Chapter XI Muscular Dystrophy of the Chicken*

Julian, L. M.; Asmundson, V. S.

doi:10.1159/000388062

Cited by 11 publications

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“…There is, therefore, no simple uncomplicated correlation between DNA content and DNAse II activity in this form of dystrophy. However, in general, throughout most of the course of the disease, both DNA content and DNAse II activity are increased over control values, and in the older dystrophic chickens the increase in DNA content is of the same magnitude as the increase in the number of muscle-cell nuclei [9].…”

Section: Discussionmentioning

confidence: 91%

Enzyme Studies in Muscular Dystrophy VI

Weinstock

Lukacs

1965

Enzymol Biol Clin

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Alterations in the activities of two acid hydrolases, cathepsin and acid deoxyribonuclease, and in noncollagen protein nitrogen and deoxyribonucleic acid content of breast muscle of chickens with hereditary muscular dystrophy have been investigated from the 14-day embryo to 1-year-old chickens. In general, dystrophic muscle has a lower noncollagen protein nitrogen content, and higher deoxyribonucleic acid content, deoxyribonuclease, and cathepsin activity than does control muscle. The relative order of appearance of these changes is deoxyribonucleic acid content, deoxyribonuclease activity, noncollagen protein nitrogen content, cathepsin activity. Cathepsin and deoxyribonuclease values for heterozygous and homozygous controls are essentially the same. Noncollagen protein nitrogen and deoxyribonucleic acid content of heterozygous control muscle are generally similar to those of the homozygous, although by 1 to 3 months they tend to approach dystrophic levels.

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Section: Discussionmentioning

confidence: 91%

Enzyme Studies in Muscular Dystrophy VI

Weinstock

Lukacs

1965

Enzymol Biol Clin

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“…In the case of the dystrophic mouse, at least, this appears to result from altered permeability of the skeletal muscle fibers [18]. Chickens with inherited muscular dystrophy [1,8] exhibit increased plasma aldolase and glutamate-oxaloacetate transaminase activity [4], In this as well as other respects, therefore, the disease of chickens re sembles the muscular dystrophies of man [5] and of the mouse [16]. Because of the high specificity of creatine phosphokinase (CPK) for striated muscle, i.e., high concentration relative to other tissues [3], determination of serum or plasma CPK activity has become useful in clinical and experimental investigations of muscle diseases.…”

mentioning

confidence: 99%

Plasma Creatine Phosphokinase Activity of Chickens with Hereditary Muscular Dystrophy

Ta¹,

Vs²,

Lm³

1965

Enzymol Biol Clin

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Plasma creatine phosphokinase activity (CPK) of hereditarily muscular dystrophic, normal and heterozygous chickens was determined using a method modified from that of Tänzer and Gilvarg. Plasma CPK activity of homozygous dystrophic chickens was significantly higher than that of normal chickens at 27-35 days of age and continued to rise to 131-134 days of age. At ten to 16 months of age plasma CPK activity was lower than at 131-134 days of age, yet still significantly higher than normal. Heterozygotes, sampled at 10 to 16 months of age, revealed significantly higher than normal plasma CPK activity despite great variability with some individual values falling within the normal range.

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“…True or "probable" dystrophies are known in the pig [5], sheep [28,29], goat [4,25]. dog [4], chicken [26], turkey [38], duck [34],mouse [18], mink [20], and Syrian hamster [23]. To our knowledge there are no descriptions of dystrophies in cattle in the literature.…”

Section: Discussionmentioning

confidence: 99%

Dystrophy of the Diaphragmatic Muscles in Adult Meuse-Rhine-Yssel Cattle: Electromyographical and Histological Findings

1983

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Abstract. Electromyographic investigation ofdiaphragmatic muscles of Meuse-Rhine-Yssel cattle revealed a significant decreased duration of action potentials, while the number of polyphasic potentials was increased in four of seven cows. Histologically, the diaphragmatic muscles in all cows were affected severely, as characterized by variation in size of individual fibers, abundant vacuolar and hyaline degeneration with occasional fragmentation and phagocytosis, fiber splitting, apparent increase in internal nuclei, vesicular nuclei, chains of central nuclei, absence of regeneration, and proliferation of endomysial and perimysial connective tissue. Core-like structures seemed to be a hallmark of the disease. The intercostal muscles in all cows had core-like structures and some variation in fiber size; degenerative lesions did occur, but were less severe than in diaphragmatic muscles. In other skeletal muscles and cardiac muscles, core-like structures were present predominantly, indicating a generaIized muscle disorder. No lesions were detected in the peripheral or central nervous systems.The muscular alterations were classified as a progressive muscular dystrophy, with a suspicion of hereditary transmission. This dystrophy may be an important animal model.

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Chapter XI Muscular Dystrophy of the Chicken*

Cited by 11 publications

References 0 publications

Enzyme Studies in Muscular Dystrophy VI

Enzyme Studies in Muscular Dystrophy VI

Plasma Creatine Phosphokinase Activity of Chickens with Hereditary Muscular Dystrophy

Dystrophy of the Diaphragmatic Muscles in Adult Meuse-Rhine-Yssel Cattle: Electromyographical and Histological Findings

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