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Adhesion molecules play important roles in airway hyperresponsiveness or airway inflammation. Our previous study indicated catenin alpha-like 1 (CTNNAL1), an alpha-catenin-related protein, was downregulated in asthma patients and animal model. In this study, we observed that the expression of CTNNAL1 was increased in lung tissue of the ozone-stressed Balb/c mice model and in acute ozone stressed human bronchial epithelial cells (HBEC). In order to identify the possible DNA-binding proteins regulating the transcription of CTNNAL1 gene in HBEC, we designed 8 oligo- nucleotide probes corresponding to various regions of the CTNNAL1 promoter in electrophoretic mobility shift assays (EMSA). We detected 5 putative transcription factors binding sites within CTNNAL1 promoter region that can recruit LEF-1, AP-2α and CREB respectively by EMSA and antibody supershift assay. Chromatin immunoprecipitation (ChIP) assay verified that AP-2 a and LEF-1 could be recruited to the CTNNAL1 promoter. Therefore we further analyzed the functions of putative AP-2 and LEF-1 sites within CTNNAL1 promoter by site-directed mutagenesis of those sites within pGL3/FR/luc. We observed a reduction in human CTNNAL1 promoter activity of mutants of both AP-2α and LEF-1 sites. Pre-treatment with ASOs targeting LEF-1and AP-2α yielded significant reduction of ozone-stress-induced CTNNAL1 expression. The activation of AP-2α and LEF-1, followed by CTNNAL1 expression, showed a correlation during a 16-hour time course. Our data suggest that a robust transcriptional CTNNAL1 up-regulation occurs during acute ozone-induced stress and is mediated at least in part by ozoneinduced recruitments of LEF-1 and AP-2α to the human CTNNAL1 promoter. [ABSTRACT FROM AUTHOR]

Bombesin receptor subtype 3 (BRS-3), the orphan bombesin receptor, may play a role in the regulation of stress responses in lung and airway epithelia. Bombesin receptor activated protein (BRAP )is a novel protein we found in our previous study which interacts with BRS-3. This study was designed to observe the subcellular location and wound repair function of BRAP in human bronchial epithelial cells (HBECs). BRAP ORF was amplified by RT-PCR and ligated to pEGFP-C1 vector, and then the recombinant plasmid pEGFP-C1-BRAP was transfected into Hela cells. The location of BRAP protein was observed by laser confocal microscope, and the expression of it was analyzed by Western-blot. At the same time,we built the recombinant plasmid pcDNA3.1(+)-BRAP, transfected it into HBECs and observed its impact on cell cycle and wound repair of HBECs. The results showed that BRAP locates in membrane and cytoplasm and increases significantly in transfected cells. Flow cytometry results demonstrated that the recombinant plasmid increases S phase plus G2 phase of cell cycle by 25%. Microscopic video analysis system showed that the repair index of wounded HBECs increases by 20% through stable expression of BRAP. The present study demonstrated that BRAP locates in the membrane and cytoplasm, suggesting that this protein is a cytoplasm protein, which promotes cell cycle and wound repair of HBECs. [ABSTRACT FROM AUTHOR]

Nickel coating on the carbon–polythene composite plate was prepared by electrodeposition in a nickel sulfate solution in this work. The morphology and cross-sectional microstructure of the nickel coating were examined by scanning electron microscope (SEM) and optical microscope (OM), respectively. The influence of bath temperature on the nickel deposition rate was investigated experimentally. The adhesion between the coating and the substrate was evaluated by the pull-off test. The corrosion behavior of the coating in an aqueous solution of NaCl was studied by electrochemical methods. The results showed that the nickel electrodeposition rate could reach up to 0.68 μm min−1 on average under conditions of cathodic current density of 20 mA cm−2 and bath temperature of 60 °C. It was confirmed that increasing the bath temperature up to 50 °C had a positive effect on the nickel deposit rate, while an adverse effect was observed beyond 60 °C. The adhesion strength between the nickel coating and the substrate can be more than 2.3 MPa. The corrosion potential of the bright coating in the NaCl solution was more positive than that of the dull coating, and the anodic dissolution rate of the bright coating was also far lower at the same polarization potential compared with the dull coating. [ABSTRACT FROM AUTHOR]

