Repair of schneiderian membrane perforation through membrane fixation with simultaneous implant placement: a case report.

Perforation of the maxillary sinus membrane is a common complication during maxillary sinus elevation. Intraoperative perforation of the maxillary sinus membrane may complicate the procedure and indirectly lead to implant failure. Timely repair of the perforated maxillary sinus membrane can effectively improve the implant survival rate. This case describes a method of repairing a maxillary sinus membrane perforation with a suture-attached collagen membrane and shows stable repair results at a 31-month follow-up.

Circular RNA MAPK4 (circ-MAPK4) inhibits cell apoptosis via MAPK signaling pathway by sponging miR-125a-3p in gliomas.

BACKGROUND: Recent evidences have shown that circular RNAs (circRNAs) are frequently dysregulated and play paramount roles in various cancers. circRNAs are abundant in central nervous system (CNS); however, few studies describe the clinical significance and role of circRNAs in gliomas, which is the most common and aggressive primary malignant tumor in the CNS. METHODS: A bioinformatics analysis was performed to profile and screen the dyregulated circRNAs during early neural development. Quantitative real-time PCR was used to detect the expression of circ-MAPK4 and target miRNAs. Glioma cells were transfected with circ-MAPK4 siRNAs, then cell proliferation, apoptosis, transwell assays, as well as tumorigenesis and TUNEL assays, were performed to examine effect of circ-MAPK4 in vitro and vivo. Biotinylated-circ-MAPK4 probe based pull-down assay was conducted to confirm the relationship between circ-MAPK4 and miR-125-3p. RESULTS: In this study, we identified a circRNA, circ-MAPK4 (has_circ_0047688), which was downregulated during early neural differentiation. In gliomas, circ-MAPK4 acted as an oncogene, was inversely upregulated and linked to clinical pathological stage of gliomas (P < 0.05). Next, we verified that circ-MAPK4 promoted the survival and inhibited the apoptosis of glioma cells in vitro and in vivo. Furthermore, we proved that circ-MAPK4 was involved in regulating p38/MAPK pathway, which affected glioma proliferation and apoptosis. Finally, miR-125a-3p, a miRNA exhibited tumor-suppressive function through impairing p38/MAPK pathway, which was increased by inhibiting circ-MAPK4 and could be pulled down by circ-MAPK4. Inhibition of miR-125a-3p could partly rescue the increased phosphorylation levels of p38/MAPK and the elevated amount of apoptosis inducing by knockdown of circ-MAPK4. CONCLUSIONS: Our findings suggest that circ-MAPK4 is a critical player in glioma cell survival and apoptosis via p38/MAPK signaling pathway through modulation of miR-125a-3p, which can serve as a new therapeutic target for treatment of gliomas.

Do Selected Blood Inflammatory Markers Combined with Radiological Features Predict Proliferation Index in Glioma Patients?

BACKGROUND: The tumor microenvironment is partially characterized by a state of chronic inflammation, and radiologic features are related to the tumor's biological behavior. This study was conducted to explore whether peripheral blood inflammatory markers combined with radiologic features could predict proliferation potency. METHODS: This study retrospectively reviewed 183 patients with a primary diagnosis of glioma. Clinical characteristics, preoperative peripheral full blood count data, and brain magnetic resonance imaging findings were reviewed to analyze the expression of inflammatory markers neutrophil lymphocyte ratio (NLR), monocyte lymphocyte ratio, and platelet lymphocyte ratio (PLR), as well as radiologic features such as location, peritumor edema, and contrast enhancement. Immunohistochemical staining was performed to determine the proliferation index (i.e., expression of Ki-67). Receiver operating characteristic curves for cutoff value, various bivariate tests, and binary logistic regression analyses were applied. RESULTS: Proliferation index was highly associated with tumor grade, showing a gradually increasing tendency. A Ki-67 cutoff value >9% predicted high-grade glioma (HGG). Mean NLR and PLR were significantly higher in the HGG group compared with the low-grade glioma group (NLR: 3.11 ± 0.59 vs. 4.27 ± 1.13; PLR: 133.07 ± 13.17 vs. 161.51 ± 38.99; P < 0.01 for both). Contrast enhancement was more likely in the HGG group, but there was no significant between-group difference in peritumor edema. Logistic regression analysis identified the following risk factors for prediction of proliferation potency: age, Karnofsky Performance Score, NLR, PLR, and contrast enhancement. However, age >43 years, NLR >3.68, and positive contrast enhancement independently predicted a higher proliferation rate. CONCLUSIONS: NLR and contrast enhancement were positively correlated with the proliferation potency of gliomas.

IDH1 R132H mutation regulates glioma chemosensitivity through Nrf2 pathway.

PURPOSE: Numerous studies have reported that glioma patients with isocitrate dehydrogenase 1(IDH1) R132H mutation are sensitive to temozolomide treatment. However, the mechanism of IDH1 mutations on the chemosensitivity of glioma remains unclear. In this study, we investigated the role and the potential mechanism of Nrf2 in IDH1 R132H-mediated drug resistance. METHODS: Wild type IDH1 (R132H-WT) and mutant IDH1 (R132H) plasmids were constructed. Stable U87 cells and U251 cells overexpressing IDH1 were generated. Phenotypic differences between IDH1-WT and IDH1 R132H overexpressing cells were evaluated using MTT, cell colony formation assay, scratch test assay and flow cytometry. Expression of IDH1 and its associated targets, nuclear factor-erythroid 2-related factor 2 (Nrf2), NAD(P)H quinine oxidoreductase 1 (NQO1), multidrug resistant protein 1 (MRP1) and p53 were analyzed. RESULTS: The IDH1 R132H overexpressing cells were more sensitive to temozolomide than WT and the control, and Nrf2 was significantly decreased in IDH1 R132H overexpressing cells. We found that knocking down Nrf2 could decrease resistance to temozolomide. The nuclear translocation of Nrf2 in IDH1 R132H overexpressing cells was lower than the WT and the control groups after temozolomide treatment. When compared with WT cells, NQO1 expression was reduced in IDH1 R132H cells, especially after temozolomide treatment. P53 was involved in the resistance mechanism of temozolomide mediated by Nrf2 and NQO1. CONCLUSIONS: Nrf2 played an important role in IDH1 R132H-mediated drug resistance. The present study provides new insight for glioma chemotherapy with temozolomide.

