Abrupt metal-insulator transition observed in VO2 thin films induced by a switching voltage pulse

An abrupt metal-insulator transition (MIT) was observed in VO2 thin films during the application of a switching voltage pulse to two-terminal devices. Any switching pulse over a threshold voltage for the MIT of 7.1 V enabled the device material to transform efficiently from an insulator to a metal. The characteristics of the transformation were analyzed by considering both the delay time and rise time of the measured current response. The extrapolated switching time of the MIT decreased down to 9 ns as the external load resistance decreased to zero. Observation of the intrinsic switching time of the MIT in the correlated oxide films is impossible because of the inhomogeneity of the material; both the metallic state and an insulating state co-exist in the measurement volume. This indicates that the intrinsic switching time is in the order of less than a nanosecond. The high switching speed might arise from a strong correlation effect (Coulomb repulsion) between the electrons in the material.Comment: 5 pages, 5 figure

Radar-based nowcasting by combining centroid tracking and motion vector of convective storm

Póster presentado en: 3rd European Nowcasting Conference, celebrada en la sede central de AEMET en Madrid del 24 al 26 de abril de 2019

Observation of First-Order Metal-Insulator Transition without Structural Phase Transition in VO_2

An abrupt first-order metal-insulator transition (MIT) without structural phase transition is first observed by current-voltage measurements and micro-Raman scattering experiments, when a DC electric field is applied to a Mott insulator VO_2 based two-terminal device. An abrupt current jump is measured at a critical electric field. The Raman-shift frequency and the bandwidth of the most predominant Raman-active A_g mode, excited by the electric field, do not change through the abrupt MIT, while, they, excited by temperature, pronouncedly soften and damp (structural MIT), respectively. This structural MIT is found to occur secondarily.Comment: 4 pages, 4 figure

Inhibition of autophagy promotes salinomycin-induced apoptosis via reactive oxygen species-mediated PI3K/AKT/mTOR and ERK/p38 MAPK-dependent signaling in human prostate cancer cells

Recently, the interplay between autophagy and apoptosis has become an important factor in chemotherapy for cancer treatment. Inhibition of autophagy may be an effective strategy to improve the treatment of chemo-resistant cancer by consistent exposure to chemotherapeutic drugs. However, no reports have clearly elucidated the underlying mechanisms. Therefore, in this study, we assessed whether salinomycin, a promising anticancer drug, induces apoptosis and elucidated potential antitumor mechanisms in chemo-resistant prostate cancer cells. Cell viability assay, Western blot, annexin V/propidium iodide assay, acridine orange (AO) staining, caspase-3 activity assay, reactive oxygen species (ROS) production, and mitochondrial membrane potential were assayed. Our data showed that salinomycin alters the sensitivity of prostate cancer cells to autophagy. Pretreatment with 3-methyladenine (3-MA), an autophagy inhibitor, enhanced the salinomycin-induced apoptosis. Notably, salinomycin decreased phosphorylated of AKT and phosphorylated mammalian target of rapamycin (mTOR) in prostate cancer cells. Pretreatment with LY294002, an autophagy and PI3K inhibitor, enhanced the salinomycin-induced apoptosis by decreasing the AKT and mTOR activities and suppressing autophagy. However, pretreatment with PD98059 and SB203580, an extracellular signal-regulated kinases (ERK), and p38 inhibitors, suppressed the salinomycin-induced autophagy by reversing the upregulation of ERK and p38. In addition, pretreatment with N-acetyl-L-cysteine (NAC), an antioxidant, inhibited salinomycin-induced autophagy by suppressing ROS production. Our results suggested that salinomycin induces apoptosis, which was related to ROS-mediated autophagy through regulation of the PI3K/AKT/mTOR and ERK/p38 MAPK signaling pathways