Behaviour of zinc in electropolished and etched Al-Zn alloys and effect on corrosion potential

The enrichments of zinc developed in binary, solid solution Al–0.3at.%Zn, Al–0.4at.%Zn and Al–1at.%Zn alloys by electropolishing and alkaline etching are examined using Rutherford backscattering spectroscopy and medium energy ion scattering with additional interest in how such enrichments affect the corrosion potentials of the alloys. During alkaline etching in 0.1 M sodium hydroxide solution, significant enrichments of zinc arise in the alloy, similar to that achieved by an anodizing treatment. However, enrichment is unusually low following electropolishing in perchloric acid solution. Contrary to the effect of enriched copper in Al–Cu alloys, zinc enrichment has minor influence on the corrosion potentials of etched alloys in ammonium pentaborate solution, which remain roughly within ±100 mV of those of non-enriched alloys

Up-regulation of prostaglandin E receptor EP2 and EP4 subtypes in rat synovial tissues with adjuvant arthritis

To evaluate the role of the prostaglandin E receptor (EP) subtypes in the development of inflammatory synovitis, we examined EP subtype mRNA distribution in the synovial tissue of rats with adjuvant arthritis and the effect of selective EP agonists on cytokine production by cultured rat synovial cells. We used reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization to measure the level of EP subtype (EP1, EP2, EP3, and EP4) mRNA expression in synovial tissues and cultured synovial cells from the arthritic joints of rats. RT-PCR and ELISA were used to analyse the effects of two selective EP agonists on IL-6 production by cultured rat synovial cells. EP2 and EP4 mRNA expression in inflamed synovial tissues was up-regulated. EP2 and EP4 mRNA were co-expressed in synovial macrophages and fibroblasts in inflamed tissues. EP4 and EP2 agonists both inhibited IL-1-induced IL-6 production. Our results suggest that prostaglandin E2 regulates the functions of synovial macrophages and fibroblasts through EP2 and EP4, which are induced by inflammatory stimuli in rats with adjuvant arthritis