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Biomedical subjects

F Hirata

Publications and source records attributed to F Hirata.

At least 73 records · Page 4Linked to original sources
PubMed1984

[Non-invasive estimates of hemodynamics in normal pregnancy].

Pregnancy provides excellent opportunities for observing the hemodynamic alterations in cardiac function occurring during the physiologic stress imposed on the normal myocardium. Hemodynamically, the most important change in the maternal circulation during pregnancy is an increase in the circulating blood volume and cardiac output. In the average woman, the cardiac output at rest rises 30-50% above the normal non-gestational resting value. Echocardiography was performed for 25 normal pregnant women, ranging in age from 21 to 36 years (mean age of 28.7 years). Echocardiography was performed periodically through out pregnancy, at the gestational ages of the 10th, 24th, 32nd, 36th, and the 3rd postpartal weeks. Tracings were obtained in the left lateral and supine positions. All pregnancies were uncomplicated, and there was no twin pregnancy. The heart rate increased throughout gestation. However, the systolic and diastolic blood pressures did not change significantly throughout pregnancy. End-diastolic left ventricular dimension (LVDd) increased throughout gestation, with the peak at the 36th week of gestation. Left atrial dimension (LAD) and mVCF increased at the 36th week of gestation. Throughout gestation, the ejection fraction (EF) showed no significant change. There were no measurable differences in the cardiac size and function in the left lateral and supine positions. Increased LVDd and LAD throughout gestation were thought the reflexion of the increased blood volume and venous return which had its peak in the 36th week of gestation. The slightly larger cardiac size and end-diastolic volume seemed to induce the increased myocardial fiber stretch and, in turn, the increased mVCF. Our results indicated that chronic volume overload with increased circulating blood volume occurs in normal pregnancy, resulting in the large cardiac size and increased contractility of myocardial fiber.

Adult↗
PubMed1984

Quinacrine inhibits the primary but not secondary proliferative response of human cytotoxic T cells to allogeneic non-T cell antigens.

Quinacrine inhibited the generation of cytotoxic T lymphocytes from human peripheral blood T cells stimulated by allogeneic non-T cells as measured by [3H]thymidine incorporation as well as by cytolytic reactions against 51Cr-labeled allogeneic lymphocytes. These observations were further supported by the finding that quinacrine inhibited the expression of Tac antigen, the receptor for growth factor(s). Because other phospholipase A2 inhibitors such as tetracaine and p-bromophenacyl bromide could inhibit these reactions, the inhibition of cytotoxic T lymphocyte responses by quinacrine appeared to be attributable to the inhibition of phospholipase A2 in these cells. In keeping with this interpretation, arachidonate release from phospholipids in cytotoxic T cells stimulated by allogeneic non-T cells was inhibited by quinacrine. In contrast, the pretreatment of T cells with quinacrine did not result in the inhibition of their secondary proliferative response to the same stimulation with allogeneic non-T cells. These results, taken together, suggest that quinacrine does not inhibit the recognition of antigens by cytotoxic T cells, while it blocks the mitogenic response of T cells to allogeneic antigens.

Cytotoxicity Tests, Immunologic↗
PubMed1984

[Ferritin levels of ascites and the contents of cystic ovarian tumors--possibilities of ferritin production and secretion by malignant tumor cells].

In this paper, we presented an interesting case with a cystic ovarian tumor, which consisted of the mucinous cystadenoma and the mucinous cystadenocarcinoma separated by a partition. The determination of ferritin concentrations in the both displayed ferritin levels of 87.5 ng/ml in the former and 14,812.0 ng/ml in latter respectively. This fact suggested the production of ferritin by the malignant tumor cells. To clarify this possibility, measurement of ferritin levels in the content of cystic ovarian tumors in fifteen cases and in the ascites of various origin in sixty-five cases was done. This study also supported a possibility that malignant tumor cells produce and/or secrete much more ferritin into the body fluid than benign tumor cells.

Ascitic Fluid↗
PubMed1983

Differentiation of a histiocytic lymphoma cell line by lipomodulin, a phospholipase inhibitory protein.

When U 937 cells, a human histiocytic lymphoma cell line, were cultured with purified lipomodulin for 3 days, morphological and functional differentiation was induced as detected by microscopical examination of Giemsa stained smears, expression of mature monocyte antigen, and antibody dependent cellular cytotoxicity tests. Essentially similar differentiation was observed by the treatment with dexamethasone for 6 days and this differentiation by dexamethasone was blocked by monoclonal anti-lipomodulin antibody. Furthermore, the synthesis of immunoprecipitable lipomodulin in these cells was induced by dexamethasone treatment. These results, taken together, suggest that the induction of lipomodulin synthesis might be the primary event in dexamethasone-induced cellular differentiation of U 937 cells.

Annexins↗
PubMed1983

Adherence and regulation of leukotaxis.

