4,132 research outputs found

    Autocracy, democracy, bureaucracy, or monopoly: can you judge a government by its size?

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    We develop a simple theoretical framework to examine on an integrated basis how the form of government affects its power and size. The analytical framework abstracts from distortions that arise from the means ofgovernment finance and separates government power into two dimensions-pure coercive power and pure monopoly power. A government can exert its coercive power to shift the demand for its services outward and/or its monopoly power to restrict the output along a given demand curve to earn rents. Among the implications drawn from the analysis are that government officials have an incentive to provide a non-optimal combination of taxes and services, and that neither size nor rents alone are reliable indicators of the extent to which government fails to achieve optimality in its provision of services.Finance ; Power resources

    THE EFFECT OF RETRIBUTION ON SHAREHOLDER LITIGATION AND MANAGERS' REPORTS

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    Shareholder litigation is important because it is costly and can influence firms' reporting behavior. Prior research finds that attorneys' incentives and specific firm characteristics drive shareholder litigation. In this study, I control for these known drivers in order to examine whether an additional behavioral factor, investor retribution, also drives shareholder litigation. Retribution theory suggests that investors will initiate litigation to punish managers for misreporting even when there is no financial incentive to do so. My study uses experimental markets to examine whether retribution plays a role in investors' litigation decisions, and if this, in turn, affects managers' reporting decisions. Consistent with economic theory, I find that when investors do not have an option to initiate litigation, managers frequently misreport and investors do not find their reports credible. Further, when investors have an option to initiate litigation and a financial incentive to do so (similar to current securities laws), misreporting decreases and the credibility of managers' reports increases. However, inconsistent with economic theory but consistent with retribution theory, when investors have an option to initiate litigation but have no financial incentive to do so, misreporting decreases and the credibility of managers' reports increases to approximately the same level as when investors have a financial incentive to initiate litigation. These findings have important implications for regulators and managers who need to accurately anticipate investors' litigation decisions in order to make optimal policy and reporting decisions

    Biofilm-stimulated epithelium modulates the inflammatory responses in co-cultured immune cells

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    The gingival epithelium is a physical and immunological barrier to the microbiota of the oral cavity, which interact through soluble mediators with the immune cells that patrol the tissue at the gingival epithelium. We sought to develop a three-dimensional gingivae-biofilm interface model using a commercially available gingival epithelium to study the tissue inflammatory response to oral biofilms associated with “health”, “gingivitis” and “periodontitis”. These biofilms were developed by sequential addition of microorganisms to mimic the formation of supra- and sub-gingival plaque in vivo. Secondly, to mimic the interactions between gingival epithelium and immune cells in vivo, we integrated peripheral blood mononuclear cells and CD14+ monocytes into our three-dimensional model and were able to assess the inflammatory response in the immune cells cultured with and without gingival epithelium. We describe a differential inflammatory response in immune cells cultured with epithelial tissue, and more so following incubation with epithelium stimulated by “gingivitis-associated” biofilm. These results suggest that gingival epithelium-derived soluble mediators may control the inflammatory status of immune cells in vitro, and therefore targeting of the epithelial response may offer novel therapies. This multi-cellular interface model, both of microbial and host origin, offers a robust in vitro platform to investigate host-pathogens at the epithelial surface

    Economic inequality increases risk taking

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    Income inequality is rising around the world. Increased income inequality has been linked with higher rates of crime, greater debt, and poorer health, but the mechanisms linking inequality to poor outcomes among individuals are poorly understood. This research tested a behavioral account linking inequality to individual decision making. The account suggests that more unequal outcomes lead people to perceive that they need more resources to be satisfied. Higher perceived needs, in turn, motivate greater risk taking to meet those needs. Results of three experiments and an analysis of large-scale internet search data supported the proposed account. Results suggest that inequality may promote a range of poor outcomes, in part, by increasing risky behavior

    A Positive Relationship Between Religious Faith and Forgiveness: Faith in the Absence of Data?

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    Religious faith and beliefs appear to play an important role in the lives of many individuals and are the topic of much research. The present study investigated the relationship between religious faith and forgiveness in a sample (n = 196) of college students. Students were asked to complete the Heartland Forgiveness Scale and the Santa Clara Strength of Religious Faith Questionnaire. Analyses of scores on both measures revealed a positive, significant correlation between these constructs, suggesting that there is a meaningful relationship between religious faith and the tendency to forgive. Implications and directions for further research are discussed

    Subcompartments of the macrophage recycling endosome direct the differential secretion of IL-6 and TNFα

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    Activated macrophages secrete an array of proinflammatory cytokines, including tumor necrosis factor-α (TNFα) and interleukin 6 (IL-6), that are temporally secreted for sequential roles in inflammation. We have previously characterized aspects of the intracellular trafficking of membrane-bound TNFα and its delivery to the cell surface at the site of phagocytic cups for secretion (Murray, R.Z., J.G. Kay, D.G. Sangermani, and J.L. Stow. 2005. Science. 310:1492–1495). The trafficking pathway and surface delivery of IL-6, a soluble cytokine, were studied here using approaches such as live cell imaging of fluorescently tagged IL-6 and immunoelectron microscopy. Newly synthesized IL-6 accumulates in the Golgi complex and exits in tubulovesicular carriers either as the sole labeled cargo or together with TNFα, utilizing specific soluble NSF attachment protein receptor (SNARE) proteins to fuse with the recycling endosome. Within recycling endosomes, we demonstrate the compartmentalization of cargo proteins, wherein IL-6 is dynamically segregated from TNFα and from surface recycling transferrin. Thereafter, these cytokines are independently secreted, with TNFα delivered to phagocytic cups but not IL-6. Therefore, the recycling endosome has a central role in orchestrating the differential secretion of cytokines during inflammation

    Regulation of succinate-fuelled mitochondrial respiration in liver and skeletal muscle of hibernating thirteen-lined ground squirrels.

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    Hibernating ground squirrels (Ictidomys tridecemlineatus) alternate between two distinct metabolic states throughout winter: torpor, during which metabolic rate (MR) and body temperature (Tb) are considerably suppressed, and interbout euthermia (IBE), during which MR and Tb briefly return to euthermic levels. Previous studies showed suppression of succinate-fuelled respiration during torpor in liver and skeletal muscle mitochondria; however, these studies used only a single, saturating succinate concentration. Therefore, they could not address whether mitochondrial metabolic suppression occurs under physiological substrate concentrations or whether differences in the kinetics of mitochondrial responses to changing substrate concentration might also contribute to mitochondrial metabolic regulation during torpor. The present study confirmed that succinate oxidation is reduced during torpor in liver and skeletal muscle at 37 and 10°C over a 100-fold range of succinate concentrations. At 37°C, this suppression resulted from inhibition of succinate dehydrogenase (SDH), which had a greater affinity for oxaloacetate (an SDH inhibitor) during torpor. At 10°C, SDH was not inhibited, suggesting that SDH inhibition initiates but does not maintain mitochondrial suppression during torpor. Moreover, in both liver and skeletal muscle, mitochondria from torpid animals maintained relatively higher respiration rates at low succinate concentrations, which reduces the extent of energy savings that can be achieved during torpor, but may also maintain mitochondrial oxidative capacity above some lower critical threshold, thereby preventing cellular and/or mitochondrial injury during torpor and facilitating rapid recruitment of oxidative capacity during arousal
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