Managing intraoperative rupture of internal carotid pseudoaneurysms during endoscopic transnasal optic canal decompression: a case report.

Background: Endoscopic transnasal optic canal decompression is widely used in the treatment of traumatic optic neuropathy (TON) following head and craniofacial trauma. Intraoperative hemorrhage is a catastrophic surgical complication during optic canal decompression. Case description: We present two cases of patients with TON who suffered unexpected intra-operative massive bleeding during endoscopic transnasal optic canal decompression. After intraoperative hemostasis was achieved, emergent cerebral angiograms demonstrated the formation of internal carotid pseudoaneurysms, which were immediately embolized with coils combined with or without Onyx with balloon assistance. One of these cases was also complicated by a postoperative cerebrospinal fluid leak, which failed to be treated with lumbar drainage but was successfully repaired with endoscopic transnasal surgery. Conclusion: The intra-operative rupture of ICA pseudoaneurysm is a rare but catastrophic complication in TON patients. Intraoperative massive bleeding indicates rupture of ICA pseudoaneurysm. Postoperative emergency angiography and endovascular therapy should be arranged to evaluate and repair the cerebral vascular injury. Endoscopic trans-nasal surgery repairing CSF leaks resistant to lumbar drainage could be efficient and safe following pseudoaneurysm embolization.

Transcatheter closure for postinfarction ventricular septal defect: A meta-analysis of the current evidence.

OBJECTIVE: Postinfarction ventricular septal defect (PIVSD) is a severe complication of acute myocardial infarction (AMI). Transcatheter closure (TCC) is an alternative option to surgical repair. This study was undertaken to examine the published literature to provide objective evidence for TCC using a meta-analysis. METHODS: We searched for significant medical and publisher databases. Two reviewers checked the quality of the studies and extracted data. Eligible studies included single-arm studies and comparative studies. Weighted means, pooled event rates, efficacy outcomes and odds ratios (ORs) for immediate shunt reduction (ISR), presence of cardiogenic shock (CS), New York Heart Association (NYHA) class IV, time from AMI to ventricular septal defect (VSD), and time to VSD closure was estimated. RESULTS: A total of 27 single-arm articles (462 patients) were included. The pooled event rate was 89.7% (95% confidence interval [CI]: 0.772-1.021) for successful device implantation, 80.9% (95% CI: 0.645-0.972) for ISR, 31.5% (95% CI: 0.149-0.482) for 30-day mortality, and 25.3% (95% CI: 0.072-0.434) for 30-day mortality of primary closure at the acute phase. CS (OR = 3.607, 95% CI: 2.301-5.653), NYHA class IV (OR = 6.491, 95% CI: 1.444-29.188) and time to VSD closure were risk predictors for TCC. There was no correlation between defect size (OR = 2.592, 95% CI: 0.380-17.661) and mortality. CONCLUSION: TCC should be a relatively safe and minimally invasive method for PIVSD, with an excellent successful device implantation rate and acceptable low 30-day mortality. The procedure appears promising, but its safety and efficacy could only be demonstrated by randomized controlled trials. Therefore, the mortality of data comparing surgery to TCC compels the need for future comparative trials.

The lncRNA RP3-439F8.1 promotes GBM cell proliferation and progression by sponging miR-139-5p to upregulate NR5A2.

BACKGROUND: Nuclear Receptor Subfamily 5 Group A Member 2 (NR5A2, LRH-1) is an oncogene in a wide range of cancer types. Bioinformatics analysis on glioblastoma multiforme (GBM) tumors has revealed that the miR-139-5p-NR5A2 axis may be putatively regulated by the long non-coding RNA (lncRNA) RP3-439F8.1. This led us to hypothesize the existence of a RP3-439F8.1-miR-139-5p-NR5A2 regulatory axis in GBM cells. METHODS: Gene expression analysis was performed in GBM tumor samples and normal controls from our hospital, the Cancer Genome Atlas Glioblastoma Multiforme (TCGA-GBM) cohort, and the Gene Expression Omnibus (GEO) database (GSE7696). Cell proliferation, apoptosis, Matrigel Transwell, colony formation, and cell cycle assays were performed in T98 G and U251 cells in vitro. An orthotopic U251 xenograft murine model was employed to test the effects of RP3-439F8.1 knockdown in vivo. RESULTS: NR5A2 was upregulated in the three independent GBM tumor cohorts. In vitro, NR5A2 overexpression enhanced GBM cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating ß-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice. Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. These findings were clinically validated by a positive correlation between RP3-439F8.1 and NR5A2 and a negative correlation between RP3-439F8.1 and miR-139-5p in GBM tumors. CONCLUSIONS: Our study supports a tumorigenic role for RP3-439F8.1 in GBM through the RP3-439F8.1/miR-139-5p/NR5A2 axis.

Anti-neuroinflammatory effects of tannic acid against lipopolysaccharide-induced BV2 microglial cells via inhibition of NF-κB activation.

Microglia mediated neuroinflammation is known to cause various neurodegenerative and neurological ailments. Tannic acid is a natural polyphenol which has been reported to possess antioxidant, anti-inflammatory, anticarcinogenic, antimutagenic, antitumor, and antimicrobial activities. As there are no reports till date on the anti-neuroinflammatory effects of tannic acid, this study was conducted to analyze the possible mechanism and pathway involved in the prevention of neuroinflammation by tannic acid in BV2 microglial cells. BV2 microglial cells were pretreated with tannic acid (10, 25, and 50 µM/mL) and induced with lipopolysaccharide (LPS; 1 µM/mL) to assess the production of reactive oxygen species (ROS), nitric oxide (NO), prostaglandin E2 (PGE2), pro-inflammatory cytokines (IL-6, IL-1ß, and TNF-α), and nuclear factor-kappa B (NF-κB) protein expressions through western blotting. The results showed that LPS significantly activated the BV2 cells via toll-like receptor 4 to induce elevated productions of ROS, NO, PGE2, IL-6, and IL-1ß. However, tannic acid was able to reverse all the neuroinflammatory effects of LPS-induced BV2 cells in a dose-dependent manner. Collectively, the anti-inflammatory effects of tannic acid on LPS-induced BV2 microglial cells are attributed to the inhibition of ROS formation and the suppression of NF-κB pathway activation. Tannic acid could be a potential therapeutic agent for the treatment of neurological related disorders.