Preparation and Performance Improvement Mechanism Investigation of High-Performance Cementitious Grout Material for Semi-Flexible Pavement.

Semi-flexible pavement material (SFPM) combines the advantages and avoids the disadvantages of asphalt concrete flexible pavement and cement concrete rigid pavement. However, due to the problem of interfacial strength of composite materials, SFPM is prone to cracking diseases, which limits the further application of SFPM. Hence, it is necessary to optimize the composition design of SFPM and improve its road performance. In this study, the effects of cationic emulsified asphalt, silane coupling agent and styrene-butadiene latex on the improvement of SFPM performance were compared and analyzed. The influence of modifier dosage and preparation parameters on the road performance of SFPM was investigated by an orthogonal experimental design combined with principal component analysis (PCA). The best modifier and the corresponding preparation process were selected. On this basis, the mechanism of SFPM road performance improvement was further analyzed by scanning electron microscopy (SEM) and Energy Dispersive Spectroscopy (EDS) spectral analysis. The results show that adding modifiers can significantly enhance the road performance of SFPM. Compared to silane coupling agents and styrene-butadiene latex, cationic emulsified asphalt changes the internal structure of cement-based grouting material and increases the interfacial modulus of SFPM by 242%, allowing cationic emulsified asphalt-SFPM (C-SFPM) to exhibit better road performance. According to the results of the principal component analysis, C-SFPM has the best overall performance compared to other SFPMs. Therefore, cationic emulsified asphalt is the most effective modifier for SFPM. The optimal amount of cationic emulsified asphalt is 5%, and the best preparation process involves vibration at a frequency of 60 Hz for 10 min and 28 days of maintenance. The study provides a method and basis for improving the road performance of SFPM and a reference for designing the material composition of SFPM mixes.

circFLNA promotes glioblastoma proliferation and invasion by negatively regulating miR­199­3p expression.

Glioblastoma (GBM) is one of the most common and malignant types of primary cancer in the central nervous system; however, the clinical outcomes of patients with GBM remain poor. Circular RNAs (circRNAs) have been revealed to serve important roles in diverse biological processes, such as regulating cell proliferation, epithelial­mesenchymal transition and tumor development. However, the underlying biological function of circRNA filamin A (circFLNA) and its potential role in GBM remain to be determined. The present study aimed to identify differentially expressed circRNAs in GBM. Reverse transcription­quantitative PCR was used to analyze the expression levels of circFLNA. The results demonstrated that the expression levels of circFLNA were significantly upregulated in clinical GBM samples and GBM cells compared with adjacent healthy brain tissues and normal human astrocytes, respectively. The results of the Cell Counting Kit­8 and Transwell assays revealed that circFLNA knockdown significantly inhibited the proliferative and invasive abilities of GBM cell lines. Moreover, high circFLNA expression levels were associated with a worse prognosis in GBM. MicroRNA (miR)­199­3p was subsequently predicted to be target of circFLNA. The inhibitory effect of miR­199­3p on cell proliferation and invasion was partially reversed following circFLNA knockdown. In conclusion, the findings of the present study identified novel roles for circFLNA in GBM and indicated that the circFLNA/miR­199­3p signaling axis may serve an important role in GBM progression. Therefore, circFLNA may represent a novel target for the diagnosis and treatment of GBM.

Allicin induces apoptosis through activation of both intrinsic and extrinsic pathways in glioma cells.

Allicin is an extract purified from Allium sativum (garlic), and previous research has indicated that Allicin has an inhibitory effect on many kinds of tumor cells. The aim of the present study was to explore the anticancer activity of Allicin on human glioma cells and investigate the underlying mechanism. MTT and colony-formation assays were performed to detect glioma cell proliferation, and explore the effect of Allicin at various doses and time-points. The apoptosis of glioma cells was measured by fluorescence microscopy with Hoechst 33258 staining, and then flow cytometry was used to analyzed changes in glioma cell apoptosis. Reverse transcription­quantitative polymerase chain reaction and western blot analysis were used to detect the effect of Allicin on the expression levels of Fas/Fas ligand (FasL), caspase­3, B­cell lymphoma 2 and Bcl­2­associated X protein. Allicin suppressed the proliferation and colony formation ability of U251 cells in a dose­ and time­dependent manner. A cytotoxic effect of Allicin was observed in glioma cells in a dose­dependent manner. Changes in nuclear morphology were observed in U251 cells with Hoechst 33258 staining. The activity of caspases were significantly elevated and Fas/FasL expression levels were increased following treatment with Allicin, at both the mRNA and protein level. These results demonstrated that Allicin suppresses proliferation and induces glioma cell apoptosis in vitro. Both intrinsic mitochondrial and extrinsic Fas/FasL­mediated pathways react in glioma cell after treating with Allicin, which then activate major apoptotic cascades. These results implicate Allicin as a novel antitumor agent in treating glioma.

miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1.

MicroRNAs (miRNAs) play a vital role in tumour biological and pathologic processes. In the present study, we aimed to detect the expression and biological role of miR-216b in glioma. Our data showed that miR-216b was significantly downregulated in human glioma tissues and cells. Ectopic expression of miR-216b inhibited the proliferation and invasion of U87 and U251 cells and suppressed the growth of xenograft tumours in vivo. Bioinformatic and luciferase reporter analyses identified Forkhead box protein M1 (FoxM1) as a direct target of miR-216b. Overexpression of miR-216b inhibited the expression of FoxM1 in glioma cells. Rescue experiments demonstrated that co-transfection of FoxM1 lacking the 3'-untranslated region partially prevented miR­216b-induced inhibition of glioma cell growth and invasion. In vivo studies indicated that ectopic expression of miR-216b impeded the proliferation of glioma xenograft tumours in nude mice, coupled with a decreased in FoxM1 protein expression and the percentage of Ki-67-positive tumour cells. Taken together, our results provide evidence of the suppressive activity of miR­216b in glioma, which is largely ascribed to downregulation of FoxM1. Restoration of miR-216b may provide a novel potential therapeutic agent for glioma.

miR-599 inhibits proliferation and invasion of glioma by targeting periostin.

OBJECTIVE: To explore the molecular mechanism of microRNA-599(miR-599) in the migration and invasion of glioma. RESULT: Clinicopathological characteristics of 33 patients were analyzed. Based on reverse transcription-PCR, miR-599 was down-regulated in glioma tissues compared with adjacent normal brain tissues (P < 0.001). Moreover, negative correlations between miR-599 and periostin protein expression in glioma tissues (P < 0.01) and necrosis by magnetic resonance imaging (P < 0.05) were observed. Transwell and wound healing assays showed that overexpression of miR-599 inhibited glioma cell migration and invasion. miR-599 down-regulated periostin expression by targeting the 3'-untranslated region. Additionally, re-expression of periostin partial reversed the suppressive effect of miR-599 on migration and invasion in vitro and in vivo. CONCLUSION: microRNA-599 inhibits proliferation and invasion by down-regulating periostin expression in vitro and in vivo.

Baicaleininhibits VSMCs proliferation via regulating LncRNAAK021954 gene expression.

Atherosclerosis is responsible for the global medical burden of cardiovascular diseases, of which the proliferation of vascular smooth muscle cells (VSMCs) plays a key role in the development. Recent evidences demonstrated that baicalein could attenuate the proliferation of VSMCs and had no influence on VSMCs migration. However, the precise molecular mechanisms of baicalein inhibiting the proliferation of VSMCs were not clear. In this study, we investigated the viability and apoptosis behaviour of VSMCs and its downstream molecular changes with exposed to different dose of baicalein. Firstly, we observed significant reducing in the VSMCs proliferation and decreasing of FGF18 expression in a dose dependent manner after addition of baicalein for 24 h and 72 h. Moreover, the mRNA expression profile of VSMCs after treatments was evaluated by microarray analysis. Microarray analysis showed that long non-coding RNA (lncRNA) AK021954 gene expression was significantly increased in the baicalein treated group compared with the control group. Inversely, the VSMCs proliferation showed a notable increase after small silent RNA of lncRNAAK021954 treatment. These results indicated that lncRNAAK021954 gene and FGF18 involved in baicalein inhibiting the proliferation of VSMCs. It may provide a promising method in treatment of atherosclerosis.