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        Assessment of Endothelial Cell Growth Behavior in Thin Film Nitinol

        Yanfei Chen,Mahdis Shayan,여운홍,천영재 한국바이오칩학회 2017 BioChip Journal Vol.11 No.1

        Growing clinical needs for less invasive endovascular treatments necessitate the development of advanced biomaterials that exhibit low-profile and enhanced biocompatible properties. One of the endovascular devices is a stent graft, which contains a metallic backbone, covered with thin polymeric membranes such as Dacron® and expandable polytetrafluoroethylene (ePTFE). This device has been widely used for treating various vascular diseases and injuries. While the commercial materials including Dacron® and ePTFE have demonstrated a good feasibility, they were found to induce inflammatory vessel wall reactions with neointimal hyperplasia. Consequently, it causes re-narrowing of the lumen space and thrombogenic issues that ultimately lead the treatment failure. In this paper, we introduced a thin film nitinol (TFN) as an alternative graft material and evaluated the growth behavior of endothelial cells (EC) both qualitatively and quantitatively. As a proof-of-concept study, both untreated nonpatterned film (TFN) and surface treated TFN (S-TFN) materials were used. We compared the adhesion, growth, and proliferation of ECs on a solid (non-patterned) TFN with the two most widely-used commercial graft materials (Dacron® and ePTFE). The in vitro experimental results showed better adhesion and growth of ECs on TFN materials than either ePTFE or Dacron®. Specifically, S-TFN showed approximately twice number of ECs attached on the surface than any other materials tested in this study. In addition, in vivo swine study demonstrated that ECs had a relatively high proliferation on the micropatterrned S-TFN with ~50% surface coverage within two weeks. Both in vitro and in vivo study results of cell growth suggested that TFN materials could be a promising graft material for low-profile endovascular devices.

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        The anti-tumor efficacy of 20(S)-protopanaxadiol, an active metabolite of ginseng, according to fasting on hepatocellular carcinoma

        Wenzhen Li,YifanWang,Xinbo Zhou,Xiaohong Pan,Junhong Lu,Hongliu Sun,Zeping Xie,Shayan Chen,Xue Gao 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1

        Background: 20(S)-protopanaxadiol (20(S)-PPD), one of the main active metabolites of ginseng, performs a broad spectrum of anti-tumor effects. Our aims are to search out new strategies to enhance anti-tumor effects of natural products, including 20(S)-PPD. In recent years, fasting has been shown to be multifunctional on tumor progression. Here, the effects of fasting combined with 20(S)-PPD on hepatocellular carcinoma growth, apoptosis, migration, invasion and cell cycle were explored. Methods: CCK-8 assay, trypan blue dye exclusion test, imagings photographed by HoloMonitorTM M4, transwell assay and flow cytometry assay were performed for functional analyses on cell proliferation, morphology, migration, invasion, apoptosis, necrosis and cell cycle. The expressions of genes on protein levels were tested by western blot. Tumor-bearing mice were used to evaluate the effects of intermittent fasting combined with 20(S)-PPD. Results: We firstly confirmed that fasting-mimicking increased the anti-proliferation effect of 20(S)-PPD in human HepG2 cells in vitro. In fasting-mimicking culturing medium, the apoptosis and necrosis induced by 20(S)-PPD increased and more cells were arrested at G0-G1 phase. Meanwhile, invasion and migration of cells were decreased by down-regulating the expressions of matrix metalloproteinase (MMP)-2 and MMP-9 in fasting-mimicking medium. Furthermore, the in vivo study confirmed that intermittent fasting enhanced the tumor growth inhibition of 20(S)-PPD in H22 tumor-bearing mice without obvious side effects. Conclusion: Fasting significantly sensitized HCC cells to 20(S)-PPD in vivo and in vitro. These data indicated that dietary restriction can be one of the potential strategies of chinese medicine or its active metabolites against hepatocellular carcinoma.

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