BACKGROUND:Selinexor is a selective inhibitor of exportin-1 (XPO1), a key mediator of the nucleocytoplasmic transport for molecules critical to tumor cell survival. Selinexor's lethality is generally associated with the induction of apoptosis, and in some cases, with autophagy-induced apoptosis. We performed this study to determine Selinexor's action in glioblastoma (GBM) cells, which are notoriously resistant to apoptosis. METHODS:Patient-derived GBM cells were treated with Selinexor, and drug response and autophagy levels were monitored. Homozygous C528S XPO1 mutant GBM43 cells were generated by CRISPR/Cas9 editing. Single Selinexor or combination treatment with autophagy inhibitors was evaluated. In addition, bulk-tissue, single-cell, and spatial transcriptome were analyzed, and molecular docking was performed. RESULTS:Although all cell lines exhibited a dose- and time-dependent reduction of cell viability, the most profound molecular response to Selinexor was induction of autophagy instead of apoptosis. Selinexor-induced autophagy was an on-target consequence of XPO1 inhibition, and could be mitigated by expression of a mutant, Selinexor-resistant form of XPO1, and Selinexor-induced autophagy was related at least in part to nuclear trapping of the transcription factor TFEB. Furthermore, genetic or pharmacologic suppression of autophagy sensitized the cells to Selinexor-induced toxicity in association with the induction of apoptosis. Finally, in intracranial PDX studies, the combination of Selinexor with the autophagy inhibitor chloroquine significantly impeded tumor growth and extended mouse survival relative to single-agent treatment. CONCLUSION:These results suggest that activation of autophagy confers a protective mechanism against Selinexor in GBM cells, and that the combination of Selinexor with autophagy inhibitors may serve as a viable means to enhance Selinexor-induced cell death.

MicroRNAs (miRs) are a class of small non-coding RNAs that function as mediators of gene expression. Dysregulations of miRs have been implicated in the development and progression of glioma. In the present study, we investigated the role of miR-133b in mediating the proliferation and invasion of glioma cells, and the potential mechanism. Real-time RT-PCR results showed that miR-133b expression was significantly decreased in glioma tissues compared with normal brain tissues. Luciferase reporter assay further identified silent information regulator 1 (Sirt1) as a novel direct target of miR-133b in glioma U87 cells. Overexpression of miR-133b suppressed Sirt1 expression and reduced the proliferation and invasion of U87 cells, which could be partly rescued by forced expression of Sirt1. In addition, the Sirt1 mRNA level was significantly higher in glioma tissues than in normal brain tissues, and was inversely correlated with miR-133b level in glioma tissues. In summary, our study sheds light on the regulatory mechanism of miR-133b in glioma growth and metastasis via direct mediation of Sirt1 expression, and suggests that Sirt1 may serve as a potential therapeutic target for glioma.

Objective: Investigate the impact of diaphragm sellae competence on surgical outcomes and risk factors for postoperative hypothalamic injury (HI) in patients undergoing endoscopic transsphenoidal surgery (ETS) for infra-diaphragmatic craniopharyngiomas (ICs). Methods: A retrospective analysis of 54 consecutive patients (2016-2023) with ICs treated by ETS was conducted. All tumors originated from the sellar region inferior to the diaphragm sellae and were classified into two subtypes in terms of diaphragm sellae competence: IC with competent diaphragm sellae (IC-CDS) and IC with incompetent diaphragm sellae (IC-IDS). Clinical features, intraoperative findings, and follow-up data were compared between subtypes. Postoperative HI was assessed using a magnetic resonance imaging-based scoring system. Results: Fifty-four patients (29 males, 25 females) were included in this study, with 12 (22.2%) under 18 years old. Overall, 35 cases were IC-CDS, while 19 were IC-IDS. Compared with IC-CDS, patients with IC-IDS tended to have hormone hypofunction before surgery (p = 0.03). Tumor volume in IC-IDS group (9.0 ± 8.6 cm3) was also higher than that in IC-CDS group (3.3 ±3.4 cm, p = 0.011). Thirty-seven patients underwent standard endoscopic transsphenoidal approach (SEA) and 17 underwent an extended endoscopic transsphenoidal approach (EEA). Gross total resection (GTR) was achieved in 50 cases (92.6%). Postoperative CSF leak was observed in four patients (7.4%). Permanent diabetes insipidus (DI) occurred in 13 patients (27.7%), six in IC-CDS and seven in IC-IDS. Postoperative HI occurred in 38.9% of patients. Univariate analysis revealed that large tumor size (p = 0.014), prior hypopituitarism (p = 0.048) and IC-IDS (p < 0.001) were significantly associated with postoperative HI. Multivariate analysis revealed that IC- IDS was the sole predictor of postoperative HI. Conclusion: To our knowledge, this is the largest case series in the literature to describe IC resected by endoscopic surgery in a single institution. Classification based on diaphragm sellae competence highlights distinct clinical features and surgical outcomes between IC-CDS and IC-IDS subtypes. Notably, IC-IDS is an independent risk factor for postoperative HI. Preoperative identification of subtype can guide surgical strategy and potentially minimize complications.

