[Dental treatment for children in the Nagasaki prefecture].
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Biomedical subjects
Publications and source records attributed to F Matsumoto.
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The mechanism of [3H]Leu-enkephalin uptake into synaptic vesicle fraction from bovine caudate nucleus was investigated. The simultaneous addition of 2 mM MgCl2, 2 mM CaCl2, and 2 mM ATP stimulated the uptake 22 times over the control, whereas the separate addition of these agents augmented the uptake 2.4 times at most. The addition of 2 mM MGCl2 plus 2 mM ATP and of 2 mM CaCl2 plus 2 mM ATP increased the uptake 6.6 times and 4.5 times, respectively. The cation, ATP-dependent uptake reached its half-maximal level within 10 min after the initiation of incubation at 25 degrees C, and little Leu-enkephalin was taken up at 0 degree C. The apparent Km for the uptake of [3H]Leu-enkephalin was 1.8 x 10(-7) M. Guanosine triphosphate stimulated the uptake as well as ATP, whereas CTP and ITP were only one-fourth effective of ATP. The cation, ATP-dependent uptake was inhibited by 25% and 20% in the presence of 0.1 mM colchicine and 1 microM reserpine, respectively.
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Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency was identified in three children who were evaluated because of chronic nonspherocytic hemolytic anemia. One child is of German extraction, another Puerto Rican, and the third Mexican. In each of the patients the hemolytic process was well compensated, but each had one or more episodes of anemia following exposure to an oxidant drug or with infections. The electrophoretic, functional, and kinetic properties of the mutant enzymes, derived both from the patients' erythrocytes and from cultured fibroblasts, allowed each to be distinguished from G-6-PD variants previously described.
The question of whether separate "membrane" and "soluble" pools of ATP exist in erythrocytes has been examined. Phosphoglycerate kinase (EC 2.7.2.3)-derived ("membrane") ATP was labeled by short-term incubation with inorganic [32P]phosphate. Pyruvate kinase (EC 2.7.1.40)-derived ("soluble")ATP is not labeled under these circumstances. The specific activity of the gamma-phosphate of "soluble" ATP was then evaluated by the addition of 2-deoxyglucose and measurement of the specific activity of 2-deoxyglucose-6-[32P]phosphate formed. This specific activity was essentially the same as the overall specific activity of erythrocyte ATP gama-phosphate, indicating that no functional pools of phosphoglycerate kinase-derived and pyruvate kinase-derived ATP exist in erythrocytes.
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An 11-yr-old child with mild chronic hemolytic anemia was found to have decreased red cell hexokinase activity in spite of the reduced mean age of her red cell population. Similar decreases in red cell hexokinase activity were documented in the patient's parents and in one sib. The red cells were morphologically normal. Red cell 2,3-DPG levels were normal and ATP and glucose-6-phosphate levels were diminished. The kinetic properties, electrophoretic mobility, and thermal stability of the residual red cell hexokinase were normal or nearly so. Glucose consumption of the hexokinase-deficient cells was not appreciably decreased, probably because less of the potent inhibitor glucose-6-phosphate was present in the erythrocytes. It is likely, although not certain, that in this patient nonspherocytic hemolytic anemia resulted from hexokinase deficiency.
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Glutathione peroxidase (GSHPx) activity was found to be greatly elevated in members of a family with alpha-thalassemia. Eleven other families with proven alpha-thalassemia were investigated, and all but one subject with hemoglobin H disease had increased red cell GSHPx. Most persons with alpha-thalassemia trait also had increased activity of red cell GSHPx. In contrast, only very modest increases in glutathione peroxidase activity were observed in subjects with various forms of beta-thalassemia.
Lymphocytes, monocytes, neutrophilic granulocytes and platelets were each separated to greater than 95% purity from six normal subjects, three patients with Gaucher's disease, two heterozygotes for Gaucher's disease, and one patient with Fabry's disease. Activities of the following acid hydrolases were determined: "acid" (pH 4.0) beta-glucosidase, pH 5.0 beta-glucosidase, alpha-galactosidase, alpha-arabinosidase, alpha-mannosidase, alpha-glucosidase, beta-glucuronidase, beta-galactosidase, beta-hexosaminidase, and acid phosphatase. Enzymatic activity varied greatly with cell type and the enzyme being measured; the importance of assaying pure preparations especially for heterozygote detection is emphasized. Gaucher's disease patients' cells were found to be deficient in the pH 4.0 acid beta-glucosidase, variable in the pH 5.0 beta-glucosidase, and normal in all other acid hydrolases tested, including acid phosphatase, the activity of which is known to be elevated in plasma. Blood cells of a patient with Fabry's disease were deficient in alpha-galactosidase and normal in all other acid hydrolases tested.
UNLABELLED: Gentamicin (GM) was studied for on its antibacterial activity, absorption, and excretion, effect on the kidney and clinical effects. The results obtained are as follows: 1. Antibacterial activity: The susceptibility of E. coli, Klebsiella, Proteus mirabilis to GM was almost the same between the periods of 1964 to 1966 and 1972 to 1974: No tendency of increase of resistance by year was noted. However, against Pseudomonas aeruginosa, strains showing sensitivity to a concentration of more than 25 mcg/ml were isolated in 12.7%, in the latter period (1972-1974), as compared with the former period (1964-1966), which was 0%. 2. Blood levels: The peak level of GM in blood was obtained at 30 minutes after intramuscular injection to a healthy human. The peak level was 7.6 mcg/ml with 40 mg dose, 8.7 mcg/ml with 60 mg and 10.6 mcg/ml with 80 mg, showing a dose-responding curve. The half-life of GM absorption was 1.1 hours with 40 mg dose, 1.3 hours with 60 mg and 1.6 hours with 80 mg, showing also a dose related tendency. 3. Urinary levels: The peak level of GM in urine, about 200 mcg/ml, was noted in 0-2 hours after intramuscular injection of GM to a healthy human. The urinary recovery was about 44% in 6 hours. 4. Effect on the kidney: The effects of GM on the kidney was studied in rats administering 20 mg/kg once a day for 21 days consecutively. The results obtained are a slight increase (20 mg/dl) in BUN and a slight decrease (2,600 mosm/kg H2O) in urinary osmotic pressure; and urea lysozyme showed tendency to increase from the third day, the same as with kanamycin. Meanwhile, in the histopathological findings of the kidney tissue, the vacuolar degeneration and flattening of renal tubules were noted. Similar findings were obtained with kanamycin in a similar type of experiment. These results indicate that nephrotoxicity of GM is considered to be approximately the same as that of kanamycin. 5. CLINICAL RESULTS: GM was injected into 22 patients with various infectious diseases (respiratory tract infections 7, liver abscess 1, urinary tract infections 14). Excellent efficacy was noted in 7 patients, good in 13 and no effect in 2. The effective rate was 90.9%. No serious side effect was noted in this clinical trial.