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Influence of Methylcellulose on Properties of Wheat Gliadin Film Cast from Aqueous Ethanol
Yihu Song,Lingfang Li,Qiang Zheng 한국식품과학회 2009 Food Science and Biotechnology Vol.18 No.4
Present work was focused on the influence of methylcellulose (MC) on steady rheology of wheat gliadin solution and the properties of glycerol plasticized gliadin films. The presence of MC below 0.99 wt% improved viscosity and flow activation energy of the 10 wt% gliadin solution significantly. In the casting films containing 0.2 g glycerol/g dry protein, the MC component aggregated in the gliadin matrix. The blend films containing less than 7.7 wt% MC exhibited higher Young’s modulus (E) and tensile strength (σb) and lower elongation at break (εb) in comparison with the pure gliadin film, which was related to the intermolecular interaction between MC and gliadins, the brittle fracture of the aggregated MC component, and the increase in glass transition temperature (Tg) of the gliadin phase. Increasing MC content led to a slight increase in water vapor permeability (WVP) without significant influence on the moisture absorption (MA).
Huajie Cai,Yihu Zheng,Zhengde Wen,Yingnan Yang,Shouzhang Yang,Qiyu Zhang 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.4
Long non-coding RNAs (LncRNAs) havebeen implicated in the pathogenesis of various human diseases. In this study, we probed into the role and potentialmechanisms of the antisense of IGF2R non-protein codingRNA (LncRNA AIRN) in the progression of hepatocellularcarcinoma (HCC). Using a quantitative real-timepolymerase chain reaction, we corroborated that LncRNAAIRN expression was raised in the HCC tissues and cells. The bioinformatic analysis revealed that a potential interactionbetween LncRNA AIRN and STAT1, which wasverifi ed by the RNA pull-down and RNA immunoprecipitation. In the cycloheximide-chase assay, the knockdown ofLncRNA AIRN enhanced the stability of STAT1 protein. Inthe immunoprecipitation assay, the knockdown of LncRNAAIRN restrained the cullin 4A (CUL4A)-mediated ubiquitinationof STAT1 protein. The cell transfection, MTT andfl ow cytometry assays expounded that the LncRNA AIRN/STAT1 axis was bound up with the regulation of the proliferationand apoptosis of HCC cells. The in vivo experimentscorroborated that the knockdown of LncRNA AIRNrestrained the tumor growth of HCC. Our data expoundedthat the knockdown of LncRNA AIRN restrained HCC cellproliferation and boosted cell apoptosis by restraining theCUL4A-mediated ubiquitination of STAT1 protein.