Diffuse gliomas in adults are highly infiltrative and largely incurable. Whole exome sequencing (WES) has been demonstrated very useful in genetic analysis. Here WES was performed to characterize genomic landscape of adult-type diffuse gliomas to discover the diagnostic, therapeutic and prognostic biomarkers. Somatic and germline variants of 66 patients with adult-type diffuse gliomas were detected by WES based on the next-generation sequencing. TCGA and CGGA datasets were included to analyze the integrated diagnosis and prognosis. Among 66 patients, the diagnosis of 9 cases was changed, in which 8 cases of astrocytoma were corrected into IDH-wildtype glioblastoma (GBM), and 1 oligodendroglioma without 1p/19q co-deletion into astrocytoma. The distribution of mutations including ATRX/TP53 differed in three cohorts. The genetic mutations in GBM mainly concentrated on the cell cycle, PI3K and RTK pathways. The mutational landscape of astrocytoma was more similar to that of GBM, with the highest frequency in germline variants. Patients with IDH-mutant astrocytoma harboring SNVs of PIK3CA and PIK3R1 showed a significantly worse overall survival (OS) than wild-type patients. AEBP1 amplification was associated with shorter OS in GBM. Our study suggests that clinical sequencing can recapitulate previous findings, which may provide a powerful approach to discover diagnostic, therapeutic and prognostic markers for precision medicine in adult-type diffuse gliomas.

Macrophage polarization plays an essential role in tumour immune cell infiltration and tumour growth. In this study, we selected a series of genes distinguishing between M1 and M2 macrophages and explored their prognostic value in gliomas. A total of 170 genes were included in our study. The CGGA database was used as the training cohort and the TCGA database as the validation cohort. The biological processes and functions were identified by GO and KEGG analysis. Kaplan-Meier analysis was used to compare survival differences between groups. Importantly, we built a risk score model using Cox regression analysis based on the CGGA and verified it in the TCGA database and our sequencing data. Patients with gliomas in the high-risk group were associated with high pathologic grade, IDH WT status, MGMT promoter unmethylation, 1p19q non-codeletion and prone to have a poor outcome. GEPIA results revealed that CD300C, CNRIP1 and MYO1F are the most related genes of immune infiltrations. The differential expression of these genes between low-grade gliomas and glioblastomas was confirmed by q-RT-PCR. Macrophage polarization-related gene signatures can predict the malignancy and outcome of patients with gliomas and might act as a promising target for glioma immunotherapy in the future.

