A unique 1D nanostructure of Pt@CeO 2 −BDC was prepared from Pt@CeBDC MOF. The Pt@CeO 2 −BDC was rich in oxygen vacancies (i.e., XPS O β /(O α + O β ) = 39.4%), and on the catalyst, the 2 nm Pt clusters were uniformly deposited on the 1D mesoporous polycrystalline CeO 2 . Toluene oxidation was conducted in a spectroscopic operando Raman−online FTIR reactor to elucidate the reaction mechanism and establish the structure−activity relationship. The reaction proceeds as follows: (I) adsorption of toluene as benzoate intermediates on Pt@CeO 2 −BDC at low temperature by reaction with surface peroxide species; (II) reaction activation and ring-opening involving lattice oxygen with a concomitant change in defect densities indicative of surface rearrangement; (III) complete oxidation to CO 2 and H 2 O by lattice oxygen and reoxidation of the reduced ceria with consumption of adsorbed oxygen species. The Pt clusters, which mainly exist as Pt 2+ with minor amounts of Pt 0 and Pt 4+ on the surface, facilitated the adsorption and reaction activation. The Pt-CeO 2 interface generates reduced ceria sites forming nearby adsorbed peroxide at low temperature that oxidize toluene into benzoate species by a Langmuir−Hinshelwood mechanism. As the reaction temperature increases, the role of lattice oxygen becomes important, producing CO 2 and H 2 O mainly by the Mars-van Krevelen mechanism.

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ObjectiveThe development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We tried to provide fundamental data to determine differences in cytotoxicity induced by ambient UFPs and engineered metal oxide NPs (ZnO, NiO, and CeO2).MethodsUFPs were sampled by using of a nano micro-orifice uniform deposit impactor. Physicochemical characterization of the UFPs and nano metal oxide particles were studied by scanning electron microscopy and transmission electron microscopy. Cellular toxicity induced by the different particles was assessed by using of comprehensive approaches and compared after A549 cells were exposured to the particles.ResultsAll of the measured particles could damage A549 cells at concentrations ranging from 25 to 200 μg/mL. The lowest survival ratio and the highest lactate dehydrogenase level were caused by nano-ZnO particles, but the highest levels of intracellular reactive oxygen species (ROS) and percentages of apoptosis were observed in cells treated with the soluble fraction of ambient fine particles (PM1.8) at 200 μg/mL. Relatively high concentrations of anthropogenic metals, including Zn, Ni, Fe, and Cu, may be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and UFPs. The selected heavy metals (Zn, Ni, Fe, and Cu) were found to be located in the perinuclear and cytoplasmic areas of A549 cells. The distribution pattern of metals from ambient particles showed that distributions of the metals in A549 cells were not uniform and followed the pattern Cu > Zn > Fe > Ni, suggesting that Cu was absorbed by A549 cells more easily than the other metals.ConclusionsMetal nanoparticles oxides and UFPs at low concentration could damage to cells, but the manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles. The local concentration effect of heavy metals in A549 cells, as well as the induction of oxidative stress by the particles, may be responsible for the damage observed to the cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-015-0082-8) contains supplementary material, which is available to authorized users.

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Glioma is the most common primary malignant tumor of the central nervous system, which results in both a poor prognosis and outcome because of the aggressive progression of disease, growth and resistance to surgery, chemotherapy, and radiotherapy. MiR-140-5p is a small, non-coding single-stranded RNA molecule, which was previously studied in the settings of human tongue cancer, hepatocellular carcinoma, and colorectal cancer. However, detailed data that formally demonstrate the contribution of miR-140-5p to glioma development are missing. Similarly, relatively little is known about the relationship of miR-140-5p, vascular endothelial growth factor A, and matrix metalloproteinase-2 in glioma progression. In this study, we found that miR-140-5p expression was significantly decreased in glioma tissues and in the glioma cell-lines U87 and U251 as compared with non-cancerous brain tissues by quantitative real-time polymerase chain reaction. In addition, miR-140-5p inhibited glioma cell proliferation and invasion and promoted glioma cell apoptosis both in vivo and in vitro. Interestingly, while the expression levels of miR-140-5p were higher in glioma cells, the messenger RNA or protein expression levels of vascular endothelial growth factor A and matrix metalloproteinase-2 were lower in glioma cells as determined by quantitative real-time polymerase chain reaction, western blot assay, and immunohistochemistry. By contrast, downregulation in the expression levels of miR-140-5p augmented the messenger RNA and protein expression levels of both vascular endothelial growth factor A and matrix metalloproteinase-2. These findings suggested that miR-140-5p inhibited glioma proliferation and invasion by regulating the vascular endothelial growth factor A/matrix metalloproteinase-2 signaling pathway both in vitro and in vivo.

In Japan, Cryptomeria japonica pollen (with diameter *30 lm) is scattered during each spring season. Daughter allergenic particles, which are smaller in size than their parent pollen grain and are abundant in fine particles (the particle sizes \ 1.