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Biomedical subjects

H Mizoguchi

Publications and source records attributed to H Mizoguchi.

At least 415 records · Page 23Linked to original sources
PubMed1983

Paroxysmal nocturnal hemoglobinuria terminating in TdT-positive acute leukemia.

A case of paroxysmal nocturnal hemoglobinuria (PNH) which developed terminal transferase (TdT)-positive leukemia 5 years after the diagnosis of PNH was studied. Most of the leukemic cells were suggestively lymphoid by cytochemistry and electron microscopy, and TdT-positive by immunofluorescence studies. The development of acute lymphoblastic leukemia during the course of PNH suggests that in PNH the clonal abnormality may involve lymphoid cells as well as myeloid cells, thus raising the possibility of the disease being a disorder of the pluripotential stem cell.

Aged↗
PubMed1983

Erythroid and granulocyte/macrophage progenitor cells in primary acquired sideroblastic anemia.

In order to study the pathogenesis of primary acquired sideroblastic anemia (PASA), bone marrow and/or peripheral blood specimens obtained from four patients with PASA were cultured for erythroid colony-forming units (CFU-E), erythroid burst-forming units (BFU-E), and granulocyte/macrophage colony-forming units (GM-CFU). The number of CFU-E was markedly decreased in all four patients. CFU-E colonies consisted exclusively of normal-appearing erythroblasts, while ringed sideroblasts were observed only in scattered single erythroblasts or in small erythroblast aggregates. In one case, very few BFU-E colonies containing both normal-appearing erythroblasts and ringed sideroblasts were detected. In addition, the number of GM-CFU was significantly decreased in three out of the four cases. These findings may suggest that there are abnormalities in the pluripotent hemopoietic stem cells at least in some cases of PASA.

Aged↗
PubMed1983

Degeneration of archenteron in sea urchin embryos caused by alpha,alpha'-dipyridyl.

Degeneration of the archenteron in middle gastrulae occurred in the presence of alpha,alpha'-dipyridyl or Zn2+, inhibitors of prolyl hydroxylase. In the presence of these substances the archenteron degenerated and was eventually destroyed. Adding Fe2+ to the embryo culture containing alpha,alpha'-dipyridyl protected the archenteron from further degeneration, but the collapsed archenteron was not restored to the upright position. At the late gastrula stage, alpha,alpha'-dipyridyl did not cause the degeneration of the archenteron. Treatment of the embryos by alpha,alpha'-dipyridyl, starting at the swimming blastula state, resulted in the production of many mesenchyme-like cells but archenteron was not produced in the embryos. Addition of Fe2+ to alpha, alpha'-dipyridyl culture, just before the beginning of gastrulation of normal embryos, resulted in the formation of normal archenteron. alpha,alpha'-Dipyridyl inhibited hydroxylation of proline residues of collagen in sea urchin embryos and Fe2+ prevented the inhibition by alpha,alpha'-dipyridyl. Respiration was not inhibited by alpha,alpha'-dipyridyl.

2,2'-Dipyridyl↗
PubMed1983

Effect of intrarenal administration of dopamine on renin release in conscious dogs.

We investigated the effect of intrarenal administration of dopamine on renin release in conscious dogs. Dopamine in doses ranging from 0.28 to 3.0 micrograms . kg(-1) . min(-1) produced a significant increase in systemic plasma renin activity (PRA) and renin secretion rate without altering systemic blood pressure. Dopamine also induced renal vasodilatation and natriuresis within this dose range. To determine if the dopamine-induced renin release is related to its vasodilatory action, two other vasodilators, papaverine and acetylcholine, were infused into the renal artery, but neither, in doses that produced a rise in renal blood flow similar to that of dopamine, had any effect on PRA. As dopamine can activate alpha- and beta-adrenergic receptors in addition to dopaminergic receptors, experiments were also performed to characterize the type of receptors involved in dopamine-induced renin release. Intrarenal infusion of sulpiride and haloperidol, dopamine antagonists, significantly inhibited dopamine-induced renin release and renal vasodilatation. In contrast, intrarenal infusion of propranolol failed to alter dopamine-induced rise in PRA or renal blood flow. Simultaneous infusion of phentolamine and dopamine, on the other hand, produced a significant potentiation of dopamine-induced renin release and renal vasodilatation. In conclusion, our studies demonstrate that dopamine is capable of inducing renin release and renal vasodilatation in conscious dogs. Moreover, such actions of dopamine are mediated through activation of specific dopamine receptors in the kidney. Finally, we present evidence for the existence of the intrarenal alpha-adrenergic mechanism that is inhibitory to renin release.

Animals↗
PubMed1983

Lysis of leukemia and lymphoma cells by autologous and allogeneic interferon-activated blood mononuclear cells.

Studies were undertaken to determine whether leukemia and lymphoma cells would be lysed by autologous and allogeneic interferon (IFN) activated peripheral blood mononuclear cells (PBMC). PBMC from healthy donors and from patients were cultured with and without 500 U of highly purified human fibroblast IFN/ml for 24 hr, and then their cytotoxic activity was assayed by a 5-hr 51Cr-release test. Of primary tumor cells isolated from patients, the cells of 5 of 15 patients with acute nonlymphocytic leukemia (ANLL), 5 of 9 patients with acute lymphocytic leukemia (ALL), 2 of 3 patients with chronic phase chronic myelogenous leukemia (CML), 2 of 3 patients with blastic phase CML, 1 patient with hairy cell leukemia, and 6 patients with diffuse non-Hodgkin's lymphoma were sensitive to IFN-activated PBMC of healthy donors, whereas the cells of 3 of the ANLL patients, 2 of the ALL patients, and 3 of the lymphoma patients were sensitive to unstimulated PBMC. Of the ANLL cells tested, myeloblasts, promyelocytes, and monoblasts were sensitive to either unstimulated or IFN-activated PBMC. Compared with the ANLL cells, the lymphoma cells were statistically significantly sensitive to activated effector cells (p less than 0.025). On the basis of the unlabeled target competition test and the recovery of cytotoxic cells within the fractions enriched in natural killer (NK) cells, NK cells appeared to mediate the above unstimulated and IFN-boosted cytotoxicity. In experiments using autologous effector-target cells from 11 patients, the addition of 500 U of IFN/ml enhanced the lytic activity of PBMC against autologous lymphoma cells in 1 patient, and higher concentrations of IFN, i.e., 2500 or 3500 U/ml, enhanced their cytotoxic activity against autologous leukemia or lymphoma cells in 4 of 8 patients. These data indicate that IFN-activated allogeneic PBMC are able to lyse both myeloid and lymphoid tumor cells, whereas higher concentrations of IFN are required to enhance lytic activity against autologous tumor cells.

Cytotoxicity, Immunologic↗