Glioma stem cells (GSCs) remodel their tumor microenvironment to sustain a supportive niche. Identification and stratification of stemness related characteristics in patients with glioma might aid in the diagnosis and treatment of the disease. In this study, we calculated the mRNA stemness index in bulk and single-cell RNA-sequencing datasets using machine learning methods and investigated the correlation between stemness and clinicopathological characteristics. A glioma stemness-associated score (GSScore) was constructed using multivariate Cox regression analysis. We also generated a GSC cell line derived from a patient diagnosed with glioma and used glioma cell lines to validate the performance of the GSScore in predicting chemotherapeutic responses. Differentially expressed genes (DEGs) between GSCs with high and low GSScores were used to cluster lower-grade glioma (LGG) samples into three stemness subtypes. Differences in clinicopathological characteristics, including survival, copy number variations, mutations, tumor microenvironment, and immune and chemotherapeutic responses, among the three LGG stemness-associated subtypes were identified. Using machine learning methods, we further identified genes as subtype predictors and validated their performance using the CGGA datasets. In the current study, we identified a GSScore that correlated with LGG chemotherapeutic response. Through the score, we also identified a novel classification of the LGG subtype and associated subtype predictors, which might facilitate the development of precision therapy.

Introduction: SEM1, a 26 S proteasome complex subunit, is an essential regulator of tumor growth. However, the underlying mechanism of SEM1 mediated glioma progression remains to be elucidated.Methods: Data from bulktumor, single-cell, and spatial sequencing were analyzed to reveal correlations between SEM1 and clinical traits, cell types, and functional enrichment in gliomas. Immunohistochemistry was used to assess SEM1 expression. MTT, flow cytometry, apoptosis signature, epithelial-mesenchymal transition signature, Transwell, and organoid assays were used to study SEM1's effect on the malignant behavior of glioma (U251 and LN229) cells. Weighted gene co-expression network analysis (WGCNA) was conducted to construct an SEM1-mediated malignant regulatory network. Accordingly, survival analysis, therapeutic response, drug prediction, and molecular docking analyses were performed.Results: High SEM1 expression was observed in gliomas and correlated with worse clinical features and prognosis. Moreover, SEM1 is mainly localized in malignant cells (glioma cells). SEM1 knockout inhibited the proliferation, invasion, and migration of glioma cells and promoted their apoptosis. We also constructed an SEM1 malignant regulatory network that was bridged by the PI3K-Akt pathway. The network had a high prognostic value. Finally, drugs potentially targeting SEM1 were screened and docked to SEM1. Conclusions: SEM1 is critically involved in the proliferation, apoptosis, invasion, and migration of glioma cells. The SEM1 malignant regulatory network shows high significance for the prognosis and treatment of gliomas.

Background: Hemodynamics plays a crucial role in the initiation, enlargement, and rupture of intracranial aneurysms (IAs). This bibliometric analysis aimed to map the knowledge network of IA hemodynamic research.Methods: Studies on hemodynamics in IAs published from 1999 to 2022 were retrieved from the Web of Science Core Collection (WoSCC). The contributions of countries, institutions, authors, and journals were identified using VOSviewer, Scimago Graphica, and Microsoft Excel. Tendencies, frontier topics, and knowledge networks were analyzed and visualized using VOSviewer and CiteSpace.Results: We identified 2,319 publications on hemodynamics in IAs. The annual number of publications exhibited an overall increasing trend. Among these, the United States, Japan, and China were the three major contributing countries. Capital Medical University, State University of New York (SUNY) Buffalo University, and George Mason University were the three most productive institutions. Meng H ranked first among authors regarding the number of articles and citations, while Cebral JR was first among co-cited authors. The American Journal of Neuroradiology was the top journal in terms of the number of publications, citations, and co-citations. In addition, the research topics can be divided into three clusters: hemodynamics itself, the relationship of hemodynamics with IA rupture, and the relationship of hemodynamics with IA treatment. The frontier directions included flow diverters, complications, morphology, prediction, recanalization, and four-dimensional flow magnetic resonance imaging (4D flow MRI).Conclusion: This study drew a knowledge map of the top countries, institutions, authors, publications, and journals on IA hemodynamics over the past 2 decades. The current and future hotspots of IA hemodynamics mainly include hemodynamics itself (4D flow MRI), its relationship with IA rupture (morphology and prediction), and its relationship with IA treatment (flow diverters, complications, and recanalization).

