Controlled Synthesis and Enhanced Gas Sensing Performance of Zinc-Doped Indium Oxide Nanowires.

Indium oxide (In2O3) is a widely used n-type semiconductor for detection of pollutant gases; however, its gas selectivity and sensitivity have been suboptimal in previous studies. In this work, zinc-doped indium oxide nanowires with appropriate morphologies and high crystallinity were synthesized using chemical vapor deposition (CVD). An accurate method for electrical measurement was attained using a single nanowire microdevice, showing that electrical resistivity increased after doping with zinc. This is attributed to the lower valence of the dopant, which acts as an acceptor, leading to the decrease in electrical conductivity. X-ray photoelectron spectroscopy (XPS) analysis confirms the increased oxygen vacancies due to doping a suitable number of atoms, which altered oxygen adsorption on the nanowires and contributed to improved gas sensing performance. The sensing performance was evaluated using reducing gases, including carbon monoxide, acetone, and ethanol. Overall, the response of the doped nanowires was found to be higher than that of undoped nanowires at a low concentration (5 ppm) and low operating temperatures. At 300 °C, the gas sensing response of zinc-doped In2O3 nanowires was 13 times higher than that of undoped In2O3 nanowires. The study concludes that higher zinc doping concentration in In2O3 nanowires improves gas sensing properties by increasing oxygen vacancies after doping and enhancing gas molecule adsorption. With better response to reducing gases, zinc-doped In2O3 nanowires will be applicable in environmental detection and life science.

Chemical Vapor Deposition-Fabricated Manganese-Doped and Potassium-Doped Hexagonal Tungsten Trioxide Nanowires with Enhanced Gas Sensing and Photocatalytic Properties.

Owing to its unique and variable lattice structure and stoichiometric ratio, tungsten oxide is suitable for material modification; for example, doping is expected to improve its catalytic properties. However, most of the doping experiments are conducted by hydrothermal or multi-step synthesis, which is not only time-consuming but also prone to solvent contamination, having little room for mass production. Here, without a catalyst, we report the formation of high-crystallinity manganese-doped and potassium-doped tungsten oxide nanowires through chemical vapor deposition (CVD) with interesting characterization, photocatalytic, and gas sensing properties. The structure and composition of the nanowires were characterized by transmission electron microscopy (TEM) and energy-dispersive spectroscopy (EDS), respectively, while the morphology and chemical valence were characterized by scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS), respectively. Electrical measurements showed that the single nanowires doped with manganese and potassium had resistivities of 1.81 × 0-5 Ω·m and 1.93 × 10-5 Ω·m, respectively. The doping contributed to the phase transition from monoclinic to metastable hexagonal for the tungsten oxide nanowires, the structure of which is known for its hexagonal electron channels. The hexagonal structure provided efficient charge transfer and enhanced the catalytic efficiency of the tungsten oxide nanowires, resulting in a catalytic efficiency of 98.5% for the manganese-doped tungsten oxide nanowires and 97.73% for the potassium-doped tungsten oxide nanowires after four hours of degradation of methylene blue. Additionally, the gas sensing response for 20 ppm of ethanol showed a positive dependence of doping with the manganese-doped and potassium-doped responses being 14.4% and 29.7%, respectively, higher than the pure response at 250 °C. The manganese-doped and potassium-doped tungsten oxide nanowires are attractive candidates in gas sensing, photocatalytic, and energy storage applications, including water splitting, photochromism, and rechargeable batteries.

Endoplasmic reticulum stress mediates the arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells.

Arsenic trioxide has been proven to trigger apoptosis in human hepatocellular carcinoma cells. Endoplasmic reticulum stress has been known to be involved in apoptosis through the induction of CCAAT/enhancer-binding protein homologous protein. However, it is unknown whether endoplasmic reticulum stress mediates arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells. Our data showed that arsenic trioxide significantly induced apoptosis in human hepatocellular carcinoma cells. Furthermore, arsenic trioxide triggered endoplasmic reticulum stress, as indicated by endoplasmic reticulum dilation, upregulation of glucose-regulated protein 78 and CCAAT/enhancer-binding protein homologous protein. We further found that 4-phenylbutyric acid, an inhibitor of endoplasmic reticulum stress, alleviated arsenic trioxide-induced expression of CCAAT/enhancer-binding protein homologous protein. More important, knockdown of CCAAT/enhancer-binding protein homologous protein by siRNA or inhibition of endoplasmic reticulum stress by 4-phenylbutyric acid alleviated apoptosis induced by arsenic trioxide. Consequently, our results suggested that arsenic trioxide could induce endoplasmic reticulum stress-mediated apoptosis in hepatocellular carcinoma cells, and that CCAAT/enhancer-binding protein homologous protein might play an important role in this process.

Inactivation of Akt by arsenic trioxide induces cell death via mitochondrial-mediated apoptotic signaling in SGC-7901 human gastric cancer cells.

Arsenic trioxide (As2O3) has been recognized as a potential chemotherapeutic agent, yet the details concerning its mechanism of action in solid cancers remain undetermined. The present study assessed the role of Akt in the cell death induced by As2O3. The MTT assay showed that As2O3 suppressed the proliferation of SGC-7901 cells in a dose- and time-dependent manner. Characteristic apoptotic changes were observed in the As2O3­treated cells by Hoechst 33342 staining, and FACS analysis showed that As2O3 caused dose-dependent apoptotic cell death. As2O3 activated caspase-3 and -9, and PARP cleavage in a dose-dependent manner. Compromised mitochondrial membrane potential and an increased protein level of Bax indicated involvement of mitochondia. As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3ß (Ser9), suggesting that As2O3 inactivated Akt kinase. In addition, LY294002 (a PI3 kinase inhibitor) augmented the apoptosis induced by As2O3. These results demonstrated that inhibition of PI3K/Akt signaling was involved in As2O3-induced apoptosis of gastric cancer SGC-7901 cells.