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Biomedical subjects

A Kuramoto

Publications and source records attributed to A Kuramoto.

At least 163 records · Page 9Linked to original sources
PubMed1989

Cytokines as autocrine growth factors in malignancies.

Interleukin 6 (IL-6) was originally characterized as a B-cell differentiation factor, responsible for the terminal maturation of activated B cells to immunoglobulin producing cells. Recent works reveal that IL-6 has a wide variety of biological functions on various cells. In particular, IL-6 has been shown to augment the growth of freshly isolated human myeloma cells, and the myeloma cells constitutively produce IL-6 and express IL-6 receptors. Moreover, it has been shown that anti-IL-6 antibody can inhibit the in vitro growth of the myeloma cells. This is direct evidence that an autocrine loop is operating in freshly isolated myeloma cells, and that a constitutive production of IL-6 and activation of the IL-6 gene could be involved in the oncogenesis of human myeloma.

Animals↗
PubMed1989

Progression activity for platelet-derived growth factor in plasma of patients with idiopathic thrombocytopenic purpura and aplastic anemia.

Progression activity for competence induced by platelet-derived growth factor (PDGF) was measured in plasma of patients with idiopathic thrombocytopenic purpura (ITP) and aplastic anemia (AA), in order to clarify the mechanism operating to maintain the wound healing system of these chronically thrombocytopenic patients. Progression activity in both ITP and AA patients was significantly higher than in normal subjects. There was a positive correlation between the activity and the duration of thrombocytopenia in AA patients who had thrombocytopenia for less than 100 months. The level of insulin like growth factor-I (IGF-I), which is a progression factor for PDGF, was lower in patients, than in normal controls. These results suggest that some plasma progression factor(s) for PDGF, other than IGF-I, plays an important role in maintaining the wound healing system of blood vessels in chronically thrombocytopenic patients.

Adolescent↗
PubMed1989

Low intracellular calcium concentration in the platelets after stimulation in patients with myeloproliferative disorders.

Intracellular calcium levels in the platelets of patients with myeloproliferative disorders (MPD) were measured by the Aequorin method. In the patients with MPD, the maximum intracellular calcium level [Ca2+]i was significantly lower and the time required to reach the peak calcium level was significantly longer than in normal controls after thrombin (0.5 U/ml) and collagen (2.5 micrograms/ml) stimulation. The rate of increase in intracellular calcium levels after thrombin (0.5 U/ml) stimulation in the presence of various concentrations of extracellular calcium was lower than in the normal controls, which suggests that the low level of intracellular [Ca2+]i after stimulation is caused mainly by a low Ca2+ influx. These results suggest the relationship between abnormalities of membrane glycoprotein and the impaired calcium influx of MPD platelets.

Blood Platelets↗
PubMed1989

Interleukin-1 accelerates autocrine growth of myeloma cells through interleukin-6 in human myeloma.

Recombinant interleukin 1 alpha (rIL-1 alpha) augmented proliferation of freshly isolated myeloma cells as well as B-cell stimulatory factor 2 (BSF-2)/interleukin-6 (IL-6). Recombinant IL-1 alpha-induced proliferation was partially inhibited by anti-IL-6 antibody. In the culture supernatants of rIL-1 alpha-stimulated myeloma cells, IL-6 activities, which were measured by using an IL-6-dependent murine hybridoma clone, MH60.BSF2, were increased, when compared with those in the culture supernatants of nonstimulated myeloma cells. Furthermore, IL-6 messenger RNA (mRNA) expression was also augmented in IL-1 alpha-stimulated myeloma cells. Therefore rIL-1 alpha stimulates myeloma cells to produce IL-6, which consequently augments proliferation of myeloma cells. Thus, IL-1 can accelerate autocrine growth of myeloma cells through IL-6.

Adjuvants, Immunologic↗
PubMed1989

Sensitive inhibitory effect of interferon-alpha on M-protein secretion of human myeloma cells.

The effects of interferon-alpha (IFN alpha) on in vitro proliferation and M-protein secretion in human myeloma cells were investigated. Human myeloma cells were purified from bone marrow aspirates in 12 multiple myeloma patients. Purified myeloma cells were cultured for 48 hours with IFN alpha at its lower concentrations (0.1 to 100 U/mL). The cells were then pulsed with 3H-TdR for the last 12 hours and 3H-TdR uptake was measured (in vitro proliferation). After 48-hour culture, supernatants were harvested and the amount of M-protein in these fluids were measured by enzyme-linked immunosorbent assay (ELISA) (in vitro M-protein secretion). In vitro M-protein secretions of myeloma cells were significantly suppressed even at 0.1 U/mL of IFN alpha, while 3H-TdR uptakes were not so suppressed until 10 or 100 U/mL of IFN alpha were added. The expressions of secretory immunoglobulin (Ig) mRNA of these myeloma cells were also selectively suppressed by IFN alpha. Furthermore, after IFN alpha had been administered intramuscularly, 3 to 6 x 10(6) U/d for at least 1 month, in vitro M-protein secretions of these myeloma cells were decreased compared with those before IFN alpha administration. Therefore, these results suggest that IFN alpha has more sensitive inhibitory effect on M-protein secretion of human myeloma cells rather than on myeloma cell proliferation.

Blood Proteins↗
PubMed1989

[Multiple myeloma following chronic neutrophilia terminated with acute monocytic leukemia (AML, M 5 b)].