Lacking appropriate model impedes basic and preclinical researches of brain tumors. Organoids technology applying on brain tumors enables great recapitulation of the original tumors. Here, we compared brain tumor organoids (BTOs) with common models including cell lines, tumor spheroids, and patient-derived xenografts. Different BTOs can be customized to research objectives and particular brain tumor features. We systematically introduce the establishments and strengths of four different BTOs. BTOs derived from patient somatic cells are suitable for mimicking brain tumors caused by germline mutations and abnormal neurodevelopment, such as the tuberous sclerosis complex. BTOs derived from human pluripotent stem cells with genetic manipulations endow for identifying and understanding the roles of oncogenes and processes of oncogenesis. Brain tumoroids are the most clinically applicable BTOs, which could be generated within clinically relevant timescale and applied for drug screening, immunotherapy testing, biobanking, and investigating brain tumor mechanisms, such as cancer stem cells and therapy resistance. Brain organoids co-cultured with brain tumors (BO-BTs) own the greatest recapitulation of brain tumors. Tumor invasion and interactions between tumor cells and brain components could be greatly explored in this model. BO-BTs also offer a humanized platform for testing the therapeutic efficacy and side effects on neurons in preclinical trials. We also introduce the BTOs establishment fused with other advanced techniques, such as 3D bioprinting. So far, over 11 brain tumor types of BTOs have been established, especially for glioblastoma. We conclude BTOs could be a reliable model to understand brain tumors and develop targeted therapies.

Glioma is the most lethal primary brain tumor with a poor prognosis and high recurrence rate. Enormous efforts have been made to find therapeutic targets for gliomas. In the current study, we identified m5C-related lncRNAs through Pearson correlation analysis by the criteria |R|>0.5 and p<0.001 in TCGA LGG and CGGA325 datasets. We then established an eight-lncRNA m5C-related prognostic signature (m5C LPS) through lasso cox regression analysis and multivariate analysis. The performance of the signature was confirmed in the CGGA325 dataset and evaluated in differential subgroups divided by relevant clinicopathological characteristics. Patients were then divided into high and low risk groups using risk scores calculated with the signature. Next, we performed GO, KEGG and gene set enrichment analysis (GSEA) and identified the m5C LPS to be related with glioma microenvironment, immune response, EMT, cell cycle, and hypoxia. Correlation of the risk groups with immune cell infiltration, somatic mutation, and CNVs was then explored. Responses to immuno- and chemotherapies in different risk groups were evaluated using submap and pRRophetic R packages respectively. The high-risk group was more sensitive to anti-CTLA4 therapy and to compounds including Temozolomide, Bleomycin, Cisplatin, Cyclopamine, A.443654 (Akt inhibitor), AZD6482 (PI3K inhibitor), GDC0941(PI3K inhibitor), and metformin. We present for the first time a m5C-related lncRNA signature for lower grade glioma patient prognosis and therapy response prediction with validated performance, providing a promising target for future research.

Objective To evaluate the long-term outcomes and safety of endoscopic transsphenoidal surgery (ETS) in recurrent and residual pituitary adenomas (rrPAs), as well as the predictors of gross total resection (GTR) and intraoperative CSF leakage. Furthermore, to compare outcomes and complications with non-rrPAs cohort. Methods Clinical and radiological characteristics of patients with rrPAs who underwent ETS were collected between 2017 and 2020. Data of patients with non-rrPAs were collected from 2019 to 2020. Logistic regression analyses were performed to investigate the factors influencing gross total resection (GTR) and intraoperative CSF leakage. Between-group comparisons of outcomes and complications were performed through propensity score analysis. Results We enrolled 73 patients with rrPAs. GTR was achieved in 41 (56.1%) cases; further, GTR or near-total resection was achieved in 93.2% of patients. The mean tumor volumes for GTR and non-GTR cases were 6.2 ±7.2 cm3 and 11.1 ±9.1 cm3, respectively. Multivariate regression analysis of the GTR rate in patients with rrPAs revealed that Knosp grade was an independent factor (odds ratio [OR] = 0.324; p=0.005). Moreover, previous transcranial surgery and non-functional pituitary adenomas were risk factors for intraoperative CSF leakage in patients with rrPAs (OR=6.450, p=0.019 and OR=7.472, p=0.012, respectively). After propensity score matching, There was no significant difference in the GTR rate between patients with rrPAs and patients with non-rrPAs. Contrastingly, patients with rrPAs had a higher rate of intraoperative CSF leakage and longer postoperative hospital stay than patients with non-rrPAs. During the follow-up, vision improved in 9 (22.0%) and 24 (62.5%) patients with rrPAs and non-rrPAs, respectively. Although there was a trend that reoperation of rrPAs involved a lower hypopituitarism recovery rate and biochemical remission rate, as well as a higher hypopituitarism rate, there was no statistically significant between-group difference. Conclusions Knosp grade was an independent factor for GTR in endoscopic transsphenoidal surgery in patients with rrPAs. Previous transcranial surgery and non-functional PAs were risk factors for intraoperative CSF leakage. Although associated with longer hospital stay, rrPAs did not associate with lower GTR rate or more frequent postoperative complications than non-rrPAs cohort.

