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Davies, R. B., & Clark, G. G. (1974). Trypanosomes from elk and horse flies in New Mexico. J Wildl Dis, 10(1), 63–65.
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Jallon, J. M., Risler, Y., & Iwatsubo, M. (1975). Beef liver L-Glutamate dehydrogenase mechanism: presteady state study of the catalytic reduction of 2.oxoglutarate by NADPH. Biochem Biophys Res Commun, 67(4), 1527–1536.
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Makarov, V. V., & Bakulov, I. A. (1975). [Zoopathogenic arboviruses, their systematics and ecology]. Veterinariia, (11), 39–41.
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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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Sudia, W. D., Fernandez, L., Newhouse, V. F., Sanz, R., & Calisher, C. H. (1975). Arbovirus vector ecology studies in Mexico during the 1972 Venezuelan equine encephalitis outbreak. Am J Epidemiol, 101(1), 51–58.
Abstract: Virus vector studies were conducted in the States of Durango, Chihuahua, and Tamaulipas, Mexico, in June and July 1972. Apparently only a low level of Venzuelan equine encephalitis (VEE) virus transmission to equines occured at the time of the study, and the infection was restricted to areas which had not experienced overt activity during the preceding year. The low level of infection was associated with a scarcity of mosquitoes. The IB (epidemic) strain of VEE virus was isolated from two pools of Anopheles pseudopunctipennis (Theo.) and the blood of one symptomatic equine. The low mosquito population, the relatively few equine cases observed, and the absence of reports of VEE human disease from the outbreak area suggested VEE virus persistence through a low-level mosquito-equine transmission cycle. Other studies have already indicated that wild vertebrates play no more than a minor role in outbreaks of epidemic VEE. Mosquito collections made in areas of the states of Durango, Chihuahua, and Tamaulipas, where considerable epidemic activity of VEE had occurred in 1971, failed to reveal evidence of VEE virus persistence. Twenty-nine ioslations of other arboviruses were also made in these studies: including 22 of St. Louis encephalitis virus (SLE), 2 of Flanders virus, 1 of Turlock virus, 1 of Trivittatus virus of the California Group, 1 of western equine encephalitis virus (VEE), and 2 (from Santa Rose) which possibly represent a hitherto unknown virus in the Bunyamwera Group. These are the first reports of SLE virus isolations from mosquitoes in Mexico, and the first demonstration of Trivittatus, VEE Turlock and Flanders viruses in Mexico from any source.
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Stober, M., & Geiger, J. F. (1975). [Lamenting “moaning” in domestic cattle]. Dtsch Tierarztl Wochenschr, 82(1), 10–13.
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Houpt, K. A. (1976). Animal behavior as a subject for veterinary students. Cornell Vet, 66(1), 73–81.
Abstract: Knowledge of animal behavior is an important asset for the veterinarian; therefore a course in veterinary animal behavior is offered at the New York State College of Veterinary Medicine as an elective. The course emphasizes the behavior of those species of most interest to the practicing veterinarian: cats, dogs, horses, cows, pigs and sheep. Dominance heirarchies, animal communication, aggressive behavior, sexual behavior and maternal behavior are discussed. Play, learning, diurnal cycles of activity and sleep, and controls of ingestive behavior are also considered. Exotic and zoo animal behaviors are also presented by experts in these fields. The critical periods of canine development are related to the optimum management of puppies. The behavior of feral dogs and horses is described. The role of the veterinarian in preventing cruelty to animals and recognition of pain in animals is emphasized. Whenever possible behavior is observed in the laboratory or on film.
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Clutton-Brock, T. H., Greenwood, P. J., & Powell, R. P. (1976). Ranks and relationships in Highland ponies and Highland Cows. Z. Tierpsychol., 41(2), 202–216.
Abstract: Recent studies of primates have questioned the importance of dominance hierarchies in groups living under natural conditions. In a herd of Highland ponies and one of Highland cattle grazing under free-range conditions on the Isle of Rhum (Inner Hebrides) well defined hierarchies were present. The provision of food produced a marked increase in the frequency of agonistic interactions but had no effect on the rank systems of the two herds. While rank was clearly important in affecting the distribution of agonistic interactions, it was poorly related to behaviour in non-agonistic situations.
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Grafner, G., Zimmermann, H., Karge, E., Munch, J., Ribbeck, R., & Hiepe, T. (1976). [Incidence and damages inflicted by simuliid flies in the GDR district of Schwerin]. Angew Parasitol, 17(1), 2–6.
Abstract: Systematic faunal studies in the district Schwerin showed at the present time there are 3 more or less damage-biotopes existing in the districts of Perleberg, Ludwigslust and Parchim; 5 river sources can be considered as potential sources, 5 are temporary and 2 are ephemeral whilst in 3 further areas environmental influences such as effluent impairs the flow of the river and the developmental stages of Simuliidae were not observed.--The following species were found: Boophthora erythrocephala, Wilhelmia salopiensis, Wilhelmia equina, Odagmia ornata, Eusimulium aureum and Eusimulium lundstroemi.--The damage statistics covering the period 1966--1971 showed in the district of Schwerin, due to Simuliid attacks, 38 cattle died, 170 were seriously ill; in 1967 5 horses were seriously ill; in 1971, 3 pigs died and 27 were seriously ill.--The symptoms were manifested by pathological petechiae, scabs and oedema, also by insufficiency of the heart and circulatory system, diminished performance and growth disturbance. In severe cases heart and circulation failure occurred, paresis, coma and death followed.--The real economic significance of the Simuliid attacks rest with its strong and prolonged distrubance in young animals, as well as in pronounced irreparable diminished performance in diseased dairy cattle.
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Dowdle, W. R., & Schild, G. C. (1976). Influenza: its antigenic variation and ecology. Bull Pan Am Health Organ, 10(3), 193–195.
Abstract: Influenza viruses have two surface antigens, the glycoprotein structures hemagglutinin (HA) and neuraminidase (NA). Antibodies to each of these are associated with immunity, but the structures themselves are antigenically variable. When an antigenic change is gradual over time it is referred to as a drift, while a sudden complete or major change in either or both antigens is termed a shift. The mechanism of antigenic drift is usually attributed to selection of preexisting mutants by pressure from increasing immunity in the human population. The mechanism of antigenic shift is less clear, but one tentative hypothesis is that shifts arise from mammalian or avian reservoirs, or through genetic recombination of human and animal influenza strains.
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