By Karl Maramorosch
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Additional resources for Advances in cell culture. Volume 4
1979a). However, the results were variable even with these methods. Thompson et al. (1977) found a peculiar clustering and piling up of cells in DMD muscle cultures, but similar cell clumps were also seen occasionally in cultures from controls or patients with other neuromuscular disorders, suggesting that this growth pattern, even if related to the primary DMD lesion, is not a sensitive morphologic maker of the disease (Ecob-Johnston and Brown, 1981; Thompson et al, 1981). , 1982). , 1982). More recent clonal analysis by Blau et al.
Am. J. Hum. Genet. 26, 59-64. , and DiMauro, S. (1977). Neurology 27, 178-184. Meienhofer, M. , Dreyfus, J - C , and Engel, W. K. (1977). Arch. NeuroL 34, 7 9 9 - 7 8 1 . , and Appel, S. (1982). In "(Disorders of the Motor Unit" (D. L. ), pp. 889-898. Wiley, New York. Miranda, A. F. (1974). J. Cell. Biol. ). Miranda, A. , and Godman, G. C. (1973). Tissue Cell 5, 1-22. Miranda, A. , and Mongini, T. (1983). In "Neuromuscular Diseases" (G. ), pp. 3 6 5 - 3 7 1 . Raven, New York. Miranda, A. , and Mongini, T.
4. Hereditary metabolic myopathies in which the biochemical defect is not known and which are not apparently expressed in muscle cultures may well be due to genetic defects of mature muscle isozymes. 3. Lysosomal Disorders Affecting Muscle a. Acid Maltase (AM:a-Glucosidase) Deficiency. AM is a lysosomal hydrolase that catalyzes the degradation of glycogen, acting on a-1-4 and on a-1-6 glycosyl linkages (Engel, 1984a; Fig. 2). , 1979). Normal muscle does not contain many lysosomes, but lysosomal glycogen degradation is nevertheless crucial for normal muscle function, since deficiency of AM (AMD) in its most severe form (Pompe disease) is generally lethal within the first year of life.
Advances in cell culture. Volume 4 by Karl Maramorosch