Biomedical subjects
Publications and source records attributed to A Kuramoto.
A system useful for the collection and analysis of a large number of abnormal karyotypes and for studies on the relationship between cytogenetic abnormalities and clinical features of diseases is reported. The program is based on the disintegration and rearrangement of abnormal karyotypes recorded according to the 1978 International System for Human Cytogenetic Nomenclature (ISCN).
An increased activity of spermidine N1-acetyltransferase was induced in bovine lymphocytes by stimulation with either sodium n-butyrate or phytohemagglutinin (PHA). The acetylase activity was elevated by 2- to 3-fold 24 h after the addition of butyrate, whereas a similar increase of the enzyme activity was found 48 h after stimulation with PHA. When butyrate and PHA were added to the lymphocyte suspensions simultaneously, the peak of enzyme induction was observed at 24 h after the addition and the increase (9-fold) was found to be more than additive. Since the increases in acetylase activity by both butyrate and PHA were markedly inhibited by actinomycin D or cycloheximide, they appear to have resulted from the synthesis of new protein rather than the release of the enzyme from a cryptic inactive form. The enzyme induced by the two agents was most active with spermidine as a substrate, but spermine was also acetylated to a smaller extent (25% of spermidine). Virtually no acetylation was observed with putrescine. Also, the product formed from spermidine and acetyl CoA was more than 90% N1-acetylspermidine. These results indicate that the acetylases induced by the two agents are similar. Although the addition of indomethacin or 8-bromocyclic AMP to PHA-stimulated lymphocytes caused an inhibition of the enzyme induction, no such inhibitory effect was found in the case of enzyme induction by butyrate. These results indicate that both sodium n-butyrate and PHA induce spermidine N1-acetyltransferase in bovine lymphocytes, but the induction mechanisms are different from each other.
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Enzymatic and electron microscopical studies were performed on the muscle of a proband with phosphofructokinase deficiency. Enzymatic studies showed that muscle phosphofructokinase activity of the proband was decreased to about a half of normal. This enzyme was quite thermolabile and had low affinity for fructose 6-phosphate. Electron microscopical studies showed the accumulation of glycogen granules beneath the sarcolemma and between the myofibrils in spite of a lack of accumulation of the intermediates before the step of phosphofructokinase. The proband's clinical symptoms, i.e., hemolytic anemia and myopathy, were considered to be due to the unstable, mutant, muscle-type phosphofructokinase in the red blood cells and muscle.
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The prognostic value of several clinical and hematologic features, recorded at diagnosis, in chronic phase Ph1 positive chronic myelocytic leukemia (CML), was analyzed in 135 patients using life-table analysis. About one third of patients were atomic bomb survivors and they had been examined twice a year before the diagnosis of CML. In general, features representing tumor cell burden, i.e., leukocyte count, spleen sizes, and absolute differential cell counts of all granulocyte series cells except myeloblasts affected survival significantly, while sex, age, hemoglobin, platelets and features representing quality of leukemia, i.e. neutrophils alkaline phosphatase score, percent Ph1 positive cells in bone marrow, and percent differentials of all granulocyte series cells except promyelocytes and segmented neutrophils were all insignificant. Multivariate life-table analysis was also performed using age, sex, hemoglobin, platelets, and leukocyte count as predictor variables. The result was that leukocyte was the single most important factor in this analysis and annual death rates between low risk (risk ratio less than 0.8) and high risk (risk ratio greater than 1.4) differed considerably up to four years from diagnosis, indicating our formula to calculate risk ratio is valid as a grading parameter of chronic phase Ph1 positive CML within four years from diagnosis.
