Hierarchically ordered materials with core/shell structures were synthesized through a layer-by-layer approach. The novel microporous/mesoporous hybrid materials were composed of a TS-1 zeolite particle for the core and mesoporous silica for the shell. The as-synthesized TS-1 crystals were modified with polydiallyldimethylammonium chloride to make their external surface positively charged, which induced an oriented self-assembly of tetraethoxysilane (TEOS) with cetyltrimethyl ammonium bromide on the TS-1 particle surface to form a shell of mesophase silica. The thickness of the mesoporous silica shell was controlled to be in the range 30-55 nm by changing the amount of TEOS added in the synthesis. The mesoporous channels in the shell were perpendicular to the zeolite core, which made the micropores inside the core accessible from the outside through the mesopores. Taking advantage of the confining effect of the mesopores, Au nanoparticles were incorporated into the shell, resulting in bifunctional catalysts which were more selective than conventional Au/TS-1 catalysts in the direct epoxidation of propylene to propylene oxide with H 2 and O 2 .
Highly ordered mesoporous carbon-titania nanocomposites with nanocrystal-glass frameworks have been synthesized via the organic-inorganic-amphiphilic coassembly followed by the in situ crystallization technology. A soluble resol polymer was used as a carbon precursor, prehydrolyzed TiCl 4 as an inorganic precursor, and triblock copolymer F127 as a template. The carbon-titania nanocomposites with controllable texture properties and composition can be obtained in a wide range from 20 to 80 wt% TiO 2 by adjusting the initial mass ratios. The C-TiO 2 nanocomposites with "bricked-mortar"frameworks exhibit highly ordered 2D hexagonal mesostructure and high thermal stability up to 700°C. The nanocomposites have high surface area (465 m 2 g -1 ) and large pore size (∼4.1 nm). Additionally, the nanocomposites show good performance in degradation of Rhodamine B due to the photocatalytic activity of the titania nanocrystals and the strong adsorptive capacity of the glasslike carbon.
Tumour cell proliferation, invasion and apoptosis are crucial steps in tumour metastasis. We evaluated the effect of serum from patients undergoing colon cancer surgery receiving thoracic epidural and propofol anaesthesia on colon cancer cell biology. Patients were randomly assigned to receive propofol anaesthesia with a concomitant thoracic epidural (PEA, n = 20) or sevoflurane anaesthesia with opioid analgesia (SGA, n = 20). Venous blood was obtained before induction of anaesthesia and 24 hours postoperatively. The LoVo colon cancer cells were cultured with patient serum from both groups and the effects on proliferation, invasion and apoptosis were measured. Twenty-four hours after surgery, the absorbance value of LoVo cells at 10% serum concentration from PEA was decreased when compared with SGA (0.302 (0.026) vs 0.391 (0.066), p = 0.005). The inhibitory rate of LoVo cells at 10% serum concentration from PEA was higher than that from SGA (p = 0.004) 24 h after surgery. The number of invasive LoVo cells at 10% serum concentration from PEA was reduced when compared with SGA (44 (4) vs 62 (4), p < 0.001). Exposure of LoVo cells to postoperative serum from patients receiving PEA led to a higher luminescence ratio (apoptosis) than those receiving SGA (0.36 (0.04) vs 0.27 (0.05), p < 0.001). Serum from patients receiving PEA for colon cancer surgery inhibited proliferation and invasion of LoVo cells and induced apoptosis in vitro more than that from patients receiving SGA. Anaesthetic technique might influence the serum milieu in a way that affects cancer cell biology and, thereby, tumour metastastasis.
Propofol is one of the most extensively used intravenous anesthetic agents and it can influence the biological behavior of gastric cancer. However, the underlying mechanism is poorly understood. In the present study, we found that propofol significantly inhibited cell proliferation, invasion and migration, and also promoted apoptosis in gastric carcinoma cell lines SGC-7901 and MGC-803, as detected using MTT, colony formation and flow cytometry assays, respectively. Moreover, propofol (10 and 20 µM) markedly upregulated the expression of inhibitor of growth 3 (ING3), which was lower in SGC-7901 and MGC-803 cells compared with that noted in normal human gastric epithelial cell lines GES-1 and HFE145. Furthermore, we transfected SGC-7901 and MGC-803 cells with ING3 overexpression vectors or ING3 small interference RNA (siING3), respectively, to assess the role of ING3 in propofol-induced antitumor activity. The siING3 transfection reversed the effects of propofol on the biological behavior of gastric cancer cells, while transfection of ING3 promoted the effects of propofol. In conclusion, our results indicate that propofol exerts an inhibitory effect on the growth and survival of gastric cancer cells by interfering with ING3 degradation.
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