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Hardy, J. L. (1987). The ecology of western equine encephalomyelitis virus in the Central Valley of California, 1945-1985. Am J Trop Med Hyg, 37(3 Suppl), 18s–32s.
Abstract: Reeves' concept of the summer transmission cycle of western equine encephalomyelitis virus in 1945 was that the virus was amplified in a silent transmission cycle involving mosquitoes, domestic chickens, and possibly wild birds, from which it could be transmitted tangentially to and cause disease in human and equine populations. Extensive field and laboratory studies done since 1945 in the Central Valley of California have more clearly defined the specific invertebrate and vertebrate hosts involved in the basic virus transmission cycle, but the overall concept remains unchanged. The basic transmission cycle involves Culex tarsalis as the primary vector mosquito species and house finches and house sparrows as the primary amplifying hosts. Secondary amplifying hosts, upon which Cx. tarsalis frequently feeds, include other passerine species, chickens, and possibly pheasants in areas where they are abundant. Another transmission cycle that most likely is initiated from the Cx. tarsalis-wild bird cycle involves Aedes melanimon and the blacktail jackrabbit. Like humans and horses, California ground squirrels, western tree squirrels, and a few other wild mammal species become infected tangentially with the virus but do not contribute significantly to virus amplification.
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Sabattini, M. S., Monath, T. P., Mitchell, C. J., Daffner, J. F., Bowen, G. S., Pauli, R., et al. (1985). Arbovirus investigations in Argentina, 1977-1980. I. Historical aspects and description of study sites. Am J Trop Med Hyg, 34(5), 937–944.
Abstract: This is the introductory paper to a series on the ecology of arboviruses in Argentina. Epizootics of equine encephalitis have occurred since at least 1908, principally in the Pampa and Espinal biogeographic zones, with significant economic losses; human cases of encephalitis have been rare or absent. Both western equine and eastern equine encephalitis viruses have been isolated from horses during these epizootics, but the mosquitoes responsible for transmission have not been identified. A number of isolations of Venezuelan equine encephalitis (VEE) virus were reported between 1936 and 1958 in Argentina, but the validity of these findings has been seriously questioned. Nevertheless, serological evidence exists for human infections with a member of the VEE virus complex. Serological surveys conducted in the 1960s indicate a high prevalence of infection of humans and domestic animals with St. Louis encephalitis (SLE), and 2 SLE virus strains have been isolated from rodents. Human disease, however, has rarely been associated with SLE infection. Only 7 isolations of other arboviruses have been described (3 of Maguari, 1 of Aura, 2 of Una, and 1 of an untyped Bunyamwera group virus). In 1977, we began longitudinal field studies in Santa Fe Province, the epicenter of previous equine epizootics, and in 1980 we extended these studies to Chaco and Corrientes provinces. The study sites are described in this paper.
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Bast, T. F., Whitney, E., & Benach, J. L. (1973). Considerations on the ecology of several arboviruses in eastern Long Island. Am J Trop Med Hyg, 22(1), 109–115.
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Scherer, W. F., & Dickerman, R. W. (1972). Ecologic studies of Venezuelan encephalitis virus in southeastern Mexico. 8. Correlations and conclusions. Am J Trop Med Hyg, 21(2), 86–89.
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Manning, G. S., & Ratanarat, C. (1970). Fasciolopsis buski (Lankester, 1857) in Thailand. Am J Trop Med Hyg, 19(4), 613–619.
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Scherer, W. F., Dickerman, R. W., & Ordonez, J. V. (1970). Discovery and geographic distribution of Venezuelan encephalitis virus in Guatemala, Honduras, and British Honduras during 1965-68, and its possible movement to Central America and Mexico. Am J Trop Med Hyg, 19(4), 703–711.
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Lonon, A. M., & Zentall, T. R. (1999). Transfer of value from S+ to S- in simultaneous discriminations in humans. Am J Psychol, 112(1), 21–39.
Abstract: When animals learn a simultaneous discrimination, some of the value of the positive stimulus (S+) appears to transfer to the negative stimulus (S-). The present experiments demonstrate that such value transfer can also be found in humans. In Experiment 1 humans were trained on 2 simple simultaneous discriminations, the first between a highly positive stimulus, A (1,000 points); and a negative stimulus, B (0 points); and the second between a less positive stimulus, C (100 points); and a negative stimulus, D (0 points). On test trials, most participants preferred B over D. In Experiments 2 and 3 the value of the 2 original discriminations was equated in training (A[100]B[0] and C[100]D[0]). In Experiment 2 the values of the positive stimuli were then altered (A[1,000]C[0]); again, most participants preferred B over D. In Experiment 3, however, when the values of B and D were altered (B[1,000]D[0]), participants were indifferent to A and C. Thus, the mechanism that underlies value transfer in humans appears to be related to Pavlovian second-order conditioning. Similar mechanisms may be involved in assimilation processes in social contexts.
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Previc, F. H. (2002). Thyroid hormone production in chimpanzees and humans: implications for the origins of human intelligence. Am J Phys Anthropol, 118(4), 402–3; discussion 404–5.
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Scott, L. D. (2006). Living donor liver transplant--is the horse already out of the barn? Am J Gastroenterol, 101(4), 686–688.
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Scherer, W. F., Madalengoitia, J., Flores, W., & Acosta, M. (1975). Ecologic studies of Venezuelan encephalitis virus in Peru during 1970-1971. Am J Epidemiol, 101(4), 347–355.
Abstract: Venezuelan encephalitis (VE) virus has intermittently produced epidemics and equine epizootics on the dry Pacific coastal plain of Peru since at least the 1930's. However, evidence that the virus exists in the Amazon region of Peru to the east of the Andes mountains was not obtained until antibodies were found in human sera collected in 1965, and 10 strains of the virus were isolated in a forest near the city of Iquitos, Peru during February and March 1971. Eight strains came from mosquitoes and two from dead sentinel hamsters. Three hamsters exposed in forests near Iquitos developed VE virus antibodies suggesting that hamster-benign strains also exist there. Antibody tests of equine sera revealed no evidence that VE virus was actively cycling during the late 1950's or 1960's in southern coastal Peru, where equine epizootics had occurred in the 1930's and 1940's. In northern coastal Peru bordering Ecuador, antibodies were present in equine sera, presumably residual from the 1969 outbreak caused by subtype I virus, since neutralizing antibody titers were higher to subtype I virus than to subtypes III or IV. No VE virus was detected in this northern region during the dry season of 1970 by use of sentinel hamsters. The possibility is considered that VE epidemics and equine epizootics on the Pacific coast of Peru are caused by movements of virus in infected vertebrates traversing Andean passes or in infected vertebrates or mosquitoes carried in airplanes from the Amazon region.
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