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Biomedical subjects

K R Tanaka

Publications and source records attributed to K R Tanaka.

At least 73 records · Page 4Linked to original sources
PubMed1980

Genetic influence on serum igd levels.

In order to better understand the factors determining serum levels of IgD, total serum IgD and IgE were studied in 23 nonallergic twin pairs, consisting of 16 monozygotic (Mz and 7 same-sex dizygotic (Dz) pairs. Both immunoglobulins were measured by a paper disc solid phase radioimmunoassay, sensitive to 1 microgram/dl of IgD and 1 I.U./ml of IgE. Also studied were 10 paired sera taken at different times from 10 healthy subjects of similar mean age to the twins and 21 randomly paired sera from unrelated subjects. The intrapair variance of both serum IgD and serum IgE levels were significantly less in Mz than in Dz twins (P less than 0.05). Thus, there appears to be a genetic influence over serum IgD levels, probably to a similar degree to that previously shown to exist for serum IgE levels. Heritability was calculated to be 0.759 for IgD and 0.697 for IgE. Also, the intraclass correlation coefficient (rI) for IgD in monozygotic twin pairs was 0.9370 (P less than 0.001) and for IgE was 0.8602 (P less than 0.001). It appears likely that the number of genetic loci controlling serum IgD levels is similar to, or less than, the number controlling serum IgE levels because the random pair/Dz pair variance ratio was lower for IgD than for IgE.

Adolescent↗
PubMed1980

Pyruvate kinase deficiency hemolytic anemia: enzymatic characterization studies in twelve patients.

Erythrocyte pyruvate kinase from twelve patients with hereditary erythrocyte pyruvate kinase (PK) deficiency was investigated according to the recommended methods for the characterization of red cell pyruvate kinase variants. Family members were also studied. Abnormalities were frequently noted in the affinity for the substrate, phosphoenolpyruvate; allosteric activator, fructose-1,6-diphosphate; allosteric inhibitor, ATP; and also in heat stability and electrophoretic pattern. Several different PK variants were identified. Polyacrylamide gel electrophoresis revealed the presence of immature activity bands in the red cells of some patients. These bands presumably represent residuals of isozymes produced during the evolution of erythrocyte PK, and may occur as a compensatory mechanism for the defective isozyme.

Adenosine Triphosphate↗
PubMed1980

The effects of adriamycin (doxorubicin HCl) on human red blood cells.

We have studied the effects of adriamycin (doxorubicin HCl) on human red blood cells. The peroxidizing effect of adriamycin on the thiols of red cell constituents resulted in decreased glutathione stability, and oxidation of hemoglobin and membrane protein components 1, 2, and 3, forming large molecular weight complexes. Membrane lipids were also peroxidized. Adriamycin itself did not inhibit the enzymes of the reductions system (glucose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase) of the red cells. Because adriamycin has the potential of inhibiting ATPase, including both Na-K-dependent ATPase and ouabain insensitive ATPase, at concentrations not inhibitory to other enzymes, the net sodium content increased, and potassium content decreased after incubation of red cells with adriamycin at high concentrations. The experimental results described with adriamycin may serve as a model for the possible mechanism of cardiotoxicity observed in its clinical use, and also explain the potential hemolyzing effect on red cells. There was greater oxidizing effect on glucose-6-phosphate dehydrogenase (G-6-PD) deficient than on normal erythrocytes. It is suggested that adriamycin be used with caution in individuals with G-6-PD deficient red cells.

Adenosine Triphosphatases↗
PubMed1979

Kinetic and electrophoretic studies of human erythrocytes deficient in pyrimidine 5'-nucleotidase.

The mutant enzyme of a patient with hereditary pyrimidine 5'-nucleotidase deficiency was analyzed biochemically. Partially purified by DEAE-Sephadex and concentrated by ultrafiltration, the enzyme had a high Km for the substrate uridine monophosphate. Utilization of the substrate cytidine monophosphate was normal, but utilization of adenosine monophosphate was greatly increased. The enzyme was stable to heat; the pH optimum was acidic. Electrophoresis of the enzyme revealed a very faint, slower than normal band.

Adult↗
PubMed1979

Mechanism of inhibition of red blood cell glutathione reductase activity by BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea).

A study of the mechanism of inhibition of glutathione reductase activity by BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) demonstrated that the enzyme was protected from inhibition by mercaptoethanol. N-Ethylmaleimide competes with BCNU and also protects the enzyme from inhibition. The inhibited enzyme showed decreased affinity for NADPH. Our data suggest that the inhibition of glutathione reductase is due to an alteration of the redox state. Several other red cell enzymes were inhibited by high concentrations of BCNU; these enzymes were also protected by mercaptoethanol. Among alkylating agents tested, only BCNU inhibited glutathione reductase at therapeutic levels.