Objective This study aimed to investigate the expression and proinflammation effect of nitric oxide in the edema of astrocytoma. Methods WHO II (10 cases), II-III (7 cases), and IV (10 cases) grade astrocytoma peritumor edema tissues were identified by magnetic resonance imaging (MRI) and collected after surgery. The content of nitrite was detected by Grice reagent; HPLC-MS/MS was applied to identify inflammatory molecules in edema zone (5 cases of each grade); ClusterProfiler, Proteomaps and Metascapedatasets were used to investigate the potential protein network between NO and microenvironment. Results There was NO in astrocytoma and edema zone, and NO in glioma was higher than that in edema zone, which had cytochrome coxidase (COX), heat shock protein (HSP), CD44 antigen (CD44), interleukin-8 (IL-8), interleukin-24 (IL-24), gelsolin (GSN), stress-induced-phosphoprotein 1 (STIP1), mitogen-activated protein kinase 1 (MAPK1), peroxiredoxin (PRDX), protein S100, and superoxide dismutase (SOD). Enrichment analysis demonstrated that proteins in glioblastoma were more involved in anaerobic metabolism than grade II-III astrocytoma, such as glycolysis. More importantly, these proteins were significantly involved in various redox reactions, such as oxidoreductase activity and peroxidase activity among which iNOS, NO, ONOO- and SOD-1 played a vital role in redox reactions. Conclusion The formation of edema zone around astrocytoma was formed by inflammatory reaction. Astrocytoma cells regulated SOD-1 and other inflammatory molecules by secreting NO to promote the formation of invasive inflammatory tumor microenvironment.

CD47 performs a vital function in cancer therapy by binding to different SIRPα, thrombospondin 1, and integrin. However, its role in tumor immunity and its correlation with prognosis among many cancer types remain unknown. The raw mRNA expression data of CD47 in cancer patients was downloaded from TCGA and GTEx datasets. The protein expression of CD47 was detected using a microarray. Kaplan Meier analysis and forest plot were performed to compare the effects of high and low expression of CD47 on overall survival in different cancers. In addition, the correlations between CD47 expression and immune cell infiltration, stromal components, immune checkpoint genes, tumor mutational burden (TMB), and microsatellite instability (MSI) were analyzed from the public database. The gene function was determined by Gene Set Enrichment Analysis (GSEA). The expressions of CD47 in CHOL, COAD, ESCA, HNSC, KIRC, STAD, and THCA were higher compared with normal tissues. Elevated expression of CD47 predicted poor prognosis in ACC, KICH, KIRP, LGG, PAAD and UCEC. CD47 expression was strongly associated with immune infiltrating cells among KICH, KIRP, LGG, and PAAD. In addition, significant positive correlations with most immune checkpoint genes including PDCD 1 (PD-1), CD274 (PD-L1), CTLA4 in BLCA, DLBC, KICH, KIRC, LUAD, LUSC, PAAD, PCPG, SKCM, STAD, UCEC, and UVM was noted for the expression of CD47. GSEA analysis demonstrated that CD47 was a key regulator in metabolism-related pathways. These findings provide novel evidence that CD47 could be utilized as a promising prognostic biomarker and combination treatment target in various cancers.

