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One-dimensional BiFeO 3 /TiO 2 heterostructure nanofibers with high visible-light photocatalytic activity have been successfully obtained via a facile hydrothermal process followed by an electrospinning technique. The results show that the BiFeO 3 /TiO 2 nanofibers are as long as dozens of micrometers with the diameters of about 100-300 nm, where BiFeO 3 nanoparticles are surrounded by anatase-type TiO 2 nanocrystals. Compared with the corresponding pure BiFeO 3 nanoparticles, and TiO 2 nanofibers, the asprepared BiFeO 3 /TiO 2 nanofibers exhibit a markedly enhanced photocatalytic activity in the degradation of methyl blue under visible light irradiation. The enhanced photocatalytic activity is attributed to the formed p-n heterojunction between BiFeO 3 and TiO 2 , which results in synergistic enhancement.Notably, the BiFeO 3 /TiO 2 nanofibers could be easily recycled without the decrease in the photocatalytic activity because of their one-dimensional nanostructural property. With their high degradation efficiency and fine recyclability, the BiFeO 3 /TiO 2 heterostructure nanofibers will have wide application in photodegradation of various organic pollutants.

Melanoma has traditionally been viewed as a radioresistant cancer. However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivity. The newly discovered mammalian CTC1-STN1-TEN1 (CST) complex has been demonstrated to be an important telomere maintenance factor. In this study, by establishing a radiosensitive/radioresistant human melanoma cell model, MDA-MB-435/MDA-MB-435R, we aimed to investigate the association of CTC1 expression with radiosensitivity in human melanoma cell lines, and to elucidate the possible underlying mechanisms. We found that CTC1 mRNA and protein levels were markedly increased in the MDA-MB-435R cells compared with the MDA-MB-435 cells. Moreover, the downregulation of CTC1 enhanced radiosensitivity, induced DNA damage and promoted telomere shortening and apoptosis in both cell lines. Taken together, our findings suggest that CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. Thus, CTC1 may be an attractive target gene for the treatment of human melanoma.

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