We have carried out O K- and Co L2,3-edge x-ray absorption studies on misfit-layered oxides of polycrystalline Ca3Co4−xFexO9+δ (x=0,0.05,0.1,0.15). The analyses of integrated absorption intensity show that the number of Co 3d unoccupied states decreases upon partial substitution of Fe for Co, which correlates well the variation trend of the room-temperature resistivity with x. Nevertheless, the number of O 2p unoccupied states increases with x. Both Hall and thermopower measurements indicate that the majority carrier is of hole type for Ca3Co4−xFexO9+δ. Therefore, the decrease of O 2p occupancy should be responsible for the increase of the hole carrier concentration upon partial substitution of Fe for Co.
ZnO films with and without Mg doping (Zn1−xMgxO) were deposited on substrates by the sol-gel technique. X-ray photoelectron spectroscopy, x-ray diffraction, photoluminescence, and conductivity measurements were used to characterize the Zn1−xMgxO semiconductors. It is worth noting that the intensity of the band-edge luminescence (BEL) of the Zn0.973Mg0.027O film at room temperature was nearly six times the ZnO film. The enhanced BEL intensity has been attributed to the suppression of capacitance variation related to trapping/detrapping of charges, a decrease in the number of nonradiative recombination defects, and an increase in the nonradiative recombination lifetime.
Morphological changes of hepatocyte death have so far only been described on cells in culture or in tissue sections. Using a high-resolution and high-magnification multiphoton microscopic system, we recorded in living mice serial changes of acetaminophen (APAP)-induced hepatocyte necrosis in relevance to metabolism of a fluorogenic bile solute. Initial changes of hepatocyte injury included basal membrane disruption and loss of mitochondrial membrane potential. An overwhelming event of rupture at adjacent apical membrane resulting in flooding of bile into these hepatocytes might ensue. Belbs formed on basal membrane and then dislodged into the sinusoid circulation. Transmission electron microscopy disclosed a necrotic hepatocyte depicting well the changes after apical membrane rupture and bile flooding. Administration of the antidote N-acetylcysteine dramatically reduced the occurrence of apical membrane rupture. The present results demonstrated a hidden but critical step of apical membrane rupture leading to irreversible APAP-induced hepatocyte injury.
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