INTRODUCTION:Glioma stem cells (GSCs) play an important role in glioma recurrence and chemo-radiotherapy (CRT) resistance. Currently, there is a lack of efficient treatment approaches targeting GSCs. This study aimed to explore the potential personalized treatment of patients with GSC-enriched gliomas.METHODS:Single-cell RNA sequencing (scRNA-seq) was used to identify the GSC-related genes. Then, machine learning methods were applied for clustering and validation. The least absolute shrinkage and selection operator (LASSO) and COX regression were used to construct the risk scores. Survival analysis was performed. Additionally, the incidence of chemo-radiotherapy resistance, immunotherapy status, and tumor treating field (TTF) therapy response were evaluated in high- and low-risk scores groups.RESULTS:Two GSC clusters exhibited significantly different stemness indices, immune microenvironments, and genomic alterations. Based on GSC clusters, 11-gene GSC risk scores were constructed, which exhibited a high predictive value for prognosis. In terms of therapy, patients with high GSC risk scores had a higher risk of resistance to chemotherapy. TTF therapy can comprehensively inhibit the malignant biological characteristics of the high GSC-risk-score gliomas.CONCLUSION:Our study constructed a GSC signature consisting of 11 GSC-specific genes and identified its prognostic value in gliomas. TTF is a promising therapeutic approach for patients with GSC-enriched glioma.

Objective To summarize the key points of neuroendoscopic transcranial resection for cerebellopontine angle (CPA) tumors. Methods Twenty⁃eight patients with CPA tumors diagnosed and treated in Xiangya Hospital Central South University from January 2019 to December 2020 were included, and all of them underwent neuroendoscopic transcranial surgery to remove CPA tumors. Results All the 28 patients were successfully treated with neuroendoscopic transcranial resection of tumors in CPA region, and the tumors were totally removed. After operation, 9 cases of acoustic neuroma, 8 cases of meningioma, 9 cases of cholesteatoma, one case of hemangioblastoma, and one case of trigeminal neurinoma were confirmed by postoperative pathology. Postoperative facial nerve function was grade Ⅲ in 3 cases, grade Ⅱ in 6 cases, and grade Ⅰ in 19 cases. One patient had no obvious recovery of auditory nerve function injury, and 2 patients had dizziness, vertigo and nausea after operation. No complications such as cerebrospinal fluid leakage, meningitis and incision infection occurred, and no death occurred. At 3 months of follow ⁃ up, no tumor recurrence was seen on MRI, and no new neurological symptoms occurred. Conclusions Neuroendoscopic transcranial resection of CPA tumors has many advantages, but also has some shortcomings, and has a good development in the future.

Angiogenesis is more prominent in anaplastic gliomas and glioblastoma (GBM) than that in pilocytic and diffuse gliomas. Caldesmon (CALD1) plays roles in cell adhesion, cytoskeletal organization, and vascularization. However, limited information is available on mechanisms underlying the effect of CALD1 on the microvascular facilitation and architecture in glioma. In this study, we explored the role of CALD1 in gliomas by integrating bulk RNA-seq analysis and single cell RNA-seq analysis. A positive correlation between CALD1 expression and the gliomas' pathological grade was noticed, according to the samples from the TCGA and CGGA database. Moreover, higher CALD1 expression samples showed worse clinical outcomes than lower CALD1 expression samples. Biofunction prediction suggested that CALD1 may affect glioma progression through modulating tumor angiogenesis. The map of the tumor microenvironment also depicted that more stromal cells, such as endothelial cells and pericytes, infiltrated in high CALD1 expression samples. CALD1 was found to be remarkably upregulated in neoplastic cells and was involved in tumorigenic processes of gliomas in single cell sequencing analysis. Histology and immunofluorescence analysis also indicated that CALD1 associates with vessel architecture, resulting in glioma grade progression. In conclusion, the present study implies that CALD1 may serve as putative marker monitoring the progress of glioma.

