Predictive value of suprasellar extension for intracranial infection after endoscopic transsphenoidal pituitary adenoma resection.

OBJECTIVE: To investigate the relationship between suprasellar extension (SSE) and intracranial infection after endoscopic endonasal transsphenoidal approach (EETA) for pituitary adenoma resection. METHODS: We retrospectively analyzed 94 patients with suprasellar extended pituitary adenoma admitted to the Department of Neurosurgery of the Affiliated Hospital of Guilin Medical College from January 2018 to December 2021. We measured the preoperative magnetic resonance sagittal SSE and collected clinical data and divided the patients into groups according to the presence of postoperative intracranial infection. The critical value for the SSE was calculated by using a working characteristic curve for the subjects. The risk factors for intracranial infection after EETA resection of pituitary adenomas were analyzed by multivariate regression analysis. RESULTS: Among the 94 patients, 12 cases (12.8%) were placed in the infection group and 82 cases (87.2%) in the non-infection group. The cut-off value for the SSE in the sagittal position was 15.6 mm, the sensitivity was 75%, the specificity was 87.8%, and the area under the curve (AUC) was 0.801. The coronary cut-off value for the SSE was 15.8 mm, the sensitivity was 66.7%, the specificity was 79.3%, and the AUC was 0.787. The SSE values in the sagittal and coronal positions were correlated with postoperative intracranial infection (P < 0.05). After univariate analysis, those with significant differences were included in the multivariate regression analysis. It was concluded that the extension distance of the tumor above the sella in the sagittal position was ≥ 15.6 mm, the tumor texture was hard, and the postoperative cerebrospinal fluid leakage were the independent risk factors for intracranial infection after EETA resection of suprasellar extended pituitary tumors (P < 0.05). CONCLUSIONS: The value of SSE on sagittal MRI can predict intracranial infection in patients with suprasellar extended pituitary adenoma after endoscopic endonasal transsphenoidal resection. This finding recommends neurosurgeons pay more attention to the imaging characteristics of pituitary adenomas and select appropriate treatment plans in combination with the intraoperative conditions to reduce the incidence of intracranial infection.

Overexpression of miR-31-5p inhibits human chordoma cells proliferation and invasion by targeting the oncogene c-Met through suppression of AKT/PI3K signaling pathway.

Altered microRNA (miRNAs) expression has been reported in chordoma which has been considered as an important and complex disease. The study aims to explore the mechanism of miR-31-5p in chordoma in vitro. We firstly verified miR-31-5p level after mimics transfection using real-time PCR and found over-expressed miR-31-5p could inhibit cell growth and invasive ability, while induce cell apoptosis in vitro as detected by CCK8 assay, flow cytometry assay and transwell assay, respectively. Based on prediction result in silico, we validated the target gene C-met using dual-luciferase assay and detected the alternation of miR-31-5p as evidence. Using recombinant plasmid, we also found over-expressed c-Met could reduce the effect of over-expressed miR-31-5p on cell growth, cell cycle change, cell apoptosis and invasive ability as detected by CCK8 assay, flow cytometry assay and transwell assay respectively. Meanwhile, it was also appeared that the PI3K/AKT signaling pathway relevant proteins had alternation through WB assays in U-CH1 cells with treatment of miR-31-5p and c-met recombinant plasmid. miR-31-5p may play a protective role in chordoma patients by targeting c-met and then activating PI3K/AKT signaling pathway which suggested that alterations of miR-31-5p might be a useful biomarker and a potential therapy for early detection of chordoma as disease-related molecular and genetic changes.

Biochanin A protects against focal cerebral ischemia/reperfusion in rats via inhibition of p38-mediated inflammatory responses.

Biochanin A, an O-methylated natural isoflavonoid classified as phytoestrogen, has been reported to show anti-tumorigenesis, anti-oxidation, and anti-inflammatory properties. However, little is known about the effects of biochanin A on cerebral ischemia/reperfusion. In this study, the neuroprotective and anti-inflammatory effects of biochanin A against ischemia/reperfusion injury, as well as the related molecular mechanisms, were investigated in rat models. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2h, followed by 24h of reperfusion. Then neurological deficits, infarct volume and brain edema were evaluated. The MPO activity and TNF-α and IL-1ß levels in ischemic boundary zone were determined by a spectrophotometer and the enzyme-linked immunosorbent assay (ELISA). The expressions of TNF-α, IL-1ß, and phosphorylation of p38 were measured by RT-PCR or Western blotting. Consequently, our findings showed that biochanin A treatment for 14 days had significantly reduced infarct volume and brain edema, and improved neurological deficits in focal cerebral ischemia/reperfusion rats. The MPO activity and TNF-α and IL-1ß levels were greatly increased after ischemia/reperfusion injury, while treatment with biochanin A dramatically suppressed these inflammatory processes. Furthermore, biochanin A attenuated the increase in p-p38 level in the ischemia/reperfusion brain tissue. Taken together, biochanin A has been shown to have neuroprotective effects in cerebral ischemia/reperfusion, and the mechanisms may correlate with inhibiting inflammatory response, as well as the inactivation of p38 signaling pathway.