PubMed · 15459155
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G P Currie, D K C Lee. 2004. Methacholine and macrolides.. https://doi.org/10.1183/09031936.04.10057104
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While titanium implants are generally recognized as having excellent biocompatibility, the mechanistic basis for this has yet to be established. We previously demonstrated that TiO2, found on surfaces of titanium, has antioxidant properties that degrade the reactive oxygen species (ROS) which mediate the inflammatory response. We hypothesized that the antioxidant mechanism was similar to that known to mediate photocatalysis by titanium oxides. Specifically, we investigated whether the electronic or valence state of the surface titanium atoms mediates the catalytic degradation of ROS. Surface Ti(IV) atoms in TiO2 and SrTiO3 single crystal substrates were converted into Ti(III) while maintaining the bulk crystalline structure by vacuum annealing or Niobium doping. The degradation of both chemically-induced and neutrophil-derived ROS were significantly increased by changing the valence state of surface titanium. These results suggest that titanium-mediated degradation of ROS is through a catalytic mechanism. Furthermore, we describe a series of novel biomaterials that have antioxidant properties superior to those of titanium.
The aim of this study was to analyze the change of serum chemokins levels of CXCL16, CX3CL1/Fractalkine, and CXCL10/interferon-gamma inducible protein-10 (IP-10) with rheumatoid arthritis (RA), by infliximab treatment. The effects of infliximab treatment were studied in 23 patients with RA, over a period of 30 weeks. The serum levels of CXCL16, Fractalkine, and IP-10, were measured at the baseline, just before initial treatment, and at 14 and 30 weeks after the initial treatment, with infliximab by ELISA. The higher levels of serum CXCL16 in the RA patients before treatment with infliximab significantly decreased at 14 and 30 weeks after the initial treatment with infliximab, but the serum Fractalkine and IP-10 levels did not decrease significantly. Infliximab treatment significantly lowered the serum levels of CXCL16 in patients with RA. CXCL16 is one of the crucial chemokines regulated by infliximab treatment.
PURPOSE OF REVIEW: To outline recent findings on the efficacy of n-3 polyunsaturated fatty acids in the prevention/treatment of inflammatory bowel disease and colorectal cancer. RECENT FINDINGS: Compelling data indicate a functional link between chronic inflammation and colon cancer. With respect to environmental risk factors, there is growing evidence that long-chain n-3 polyunsaturated fatty acids found in fish oil suppress inflammatory bowel diseases and colon cancer risk in humans. Unfortunately, the molecular basis of the effect of n-3 polyunsaturated fatty acids on inflammation/colitis-associated colon cancer risk is still largely obscure. In this review, we focus on recent studies which address three emerging mechanisms of n-3 polyunsaturated fatty acids action: (1) metabolic interconversion into bioactive eicosanoids, (2) modulation of nuclear receptor activation, and (3) alteration of membrane phospholipid composition and functionality of lipid microdomains. SUMMARY: The consumption of dietary fish oil may prove to be an effective adjuvant therapy in colon cancer. Therefore, it is both appropriate and timely to determine precisely how n-3 polyunsaturated fatty acids modulate cell signaling networks, and reduce the risk of developing colon cancer and inflammatory disorders of the intestine.