Laparoscopy versus mini-laparotomy peritoneal catheter insertion of ventriculoperitoneal shunts: a systematic review and meta-analysis.

OBJECTIVE Ventriculoperitoneal (VP) shunt treatment is the main treatment method for hydrocephalus. The traditional operative approach for peritoneal catheter insertion is mini-laparotomy. In recent years, laparoscopy-assisted insertion has become increasingly popular. It seems likely that use of an endoscope could lower the incidence of shunt malfunction. However, there is no consensus about the benefits of laparoscopy-assisted peritoneal catheter insertion. METHODS A systematic search was performed using the PubMed, Embase, ScienceDirect, and Cochrane Library databases. A manual search for reference lists was conducted. The protocol was prepared according to the interventional systematic reviews of the Cochrane Handbook, and the article was written on the basis of the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) guidelines. RESULTS Eleven observational trials and 2 randomized controlled trials were included. Seven operation-related outcome measures were analyzed, and 3 of these showed no difference between operative techniques. The results of the meta-analysis are as follows: in the laparoscopy group, the rate of distal shunt failure was lower (OR 0.41, 95% CI 0.25-0.67; p = 0.0003), the absolute effect is 7.11% for distal shunt failure, the number needed to treat is 14 (95% CI 8-23), operative time was shorter (mean difference [MD], -12.84; 95% CI -20.68 to -5.00; p = 0.001), and blood loss was less (MD -9.93, 95% CI -17.56 to -2.31; p = 0.01). In addition, a borderline statistically significant difference tending to laparoscopic technique was observed in terms of hospital stay (MD -1.77, 95% CI -3.67 to 0.13; p = 0.07). CONCLUSIONS To some extent, a laparoscopic insertion technique could yield a better prognosis, mainly because it is associated with a lower distal failure rate and shorter operative time, which would be clinically relevant.

Combination treatment with fasudil and clioquinol produces synergistic anti-tumor effects in U87 glioblastoma cells by activating apoptosis and autophagy.

Survival of patients with glioblastoma (GBM) remains poor, and novel treatment methods are urgently needed. In this study, we tested the effects of a combination of fasudil, a ROCK inhibitor, and clioquinol, an 8-hydroxyquinoline derivative with antimicrobial properties, on human GBM U87 cells. Combination treatment synergistically inhibited the viability of glioma cells but not mouse normal neuron HT22 cells and significantly induced mitochondria-mediated apoptosis. Moreover, the combination was also found to trigger macro-autophagy (henceforth referred to as autophagy) by increasing the expression levels of several proteins involved in the induction of autophagy. Further studies showed that 3-methyladenine (3-MA) or chloroquine (CQ), two autophagy inhibitors, abrogated the cytotoxic effects of the combination treatment as well as the autophagy. Overall, we demonstrated that fasudil and clioquinol show synergistic anti-cancer effects, providing evidence for the further development of combination therapy for GBM.

CXCL12-induced upregulation of FOXM1 expression promotes human glioblastoma cell invasion.

Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor; it is highly aggressive and is associated with a poor prognosis. Binding of the chemokine CXCL12 to its receptors (CXCR4 and CXCR7) contributes to the activation of many downstream signaling pathways and promotes the invasion of various malignant tumor cells, including GBM cells. FOXM1, a transcription factor involved in cell cycle regulation, is overexpressed in GBM and is involved in GBM progression. However, the molecular mechanisms by which CXCL12 promotes the invasion of human GBM cells remain unclear. In this study, we demonstrate that CXCL12 increases the production of FOXM1 by binding to CXCR4 in GBM cell lines. Furthermore, pretreatment with an inhibitor of the PI3K/AKT pathway abrogated the CXCL12-induced expression of FOXM1. In addition, there was a positive correlation between CXCL12/CXCR4 expression and FOXM1 expression in human malignant glioma tissues. Finally, a functional assay revealed that CXCL12 does not stimulate GBM cell invasion when FOXM1 expression is silenced using a small interfering RNA (siRNA). Collectively, these findings suggest that CXCL12 promotes GBM cell invasion in part by increasing the expression of FOXM1, which is mediated in part by a PI3K/AKT-dependent mechanism in vitro.

Adenovirus-mediated transfection with glucose transporter 3 suppresses PC12 cell apoptosis following ischemic injury.

In this study, we investigated the effects of adenovirus-mediated transfection of PC12 cells with glucose transporter 3 after ischemic injury. The results of flow cytometry and TUNEL showed that exogenous glucose transporter 3 significantly suppressed PC12 cell apoptosis induced by ischemic injury. The results of isotopic scintiscan and western blot assays showed that, the glucose uptake rate was significantly increased and nuclear factor kappaB expression was significantly decreased after adenovirus-mediated transfection of ischemic PC12 cells with glucose transporter 3. These results suggest that adenovirus-mediated transfection of cells with glucose transporter 3 elevates the energy metabolism of PC12 cells with ischemic injury, and inhibits cell apoptosis.