Achieving cadmium selenide-decorated zinc ferrite@titanium dioxide hollow core/shell nanospheres with improved light trapping and charge generation for photocatalytic hydrogen generation.

We report the rational design and fabrication of magnetically separable zinc ferrite@titanium dioxide (ZnFe2O4@TiO2) hollow core/shell nanospheres as photocatalysts for efficient H2 evolution by loading the TiO2 shell layer on the prepared ZnFe2O4 hollow nanospheres using the kinetics-controlled coating method. Meanwhile, the incident light absorption, photogenerated charge transfer and separation and photocatalytic hydrogen evolution activity were remarkably improved by well anchoring cadmium selenide (CdSe) quantum dots on the ZnFe2O4@TiO2 hollow core/shell nanospheres. This unique design integrates the structural and functional merits of the ZnFe2O4, TiO2, and CdSe quantum dots into porous hollow nanospheres with the double-shell heterostructure. This design significantly accelerates the separation and transport of photogenerated charge carriers, enhances the light absorption, and offers more active sites for the photocatalytic H2 evolution reaction. Benefitting from the unique structural and component merits, the optimized magnetically separable ZnFe2O4@TiO2/CdSe hollow core/shell nanospheres exhibit excellent photocatalytic hydrogen evolution performance with a high H2 generation rate (266.0 µmol h-1·g-1) and high stability.

Low dosage of arsenic trioxide inhibits vasculogenic mimicry in hepatoblastoma without cell apoptosis.

Hepatoblastoma (HB) is the most common type of pediatric liver malignancy, which predominantly occurs in young children (aged <5 years), and continues to be a therapeutic challenge in terms of metastasis and drug resistance. As a new pattern of tumor blood supply, vasculogenic mimicry (VM) is a channel structure lined by tumor cells rather than endothelial cells, which contribute to angiogenesis. VM occurs in a variety of solid tumor types, including liver cancer, such as hepatocellular carcinoma. The aim of the present study was to elucidate the effect of arsenic trioxide (As2O3) on VM. In vitro experiments identified that HB cell line HepG2 cells form typical VM structures on Matrigel, and the structures were markedly damaged by As2O3 at a low concentration before the cell viability significantly decreased. The western blot results indicated that As2O3 downregulated the expression level of VM­associated proteins prior to the appearance of apoptotic proteins. In vivo, VM has been observed in xenografts of HB mouse models and identified by periodic acid­Schiff+/CD105­ channels lined by HepG2 cells without necrotic cells. As2O3 (2 mg/kg) markedly depresses tumor growth without causing serious adverse reactions by decreasing the number of VM channels via inhibiting the expression level of VM­associated proteins. Thus, the present data strongly indicate that low dosage As2O3 reduces the formation of VM in HB cell line HepG2 cells, independent of cell apoptosis in vivo and in vitro, and may represent as a candidate drug for HB targeting VM.