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The method for producing polyvinyl alcohol (PVA) by the solution polymerization of vinyl acetate first and then alcoholysis strategy is industrial. Where solvent plays a vital role in control over stereoregularity, molecular weight and its distribution, crystallinity and so on. In this report, when methyl acetate was used as a solvent in the polymerization of vinyl acetate instead of methanol, prepared PVA was characterized by Fourier‐transform infrared spectroscopy (FT‐IR), nuclear magnetic resonance (NMR), gel permeation chromatography (GPC), thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC). The results showed that PVA obtained in methyl acetate has a higher content of syndiotactic structure, crystallinity melting temperature and enhanced thermal stability compared with PVA obtained in methanol due to the formation of Π ‐ Π complex between methyl acetate and vinyl acetate and the enhanced steric hindrance effect during polymerization. Additionally, methyl acetate has a smaller chain transfer constant (1.31 × 10−4), which benefits to decrease the branching degree and molecular weight distribution index of PVA. This research provides more ideas for the choice of solvents in the industrial production of polyvinyl alcohol. [ABSTRACT FROM AUTHOR]

ABSTRACT For the first time, the main characteristics of the polymeric materials are considered for understanding their possible application in ecological sand-fixing. In this investigation, two emulsions, named as E2, a poly(vinyl acetate) emulsion, and E7, a vinyl acetate-ethylene copolymer emulsion, have been selected for a series of tests related to the practical requirements for ecological sand-fixing. Besides the sand-fixing properties and the thermal aging and freeze-thaw stabilities of the emulsions, their effects in increasing the growth of both microbes and plants in sandy lands have been evaluated by field experiments in Kerqin Sandy Land of China, and the relationship between the performance and structure of the two emulsions has also been described. The experimental results show that both emulsions could significantly improve the compressive strength of treated sand and could withstand the changes in temperature of the Kerqin Sandy Land. However, different effects were exhibited in promoting the growth of microbes, in facilitating the accumulation of organic fertilizer and soluble salt, and in increasing the crop yield. All of the differences are attributed to their different molecular chain structures. These findings suggest that the structure of a polymeric emulsion should be the first consideration for the materials used in ecological sand-fixing, and ecological sand-fixing is a successful method for the stabilization of sandy land and the restoration of desertified land in semiarid regions. © 2016 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2016, 133, 44102 [ABSTRACT FROM AUTHOR]

Aims To validate whether the anti-cancer effect of micro RNA-122 ( miR-122) on hepatocellular carcinoma ( HCC) is mediated through regulating Wnt/β-catenin signalling pathways. Methods The expression levels of miR-122 in HCC tissues and varied hepatoma cells were quantified by real-time PCR. MiR-122 agomir was transfected into HepG2, Hep3B cells to over-express miR-122. The effect of over-expression miR-122 on proliferation and apoptosis of HepG2 and Hep3B cells was evaluated using CCK-8 kit and flow cytometer respectively. The 3′- UTR segments of Wnt1 containing the miR-122 binding sites were amplified by PCR and the luciferase activity in the transfected cells was assayed. Wnt1 mRNA level was quantified using RT-PCR. Protein levels of Wnt1, β-catenin and TCF-4 were detected using Western blotting. Results In comparison with the expression level of miR-122 in para-cancerous tissues or Chang liver cell, the expression level in HCC tissues or varied hepatoma cells was significantly decreased ( P < 0.05). Over-expression of miR-122 significantly inhibited the proliferation ( P < 0.05), and promoted the apoptosis of HepG2 and Hep3B cells. Over-expressed miR-122 down-regulated the protein levels of Wnt1, β-catenin and TCF-4 ( P < 0.05). MiR-122 suppressed the luciferase activity of the pmiR-Wnt1-wt by approximately 50% compared with the negative control, while mutation or removal of the miR-122 binding site using si RNA or mir-122 inhibitor blocked the suppressive effect ( P < 0.05). Conclusions MiR-122 expression is down-regulated in human HCC. Over-expression of miR-122 inhibits HCC cell growth and promotes the cell apoptosis by affecting Wnt/β-catenin- TCF signalling pathway. [ABSTRACT FROM AUTHOR]

Aims: To validate whether the anti-cancer effect of microRNA-122 (miR-122) on hepatocellular carcinoma (HCC) is mediated through regulating Wnt/β-catenin signalling pathways., Methods: The expression levels of miR-122 in HCC tissues and varied hepatoma cells were quantified by real-time PCR. MiR-122 agomir was transfected into HepG2, Hep3B cells to over-express miR-122. The effect of over-expression miR-122 on proliferation and apoptosis of HepG2 and Hep3B cells was evaluated using CCK-8 kit and flow cytometer respectively. The 3'-UTR segments of Wnt1 containing the miR-122 binding sites were amplified by PCR and the luciferase activity in the transfected cells was assayed. Wnt1 mRNA level was quantified using RT-PCR. Protein levels of Wnt1, β-catenin and TCF-4 were detected using Western blotting., Results: In comparison with the expression level of miR-122 in para-cancerous tissues or Chang liver cell, the expression level in HCC tissues or varied hepatoma cells was significantly decreased (P < 0.05). Over-expression of miR-122 significantly inhibited the proliferation (P < 0.05), and promoted the apoptosis of HepG2 and Hep3B cells. Over-expressed miR-122 down-regulated the protein levels of Wnt1, β-catenin and TCF-4 (P < 0.05). MiR-122 suppressed the luciferase activity of the pmiR-Wnt1-wt by approximately 50% compared with the negative control, while mutation or removal of the miR-122 binding site using siRNA or mir-122 inhibitor blocked the suppressive effect (P < 0.05)., Conclusions: MiR-122 expression is down-regulated in human HCC. Over-expression of miR-122 inhibits HCC cell growth and promotes the cell apoptosis by affecting Wnt/β-catenin-TCF signalling pathway., (© 2012 John Wiley & Sons A/S.)