Phase-change materials undergo rapid and reversible crystalline-to-amorphous structural transformation and are being used for nonvolatile memory devices. However, the transformation mechanism remains poorly understood. We have studied the effect of electrical pulses on the crystalline-to-amorphous phase change in a single-crystalline Ge(2)Sb(2)Te(5) (GST) nanowire memory device by in situ transmission electron microscopy. We show that electrical pulses produce dislocations in crystalline GST, which become mobile and glide in the direction of hole-carrier motion. The continuous increase in the density of dislocations moving unidirectionally in the material leads to dislocation jamming, which eventually induces the crystalline-to-amorphous phase change with a sharp interface spanning the entire nanowire cross section. The dislocation-templated amorphization explains the large on/off resistance ratio of the device.

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Cu 2 O rhombic dodecahedra, octahedra, and cubes were densely modified with conjugated 4-ethynylaniline (4-EA) for facet-dependent photocatalytic activity examination. Infrared spectroscopy affirms bonding of the acetylenic group of 4-EA onto the surface copper atoms. The photocatalytically inactive Cu 2 O cubes showed surprisingly high activity toward methyl orange photodegradation after 4-EA modification, while the already active Cu 2 O rhombic dodecahedra and octahedra exhibited a photocatalytic activity enhancement. Electron, hole, and radical scavenger experiments prove that the photocatalytic charge transport processes have occurred in the functionalized Cu 2 O cubes. Electrochemical impedance spectroscopy also indicates reduced charge transfer resistance of the functionalized Cu 2 O crystals. A band diagram constructed from UV−vis spectral and Mott−Schottky measurements reveals significant band energy shifts in all Cu 2 O samples after decorating with 4-EA. From density functional theory (DFT) calculations, a new band has emerged slightly above the valence band maximum within the band gap of Cu 2 O, which has been found to originate from 4-EA through banddecomposed charge density analysis. The increased charge density localized on the 4-EA molecule and the smallest electron transition energy to reach the 4-EA-generated band are factors making {100}-bound Cu 2 O cubes photocatalytically active. Proper molecular decoration represents a powerful approach to improving the photocatalytic efficiency of semiconductors.

Novel quinazolinone compounds have been studied in the field of drug discovery for a long time. Among their broad range of pharmacological effects, certain compounds effectively inhibit cancer cell proliferation. MJ-33 is a quinazolinone derivative with proposed anticancer activities that was synthesized in our laboratory. The present study aimed to evaluate the anticancer activity of MJ-33 in fluorouracil (5FU)-resistant colorectal cancer cells (HT-29/5FUR) and to investigate the underlying molecular mechanisms. The cell viability assay results indicated that HT-29/5FUR cell viability was inhibited by MJ-33 treatment in a concentration-dependent manner compared with the control group. The cellular morphological alterations observed following MJ-33 treatment indicated the occurrence of apoptosis and autophagy, as well as inhibition of cell proliferation in a time-dependent manner compared with the control group. The acridine orange, LysoTracker Red and LC3-green fluorescent protein staining results indicated that MJ-33 treatment significantly induced autophagy compared with the control group. The DAPI/TUNEL dual staining results demonstrated increased nuclear fragmentation and condensation following MJ-33 treatment compared with the control group. The Annexin V apoptosis assay and image cytometry analysis results demonstrated a significant increase in apoptotic cells following MJ-33 treatment compared with the control group. The western blotting results demonstrated markedly decreased Bcl-2, phosphorylated (p)-BAD, pro-caspase-9 and pro-caspase-3 expression levels, and notably increased cytochrome c and apoptotic peptidase activating factor 1 expression levels following MJ-33 treatment compared with the control group. Moreover, the expression levels of autophagy-related proteins, including autophagy related (ATG)-5, ATG-7, ATG-12, ATG-16, p62 and LC3-II, were increased following MJ-33 treatment compared with the control group. Furthermore, MJ-33-treated HT-29/5FUR cells displayed decreased expression levels of p-AKT and p-mTOR compared with control cells. The results suggested that MJ-33-induced apoptosis was mediated by AKT signaling, and subsequently modulated via the mitochondria-dependent signaling pathway. Therefore, the results suggested that suppression of AKT/mTOR activity triggered autophagy in the HT-29/5FUR cell line. In summary, the results indicated that MJ-33 inhibited HT-29/5FUR cell viability, and induced apoptosis and autophagy via the AKT/mTOR signaling pathway. The present study may provide novel insight into the anticancer effects and mechanisms underlying MJ-33 in 5FU-resistant colorectal cancer cells.