The "Marshallian" approach assumes a prohibitively high cost of monitoring the sharecropper's activities while the "monitoring" approach argues that landlords stipulate and effectively monitor sharecroppers' activities. I present new evidence using detailed data collected from eight Indian villages. Most tenants own some land of their own; this provides a controlled environment in studying the impact of contractual arrangements. The differences in input and output intensities on owned minus sharecropped land of the same household are found to be sizable and significant, suggesting a rejection of the monitoring approach and supporting the notion of the "Marshallian productive inefficiency" of sharecropping.

The al. (13, 14) indicates that STB induces a rapid short-circuit current across porcine intestinal mucosa. Evidence for chloride transport was not observed, yet electrogenic anion secretion, possibly bicarbonate, was observed in the absence of elevated cyclic nucleotides (14,15). Beyond these few studies, nothing is known of the mechanism of STB action.Evidence that suggests a receptor-mediated mode of STB action includes short-circuit current responses when toxin is delivered to the mucosal, but not serosal, side of intestinal tissue mounted in Ussing chambers (13); a rapid STB response in experiments utilizing either mounted tissue or whole animal models (15 min and 2 hr, respectively) (13,14,16); and the lack of apparent damage to the intestinal mucosa following STB treatment (17,18). Known mediators of membrane signal transduction include cAMP, cGMP, the phosphatidylinositol 4,5-bisphosphate-derived metabolites inositol 1,4,5-trisphosphate (InsP3) and diacyl glycerol, and Ca2W (for reviews, see refs. 19-21

Human and murine receptors for tumor necrosis factor alpha (TNF-a) are present on most somatic cells and have been characterized and cloned. In contrast, very little is currently known about whether TNF-cK can bind to pathogens and whether such binding results in important biological consequences for the infected host. We now report that a number of gram-negative bacteria have receptors for TNF-a. Using '25I-labeled TNF-ax, weshow that ShigeUaflexneri has 276 receptors for TNF-ax, with a Kd of 2.5 nM. The binding of labeled TNF-ae to these bacterial receptors can be inhibited by cold TNF-a but not by cold TNF-13. Binding of 125I-TNF-a to S. flexneri was inhibited by trypsin treatment of bacterial cells or incubation at 52°C for 3 min. Monoclonal antibody to either the 55-kDa or the 75-kDa TNF-aK receptor, which are present on different eukaryotic cells, had no effect on 125I-TNF-a binding to bacteria. A number of gram-negative bacteria were capable of binding 830

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