Animal model of human disease. Alpha-antitrypsin deficiecy. Animal model: Round heart disease of turkeys.
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The zinc content of the liver and the thigh muscle of the rat were measured by means of atomic absorption spectrophotometry under different conditions: standard diet, carbohydrate diet, an experimental dystrophy model and its recovery period. The influence of a parental mineral substitution on the whole body and the organ weight was studied. Carbohydrate diet caused a lower rise of the whole body weight, a decrease of the zinc content of the liver and an increase of the zinc content of the thigh muscle. In dystrophy model, the liver weight decreased to one fifth of the controls. The zinc concentration of the liver increased markedly, the zinc content of the whole liver is equal to that of control animals. The thigh muscle showed an increase of the zinc content, too. The parenteral mineral application had no effect upon the whole body weight and the organ weights. Little influences on the zinc content of the skeletal muscle were seen. The zinc content of parenchymatous organs varies markedly, and it is influenced by diets and disease. In the dystrophy model, zinc is concentrated in atrophic organs in order to protect the organism against zinc deficiency.
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The sedative effectiveness of apomorphine in a newly developed animal model of Huntington's disease was examined. The motor responses of rats with kainic acid lesions of the neostriatum to a sedative dose of apomorphine (50 micrograms/kg) was similar to that observed in intact controls. In contrast, compared to controls, a marked potentiation of the motor stimulant effects of dextroamphetamine was confirmed in the kainic acid-lesioned group. We suggest that the pathological changes underlying the symptoms observed in this animal model and in Huntington's disease do not include abnormalities in presynaptic dopamine receptors in the neostriatum.
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