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Volume 3, Number 2—June 1997

Synopsis

Polycystic Kidney Disease: An Unrecognized Emerging Infectious Disease?

Marcia A. Miller-Hjelle*, J. Thomas Hjelle*, Monica Jones*, William R. Mayberry†, Mary Ann Dombrink-Kurtzman‡, Stephen W. Peterson‡, Deborah M. Nowak*, and Frank S. Darras*
Author affiliations: *University of Illinois College of Medicine at Peoria, Peoria, Illinois, USA; †East Tennessee State University, Johnson City, Tennessee, USA; ‡U.S. Department of Agriculture, Agricultural Research Service, Peoria, Illinois, USA

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Figure 1

Cascade of biochemical interactions and reactions leading to gel clot formation in the Limulus amebocyte lysate assay. Endotoxin binding to Factor C via the Lipid A moiety results in its activation and in turn the sequential activation of Factor B, which results in the subsequent activation of the proclotting enzyme. Binding of polymyxin B to endotoxin blocks Limulus reactivity in those samples where endotoxin is the initiating molecule. In contrast, (1<!-- INSERT SHAPE PICT -->3)-ß-D-glucans bi

Figure 1. Cascade of biochemical interactions and reactions leading to gel clot formation in the Limulus amebocyte lysate assay. Endotoxin binding to Factor C via the Lipid A moiety results in its activation and in turn the sequential activation of Factor B, which results in the subsequent activation of the proclotting enzyme. Binding of polymyxin B to endotoxin blocks Limulus reactivity in those samples where endotoxin is the initiating molecule. In contrast, (13)-ß-D-glucans bind to a different component, Factor G, in the Limulus assay reagent, thereby leading to its activation and subsequent cascade of reactions to gel formation. The addition of laminarin, an inhibitor of glucan binding to Factor G, to Limulus assay reagent blocks reactivity of samples containing glucan (21).

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