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Summary: The pathogenesis of intestinal metaplasia (IM) of the human stomach remains completely unknown. Several classifications of IM have been suggested. Recent investigators have examined epithelial cell phenotypes in IM through immunohistochemistry, and revealed that gastric IM glands consist of a mixture of gastric and intestinal cell phenotypes. This implies that a heterogeneous cell population with both gastric and intestinal phenotypes would develop into a single intestinal phenotype. Recently, an intestinal stem cell marker was found to be present in the putative position of human gastric glands, whereas it was absent in gastric IM glands. This supports the assumption that IM is a consequence of abnormal stem cell differentiation, leading to lack of differentiation into any of the normal intestinal epithelial phenotypes. Recent advances in molecular biology have revealed intestinal transcriptional factors (Cdx1/Cdx2), suggesting that upregulation of Cdx2 may trigger the initiation and development of IM in the stomach. Epidemiological evidence indicates that Helicobacter pylori is a major cause of IM but might not be solely responsible for its induction. A variation in host and bacterial background that predisposes to the development of IM has been revealed. [Copyright &y& Elsevier]

Abstract: We examined whether soluble mediators regulate the expression of tachykinin receptor mRNAs in synovial fibroblasts of patients with rheumatoid arthritis (RA). mRNAs encoding long and short isomers of neurokinin 1 receptor (NK1R), and neurokinin 2 receptor (NK2R) were confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Level of long, but not the short, of NK1R mRNA was increased by treatment with 10–100ng/ml basic fibroblast growth factor (bFGF) or 20ng/ml tumor necrosis factor-α (TNF-α), but not with 1ng/ml interleukin 1β (IL-1β). TNF-α upregulated NK2R mRNA as well as long NK1R mRNA whereas bFGF had no effect on NK2R mRNA. Expression of neurokinin 3 receptor (NK3R) mRNA was not observed in RA fibroblasts, and its expression was not induced by bFGF and TNF-α. The basal and increased levels of long NK1R mRNA were inhibited by treatment with 20μM SU5402, an inhibitor of the tyrosine kinase activity of FGF receptor 1 (FGFR1), or 10ng/ml transforming growth factor-β1 (TGF-β1). SU5402 and TGF-β1 had no effect on the basal level of short NK1R mRNA. Immunocytochemistry revealed the enhancement by bFGF of immunoreactive NK1Rs in the cells at 24h after treatment. These results suggest that bFGF, TGF-β1, and TNF-α in synovial tissue and fluid play a role in the regulation of long NK1R expression in synovial fibroblasts of RA patients. It appears that the pathway of downregulation by TGF-β1 is more dominant in the long NK1R mRNA expression than that of upregulation by bFGF or TNF-α. Furthermore, the regulation of short NK1R mRNA expression seems to be performed via a different pathway from that of long isomer mRNA. [Copyright &y& Elsevier]

We have examined the reaction characteristics of the shift reaction for Ni/Mo/TiO 2 catalyst (Ni/Mo/Ti) which is a sulfur-tolerant water gas shift catalyst (sour shift catalyst). We used a bench-scale apparatus and the actual coal gasification gas (actual gas) which included COS and HCN as the competing reaction materials for the shift reaction. From the catalyst inlet temperature dependence of the shift reaction at the H 2 O/CO ratio of 1.2 mol/mol, it appeared that the reaction starting temperature was less than 200 °C. In addition, for Co/Mo/Al 2 O 3 catalyst (Co/Mo/Al) as a comparison catalyst, gas hour space velocities (GHSVs) to reach chemical equilibrium was calculated by static characterization analysis using E a and A obtained from the actual experiment for the catalyst inlet temperature of 200 °C and the H 2 O/CO ratio of 1.2 mol/mol. As a result, we confirmed that GHSV of Ni/Mo/Ti was 5 times more than that of Co/Mo/Al, that is, the catalyst quantity of Ni/Mo/Ti can be decreased to 1/5 that of Co/Mo/Al for the above conditions. Furthermore, we confirmed that COS and HCN were sufficiently reacted on Ni/Mo/Ti. [ABSTRACT FROM AUTHOR]