No abstract

Cyanobacteria (blue-green algae) commonly occur in fresh- and brackish waters and may produce massive annual growths as a consequence of nutrient enrichment from natural waters, agricultural fertilizer run-off, or from domestic/industrial effluents. The cyanobacterial species which dominate these growths typically belong to the genera which produce toxins. Cyanobacterial toxins cause fatal poisonings of agricultural livestock, wild animals, birds and fish on a world-wide basis. The involvement of the toxins in human health problems has also been inferred in several countries and their presence in drinking water sources is of interest to the drinking water industry. The occurrence and properties of cyanobacterial toxins are discussed here. New methods are being developed for the purification of the toxins and for their recovery and quantification from waters. These include the use of chemical, cytotoxicity and immunological methods to complement the mouse bioassay which has hitherto been used in cyanobacterial toxin studies with laboratory cultures and water samples. Information on the regulation of cyanobacterial toxin production and on the possible biological significance of the toxins in aquatic environments is also presented. A greater awareness of cyanobacterial toxins in waters destined for human use is required.

No abstract

Hypertrophic gastropathy -that is, Menetrier's disease -was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylon gastritis in these patients.

Type B gastritis in its active form is characterized by a dense infiltration of the lamina propria with granulocytes. Since the bacterium Helicobacter pylori does not invade the epithelial barrier, a signaling pathway chemoattractive for granulocytes must exist across this mucosal boarder. One possible mechanism tested was whether granulocytes are directly activated by water-soluble membrane proteins (WSP) from H. pylori. These findings were compared with the effects of WSP from other bacteria (Helicobacter felis, Campylobacter jejuni, Escherichia coli, and Staphylococcus aureus). A unique activation pattern by H. pylori WSP was found. Like all other WSP tested, they induced an upregulation of CD11b but had no influence on CD11c and, most strikingly, CD62L expression. In contrast, E. coli WSP, e.g., not only induce a strong CD11b and CD11c expression but also lead to a loss in surface CD62L. The lack of CD62L shedding conserves rolling of granulocytes along the endothelium, creating a favorable precondition for granulocytes to stick more readily to activated endothelium after H. pylori stimulation via CD11b-CD54 receptor-counterreceptor interaction. This may explain why H. pylori infection is a very strong stimulus for granulocyte infiltration. The active fraction for the induction of CD11b on granulocytes is a heat-and protease-sensitive protein with a molecular mass between 30 and 100 kDa. One activation step involved may be the binding of WSP to CD15 determinants on granulocytes with subsequent induction of CD11b.