PROTASPIDES OF UPPER CAMBRIAN APHELASPIS (PTYCHOPARIIDA, TRILOBITA) AND RELATED SPECIES WITH THEIR TAXONOMIC IMPLICATIONS

Abstract:  The ontogeny of Aphelaspis brachyphasis is illustrated and described on the basis of newly discovered silicified material from the McGill section, Nevada, USA. Protaspides of three other Aphelaspis species are redescribed. Of ptychopariide species for which protaspides have been documented, the protaspides of those previously considered to be closely related to Aphelaspis are illustrated herein. Protaspides of Aphelaspis are most similar to those of Olenus , supporting previous taxonomic suggestions that the Aphelaspidinae is closely related to the Olenidae and may be assigned to the Olenacea. The protaspides of Housia share few similarities with those of Aphelaspis , contradicting the hypothesis that these genera are placed together within the Pterocephaliidae.     

A Model Approach for Studying Race: Provocative Theory, Sound Science, and Very Good History

The Problem of Race in the Twenty-First Century. Thomas C. Holt. Cambridge, MA: Harvard University Press, 2002. 146 pp.
Race in Mind: Race, IQ, and Other Racisms. Alexander Alland Jr. New York: Palgrave Macmillan, 2002. 219 pp.
The Funding of Scientific Racism: Wickliffe Draper and the Pioneer Fund. William H. Tucker. Urbana: University of Illinois Press, 2002. 286 pp.     

Macrolide-affected Toll-like receptor 4 expression from Helicobacter pylori-infected monocytes does not modify interleukin-8 production

Macrolide antibiotics have an anti-inflammatory effect by suppressing lipopolysaccharide-induced IL-8 production. IL-8 secretion from monocytes is observed in Helicobacter pylori infection. Although cag gene products are known to induce IL-8 secretion, whether other bacterial substances can initiate the reaction is not determined. In this study, we show that clarithromycin induced down-regulation of Toll-like receptor 4 expression and did not lead to a decrease in IL-8 production and H. pylori lipopolysaccharide. However, Toll-like receptor 4 activation was possibly not the main cause in the induction of inflammation during H. pylori infection.     

Prostaglandin E2 induces MUC8 gene expression via a mechanism involving ERK MAPK/RSK1/cAMP response element binding protein activation in human airway epithelial cells

MUC8 gene expression is overexpressed in nasal polyp epithelium and is also increased by treatment with inflammatory mediators in nasal epithelial cells. These data suggest that MUC8 may be one of important mucin genes expressed in human airway. However, the mechanisms of various inflammatory mediator-induced MUC8 gene expression in normal nasal epithelial cells remain unclear. We examined the mechanism by which prostaglandin E(2) (PGE2), an arachidonic acid metabolite, increases MUC8 gene expression levels. Here, we show that ERK mitogen-activated protein kinase is essential for PGE2-induced MUC8 gene expression in normal human nasal epithelial cells and that p90 ribosomal S 6 protein kinase 1 (RSK1) mediates the PGE2-induced phosphorylation of cAMP-response element binding protein. Our results also indicate that cAMP-response element at the -803 region of the MUC8 promoter is an important site of PGE2-induced MUC8 gene expression. In conclusion, this study gives insights into the molecular mechanism of PGE2-induced MUC8 gene expression in human airway epithelial cells.