Abstract
WITHIN the framework of our investigations of the pathogenesis of progressive muscular dystrophy (Erb)1, we assumed as a hypothesis a genetically fixed defect in electrons and energy transport of the cell, to explain the symptoms of the disease, as known so far, such as variation of myoglobin, disorder in the ionic system, enzymes leaving the cytoplasmic and mitochondrial compartment of the muscular cell, etc.
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References
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KLEINE, T. Localization of Creatine Kinase in Microsomes and Mitochondria of Human Heart and Skeletal Muscle and Cerebral Cortex. Nature 207, 1393–1394 (1965). https://doi.org/10.1038/2071393a0
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DOI: https://doi.org/10.1038/2071393a0
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