A new layered nanocomposite, which is one-to-one interstratified with a montmorillonite layer and a mixed SiO 2 /TiO 2 sol particle one, has been prepared by ion exchange reaction of the Na + ion in montmorillonite with the positively charged SiO 2 /TiO 2 sol particles. The ion exchange reaction was performed at three different temperatures of 45, 60, and 75°C by mixing an aqueous suspension of 1 wt % Na + montmorillonite with SiO 2 /TiO 2 sol solution where the molar ratio of Si/Ti was selected as 20/2. According to the powder X-ray diffraction analysis, the basal spacings of layered nanocomposites calcined at 400°C were found to increase from 35.4 Å, to 47.3 Å, and to 60.0 Å as the ion exchange reaction temperature was raised from 40°C, to 60°C, and to 75°C. Their BET and Langmuir specific surface areas and porosities, estimated from nitrogen adsorption-desorption isotherms, become larger with the increment of basal spacing, and the highest BET specific surface area and the largest porosity are found to be 683 m 2 /g and 0.50 mL/g, respectively. Despite the large increment of the basal spacing, the porous properties such as specific surface areas, porosities, and pore sizes, those which are calculated from t-plots and chemical shift of 129 Xe NMR, respectively, are determined to be almost constant. From the UV/vis spectra, the blue shift of the absorption edge was observed, indicating that the TiO 2 sol particles in the interlayer are quantum sized. It is therefore proposed that the products are intercalation-type nanocomposites with the multistacked structure of the SiO 2 /TiO 2 nanoparticles in the interlayer space of montmorillonite.

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Nitric oxide (NO) causes apoptosis and dedifferentiation of articular chondrocytes by the modulation of extracellular signal-regulated kinase (ERK), p38 kinase, and protein kinase C (PKC) ␣ and -. In this study, we investigated the effects and mechanisms of non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, ketoprofen, ibuprofen, sulindac sulfide, and flurbiprofen, in NO-induced apoptosis and dedifferentiation of articular chondrocytes. We found that all of the examined NSAIDs inhibited apoptosis and dedifferentiation. NO production in chondrocytes caused activation of ERK-1/2 and p38 kinase, which oppositely regulate apoptosis and dedifferentiation. NO production also caused inhibition of PKC␣ and -independent of and dependent on, respectively, p38 kinase, which is required for apoptosis and dedifferentiation. Among the signaling molecules modulated by NO, NSAIDs blocked NO-induced activation of p38 kinase, potentiated ERK activation, and blocked inhibition of PKC␣ and -. NSAIDs also inhibited some of the apoptotic signaling that is downstream of p38 kinase and PKC, such as NFB activation, p53 accumulation, and caspase-3 activation. The inhibitory effects of NSAIDs on apoptosis and dedifferentiation were independent of the inhibition of cyclooxygenase (COX)-2 and prostaglandin E 2 (PGE 2 ) production, as evidenced by the observation that specific inhibition of COX-2 activity and PGE 2 production or exogenous PGE 2 did not affect NO-induced apoptosis and dedifferentiation. Taken together, our results indicate that NSAIDs block NO-induced apoptosis and dedifferentiation of articular chondrocytes by the modulation of ERK, p38 kinase, and PKC␣ and -in a manner independent of their ability to inhibit COX-2 and PGE 2 production.Chondrocytes are a unique cell type in which the differentiated phenotype is reversible. The phenotype of chondrocytes is regulated by the balance between anabolic and catabolic reactions of molecules, which are involved in the maintenance of cartilage homeostasis (1). Differentiated chondrocytes both in vivo and in vitro dedifferentiate into fibroblastic cells upon exposure to interleukin-1␤ (2, 3), retinoic acid (4), or nitric oxide (NO) 1 (5). Although the molecular mechanism is not yet clear, dedifferentiation of articular chondrocytes is believed to play a role in the pathophysiology of arthritis. In addition to dedifferentiation, increased apoptotic death of chondrocytes was observed in arthritic cartilage, and apoptosis is closely related to cartilage destruction (6, 7), indicating that chondrocyte apoptosis plays an important role in the pathogenesis of arthritis.NO is generally believed to be an important mediator of the dedifferentiation and apoptosis of articular chondrocytes in arthritic cartilage (5,8,9). NO is produced in chondrocytes by the action of proinflammatory cytokines, such as interleukin-1␤. NO production in chondrocytes causes activation of matrix metalloproteinases (10), decreased production of interleukin-1 receptor antagonists (11), inhibition of ...

Temperature-dependent in situ W L 3 -edge X-ray absorption spectroscopy has been performed at 20-500 ‡C to investigate the geometric environment and electronic structure of tungsten upon the transformation of electrochromic peroxopolytungstic acid to tungsten trioxide. The temperature-dependent variation of the coordination number and bond distance of the nearest (W-O) sphere reveals that the peroxopolytungstate changes into crystalline tungsten oxide through the gradual removal of peroxo species, zeolitic water, hydroxyl groups, and terminal WLO bonds, which is also confirmed by thermal analysis, powder XRD, and FT-IR spectroscopy. It is especially emphasized that the intermediate structure of peroxopolytungstate at 120-200 ‡C is characterized by a substantial number of oxygen vacancies together with a partially formed oxide lattice. A thin film of peroxopolytungstic acid has been prepared on a transparent conducting substrate and post-annealed at 100-300 ‡C. From cyclic voltammetry and optical density measurements in a LiClO 4 -propylene carbonate electrolyte, it was found that the voltammetric exchange charges are maximized for films annealed at 150-200 ‡C, whereas the voltage response of coloration/bleaching is depressed by the increase in annealing temperature. Considering both the electrochromic kinetics and redox capacity, the optimum annealing temperature for the formation of WO 3 film was determined to be 120-200 ‡C. Such results could be well explained in terms of the structural evolution of peroxopolytungstic acid on the basis of X-ray absorption spectroscopic analysis.

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