuoles, upregulated expressions of Atg5, Beclin 1 and LC3-II, and the increase of punctate fluorescent signals in glioblastoma cells pre-transfected with GFP-tagged LC3 plasmid. After the combination treatment of autophagy inhitors and GA, GA mediated growth inhibition and apoptotic cell death was further potentiated. CONCLUSION: Our results suggested that autophagic responses play roles as a self-protective mechanism in GA-treated glioblastoma cells, and autophagy inhibition could be a novel adjunctive strategy for enhancing chemotherapeutic effect of GA as an anti-malignant glioma agent.