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Biomedical subjects

S Miwa

Publications and source records attributed to S Miwa.

At least 379 records · Page 21Linked to original sources
PubMed1980

Na,K-, Mg- and HCO3-adenosine triphosphatases in the rabbit brain choroid plexus.

Properties of adenosine triphosphatases (ATPases) in the choroid plexus of rabbit cerebral ventricles were investigated using tissue homogenates and subcellular fractions. Na,K-ATPase or HCO3-ATPase activity of choroid plexus was significantly lower than that of the brain or the kidney, respectively. Among the homogenates of choroid plexus from the lateral, third and fourth ventricles, there were no differences in the activities of Na,K-, Mg- and HCO3-ATPases. In the choroid plexus, Na,K-ATPase activity was demonstrated to be highest in 10,000 X g fraction, while the highest Mg- and HCO3-ATPase activities were observed in 8,000 X g fraction, the so-called mitochondrial fraction. Ion requirement, pH optimum and ouabain sensitivity of Na,K-ATPase in 10,000 X g fraction of choroid plexus were similar to findings in erythrocytes, brain and kidney. However, properties of Mg- and HCO3-ATPases in 8,000 X g fraction were considerably different from those found in the brain and gastric mucosa. In the choroid plexus, thiocyanate ion inhibited Mg-ATPase as well as HCO3-ATPase. These results indicate that characteristics of ATPase systems in the choroid plexus are to some extent different from those in tissues such as brain, kidney and gastric mucosa.

Adenosine Triphosphatases↗
PubMed1980

Pyruvate kinase variants characterized by the methods recommended by the International Committee for Standardization in Haematology.

Seven new pyruvate kinase (PK) variants were characterized by the recently established recommended methods by the International Committee for Standardization in Haematology (ICSH). The seven cases were all true homozygotes as evidenced by consanguineous marriages of the parents. All of them were Japanese. These variants were designated PK Tokyo, Nagasaki, Sapporo, Maebashi, Itabashi, Fukushima, and Aizu. Low substrate affinity for phosphoenolpyruvate and thermal instability seem to play a major role in causing clinical manifestation of chronic hemolysis. Product inhibition of PK by ATP may also play an additional role in some cases.

Adolescent↗
PubMed1980

Pyrimidine 5'-nucleotidase deficiency: studies of five cases in two Japanese families.

Two new families with red cell pyrimidine 5'-nucleotidase (P5N) deficiencies were found in Japan. The enzyme activities were 4.8% in case 1 and 9.7% in case 2. The propositi showed characteristic hemolytic anemia with market basophilic stippling, increased reduced glutathione content and accumulation of pyrimidine nucleotides in the red cell. High Michaelis constants for cytidine monophosphate, normal thermostability, abnormal optimum pH in both cases, and normal electrophoretic mobility in case 1 and slower mobility in case 2 were shown, suggesting that the cause of P5N deficiency, at least in these cases, is due to the structural gene mutation.

5'-Nucleotidase↗
PubMed1980

Purification and properties of adenosine deaminase in normal and hereditary hemolytic anemia with increased red cell activity.

Red cell adenosine deaminase from normal subjects and from a patient with hereditary hemolytic anemia with a 40-fold increase in activity were purified using antibody affinity chromatography. The purified enzymes were completely homogeneous on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. There were no differences in the molecular weight, specific activity, polyacrylamide gel electrophoresis, Michaelis constant for adenosine, inhibition constant for guanylurea, utilization of 2-deoxyadenosine, thermal stability, optimum pH, immunological reactivity, amino acid composition and tryptic peptide mapping. These results strongly suggest that increased red cell adenosine deaminase activity is caused by an overproduction of a structurally normal enzyme.

Adenosine Deaminase↗
PubMed1980

Glucose 6-phosphate dehydrogenase variants in Japan.

