JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology.Abstract. We investigated the spatial synchrony of outbreaks of the spruce budworm, Choristoneurafumiferana, over much of its outbreak range in eastern North America during the period 1945-1988. Spatial synchrony decreased with distance between local populations and approached zero near 2000 km. Investigation of the synchrony of local population time series with cluster analysis revealed a pattern of geographically distinct blocks of clusters oriented along an east-west axis. Spatial synchrony also was identified in monthly temperature and precipitation time series at 18 weather stations over the same time period and geographical range as the spruce budworm outbreaks. Cross correlations decreased linearly with distance between stations and approached zero near 3000 km and 1800 km, respectively. We developed a spatially explicit lattice model for a single species occupying multiple patches. Within patches, the model had first order logistic dynamics, and patches were linked by dispersal that depended upon their separation distances. Both local and regional stochasticity (i.e., a Moran effect) were present. The modeled lattice had the same spatial configuration as the outbreak region to facilitate investigating the relative effects of a Moran effect and dispersal on spatial synchrony. Simulations with and without a simple regionwide Moran effect and three levels of dispersal did not produce the decrease in spatial synchrony with distance observed with spruce budworm time series. However, when run at the highest dispersal rate, those simulations produced cluster maps similar to that observed for spruce budworm defoliation. Simulations with a spatially autocorrelated disturbance that had either zero or high local variability and three levels of dispersal produced decreases in spatial synchrony with distance similar to that observed in the historical data. When run at the highest dispersal rate, simulations yielded cluster maps similar to the cluster map for defoliation. We discuss the potential significance of the spatially autocorrelated disturbance factor in understanding regional insect outbreaks. We also consider the plausibility of dispersal rates used in our simulations. We suggest in conclusion that spruce budworm outbreaks were synchronized by a combination of a spatially autocorrelated Moran effect and a high dispersal rate.

This article discusses the early history of performance and productivity measurement. It finds sophisticated development of these tools beginning in the first decade of the twentieth century, primarily at the New York Bureau of Municipal Research. These practices grew out of accounting, the social survey, work records, and municipal statistics. The bureau built government's capacity to measure. They advocated such basic empirical practices as making observations at all, doing so systematically and routinely, and recording data at the time of observation. By 1912, performance measurement exhibited many of the features associated with the modern practice: measuring of input, output, and results; attempting to make government more productive; making reports comparable among communities; and focusing on allocation and accountability. Performance measurement was developed in the context of shifting power between the elected executive and the legislature.

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Tumor necrosis factor-alpha was detected in supernatants collected from BALB/c mouse peritoneal macrophages incubated continuously with Histoplasma capsulatum. The levels of TNF alpha measured by actinomycin D bioassay peaked within hours after exposure and then greatly declined by 24 h. TNF alpha was also measured in bronchoalveolar lavage fluid from BALB/c mice challenged intranasally with H. capsulatum. Lavage fluid TNF alpha levels exhibited the same pattern as the in vitro supernatants; they peaked within hours after challenge and lower levels were detected at 24 h. Treatment of mice with anti-TNF alpha antibody accelerated mortality in response to systemic infection and significantly increased tissue colony counts in the liver and spleen. In the murine model, TNF alpha is produced in response to H. capsulatum and appears to play some role in host defense to infection.

Athymic nude mice (nu/nu) were significantly more susceptible to pneumonia due to the agent of mouse pneumonitis (MoPn), Chlamydia trachomatis, than their heterozygous (nu/+) littermates, as judged both by a greater mortality and a decreased ability to rid their lungs of the infection. Nu/nu mice did not produce significant antibody to the MoPn agent, whereas nu/+ mice did. Thymic transplantation rendered nu/nu mice significantly more resistant to the MoPn agent than nu/nu controls. Resistance to the MoPn agent and production of specific antibody to the MoPn agent were dependent on thymus-derived cells.