Carmustine↗
PubMed1979

Hereditary deficiency of erythrocyte acetylcholinesterase.

A 36-year-old white man was found to have low erythrocyte acetylcholinesterase activity. Plasma cholinesterase activity was normal. The propositus had mild anemia and moderate elliptocytosis, but was asymptomatic. A sister, brother, father, and nephew were hematologically normal, but had slightly subnormal red cell acetylcholinesterase activities. There was no exposure to organophosphates, and paroxysmal nocturnal hemoglobinuria was excluded. Mixing experiments failed to demonstrate the absence of an activator or the presence of an inhibitor. The propositus enzyme showed normal kinetics for the substrate and various inhibitors, normal thermostability, and electophoretic migration. Major protein bands of the red cell membrane were normal by electrophoresis. Membrane cholesterol and phospholipid content were also normal. The mild anemia is presumably secondary to the presence of moderate elliptocytosis. The pattern of inheritance of the variant gene is unclear, but the propositus may be homozygous for the abnormal allele, and other family members may be heterozygous.

Acetylcholinesterase↗
PubMed1979

Acute leukemia in pregnancy: transient neonatal myelosuppression after combination chemotherapy in the mother.

An 18-year-old primagravida received combination chemotherapy with vincristine, prednisone, L-asparaginase, cyclophosphamide, daunomycin, 6-mercaptopurine and central nervous system (CNS) prophylaxis with intrathecal methotrexate and whole-brain irradiation for acute lymphoblastic leukemia (ALL) beginning in the 12th week of pregnancy. Therapy resulted in sustained complete remission of the leukemia and delivery of a normally developed female infant whose immediate neonatal course was complicated by transient severe bone marrow hypoplasia. Our experience confirms the reports of others that intensive chemotherapy can be administered in the last two trimesters of pregnancy without serious teratogenic complications. However, we conclude that such therapy may cause significant myelosuppression in the newborn.

Antineoplastic Agents↗
PubMed1979

Erythrocyte enzymes in groups of Rattus norvegicus with genetic differences in 2,3-diphosphoglycerate levels.

1. A major locus with two alleles is responsible for large differences in erythrocyte 2,3-diphosphoglycerate (DPG) levels in Rattus norvegicus. Blood from homozygous High-DPG, homozygous Low-DPG and heterozygous animals was used to measure blood indices and red cell enzyme activities. 2. Significant differences between groups were found in DPG levels, white blood cell counts and hemoglobin levels. 3. The results suggest that none of the red cell enzymes assayed is structurally or quantitatively different in the three groups.

2,3-Diphosphoglycerate↗
PubMed1979

Bone marrow granulomas in Q fever.

This report describes the case of a patient who had a fever of unknown origin and granulomatous hepatitis. Numerous granulomas were present in sections from a bone-marrow biopsy and bone-marrow clot obtained as a part of the diagnostic evaluation. Subsequent serologic studies proved the patient had Q fever. The authors re-emphasize that a distinctive form of granuloma occurs in the bone marrow with Q fever and that Q fever should always be a consideration in the differential diagnosis of bone-marrow granulomas.

Adult↗
PubMed1978

Leukocyte alkaline phosphatase.

In summary, LAP is an intriguing enzyme and its control is related to pituitary-adrenal function. A review of the changes in LAP activity which occur in some physiological conditions and in disease states has been presented. The function of LAP, however, is unknown. Table I summarizes those conditions in which the LAP is consistently altered enough so to help in the diagnosis of the disorder. Of prime importance is the differentiation of CML from a leukemoid reaction or agnogenic myeloid metaplasia with a leukocytosis. However, in no instance is the LAP value alone diagnostic of any disease. It remains a laboratory test to be utilized in conjunction with all other available clinical data.

Alkaline Phosphatase↗
PubMed1978

Relationship of density distribution and pyruvate kinase electrophoretic pattern of erythrocytes in sickle cell diseases and other disorders.

The density distributions of red cells from sickle cell disorders and other hematological diseases were determined. In sickle cell anemia there was an increase in the proportion of cells in both the heaviest and lightest fractions. In hemoglobin SC disease, a small fraction was shifted to heavier cells. Sickle cell trait blood had a normal density pattern. In hereditary spherocytosis an increase in the number of heavy cells was observed. Thin-layer polyacrylamide gel electrophoresis of red cell pyruvate kinase demonstrated that the pyruvate electrophoretic pattern was related to density distribution.

Anemia↗