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Biomedical subjects

E Satoyoshi

Publications and source records attributed to E Satoyoshi.

At least 73 records · Page 4Linked to original sources
PubMed1983

Partial purification and properties of acid sphingomyelinase from rat liver.

Acid sphingomyelinase was purified approximately 5,200-fold from the mitochondria-lysosome-enriched particles of rat liver by sequential chromatography on DEAE-cellulose, octyl-Sepharose, Sephacryl S-300, Concanavalin A-Sepharose, and CM-cellulose. The specific activity of this highly purified enzyme was 3.2 mmol per hr per mg protein. The enzyme was active against 2-hexadecanoylamino-4-nitrophenylphosphorylcholine, but bis-4-methylumbelliferyl-phosphate and bis-p-nitrophenyl-phosphate were poor substrates. The preparation was free of Mg2+-dependent neutral sphingomyelinase and eight lysosomal enzymes except for the trace amount of acid phosphatase and beta-galactosidase. Apparent molecular weight of the enzyme was 200,000, estimated by Sephadex G-200 filtration in 0.1% Triton X-100. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed three major bands corresponding to molecular weights of 45,600, 44,500, and 40,000 with several minor bands. Characterization of the enzyme revealed almost the same properties as those of human tissues reported by other investigators, including pH optimum, requirement of Triton X-100, effects of metal divalent cations, phosphate ion, EDTA, some thiol blocking reagents, and amphophilic drugs.

Animals↗
PubMed1982

Monoclonal antibody to acetylcholine receptor: cell line established from thymus of patient with Myasthenia gravis.

A human B cell line producing a monoclonal antibody to an antigenic determinant of acetylcholine receptors was established by cloning B cells that had been transformed in vitro by Epstein-Barr virus. The B cells were obtained from the thymus of a patient with myasthenia gravis. The antibody produced by the cell line precipitated acetylcholine receptors from denervated and innervated rat muscle and from human muscle, but did not show detectable response to the acetylcholine receptors from the electric organs of Narke japonica. The monoclonal antibody showed identical binding patterns in innervated and denervated rat muscles. Passive transfer of the monoclonal antibody into rats induced moderate muscle weakness and electromyographic changes characteristic of myasthenia gravis.

Animals↗
PubMed1981

Familial distal myopathy with rimmed vacuole and lamellar (myeloid) body formation.

Three cases from 2 families had muscle weakness with predilection for distal extremities, predominantly affecting the tibialis anterior muscles, and onset in early adulthood. The disorder seemed to be inherited through an autosomal recessive trait. The EMG demonstrated a myopathic pattern and CPK was mildly elevated. The striking finding in their muscle biopsies was the presence of "rimmed" vacuoles which had acid phosphatase-positive autophagic activity and which contained numerous concentric lamellar bodies in various forms (myeloid and cabbage bodies). Despite rapid clinical progression, not only necrotic fibers with phagocytosis, as seen in Duchenne dystrophy, but also evidence of regeneration were virtually absent. Continuous destruction of myofibrils by activation of certain lysosomal proteolytic enzymes might be responsible for the production of atrophic fibers.

Adult↗
PubMed1981

Hemorrhage of thiamine-deficient encephalopathy.

Hemorrhagic lesions of pyrithiamine-induced acute thiamine-deficient encephalopathy of the mouse (PIATDEM) consisted of petechiae, which often coalesced to form small hematomas. Electron microscopy showed the typical petechial lesion to be composed of a perivascular necrotic zone containing fibrin-platelet clot surrounded by a ring of erythrocytes. Endothelial cells were intact and tight junctions were closed. A study of permeability to horseradish peroxidase (HRP) revealed only a slight increase in the number of transport vesicles in the endothelial cells. A large amount of HRP present in the lesions seemed to have entered the brain by a hemorrhagic route which remains unclarified. Spherical latex particles, 0.23 micrometer in diameter, were injected intravenously into encephalopathic mice at a time when intracerebral hemorrhages frequently occurred. Two to 24 hours after the injection, a large number of latex particles penetrated the blood vessels at sites of hemorrhage. There were many particles in the phagosomes of the endothelial cells, which suggested transendothelial transport by the organelle. The possibility of endothelial phagocytic transport of erythrocytes as a main route of diapedesis is discussed.

Animals↗
PubMed1981

[Frontal pseudoataxia, discussion on its mechanism (author's transl)].

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.

Ataxia↗