The atomic structure and the magnetic properties of 5 and 10 at. % Co-doped ZnO samples prepared by a high-pressure and high-temperature method have been investigated by various techniques, including x-ray diffraction with Rietveld refinements, scanning electron microscopy, high-resolution transmission electron microscopy, nanometer-sized element mapping, x-ray photoelectron spectroscopy, near-edge x-ray absorption fine structure, and extended x-ray absorption fine structure and magnetization measurements. It is found that Co ions with a valence of 2+ substitute Zn ions in the wurtzite ZnO structure. No metallic or oxidic Co-rich clusters were detected in the samples. If Co 2+ ions substitute Zn 2+ ions, no intrinsic ferromagnetism is observed in ZnO at doping levels up to 10 at. % Co even down to 5 K. A paramagnetic behavior with partially antiferromagnetic interactions is observed. Thus, in bulk Co-doped ZnO system any observation of ferromagnetism is probably due to small clusters of second phase materials. However, in thin films the situation might be more complex, since other extrinsic influences, such as strain or proximity effects, may modify the electronic and magnetic properties.
Polycrystalline ZnO : Cu-based film photodetectors with extended detection waveband (UV and visible light) were fabricated using facile colloidal chemistry and a post-annealing process. The obtained detectors are highly sensitive to visible light and can realize the response switch between UV and visible light. A native and extrinsic trap cooperatively controlled space charge limited (SCL) transport mechanism is proposed to understand this complex photoconduction behaviour.
Aging is accompanied with behavioral and cognitive decline. Changes in the neurotransmitter level are associated with the age-related behavioral deterioration, but whether well-known longevity manipulations affect the function of neurotransmitter system in aging animals is largely unclear. Here we report that serotonin
Epithelial barrier integrity is critical to maintain the homeostasis in the body. The regulatory mechanism of the epithelial barrier function has not been fully understood. This study aims to elucidate the role of the TWIK-related potassium channel-1 (Trek1) in the regulation of the epithelial barrier function of the nasal mucosa. In this study, the levels of Trek1 were assessed by real time RT-PCR and Western blotting. The epithelial barrier function of the rat nasal epithelia was evaluated by the Ussing chamber system. The results showed that Trek1 was detected in the human and rat nasal epithelia, which were significantly lower in patients and rats with allergic rhinitis than that in healthy controls. Exposure to the signature T helper 2 cytokine, interleukin (IL)-4, markedly suppressed the expression of Trek1 in the nasal mucosa via up regulating the expression of the histone deacetylase (HDAC)1. The IL-4-induced rat nasal epithelial barrier dysfunction could be blocked by HDAC1 inhibitor (Trichostatin A), or sodium butyrate, or administration of Clostridium Butyricum. We conclude that Trek1 is critical to maintain the nasal epithelial barrier function.
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