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Preparation and characterization of superhydrophobic coatings
Hsing-I Hsiang,Ming-Tsai Liang,Yu-Lun Chang,Hung-Chin Huang,Fu-Su Yen 한양대학교 세라믹연구소 2010 Journal of Ceramic Processing Research Vol.11 No.3
To obtain a surface with water-repelling and self-cleaning abilities attracts much interest in the nanotechnology age. In this study, a perfluroalkyl surfactant (perflurodecanoic acid, PFDA) was coated on nano-sized boehmite surfaces to obtain hydrophobic nano-particles via surface modification. Then the hydrophobic boehmite was coated on a transparent plastic film using spin-coating to obtain a hydrophobic film. The effects of various amounts of hydrophobic polymer on the adsorption behavior and contact angle for hydrophobic properties were investigated using FTIR, and a contact-angle meter. The adsorption of PFDA onto the surface of boehmite takes place through ionic bonding. The contact angles of the thin film prepared by spin coating PFDA-modified-boehmite on glass substrates were above 150o as the adsorption of PFDA onto the surface of boehmite reached saturation.
Youmei Xiao,Zhanxue Xu,Yuan Cheng,Rufan Huang,Yuan Xie,Hsiang‑i Tsai,Hualian Zha,Lifang Xi,Kai Wang,Xiaoli Cheng,Yanfeng Gao,Changhua Zhang,Fang Cheng,Hongbo Chen 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Background Ferroptosis, iron-dependent cell death, is an established mechanism for cancer suppression, particularly in hepatocellular carcinoma (HCC). Sorafenib (SOR), a frontline drug for the treatment of HCC, induces ferroptosis by inhibiting the Solute Carrier family 7 member 11 (SLC7A11), with inadequate ferroptosis notably contributing to SOR resistance in tumor cells. Methods To further verify the biological targets associated with ferroptosis in HCC, an analysis of the Cancer Genome Atlas (TCGA) database was performed to find a significant co-upregulation of SLC7A11 and transferrin receptor (TFRC), Herein, cell membrane-derived transferrin nanovesicles (TF NVs) coupled with Fe3+ and encapsulated SOR (SOR@TF-Fe3+ NVs) were established to synergistically promote ferroptosis, which promoted the iron transport metabolism by TFRC/TF-Fe3+ and enhanced SOR efficacy by inhibiting the SLC7A11. Results In vivo and in vitro experiments revealed that SOR@TF-Fe3+ NVs predominantly accumulate in the liver, and specifically targeted HCC cells overexpressing TFRC. Various tests demonstrated SOR@TF-Fe3+ NVs accelerated Fe3+ absorption and transformation in HCC cells. Importantly, SOR@TF-Fe3+ NVs were more effective in promoting the accumulation of lipid peroxides (LPO), inhibiting tumor proliferation, and prolonging survival rates in HCC mouse model than SOR and TF- Fe3+ NVs alone. Conclusions The present work provides a promising therapeutic strategy for the targeted treatment of HCC.