[A study of neuromuscular disorders in type III glycogenosis (Cori-Forbes disease)].
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Biomedical subjects
Publications and source records attributed to M Osawa.
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A 77-year-old, nonalcoholic man was admitted to the Omiya Red Cross Hospital with the complaint of fever and delirium state of two days' duration. Two months prior to admission he had had cough and sputum. Chest X-ray revealed honey comb lungs. Cultures of sputum revealed mycobacterium tuberculosis after eight weeks incubation. He had no liver disease in his past history. The patient appeared cachetic. His vital signs were as follows; temperature 38 degrees C, blood pressure 132/68 mmHg, with a pulse rate of 84/min. He was delirium and excited. Findings of the cranial, motor and sensory nerve examination were normal. Initial laboratory studies showed a serum sodium value of 133 mEq/l, potassium 4.5 mEq/l, chloride 98 mEq/l; a serum GOT value of 51 units, GPT 36 units; a total protein content of 7.8 g/dl and ESR rate of 87 mm/hr. Six days after admission, the patients' consciousness level began to stupor and nuchal rigidity was appeared. Spinal fluid examination revealed opening pressure 270 mm H2O, cell counts 720 (N 712, L 8)/cumm, sugar 57 mg/dl and protein 170 mg/dl. Spinal fluid cultures were positive in mycobacterium tuberculosis after eight weeks incubation. Laboratory studies showed a serum sodium value of 114 mEq/l, potassium 4.4 mEq/l, chloride 86 mEq/l, a serum osmorality (SeOs) 225 mOsm/l and urine osmorality (UOs) 958 mOsm/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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The Fukuyama type congenital muscular dystrophy (FCMD), which was firstly described by one of the authors in 1960, is now recognized as an independent subtype of progressive muscular dystrophy in Japan. Recent advances in clinical, pathological and etiological studies of this syndrome were extensively reviewed. A long-term observation on a large number of cases revealed a wide spectrum of clinical features and courses, and comprehensive laboratory examinations including cranial computed tomography disclosed several new findings. A sharp dichotomy exists in the study of etiology; the genetic or intrauterine infection theories, with reasonable grounds for each. The most conspicuous is the fact that FCMD had been seldom described in countries other than Japan. If attention and interest on FCMD expand in a worldwide scale, the elucidation of basic pathogenesis of this disorder will be facilitated rapidly.
The effects of several anaesthetics on spinal cord nociceptive neural mechanisms and their interactions with the opiate antagonist, naloxone, were studied in acute, spinal cord transected cats. Intra-arterial injection of bradykinin was used as the noxious test stimulus. Spontaneous activity and the neural response induced by bradykinin were recorded by the multi-unit activity technique in the lateral funiculus of the spinal cord. Naloxone, 0.1 or 2.0 mg/kg i.v. had little effect on the bradykinin-induced response, but enhanced the spontaneous firing of the lateral funiculus significantly. Fentanyl, 30 micrograms/kg i.v., depressed both the bradykinin-induced response and spontaneous firing. These effects of fentanyl were antagonized completely by naloxone, 0.1 mg/kg i.v. Nitrous oxide, thiamylal, halothane and ether depressed the bradykinin-induced response considerably, but it was not antagonized by naloxone, 0.1-2.0 mg/kg i.v. Enflurane had little effect on the bradykinin-induced response. The effects of these anesthetics on spontaneous firing were divergent: nitrous oxide enhanced it while other drugs depressed it, to various degrees. All these data suggest that the neural and/or neurochemical mechanisms of anesthetic-induced analgesia differ from mechanisms related to opioids.
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