The fabrication of controlled nanostructures such as quantum dots, nanotubes, nanowires, and nanopillars has progressed rapidly over the past 10 years. However, both bottom-up and top-down methods to integrate the nanostructures are met with several challenges. For practical applications with the high level of the integration, an approach that can fabricate the required structures locally is desirable. In addition, the electrical signal to construct and control the nanostructures can provide significant advantages toward the stability and ordering. Through experiments on the negative resistance switching phenomenon in Pt-NiO-Pt structures, we have fabricated nanofilament channels that can be electrically connected or disconnected. Various analyses indicate that the nanofilaments are made of nickel and are formed at the grain boundaries. The scaling behaviors of the nickel nanofilaments were closely examined, with respect to the switching time, power, and resistance. In particular, the 100 nm x 100 nm cell was switchable on the nanosecond scale, making them ideal for the basis for high-speed, high-density, nonvolatile memory applications.

We report the presence of defects in CH3NH3PbI3, which is one of the main factors that deteriorates the performance of perovskite solar cells.

Quercetin, a plant-derived flavonoid found in fruits, vegetables and tea, has been known to possess bioactive properties such as anti-oxidant, anti-inflammatory and anti-cancer. In this study, anti-cancer effect of quercetin and its underlying mechanisms in triple-negative breast cancer cells was investigated. MTT assay showed that quercetin reduced breast cancer cell viability in a time and dose dependent manner. For this, quercetin not only increased cell apoptosis but also inhibited cell cycle progression. Moreover, quercetin increased FasL mRNA expression and p51, p21 and GADD45 signaling activities. We also observed that quercetin induced protein level, transcriptional activity and nuclear translocation of Foxo3a. Knockdown of Foxo3a caused significant reduction in the effect of quercetin on cell apoptosis and cell cycle arrest. In addition, treatment of JNK inhibitor (SP 600125) abolished quercetin-stimulated Foxo3a activity, suggesting JNK as a possible upstream signaling in regulation of Foxo3a activity. Knockdown of Foxo3a and inhibition of JNK activity reduced the signaling activities of p53, p21 and GADD45, triggered by quercetin. Taken together, our study suggests that quercetin induces apoptosis and cell cycle arrest via modification of Foxo3a signaling in triple-negative breast cancer cells.