Minimally invasive endoscopic hematoma evacuation is widely used in the treatment of intracerebral hemorrhage. However, this technique still has room for improvement. The intra-neuroendoscopic technique (INET) is a modified minimally invasive technique, and we report its safety and efficacy in evacuating brain parenchyma hematomas by comparing it with cranial puncture and drainage operation (CPDO). The frontal, temporal, or occipital approaches were used according to the site of bleeding. The preoperative and postoperative hematoma volumes, Glasgow Coma Scale (GCS) score, Cerebral State Index (CSI), hematoma evacuation rate, operation time, complications, and 30-day mortality and Glasgow Outcome Scale (GOS) were retrospectively compared between the two groups. A total of 98 patients were enrolled. The evacuation rate (84 ± 7.1% versus 51.0 ± 8.4%, p = 0.00), 7-day GCS (11.8 ± 1.2 versus 10.4 ± 1.5, p = 0.01), and CSI (87.1 ± 8.7 versus 80.6 ± 10.2, p = 0.02) were higher, and the 30-day mortality rate (1.9% versus 15.6%, p = 0.036) was lower in the INET group. However, the operation time was longer in the INET group than in the control group (65.2 ± 12.5 min versus 45.6 ± 10.9 min, p = 0.000). Multivariable logistic regression showed that a good medium-term outcome (GOS scores 4–5) was significantly associated with INET (odds ratio (OR) 3.514, 95% confidence interval (CI) 1.463–8.440, p = 0.005), age under 65 years (OR 1.402, 95% CI, 1.041–1.888, p = 0.026), and hematoma volume less than 50 ml (OR 1.974, 95% CI 1.302–2.993, p = 0.001). INET surgery for brain parenchyma hematoma evacuation is a safe and efficient modified technique. This technique is minimally invasive, has less complications, and may be helpful in providing optimal outcomes for selected patients. ClinicalTrials.gov , NCT02515903. Registered on 5 August 2015.

Objective: The surgical technique, safety, efficacy, and clinical application value of the intra-neuroendoscopic technique (INET) for the treatment of subacute-chronic and chronic septal subdural hematoma was investigated based on the structure and pathological features of the hematoma wall, and the critical factors of hematoma growth and recurrence were determined, in order to provide reference for clinical drug treatment. Methods: This was non-randomized concurrent control study. A total of 94 patients who met the inclusion criteria were recruited between May 2015 and February 2019 and were divided into the INET treatment group (INET group, 45 cases) and the burr hole drainage (BHD) treatment group (control group, 49 cases). The hematoma fluid components and the morphological structure and pathological characteristics of the hematoma wall were analyzed, and the surgical duration, subdural drainage tube (SDT) placement duration, intracranial infection rate, Bender grade at the 1 month post-operative follow-up and hematoma recurrence rate within the 6 months of post-operative follow-up were compared between the two groups. A multiple logistic regression model was established to analyze the risk factors associated with recurrence within 6 months. Results: Intraoperative endoscopy showed that the adhesion bands that formed early in the hematoma cavity were strip-like and that those that formed late were lock-column-like. The hematoma cavity was divided into different-sized chambers with by these strips/columns. Pathological sections of cyst wall reveled angiogenesis inside the cyst and mucus-like changes, rupture and hemorrhage in the vascular wall. Obvious inflammatory cell infiltration and fibrous connective tissue hyperplasia were observed in the cyst wall. The osmotic pressure of the hematoma fluid was not significantly different from that of the peripheral venous blood [(296.7 ± 10.3) mOsm/kg vs. (291.5 ± 12.4) mOsm/kg, p = 0.68]. However, the D-dimer contents which reflect the severity of fibrinolysis in the hematoma and the proinflammatory cytokine interleukin 6 (IL-6) were significantly higher in the hematoma fluid than in the peripheral venous blood. The surgery duration for the INET group was significantly longer than that for the control group [(60.4 ± 10.6) min vs. (44.1 ± 9.8) min, p = 0.00], but both the hematoma recurrence rate within 6 months of post-operative follow-up (4.4 vs. 24.5%, p = 0.00) and the SDT placement duration [(2.1 ± 0.6) d vs. (3.9 ± 0.7) d, p = 0.00] for the INET group were both lower than those for the control group. The intracranial infection rate did not differ significantly between the two groups (4.4 vs. 10.2%, p = 0.50). The overall effective rate of the Bender grade at 1 month of follow-up did not differ significantly between the two groups (95.6 vs. 87.8%, p = 0.32), but the proportion of patients who recovered to Bender grade 0 with no symptoms was significantly higher in the INET group than in the control group (86.7 vs. 67.3%, p = 0.03). Multiple logistic regression analysis showed that INET surgery [odds ratio (OR) 3.71, 95% confidence interval (CI) 1.31–9.62, p = 0.02], age of 65 years or younger (OR 1.51, 95% CI 1.05–2.87, p = 0.03) and unilateral subdural hematoma (OR 1.76, 95% CI 1.05–3.41, p = 0.02) were independent factors that reduced the post-operative recurrence rate. Conclusion: The INET surgical plan based on the structure and pathological features of the subacute-chronic and chronic subdural hematoma wall can reduce the recurrence rate and improve the clinical prognosis. Trial registration: ClinicalTrials.gov, NCT02515903. Registered 5 August, 2015.

