The possible role of glucose-pentapeptides extracted from erythrocyte membranes in the regulation of glucose transport [proceedings].
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Biomedical subjects
Publications and source records attributed to R J Davis.
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A retrospective study was carried out of 48 patients who underwent ankle arthrodesis for tramatic arthritis from January 1967 through January 1976. Following ankle fusion, the most common complaint was subtalar pain and the most frequent finding was limitation of subtalar motion (56%). Subtalar or triple arthrodesis was required in 12 patients, with good results in the majority of the cases. An infection rate of 22% was encountered, felt to be consequent to the failure to properly employ prophylactic antibiotics; which, when employed, were associated with less than 6% incidence of sepsis 69% of patients were improved from their status before ankle arthrodesis; 12% had come to below-knee amputation (three for resistant pain, two for chronic osteomyelitis, and one for vascular insufficiency). Fusion of the subtalar joint seems curative, and early mobilization of the subtalar joint, by ankle fusion techniques that do not immobilize the entire foot may play a preventive role.
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Cardiac conduction abnormalities are frequent in myotonic dystrophy and can result in complete heart block. In a study of 26 patients with myotonic dystrophy, first degree heart block was found to precede clinical presentation of the disease in 7 patients. His bundle electrocardiography in 11 patients demonstrated abnormalities throughout the entire conducting system, even in patients with only first degree heart block. In patients with block of the right bundle branch or anterior fascicle of the left bundle branch, slowing in the remaining fascicles was always present. Therapy of myotonia with procainamide significantly lengthened the P-R interval, and treatment with diphenylhydantoin significantly shortened the P-R interval suggesting that diphenylhydantoin may be preferable for therapy of myotonia in patients with myotonic dystrophy.
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The effects of urea on the rate of efflux of preloaded taurine and volume regulation have been examined in incubated minislices from rat superficial cerebral cortex. As external urea was increased in the range 0-100 mmol/L, there was a concentration-dependent slowing of cellular taurine efflux. Cell volumes progressively increased over the range 0-50 mmol/L urea, but decreased slightly in 100 mmol/L. Urea had no effect on cell volume in the absence of taurine. Retardation of efflux, and cell swelling in the presence of 50 mmol/L urea were entirely abolished by trimethylamine (100 mumol/L). TMA had no effect on either variable in the absence of urea. It is suggested that impaired loss of taurine and accompanying cell swelling may be factors contributing to the neurological disturbances accompanying uremia.
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