Tröger's base (TB) analogues are important building blocks in molecular engineering due to their C2 symmetry, concave Λ-shape and chirality. We have synthesized three new TB analogues with aromatic fluorene units substituted by n-butyl or/and bromine groups. The structure and packing properties of these TB analogues have been reported. The weak intermolecular forces involved in the crystal packing varying with the substitutions of the three TB analogues have been analysed and described in detail. Thermal and optical properties have also been provided for additional illustration. [ABSTRACT FROM AUTHOR]

Previously, we found that bombesin receptor subtype 3 (BRS-3) significantly increased in an ozone-stressed airway hyperresponsiveness animal model and resulted in induced wound repair and protection from acute lung injury. In the present study, we determined molecular mechanisms of BRS-3 regulation in human BECs (bronchial epithelial cells) in response to ozone stress. Ten oligonucleotide probes corresponding to various regions of the BRS-3 promoter were used in EMSA (electrophoretic mobilityshift assays). Four were found to have an enhanced mobility shift with extracts from ozone-stressed cells. On the basis of the assay of mutated probes binding with extracts and antibody supershift, they were verified as MTF-1 (metal-regulatory-element-binding transcription factor-1), PPARα (peroxisome-proliferator-activated receptor α), AP-2α (activator protein 2α) and HSF-1 (heat-shock factor 1). Next, ChIP (chromatin immunoprecipitation) assay, site-directed mutagenesis technology and antisense oligonucleotide technology were used to observe these transcription factors associated with the BRS-3 promoter. Only AP-2α and PPARα increased ozone-inducible DNA binding on the BRS-3 promoter and BRS-3 expression. The time courses of AP-2α and PPARα activation, followed by BRS-3 expression, were also examined. It was shown that ozone-inducible BRS-3 expression and AP-2α- and PPARα-binding activity correlated over a 48 h period. The translocation of PPARα was observed by immunofluorescence assay, which showed that PPARα nuclear translocation increased after ozone exposure. Our data suggest that AP-2α and PPARα may be especially involved in this ozone-inducible up-regulation mechanism of BRS-3 expression. [ABSTRACT FROM AUTHOR]

Aim: To examine the possible protective effect of ginsenoside Rg1, an active component of ginseng, on lung injury caused by glutamate in vivo. Methods: The lungs of mice receiving glutamate (0.5 g/kg) and/or ginsenoside Rg1 (0.03 g/kg) via intraperitoneal administration were collected. The indexes of lung wet weight/ body weight ratios (LW/BW), lung wet/dry weight ratios (W/D), heart rate (HR), and breathing rate (BR) were determined. The activity of nitric oxide synthase (NOS), xanthine oxidase (XOD), superoxide dismutase (SOD), catalase (CAT), the content of NO, and malondialdehyde in the lung homogenate were measured. Results: Treatment with glutamate for 2 h increased LW/BW, W/D, HR, and BR. These changes were nearly abolished by pretreatment with ginsenoside Rg1 for 30 min before glutamate injection. An analysis of the lung homogenate demonstrated the protective effect as evidenced by the inhibition of NOS (12%) and XOD (50%) inactivity, the enhanced activity of SOD (20%) and CAT (25%). Conclusion: Ginsenoside Rg1 has a potential protective role in lung diseases associated with glutamate toxicity. [ABSTRACT FROM AUTHOR]

Abstract Degradation of organic contaminants in water by high-voltage pulse discharges was investigated. The effects of gas flow rate and liquid conductivity on the degradation of 4-chlorophenol were studied. With the increase of time, the liquid conductivity increases, which have an important effect on discharge. Meanwhile, with the increase of time, the concentration of H 2 O 2 increases. Addition of 200 mg/L H 2 O 2 , the conversion of 4-chlorophenol was greatly enhanced. This may be due to the synergistic effect of high-voltage pulsed discharge and H 2 O 2 . Also, it was found that the influence of quantity of TiO 2 or CuO on degradation of acetophenone is not apparent, maybe the presence of metal oxides hinders the formation of plasma channel due to increase of collusions between metal oxides and oxygen. [ABSTRACT FROM AUTHOR]