Endoscope-Assisted Keyhole Surgery for Traumatic Subacute Subdural Hematoma Evacuation in Emergencies.

OBJECTIVE: This study aimed to investigate whether a simple endoscopic method was effective for the evacuation of traumatic subacute subdural hematomas. METHODS: A total of 51 patients with subacute subdural hematomas requiring surgery were enrolled in this study. An endoscopic hematoma evacuation was performed through a small bone window for 22 patients. Hematoma evacuation by open surgery was performed for 29 patients. The postoperative Glasgow Coma Scale scores improvement, surgery times, displacement of midline measurements, and intraoperative blood loss were recorded and analyzed for each patient. RESULTS: The average time from the initial incision to suture completion was 38.41 ± 6.97 minutes for the endoscopic surgery group and 74.66 ± 9.54 minutes for the open-surgery group (P < 0.01). The average total blood loss was 41.36 ± 10.82 ml for the endoscopic group and 250.00 ± 58.25 ml for the open-surgery group (P < 0.01). No postoperative bleeding occurred in either group. The midline displacement measurement showed significant improvement on the day after surgery, with 5.21 ± 1.98 mm in the study group versus 6.75 ± 1.37 mm in the control group (P < 0.01). At the 1-month follow-up appointment, the midline measurement was normal in both groups. Computed tomography scans revealed almost no residual hematomas, representing an average evacuation rate of 100% in both groups. The average Glasgow Coma Scale scores improvement on the day after surgery were 1.77 ± 1.93 in the endoscopic surgery group and 1.66 ± 0.77 in the open-surgery group (P = 0.766). CONCLUSION: Endoscopic subacute subdural hematoma removal through a small bone window achieved satisfactory hematoma removal using a minimally invasive method when compared with an open-surgery method.

The Prognostic Role of Peritumoral Edema in Patients with Newly Diagnosed Glioblastoma: A Retrospective Analysis.

OBJECTIVE: Previous studies on glioblastomas (GBMs) have not reached a consensus on peritumoral edema (PTE)'s influence on survival. This study evaluated the PTE index's prognostic role in newly diagnosed GBMs using a well-designed method. METHODS: Selected patients were reviewed after a rigorous screening process. Their general information was obtained from electronic medical records. The imaging metrics (MTD, TTM, TTE) representing tumor diameter, laterality, and PTE extent were obtained by manual measurement in Syngo FastView software. The PTE index was a ratio of TTE to MTD. Multiple variables were evaluated using analysis of variance and Cox regression model. RESULTS: Of 143 patients, 62 were included in this study. MGMT promoter methylation and tumor laterality were both independent prognostic factors (p = 0.020, 0.042; HR = 0.272, 2.630). The lateral tumors' index was higher than that of the medial tumors (57.7% vs. 42.6%, p = 0.027). Low-index tumors were located in relatively medial positions compared with high-index tumors (TTM, 4.9 vs. 12.8, p = 0.032). This finding indicated that the PTE index tended to increase with tumor laterality. Moreover, the patients with low-index tumors had a significant survival disadvantage in the univariate analysis but not in the multivariate analysis (p = 0.023, 0.220). However, further analysis found that the combination of tumor laterality and PTE statistically stratified the survival outcome. The patients with lateral high-index tumors survived significantly longer (p = 0.022, HR = 1.927). CONCLUSIONS: In contrast with the previous studies, this study recommends combining PTE and tumor laterality for survival stratification in newly diagnosed GBMs.

miR-26b Mimic Inhibits Glioma Proliferation In Vitro and In Vivo Suppressing COX-2 Expression.

Glioma is the most common malignant tumor of the nervous system. Studies have shown the microRNA-26b (miR-26b)/cyclooxygenase-2 (COX-2) axis in the development and progression in many tumor cells. Our study aims to investigate the effect and mechanism of the miR-26b/COX-2 axis in glioma. Decreased expression of miR-26b with increased levels of COX-2 was found in glioma tissues compared with matched normal tissues. A strong negative correlation was observed between the level of miR-26b and COX-2 in 30 glioma tissues. The miR-26b was then overexpressed by transfecting a miR-26b mimic into U-373 cells. The invasive cell number and wound closing rate were reduced in U-373 cells transfected with miR-26b mimic. In addition, COX-2 siRNA enhanced the effect of miR-26b mimic in suppressing the expression of p-ERK1 and p-JNK. Finally, the in vivo experiment revealed that miR-26b mimic transfection strongly reduced the tumor growth, tumor volume, and expression of matrix metalloproteinase-2 (MMP-2) and MMP-9. Taken together, our research indicated a miR-26b/COX-2/ERK/JNK axis in regulating the motility of glioma in vitro and in vivo, providing a new sight for the treatment of glioma.