Growth hormone-secreting pituitary adenoma (GHPA), a benign endocrine tumor located in the base of the skull, results in acromegaly. In addition to the mass effect of the tumor itself in the sellar region, GHPA can lead to the overgrowth of almost every organ. Previous findings indicated that the processes underlying acromegaly were partly attributable to hyperactivity of the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis. However, the mechanisms driving this syndrome remains largely unknown. Additionally, the roles of GHPA-derived exosomes, which contain functional microRNAs and proteins that manipulate target cell proliferation and differentiation in distal extremities, are also unknown. In this study, we demonstrated that GHPA exosomes promote bone formation in vitro and trabecula number in vivo. The mechanism of increased trabecula formation may be attributable to GHPA exosome-induced osteoblast proliferation via increased cell viability and DNA replication. We further discovered that exosomal hsa-miR-21-5p plays a distinct role from the GH/IGF-1 axis in these processes. Accordingly, the results of this study provide a novel mechanism whereby GHPA influences distal extremities and a new perspective for treating GHPA.

OBJECTIVE:To evaluate value of neuronavigator-assisted microsurgery of glioma located in cerebral functional areas.
 Methods: Patients with glioma located in cerebral functional areas were underwent operation in Xiangya Hospital. Of 64 patients, 34 patients were performed neuronavigator-assisted microsurgery, and 30 were underwent routine surgical operation.
 Results: The neuronavigator-assisted microsurgery group showed high complete resection rate with low neurological deficit and cerebral edema compared with the routine surgical group (P<0.05).
 Conclusion: Neuronavigator-assisted microsurgery is effective and characterized by accurate location, personalized operative incision design, and higher rate of tumor resection.

Objective To investigate the role of neuroglobin (NGB) and vascular endothelial growth factor (VEGF) regulated by hypoxia-inducible factor-1 (HIF-1) in promoting angiogenesis after cerebral contusion and laceration.Methods Proteomic technology was used to compare differentially expressed proteins in the frontal lobe between patients with cerebral contusion and laceration and those with non-traumatic brain injury,and bioinformatics technology was used for the analysis and identification of differentially expressed proteins.Immunohistochemistry and ELISA were used to measure the expression of HIF-1,NGB,and VEGF in cerebral tissue and serum.Results The 2-dimensional gel electrophoresis profile was established for brain tissues from patients with cerebral contu sion and laceration or non-traumatic brain injury,and 7 differentially expressed proteins were identified,including HIF-1,NGB,and VEGF.Immunohistochemistry showed that the patients with cerebral contusion and laceration had higher expression of HIF-1,NGB,and VEGF in brain tissue than those with non-traumatic brain injury.The results of ELISA showed that the patients with cerebral contu sion and laceration had higher expression of HIF-1,NGB,and VEGF in serum than those with non-traumatic brain injury.Conclusions HIF-1 regulates the release of two target genes NGB and VEGF after cerebral contusion and laceration and thus plays an important role in cerebral angiogenesis.Changes in the serum levels of HIF-1,NGB,and VEGF can be used as a reference for clinical evaluation and monitoring of the severity of hypoxic-ischemic encephalopathy.They also have important significance in the diagnosis,treatment,and outcome of cerebral contusion and laceration and await in-depth research.

Non-functioning pituitary adenomas (NFPAs) are the most frequent pituitary tumors. The elucidation of the mechanisms of aggressive NFPAs in bone destruction is required in order to guide the clinical diagnosis and treatment of NFPAs. In the present study, we investigated the differential proteomics of fibroblasts isolated from clinical specimens of NFPAs with or without bone destruction. Proteomic analysis revealed a group of molecules associated with cytoskeleton organization, including caldesmon, were differentially expressed between fibroblasts isolated from bone destruction NFPAs (BD-NFPAs) and fibroblasts isolated from non-bone destruction NFPAs (NBD-NFPAs). The secreted proteins analysis found that osteopontin was significantly upregulated in BD-NFPAs fibroblasts. Furthermore, immunohistochemical staining of the NFPAs clinical samples showed that the expression of caldesmon in stromal cells and the expression of osteopontin in both tumor cells and stroma were significantly increased in BD-NFPAs. Taken together, our results indicate a possible way that osteopontin secreted from both NFPA cells and surrounding fibroblasts modify caldesmon expression and polymerization in fibroblasts, which may contribute to bone destruction in NFPA patients.