Comparison of Supraorbital and Pterional Keyhole Approach for Clipping Middle Cerebral Artery Aneurysm: A Chinese Population-Based Study.

OBJECTIVE: Keyhole craniotomy is a minimally invasive approach for the treatment of middle cerebral artery (MCA) aneurysms. The aim of this study was to compare the clinical outcome between supraorbital keyhole approach and pterional keyhole approach (PKA) in Chinese patients with MCA aneurysm. METHODS: Consecutive patients with MCA aneurysms were reviewed between January 2013 and December 2017. Efficacy and safety between PKA and supraorbital keyhole approach were compared. Poor outcome was defined as modified Rankin Scale score of 3-6 at discharge. RESULTS: This study enrolled 260 patients; 222 (85.4%) had ruptured aneurysm, and 183 (70.4%) received PKA. The distribution of PKA in unruptured and ruptured aneurysms showed no significant difference (P > 0.05). In subgroup analyses, PKA was more likely associated with poor outcome at discharge in patients with unruptured aneurysms (odds ratio = 5.500, 95% confidence interval = 1.013-29.850, P = 0.048), whereas approach selection was not an independent factor predicting poor outcome in patients with ruptured aneurysms (P > 0.05). CONCLUSIONS: In a Chinese population, supraorbital keyhole approach was superior to PKA in improving outcome in patients with unruptured MCA aneurysms, but the 2 approaches showed comparable outcomes at discharge in patients with ruptured aneurysms.

Overexpression of the Kininogen-1 inhibits proliferation and induces apoptosis of glioma cells.

BACKGROUND: Glioma is the most common primary central nervous system tumor derived from glial cells. Kininogen-1 (KNG1) can exert antiangiogenic properties and inhibit proliferation of endothelial cells. The effect of KNG1 on the glioma is rarely reported, so our purpose in to explore its mechanism in glioma cells. METHODS: The differentially expressed genes (DEGs) were identified based on The Cancer Genome Atlas (TCGA) database. The KNG1-vector was transfected into the two glioma cells. The viability, apoptosis and cell cycle of glioma cells and microvessel density (MVD) were detected by cell counting kit-8 assay, flow cytometry and immunohistochemistry, respectively. The expression were measured by quantitative real-time PCR and Western blot, respectively. A tumor mouse model was established to determine apoptosis rate of brain tissue by terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis. RESULTS: KNG1 was identified as the core gene and lowly expressed in the glioma cells. Overexpression of KNG1 inhibited cell viability and angiogenesis of glioma cells. Overexpression of KNG1 promoted the apoptosis and G1 phase cell cycle arrest of glioma cells. Moreover, the expressions of VEGF, cyclinD1, ki67, caspase-3/9 and XIAP were regulated by overexpression of KNG1. In addition, overexpression of KNG1 inhibited the activity of PI3K/Akt. Furthermore, overexpression of KNG1 decreased the tumor growth and promoted the apoptosis of decreased by overexpression of KNG1 in vivo. . CONCLUSIONS: Overexpression of KNG1 suppresses glioma progression by inhibiting the proliferation and promoting apoptosis of glioma cells, providing a therapeutic strategy for the malignant glioma.