Fifty-four cases of glucose 6-phosphate dehydrogenase (G6PD) deficiency have so far been reported in Japan. Among them, 21 G6PD variants have been characterized. Nineteen out of the 21 variants were characterized in our laboratory and G6PD Heian and "Kyoto" by others. G6PD Tokyo, Tokushima, Ogikubo, Kurume, Fukushima, Yokohama, Yamaguchi, Wakayama, Akita, Heian and "Kyoto" were classified as Class 1, because all these cases showed chronic hemolytic anemia and severe enzyme deficiency. All these variants showed thermal instability. G6PD Mediterranean-like, Ogori, Gifu and Fukuoka were classified as Class 2, whereas G6PD Hofu, B(-) Chinese, Ube, Konan, Kamiube and Kiwa belonged to Class 3. All the 6 Class 3 variants were found as the results of the screening tests. The incidence of the deficiency in Japanese seems to be 0.1-0.5% but that of the cases which may slow drug-induced hemolysis would be much less. G6PD Ube and Konan appear to be relatively common in Japan.

Anemia, Hemolytic↗
PubMed1980

A combined system for the study of glutathione metabolism in erythrocytes.

A combined system for measuring glutathione stability, hexose monophosphate pathway activity, glutathione synthesis, glucose consumption and lactate formation in erythrocytes has been devised. By this method the results were obtained from the blood samples of six glucose 6-phosphate dehydrogenase deficiencies, one glucose phosphate isomerase deficiency and two pyruvate kinase deficiencies. These results indicate that one abnormal enzyme may exert its influence on the other several enzyme systems and that it is valuable to investigate the metabolism of erythrocytes using this system in different erythroenzymopathies as well as different variants of one enzyme deficiency.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1979

Incidence and characteristics of glucose-6-phosphate dehydrogenase variants in Japan.

A total of 3000 men living in Yamaguchi were screened for glucose-6-phosphate dehydrogenase (G6PD) deficiency using Beutler's spot test and three types of starch gel electrophoresis. These electrophoresis used a phosphate buffer system at pH 7.0, a TRIS-EDTA-borate buffer system at pH 8.6, and a TRIS-hydrochloride buffer system at pH 8.8. Fifteen G6PD-deficient variants were found at the rate of 0.5% and classified into four groups. As new variants, G6PD Konan, Kamiube, and Kiwa were identified. These three variants had a mild to moderate G6PD deficiency and were not associated with any clinical signs. G6PD Konan had fast electrophoretic mobility as compared with normal levels, G6PD Kiwa had slightly elevated electrophoretic mobility, and G6PD Kamiube had normal electrophoretic mobility. These three variants had normal levels of Km G6P, Km NADP, and Ki NADPH, normal utilizations of both 2-deoxy-G6P and deamino-NAPD, normal heat stability, and a normal pH curve. The other variant was G6PD Ube, which we had previously found in Yamaguchi (Nakashima et al., 1977). One boy with G6PD Ube was Korean.

Adolescent↗
PubMed1979

Electrophoretic and kinetic studies of a mutant red cell pyrimidine 5'-nucleotidase.

Human red cell pyrimidine 5'-nucleotidase (P5N) was studied by partial purification and condensation in a patient with an extremely low red cell P5N activity and chronic hemolytic anemia. The residual P5N in the red cell of the patient was characterized by an increased Michaelis constant for cytidine 5'-monophosphate, a marked shift of the pH optimum to the acidic side, normal electrophoretic mobility and normal heat stability. These data indicate that, in this patient, severe enzyme deficiency is caused by a structural gene mutation. This variant is clearly distinguished from a previously reported case and it is designated P5N Kagoshima.

Anemia, Hemolytic, Congenital↗
PubMed1979

Erythrophagocytosis by the sinus endothelial cell of the spleen in haemolytic anaemias.

An ultrastructural study of spleens from patients with a heterogeneous group of haemolytic anaemias was undertaken in order to determine whether sinus endothelial cells have erythrophagocytic ability. In most cases, sinus endothelial cells contained erythrocytes and various stages of intracellular degradation of engulfed erythrocytes were noted. Though the frequency of erythrophagocytosis varied from case to case, phagocytosis of erythrocytes by the endothelial cell was more frequent in cases in which cordal macrophages showed active erythrophagocytosis. These results suggest that the sinus endothelial cells have erythropagocytic ability in certain pathological states, especially when the demands for the removal of defective erythrocytes are increased. However, the bulk of erythrophagocytosis is carried out by cordal macrophages, and endothelial phagocytosis has a minor significance in the developemnt of haemolytic anaemia. Two possible processes by which erythrocytes come into contact with sinus endothelial cells are suggested.

Anemia, Hemolytic↗