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1.
Int J Biol Macromol ; 228: 311-322, 2023 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-36581025

RESUMO

In order to alleviate environmental pollution and the shortage of petroleum resources, improve the utilization of renewable materials, the research of biodegradable green composite materials has become a research hotspot. In this paper, Poplar Wood powder(PWP) and Polylactic acid(PLA) were selected, adding poly lactic acid graft maleic anhydride (MPLA) and Silane coupling agent KH-550 (KH550) as a compatibilizer and coupling agent to improve interface compatibility, at the same time, poly Butylenedioate-co-terephthalate (PBAT) and poly Butylene Succinate (PBS) were added to improve the toughness of the composites. The experimental results show that, the impact strength of 20 %-KMPP/PBAT/PBS composite modified by MPLA and KH550 was 20.70 kJ/m-2. Secondly, the hydrophobic angle of the composite material is as high as 112°. It is found that the high content of PWP with small particle size (200 mesh) can make it more evenly dispersed in the composite material, and the cross section of the composite material was smooth. The modified composite was 4.24$/kg, which reduced the cost by 28.07 %. The research results have opened up a new way to develop 3D printed biomass composites with low cost, high compatibility, high toughness and good environmental adaptability, and broadened the application scope and value of the composites.


Assuntos
Populus , Madeira , Pós , Poliésteres , Anidridos Maleicos , Impressão Tridimensional
2.
Appl Biochem Biotechnol ; 194(6): 2731-2746, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35267120

RESUMO

The purpose of this study was to investigate the role of microRNA-148a (miR-148a) in hepatocellular carcinoma (HCC) metastasis and explore its potential mechanism in HCC cells. Expression levels of miR-148a were measured using qRT-PCR in 120 HCC tissue samples and two HCC cell lines. Migration and invasion assays were used to determine the role of miR-148a in HCC cells. Flow cytometry was used to access the effect of miR-148a on cell cycle of HCC cells. Western blot was performed to analyze the effect of miR-148a on epithelial-to-mesenchymal transition (EMT) and PI3K/AKT signaling pathways in HCC cells. Luciferase reporter assay was conducted to explore the downstream targets and biological function of miR-148a in HCC cells. The results showed that level of miR-148a was significantly downregulated in both HCC tissue and plasma samples in HCC patients. A higher level of miR-148a was positively correlated with better survival time and prognosis of HCC patients. Transfection of miR-148a inhibited the proliferation, migration and invasion of HCC cell lines. Transfection of miR-148a arrested HCC cells at S phase and promoted apoptosis of HCC cells. Death receptor-5 (DR-5) was identified as a direct target of miR-148a in HCC cell lines. Western blot and qRT-PCR analyses showed that miR-148a upregulated EMT and downregulated PI3K/AKT signaling pathways in HCC cell lines. In conclusion, data in the current study indicate that miR-148a inhibits HCC cells growth via downregulation of EMT and PI3K/AKT signaling pathways by targeting death receptor. These data suggest that miR-148a may serve as a therapeutic target for HCC cancer therapy in the future.


Assuntos
Carcinoma Hepatocelular , Transição Epitelial-Mesenquimal , Neoplasias Hepáticas , MicroRNAs , Receptores do Ligante Indutor de Apoptose Relacionado a TNF , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Transição Epitelial-Mesenquimal/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética , Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo , Transdução de Sinais/genética
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