Hypervitaminosis A in the chick.
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Biomedical subjects
Publications and source records attributed to J M Howell.
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A 61-year-old white male with recurrent thrombophlebitis developed a painful left arm. He was initially diagnosed with superficial thrombophlebitis and treated conservatively for several days without improvement. He subsequently developed right-sided pulmonary embolism. Hypercoagulability was not present, and venography confirmed the left basilic vein as the sole thrombogenic source. Twelve to twenty percent of documented pulmonary emboli arise from deep veins of the upper extremity. To our knowledge, only one case of basilic vein thrombosis causing pulmonary embolism exists in the literature. Clinical vigilance to this uncommon entity may reduce attendant morbidity and mortality.
Xiphodynia is an uncommon musculoskeletal disorder that mimics a number of common abdominal and thoracic diseases. We report three cases of xiphodynia. The diagnosis is suggested when a given patient's chest or abdominal discomfort is completely or almost completely reproduced with light pressure on the xiphoid process. Local injection with an anesthetic-steroid combination is frequently curative. No more than 5 to 7 mL of solution should be injected, and results are variable when several trigger points are found on the anterior chest wall. Tack hammer deformity of the xiphoid, another cause of xiphoid pain, has been successfully treated with surgical excision.
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Generalized Glycogenosis type II has been diagnosed in seven calves from a herd of cattle maintained at the Murdoch University Veterinary School Farm. The syndromes seen are equivalent to the infantile and childhood forms of the disease in humans. In the brain and spinal cord of the calves acid alpha-glucosidase activity was depressed and glycogen deposition was markedly increased. Swelling, vacuolation and glycogen deposition was present in neurones of the central and autonomic nervous systems and retina, in glia and in Schwann cells and fibroblasts within peripheral nerves. The distribution was similar to that seen in human cases. The glycogen was both membrane bound and free within the cytoplasm. Changes similar to those seen in axonal dystrophy were present and some nerve fibres showed Wallerian degeneration. Evidence of nerve cell destruction and nerve cell loss were not seen and the predominant clinical signs were related to muscle weakness.
Progressive changes in acid alpha-glucosidase activity, glycogen content and light microscopical and ultrastructural features in skeletal muscle of calves affected by generalized glycogenosis type II were assessed in biopsies from semitendinosus muscle of nine affected, twenty-six carrier and fifteen normal calves taken at varying times between birth and 17 months of age. Affected animals could be identified by using the PAS technique on paraffin and epon embedded material or by electron microscopy. However, estimation of acid alpha-glucosidase activity was required for precise diagnosis of generalized glycogenosis type II or to distinguish between normal and carrier animals. The glycogen content of the semitendinosus muscle of affected animals was approximately three times that in non-affected animals and although storage of glycogen reached a plateau soon after birth, the muscle fibre damage seen in very young calves increased with age. Morphological evidence of glycogen accumulation, both within the cytoplasm and within membrane bound structures, was present at birth. In some animals evidence of muscle fibre regeneration and damage was seen in the same sections.
The biochemical and morphological properties of cultured skeletal muscle from calves born into a herd of cattle, which are heterozygous for glycogenosis type II, were studied over 17 days. Muscle was cultured by a modification of the explant technique in which the mononucleated cells that grew from the explants were subcultured. Skeletal muscle from animals up to 15 months of age grew in culture to produce mature, cross-striated and spontaneously contractile myotubes. The creatine kinase activity was 310 (+/- 45.4) mU/mg protein on day 7 when fusion was complete, and 210 (+/- 15.1) mU/mg protein on day 17 of culture. Mature muscle cultures from animals affected by glycogenosis type II showed the characteristic biochemical and morphological abnormalities previously observed in vivo. Acid alpha-glucosidase activity was absent whereas the activities of neutral alpha-glucosidase, lysosomal alpha-mannosidase and creatine kinase were the same as in cultures of unaffected muscle. The concentration of glycogen was higher in cultured affected muscle than in cultured unaffected muscle. On days 7, 9 and 17 of culture the glycogen concentrations were 66.7 (+/- 2.7), 89.0 (+/- 5.5) and 120.3 (+/- 34.2) micrograms/mg protein respectively in affected muscle and 51.8 (+/- 3.6), 59.9 (+/- 5.4) and 55.4 (+/- 1.0) micrograms/mg protein respectively in non-affected muscle. Electron microscopic studies showed that the glycogen accumulated within the lysosomes. These results indicate that bovine glycogenosis type II is expressed in tissue culture since the cultured skeletal muscle from affected animals shows the same abnormalities as skeletal muscle in vivo.
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