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The divalent cation ionophore, A23187, at a concentration of 0.25 microgram/ml, enhanced influx of Ca2+, activity of ornithine decarboxylase and incorporation of [3H]thymidine into DNA of guinea pig lymphocytes. Combined treatment of cells with A23187 and dibutyryladenosine 3',5'-monophosphate (Bt2cAMP) augmented these three events. A23187 at a concentration of 0.06 microgram/ml was insufficient for induction of ornithine decarboxylase stimulated neither Ca2+ influx nor [3H]thymidine incorporation, but stimulated Ca2+ efflux. A23187 (0.06 microgram/ml) in combination with Bt2cAMP caused a marked induction of ornithine decarboxylase and stimulation of [3H]thymidine incorporation into DNA. When the time of Bt2cAMP addition was delayed after A23187, the stimulation of ornithine decarboxylase activity decreased. Washout of Bt2cAMP from cell culture earlier than 4 h of incubation caused a reduction in the stimulatory effect of Bt2cAMP. These results suggest that raising concentrations of cytoplasmic Ca2+ and cellular cAMP are important to some initial events leading to induction of ornithine decarboxylase and these biochemical changes are obligatory sequential steps for stimulation of DNA synthesis.
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Induction of ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17) in phytohemagglutinin-stimulated lymphocytes was suppressed by the administration of dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine. This inhibition of ornithine decarboxylase induction was overcome by removing the chemicals from the lymphocyte culture. However, the recovery of ornithine decarboxylase induction by washout of the chemicals did not occur when actinomycin D, cordycepin or alpha-amanitin was added to the cultures, suggesting that the synthesis of mRNA directed to ornithine decarboxylase was reduced in dibutyryl cyclic AMP- and 3-isobutyl-1-methylxanthine-treated cells. Moreover, the decay of ornithine decarboxylase activity in the cells treated with phytohemagglutinin plus dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine was significantly slower than that of control cells stimulated with phytohemagglutinin alone. The difference of the decrease in ornithine decarboxylase activity between dibutyryl cyclic AMP- and 3-isobutyl-1-methylxanthine-treated and control cells was observed when actinomycin D was added to the culture, but not when cycloheximide was added. Therefore, prevention of ornithine decarboxylase decay by cyclic AMP may be post-transcriptional events, but not post-translational events.
The platelet survival time was shortened in stroke-prone spontaneously hypertensive rats (SHRSP) at 10 weeks of age on feeding the regular diet but it was normalized on administering the vitamin E-supplemented diet. Platelet survival time was normal in stroke-resistant spontaneously hypertensive rats (SHRSR) at 10 weeks of age on feeding the regular diet but it was shortened when supplying the vitamin E-free diet. The maximal uptake of 75Se-selenomethionine by platelets was increased in SHRSP at 10 weeks of age on feeding the regular diet. It was further increased in SHRSP on feeding the vitamin E-free diet. On the other hand, the increased maximal uptake of 75Se-selenomethionine by platelets was normalized in SHRSP on feeding both the vitamin E-supplemented diet and the vitamin E-supplemented diet after administering the vitamin E-free diet. Therefore, we concluded that the deficiency of vitamin E brought about the shortening of platelet survival time and enhanced platelet production.
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The biochemical activities of 8 lysosomal acid hydrolases in leukemic cells from 48 patients were examined. Characteristic alterations were found in alpha-mannosidase, beta-galactosidase and N-acetyl-beta-glucosaminidase activities of leukemic cells. The level of alpha-mannosidase activity was much higher in myelo(mono)genous leukemias (AML, AMoL, AMMoL, CML and CMMoL) than in lymphogenous ones (ALL, T-cell leukemia, hairy cell leukemia and CLL) without exception. The beta-galactosidase activity also differed as a result of alpha-mannosidase, except in T-cell leukemia. In T-cell leukemia it was within the range of normal lymphocytes, but in the other lymphogenous leukemias it was significantly below normal. N-acetyl-beta-glucosaminidase activity in myelo(mono)genous leukemic cells was above the range of normal granulocytes. The changes in these enzyme levels were consistent. The lymphocytic or myelocytic nature of three cases of acute undifferentiated leukemia could be determined by enzyme studies. In two cases it was lymphocytic and in one it was myelocytic. The enzymatic abnormalities were also found in morphologically mature neutrophils from patients but not only chronic types (CML, CMMoL) but also acute types (AMoL, AMMoL) of leukemias, and were similar to those of their respective leukemic cells. Analysis of lysosomal enzymes (at least three of those mentioned above), can elucidate one of the biochemical properties of leukemic cells and may be valuable in the differentiation of leukemias.
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