Chapter 1 Microbial pollutants and Diarrhoeal ailments: creation and evaluation (pages 1–13): R. L. Guerrant
Chapter 2 legislation of Water and Ion move in gut (pages 14–33): Don W. Powell, Helen M. Berschneider, Larry D. Lawson and Holger Martenst
Chapter three function of the Mucosal Barrier in Toxin/Microbial Attachment to the Gastrointestinal Tract (pages 34–56): W. Allan Walker
Chapter four pollution which turn on Adenylate Cyclase (pages 57–73): D. Michael Gill and Marilyn Woolkalis
Chapter five pollutants which turn on Guanylate Cyclase: Heat?Stable Enterotoxins (pages 74–93): Mrinalini C. Rao
Chapter 6 STB Enterotoxin of Escherichia coli: Cyclic Nucleotide?Independent Secretion (pages 94–115): Cynthia S. Weikel and Richard L. Guerrant
Chapter 7 Mechanisms wherein Cyclic Nucleotides and different Intracellular Mediators keep watch over Secretion (pages 116–138): Hugo R. De Jonge and Suzanne M. Lohmannt
Chapter eight Secretory Hormones of Entamoeba histolytica (pages 139–154): Katherine McGowan, Victoria Guerina, Joan Wicks and Mark Donowitz
Chapter nine The Pharmacological amendment of Secretory Responses (pages 155–174): Richard J. Miller, David R. Brown, Eugene B. Chang and David D. Friel
Chapter 10 Salmonellosis: looking back and Prospect (pages 177–192): J. Stephen, T. S. Wallis, W. G. Starkey, D. C. A sweet, M. P. Osborne and S. Haddon
Chapter eleven Shigella Toxin and the Pathogenesis of Shigellosis (pages 193–214): Gerald T. Keusch, Arthur Donohue?Rolfe and Mary Jacewicz
Chapter 12 Staphylococcus aureus Delta Toxin as an Entero Toxin (pages 215–229): Frank A. Kapral
Chapter thirteen Clostridial pollutants energetic in the neighborhood within the Gastrointestinal Tract (pages 230–241): Tracy Wilkins, Howard Krivan, Bradley Stiles, Robert Carman and David Lyerly
Chapter 14 Vaccine improvement for the keep watch over of Cholera and similar Toxin?Induced Diarrhoeal illnesses (pages 242–270): Jan Holmgren and Ann?Mari Svennerholm
Chapter 15 Chairman's Summing?Up (pages 271–274): Richard L. Guerrant
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Extra resources for Ciba Foundation Symposium 112 - Microbial Toxins and Diarrhoeal Disease
Holmgren: This complexity of cell types in the gut and the possibility of many messengers of different cellular origin operating on these cells often makes interpretation of the data difficult, even in Ussing chamber experiments. Has any systematic work been done to try to establish artificial epithelia, by using available epithelial cell lines? They are mainly malignant ones, admittedly, but there is now a good number of both colonic and small intestinal cell lines to choose from. Has anyone tried to grow them on artificial semi-porous membranes, getting them to form epithelia which could be investigated from the point of view of both what these cells produce and, more importantly, how they respond to various exogenous stimuli?
Is it known which of these three cell types are the secretory cells? Ruo: It was not the goblet cells that released fluid in the response to prostaglandin EZ, but the vesiculated columnar type of cells. Powell: Dr Krasny and Dr Frizzell (1984) have shown that one group of stimuli, including acetylcholine, do stimulate the goblet cells and result in compound exocytosis of mucus. The prostaglandins stimulated the vesiculated columnar cells, and they saw changes in the apical membrane of those cells, consisting of vesiculation and increases in surface area, much as is seen in the gastric mucosa when it is stimulated to secrete.
Kleinman R, Trier JS, Walker WA 1981b Development of gastrointestinal mucosal barrier. 11. The effect of natural versus artificial feeding on intestinal permeability to macromolecules. Pediatr Res 15:245-249 Virnig NL, Reynolds JW 1974 Epidemiological aspects of neonatal necrotizing enterocolitis. Am J Dis Child 128: 186-190 Walker WA 1981 Intestinal transport of macromolecules. In: Johnson J et al (eds) Physiology of the gastrointestinal tract. Raven Press, New York. chapter 51, p 1271-1289 Walker WA, Bloch KJ 1976 Uptake of antigen-antibody complexes prepared in antibody or antigen excess by normal rat small intestine in v i m .