{'fraction_non_alphanumeric': 0.016227180527383367, 'fraction_numerical': 0.002028397565922921, 'mean_word_length': 5.950704225352113, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Histological study of muscle in the experimental hypophosphatemic rat].

Using hypophosphatemic rat maintained on a low phosphate diet as a model for human rickets and osteomalacia, the skeletal muscle was histochemically and electron microscopically examined, in comparison with specimens obtained from normal control animals. In muscles obtained from hypophosphatemic animals, the type 2 muscle fibers were increased in number, and the type 1 fibers were atrophic. Electron microscopic studies revealed some atypical structures of mitochondria with fusion of cristae in the muscle spindles of intrafusal muscle fibers. The presynapse, the secondary cleft, and the endplate plasm were significantly atrophic in the extrafusal neuromuscular junction. Mitochondrial vacuolization was observed in the presynapse. These results indicated the presence of immature muscle fibers, dysfunction of the energy metabolism of the mitochondria and neurogenic disorders in hypophosphatemic muscles.