Background: Minimally invasive endoscopic haematoma evacuation is widely used in the treatment of intraventricular haemorrhage. However, its technique still has room for improvement. A new modified neuroendoscope technology (MNT) was used in this study and we explored its safety and efficacy in the treatment of severe acute intraventricular haemorrhage by comparing it with extraventricular drainage plus urokinase thrombolytic (EVD + UT) therapy. Methods: The following parameters were compared between the MNT group and the control group: incision design, operation time, ICU monitoring time, ventricular drainage tube (VDT) placement time, post-operative drainage tube obstruction (PDTO) rate, post-operative complications rate, 6-month mortality and Glasgow Outcome Scale (GOS). Results: A total of 85 patients were enrolled. The ICU monitoring times, VDT placement times, PDTO rate were shorter in the MNT group. Multivariable logistic regression identified that good medium-term outcome (GOS scores 4–5) was significantly associated with MNT applied (OR 1.017, 95% CI 1.005–1.029, p = 0.008), age under 65 years (OR 4.223, 95% CI, 1.322–17.109, p = 0.034) and pre-operation GCS scores more than 10 (OR 3.427, 95% CI 1.048–11.205, p = 0.040). Conclusion: MNT surgery for severe intraventricular haematoma evacuation is a safe and efficient new surgical option. This technique is minimally invasive and may be helpful to provide good outcomes for selected patients.

Tropomyosin 4 (TPM4) has been reported as an oncogenic gene across different malignancies. However, the role of TPM4 in glioma remains unclear. This study aimed to determine the clinical characterization and prognostic value of TPM4 in gliomas. Transcriptome expression and clinical information were collected from the CGGA and TCGA datasets, which included 998 glioma patients. ScRNA-seq data were obtained from CGGA. R software was utilized for statistical analyses. There was a positive correlation between TPM4 and WHO grades. IDH-wildtype and mesenchymal subtype gliomas were accompanied by TPM4 upregulation. GO and GSEA analysis suggested that TPM4 was profoundly associated with epithelial-to-mesenchymal transition (EMT). Subsequent GSVA revealed a robust correlation between TPM4 and three signaling pathways of EMT (hypoxia, TGF-β, PI3K/AKT). Furthermore, TPM4 showed a synergistic effect with mesenchymal biomarkers, particularly with N-cadherin, Slug, Snail, TWIST1, and vimentin. ScRNA-seq analysis suggested that higher TPM4 was mainly attributed to tumor cells and macrophages and associated with tumor cell progression and macrophage polarization. Finally, high TPM4 was significantly associated with unfavorable outcomes. In conclusion, our findings indicate that TPM4 is significantly correlated with more malignant characteristics of gliomas, potentially through involvement in EMT. TPM4 could predict worse survival for patients with glioma.

Background: Glioblastoma is the most common and aggressive primary tumor in the central nervous system (CNS). Patients with glioblastomas have poor prognosis due to its aggressive clinical behavior and resistance to the chemotherapeutic agent temozolomide (TMZ). Aberrant long non-coding RNAs (lncRNAs) are involved in glioma progression and its regulatory mechanisms. Analysis of sequencing data identified a new lncRNA, named lncRNA TCONS_00004099, which could derive a new microRNA and was highly expressed in glioma. Methods: To elucidate the role of lncRNA TCONS_00004099 in gliomas, Quantitative Real-time PCR (qPCR) was used to assess the differential expression of lncRNA TCONS_00004099 and its related miRNA in glioma tissues, normal brain tissues, glioma cell lines (U87 and U251 cells), and a normal human embryonic brain cell line (HEB). Cell Counting Kit-8 (CCK8) assays to assess cell proliferation, flow cytometry assays examining apoptosis and the cell cycle, colony formation assays, wound healing assay, transwell assays, and zebrafish xenograft models were performed to further clarify the effects of the lncRNA and the related miRNA. Finally, Western blots were carried out to verify the mechanisms related to PTPRF (Protein Tyrosine Phosphatase Receptor Type F). Results: LncRNA TCONS_00004099 was significantly increased in glioma tissues and glioma cell lines. A novel miRNA (miRNA TCONS_00004099) derived from the lncRNA was identified by qPCR. Knockdown of this lncRNA suppressed cell proliferation, migration, invasion and enhanced TMZ-induced apoptosis in U87 and U251 cell lines in vitro and in vivo. The miRNA mimics or inhibitor of miRNA TCONS_00004099 was used to reverse the effects of knockdown or overexpression of lncRNA TCONS_00004099, respectively. Western Blot analyses verified that PTPRF is one of the downstream targets of lncRNA TCONS_00004099. Conclusions: These results demonstrated that lncRNA TCONS_00004099 promoted malignant behaviors in gliomas, including proliferation, metastasis, and anti-apoptosis. The effect of lncRNA TCONS_00004099 was mediated through miRNA TCONS_00004099 and its target PTPRF. Thus, the lncRNA TCONS_00004099/miRNA/PTPRF axis may be a potential therapeutic target for gliomas.

Chronic subdural hematoma (CSDH) is a disease characterized by capsuled blood products that progressively occupy the intracranial space, causing intracranial hypertension and compression in the brain. CSDH frequently occurs in all demographics, especially in the elderly, but the pathogenesis of CSDH remains unclear. In this review, we discuss the origin, development, and current treatment strategies of CSDH. For the first time, we analyzed the cellular and molecular compositions of hematoma membranes with a focus on neomembrane formation, a complex early-stage interactive event in hematoma pathogenesis. We hypothesize that in patients with CSDH, dural border cells (DBCs) might be induced to synthesize collagen or serum proteins might accumulate at the dura and arachnoid layers at the site of injury, thereby encapsulating the hemorrhage. Membrane formation may trigger inflammatory responses after subdural hemorrhage, promoting fibroblast-involved extracellular matrix (ECM) deposition and aberrant angiogenesis within the outer membrane. Consequently, ECM deposition and angiogenesis mutually influence each other and are modulated by inflammatory processes. By illustrating the complex and interactive mechanism of neomembrane formation, we aim to provide a novel insight into CSDH pathogenesis and propose directions for future research as well as advancements in treatment strategies for this disease.