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Biomedical subjects

H Mizoguchi

Publications and source records attributed to H Mizoguchi.

At least 361 records · Page 20Linked to original sources
PubMed1987

Myeloproliferative disorders terminating in acute megakaryoblastic leukemia with chromosome 3q26 abnormality.

Two cases of myeloproliferative disorders terminating in acute megakaryoblastic leukemia are reported. One case began as primary myelofibrosis and the other as chronic myelogenous leukemia. Blast cells in the acute leukemic phase were identified as megakaryoblasts by the presence of platelet peroxidase. The clinical course is described, and the morphology, immunologic studies, and ultrastructure studies of the blast cells are reported. On cytogenetic analysis both cases had a translocation involving the No. 3 chromosome locus q26.2. The present data suggest that 3q26 may be associated with transformation of the megakaryocytic lineage.

Adult↗
PubMed1987

Establishment of a CSF-producing cell line from a human gastric carcinoma and characteristics of the CSF produced by that cell line.

A human cell line producing colony-stimulating factor has been established in vitro from a human gastric carcinoma. The cell line was transplantable into nude mice which developed a marked neutrophilia. The cell line has been maintained for three years. The cells grew in a monolayered sheet and produced colony-stimulating factors that enhanced the formation of granulocyte and monocyte colonies in vitro with mouse bone marrow cells as the target and granulocyte colonies with human bone marrow cells as the target.

Animals↗
PubMed1987

Improvement of culture conditions for human megakaryocytic and pluripotent progenitor cells by low oxygen tension.

The effect of low oxygen tension on the growth of human hemopoietic progenitor cells in bone marrow was investigated using the semisolid methylcellulose colony assay. The clonal growth of granulocyte-macrophage progenitors (CFU-gm), early (BFU-e) and late (CFU-e) erythroid progenitors, megakaryocyte progenitors (CFU-meg) and pluripotent progenitors (CFU-mix) improved more markedly incubation at the low oxygen tension (5%) than in conventional air (20%). The thiol compound 2-mercaptoethanol had a strong additive effect on colony growth in conventional air, but little or no effect in the low oxygen tension. These results suggest that enhancement of colony growth in the low oxygen tension may be due to a decrease in the production of oxygen intermediates.

Bone Marrow Cells↗
PubMed1987

Asymmetric distribution of arachidonic and n-3 polyunsaturated fatty acids in rat liver microsomal membranes under a fat-free diet.

Rats adapted to a corn oil or a fish oil diet were fed a fat-free diet, and changes in phospholipid polyunsaturated fatty acids (PUFA) in the inner and outer leaflets of liver microsomal membranes were followed for 18 wk. In rats previously adapted to a corn oil diet, arachidonic acid in phosphatidylcholine and phosphatidylethanolamine in the inner and outer leaflets did not decrease quickly; rather, linoleic acid decreased more than arachidonic acid for the first three weeks of feeding the fat-free diet. Even at 18 wk, 40-50% of the beginning arachidonic acid levels were still retained. In contrast, in rats previously adapted to a fish oil diet, the n-3 PUFA were quickly decreased by the fat-free diet to only 10-30% at 18 wk. Due to the appearance and increase of n-9 eicosatrienoic acid in the replacement of the n-3 and n-6 PUFA, total PUFA did not decrease in the inner and outer phosphatidylcholine in either group, but decreased somewhat in the phosphatidylethanolamine due to the insufficient increase of the n-9. On the other hand, the overall degrees of unsaturation in phosphatidylcholine fatty acids were always higher in the outer than in the inner leaflets and were not altered by feeding the fat-free diet even for 18 wk. Thus, the results appear to reveal the physiological importance of unsaturation ratio of fatty acids and the necessity of arachidonic acid in each membrane leaflet.

Animals↗
PubMed1987

Role of the kallikrein-kinin system in two-kidneyed and one-clipped hypertensive rats.

The influence of aprotinin as a kallidinogenase inactivator on the antihypertensive effect of angiotensin I converting enzyme inhibitor (CEI) was studied in two-kidneyed and one-clipped hypertensive rats. Sixteen two-kidneyed and one-clipped hypertensive rats and sham-operated normotensive rats were prepared for this experiment. They were divided into two groups: those with the aprotinin infusion and those without. The effects of the oral administration of CEI were compared as regards mean arterial pressure (MAP) and urinary kallikrein activity (UKA). In 8 hypertensive rats under glucose infusion, MAP fell from 184.4 +/- 4.5 to 106.3 +/- 5.2 mm Hg, and UKA changed from 1.37 +/- 0.18 nkat/12 h to 0.61 +/- 0.11 nkat/12 h after the administration of CEI. In the remaining hypertensive rats under aprotinin infusion, MAP decreased from 175.0 +/- 3.0 to 140.6 +/- 5.1 mm Hg, and UKA slightly changed from 0.72 +/- 0.25 nkat/12 h to 0.59 +/- 0.12 nkat/12 h. Thus, the decrease of MAP after the administration of CEI was suppressed by the aprotinin infusion, and this significant difference was supported by the decrease of UKA. As for 16 normotensive rats, CEI did not alter MAP, nor did aprotinin have any effect on it. However, UKA tended to decrease after the administration of CEI. These results suggest that both the kallikrein-kinin system and the renin-angiotensin system play an important role in the maintenance of high blood pressure in two-kidneyed and one-clipped chronically hypertensive rats.

Animals↗
PubMed1987

Effect of recombinant interferons on colony formation of blast progenitors in acute myeloblastic leukemia.

The effect of recombinant interferons (rIFNs) on primary and secondary colony formation by blast progenitors (leukemic colony-forming units, L-CFU) from the peripheral blood of patients with acute myeloblastic leukemia (AML) was examined. rIFN-alpha, rIFN-beta, and rIFN-gamma inhibited L-CFU in a dose-dependent manner. When 3000 U/ml rIFN-alpha, -beta, and -gamma were added, L-CFU were suppressed to 20%, 12%, and 40% of the control cultures, respectively. The concentrations of rIFN-alpha, -beta, and -gamma required for 50% inhibition of colony formation were 63, 29, and 250 U/ml, respectively. The self-renewal capacity of L-CFU was inhibited by rIFNs in a dose-dependent manner, the degree of inhibition being the same for all three rIFNs. These rIFNs also inhibited normal granulocyte-macrophage progenitors to a similar degree as L-CFU. Taken together, these in vitro studies indicate that these rIFNs may be efficacious in the treatment of AML, though development of granulocytopenia may be observed as a complication of IFN therapy.

Antibodies, Monoclonal↗
PubMed1987

Y chromosome abnormality in human stomach and lung cancer.

Sex chromosome abnormalities in human stomach and lung cancers from 33 male patients were examined by Southern blot hybridization with pDP34 DNA probe, which recognizes X and Y chromosome-linked restriction fragment length polymorphisms (RFLPs). Contrary to the recent cytogenetic observations showing high incidence of loss of the Y chromosome in solid tumors, loss of the Y chromosome was observed in only 3 of 21 stomach cancers and 2 of 12 lung cancers. Gain of the Y chromosome was found in one of 12 lung cancers, but not in any of the stomach cancers. No X chromosome abnormality was found in any of these 33 stomach cancers and lung cancers.

Humans↗