PMNs upon stimulation by a chemoattractant adhere to a substratum and then in amoeboid fashion migrate toward the source of the attractant. We have studied molecular events in both adherence and migration and have arrived at the following conclusions: 1) PMNs, like other motile cells such as highly metastatic tumor cells, can use laminin to attach to Type IV basement membrane collagen. PMNs may use this anchoring mechanism in their emigration from the vasculature. 2) Attached cells may be stimulated to migrate as a result of the chemo-attractant-induced inactivation of lipomodulin, a natural inhibitor of phospholipase A2, an enzyme that may be essential for chemotaxis. 3) The substrate for this enzyme is generated by both the CDP-choline and transmethylation pathways. These pathways may be regulated by another enzyme, transglutaminase (TGase). 4) Natural substrates of TGase, such as uteroglobin, inhibit leukocyte chemotaxis, again suggesting a regulatory role for TGase in chemotaxis. 5) Tumor cells also produce inhibitors of chemotaxis. In addition to protecting the tumor from the host's phagocytes, these inhibitors may be related to normal modulators of cell motility. Therefore, determination of their mode of action could increase our understanding of this type of cell behavior.

Annexins↗
PubMed1983

Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.

The biochemical events that lead to bradykinin stimulation of cAMP accumulation in human fibroblasts were examined. Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content. The dose-response curves of bradykinin for the increase in the above changes were similar. In human fibroblasts, exogenous arachidonic acid was mainly incorporated into phosphatidylcholine, followed by phosphatidylserine, phosphatidylethanolamine, and phosphatidylinositol. Bradykinin caused a release of arachidonic acid from methylated phospholipids (phosphatidylcholine) and phosphatidylinositol. 3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation. Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation. Indomethacin, a cyclooxygenase inhibitor, blocked the effect of bradykinin on cAMP accumulation. Prostaglandins E1 and E2, but not F2 alpha, increased accumulation of cAMP. These observations indicate that bradykinin generates cAMP via arachidonic acid release and subsequent formation of prostaglandins. Our findings suggest that arachidonic acid can arise from either phosphatidylcholine synthesized by the methylation pathway or phosphatidylinositol.

Arachidonic Acid↗
PubMed1983

Role of lipomodulin, a phospholipase inhibitory protein, in immunoregulation by thymocytes.

The treatment of murine thymocytes with anti-lipomodulin antibody during Con A stimulation causes selective loss of suppressor activity, but not of helper activity on PFC assay, when co-cultured with T cell-depleted spleen cells. Interaction of the antibody with responder cells in thymocyte culture were necessary in the early stage rather than in the later stage of lymphocyte activation by Con A, which suggests that anti-lipomodulin antibody acts in the stage of suppressor T cells generation. When thymocytes were cultured with purified lipomodulin for 48 hr, suppressor activity was induced. Lipomodulin as detected by radioimmunoassay was found to be released from T cells with the phenotype of I-J+, Lyt-1-, Lyt-2+. The immunoprecipitates from the media of Con A-stimulated thymocyte with anti-I-Kk antibody and anti-lipomodulin antibody were analyzed on SDS-gel electrophoresis. I-J products had m.w. 36,000 and 24,000, whereas lipomodulin had m.w. 36,000, 24,000, and 15,000. Because anti-I-Jk antibody could precipitate 125I-labeled lipomodulin purified from rabbit neutrophils, these results suggest that lipomodulin is a product of I-J genes that induces suppressor T cells.

Animals↗
PubMed1983

Lipomodulin: a possible mediator of the action of glucocorticoids.

Lipomodulin, a protein with a MW of 40,000, is induced in many cells by glucocorticoids. This protein can mimic a variety of biological activities of glucocorticoids such as anti-inflammation, immunosuppression, and promotion of cellular differentiation. Since anti-lipomodulin antibody can block these effects of both glucocorticoids and lipomodulin, it is quite possible that lipomodulin is a mediator of glucocorticoids.

Animals↗
PubMed1983

Inhibition of human natural killer (NK) activity and antibody dependent cellular cytotoxicity (ADCC) by lipomodulin, a phospholipase inhibitory protein.

A highly purified preparation of lipomodulin, a phospholipase-inhibitory protein from rabbit neutrophils treated with glucocorticoids, inhibited NK and antibody-dependent cellular cytotoxicity (ADCC) activities of human peripheral blood lymphocytes in a dose-dependent manner. The presence of lipomodulin during the early period of the cytotoxicity assay was necessary to obtain maximal inhibition. The inhibition of NK or ADCC activity by lipomodulin was greater when effector cells were treated with lipomodulin than when target cells were incubated with lipomodulin. As lipomodulin did not block binding of effector cells to target cells, our results suggest that lipomodulin inhibits the cytolytic phase of NK and ADCC activities after binding to target cells, and imply that phospholipase(s) may be involved in NK and ADCC activities.

Annexins↗