Application of wear resistant coatings by the brush plating technique

The development of cobalt molybdenum and cobalt tungsten brush plating electrolytes is described. Their optimum compositions and operating conditions for commercial applications have been determined. The effects of composition, pH, applied voltage, stylus speed and pressure upon deposit composition and efficiency have been investigated. Transmission and Scanning Electron Microscopy have been employed to study the cobalt alloy deposits produced. Evaluation of the wear resistant properties of the cobalt alloys developed in this work was carried out in the laboratory using a pin and disc technique and a simulated hot forging test, and by industrial trials involving the "on site" plating of hot forging dies and cold pressing tools. It was concluded that the electrolytes developed in tl1is work enabled cobalt alloys containing 6% Mo or 8% W to be deposited at 17-20V. Brush plated cobalt deposits possessed a mixed CPU and FCC crystallographic structure at room temperature. The application of 13µm of either of the cobalt alloys resulted in improved wear performance in both pin and disc and simulated hot forging tests. The results of the industrial trials indicated that by the use of these alloys, the life of hot forging dies may be increased by 20-100%. A commercial forging organisation is using electrolytes developed in this work to coat dies prior to forging nimonic alloys. Reductions in forging temperature and improved forging qualities have been reported. Cold pressing tools coated with the alloys showed a reduced tendency to "pick-up" and scoring of the pressed panels. Reports of a reduced need for lubrication of panels before pressing have also been received.

Antipyretic, analgesic and anti-oxidative activities of Aquilaria crassna leaves extract in rodents

In Thailand, the leaves of Aquilaria crassna have been used traditionally for the treatments of various disorders, but without any scientific analysis. In this study, the antipyretic, analgesic, anti-inflammatory and anti-oxidative properties of A. crassna leaves extract were investigated at a wide dose range in rodents. Experimental animals were treated orally with an aqueous extract of Aquilaria crassna leaves (ACE). They were tested for antipyretic (Baker′s yeast-induced fever in rats), analgesic (hot plate test in mice) and anti-inflammatory (carrageenan-induced paw edema in rats) activities. An anti-oxidative effect of ACE was evaluated by using the DPPH anti-oxidant assay. The results showed that, after 5 hours of yeast injection, 400 and 800 mg/kg ACE significantly reduced the rectal temperature of rats. Mice were found significantly less sensitive to heat at an oral dose of 800 mg/kg ACE, after 60 and 90 min. No anti-inflammatory activity of ACE at an 800 mg/kg dose could be observed in the rat paw assay. An anti-oxidative activity of ACE was observed with an IC 50 value of 47.18 g/ ml. No behavioral or movement change could be observed in mice after oral administration of ACE (800 or 8,000 mg/kg) for seven consecutive days. Interestingly, from the second day of treatment, animals had a significant lower body weight at the 8,000 mg/kg dose of ACE compared to the control. No toxicity was identified and the results of this study state clearly that Aquilaria crassna leaves extracts possess antipyretic, analgesic and anti-oxidative properties without anti-inflammatory activity.

25-hydroxycholesterol, 7β-hydroxycholesterol and 7-ketocholesterol upregulate interleukin-8 expression independently of Toll-like receptor 1, 2, 4 or 6 signalling in human macrophages

Recent studies have shown that Toll-like receptor (TLR)- signalling contributes significantly to the inflammatory events of atherosclerosis. As products of cholesterol oxidation (oxysterols) accumulate within atherosclerotic plaque and have been proposed to contribute to inflammatory signalling in the diseased artery, we investigated the potential of 7-ketocholesterol (7-KC), 7β-hydroxycholesterol (7β-HC) and 25-hydroxycholesterol (25-HC) to stimulate inflammatory signalling via the lipid-recognising TLRs 1, 2, 4 and 6. Each oxysterol stimulated secretion of the inflammatory chemokine interleukin-8 (IL-8), but not I?B degradation or tumour necrosis factor- release from monocytic THP-1 cells. Transfection of TLR-deficient HEK-293 cells with TLRs 1, 2, 4 or 6 did not increase sensitivity to the tested oxysterols. Moreover, blockade of TLR2 or TLR4 with specific inhibitors did not reduce 25-hydroxycholesterol (25-HC) induced IL-8 release from THP-1 cells. We conclude that although the oxysterols examined in this study may contribute to increased expression of certain inflammatory genes, this occurs by mechanisms independent of TLR signalling.