A case of a 70 years old female who developed multiple myeloma during a course of neutrophilia, and later on terminated with acute monocytic leukemia (AML, M 5 b) following Melphalan therapy for five years is reported. This patient was first found to have neutrophilia in 1966, After six years, she developed monoclonal gammopathy, (IgG1 kappa type) which coexisted with the neutrophilia. She was put on Melphalan regimen for 5 years which was discontinued due to anemia, leukocytopenia and the reduction of serum IgG. By routine bone marrow examination, she was diagnosed as AMoL (AML, M 5 b) in July 1984. Thereafter, a combination chemotherapy of BH-AC, 6-MP and prednisolone was started and complete remission for the AMoL was achieved after 2 months. Sixteen months later, she relapsed and a similar combination chemotherapy for reinduction regimen was administered. However, the AMoL was resistant and after 7 months, she died of pneumonia and multiple organ failure. The association of neutrophilia with multiple myeloma, the occurrence of AMoL after prolonged Melphalan therapy for the multiple myeloma and the strategy of therapy for secondary leukemia is discussed.

Aged↗
PubMed1988

Platelet-derived growth factor is decreased in patients with myeloproliferative disorders.

Platelet-derived growth factor (PDGF) has been suggested to play some role in the pathogenesis of myelofibrosis frequently encountered in patients with myeloproliferative disorders (MPD). In this study we measured PDGF activity and PF4 content in circulating platelets of patients with MPD. Both factors were lower than those of normal controls. PDGF activity in patients with myelofibrosis was slightly lower than in those without fibrosis. However, when adjusted to whole blood volume, there was a positive correlation between platelet count and PDGF activity per ml whole blood. Nevertheless, no correlation was found between activity and grade of bone marrow fibrosis. These results may support the idea that an abnormal release of PDGF occurs from platelets or megakaryocytes in the bone marrow environment, resulting in the stimulation of fibroblast proliferation, and hence, the occurrence of myelofibrosis in patients with MPD.

Adult↗
PubMed1988

Flow cytometric analysis of peroxidase negative acute leukemias by monoclonal antibodies--II. Acute megakaryoblastic and acute pro-megakaryocytic leukemias.

In this report, we have described three cases of acute megakaryoblastic leukemia (AMKL) which were demonstrated by the presence of megakaryocyte-platelet-related cell-surface antigens detected by utilizing flow cytometry and monoclonal antibodies in addition to both PPO activity which was shown by ultrastructural cytochemistry and emergence of differentiation antigens while culturing these leukemic cells. The blasts of one case possessed both platelet GpIb and GpIIb/IIIa cell-surface antigens detected by 5F1 (CD36), AN51 (CDw42), and J15, P2 and HPL2 (CDw41), respectively, whereas the remaining two cases almost completely lacked Gp1b cell-surface antigen. Hence, the former was diagnosed as immature (pro) megakaryocytic leukemia and the latter as AMKL from the viewpoint of immunophenotypic analysis as discussed in this article.

Aged↗
PubMed1988

Effects of platelet derived growth factor, epidermal growth factor and transforming growth factor-beta on the growth of human marrow fibroblasts.

The effects of three growth factors contained in platelets on human bone marrow fibroblasts as well as fibroblast colony-forming cells were investigated to clarify the pathogenesis of marrow fibrosis frequently associated with myeloproliferative disorders. Two growth factors, platelet derived growth factor (PDGF) and epidermal growth factor (EGF), cooperatively stimulated the growth of passaged fibroblasts as well as fibroblast colony-forming cells. Transforming growth factor-beta augmented the growth of fibroblasts at low concentrations in the presence of EGF and/or PDGF, but inhibited that of colony-forming cells in the presence of PDGF or EGF. These results suggest that the growth of fibroblasts causing marrow fibrosis might be finely regulated, depending on the concentrations of growth factors released or leaked from platelets or megakaryocytes into marrow environment.

Adult↗
PubMed1988

Marrow fibroblasts from patients with myeloproliferative disorders show increased sensitivity to human serum mitogens.

The growth of marrow fibroblasts from patients with myeloproliferative disorders (MPD) was investigated using platelet derived growth factor (PDGF) and human serum as mitogens in the presence of human plasma derived serum. The proliferation of fibroblasts in MPD patients was increased compared to normal individuals, especially in patients with chronic myelocytic leukaemia and essential thrombocythaemia. This increment of proliferation might be due to higher sensitivity of the fibroblasts to plasma derived serum than to PDGF, because the ratio of proliferation with PDGF to that without PDGF, when compared between patients and normals, remained unchanged. These results suggest that MPD fibroblasts are more sensitive to some factor(s) in plasma, and this fact could partially explain the pathogenesis of myelofibrosis in MPD patients.

Adult↗
PubMed1988

Analysis of peroxidase-negative acute unclassifiable leukemias by monoclonal antibodies. 1. Acute myelogenous leukemia and acute myelomonocytic leukemia.

In this study, pretreatment peripheral and/or bone marrow blasts from 12 patients with acute unclassifiable leukemia (AUL) expressing the myeloid-related cell-surface antigen (CD 11) were isolated for further analysis. Despite a lack of myeloperoxidase (MPO) activity, 1 patient's blasts contained cytoplasmic Auer rods. The circulating blasts from another patient expressed MPO while maintaining the same surface phenotype during 20 months of clinical follow-up. In addition, the blasts from 3 cases demonstrated both myelomonocytic and monocyte-specific surface antigens, whereas the remaining 9 cases completely lacked any monocyte-specific antigen detectable by monoclonal antibodies, Mo2, My4 and Leu M3 (CD 14). The first case eventually was diagnosed as acute myelomonocytic leukemia and the second as acute myelogenous leukemia by means of immunophenotypic analysis using flow cytometry (FACS IV). In addition, the presence of MPO protein was identified in the cytoplasm of blast cells from 5 patients with AUL by means of a cytoplasmic immunofluorescence test using a monoclonal antibody (MA1). Our study indicates that non-T, non-B AUL expressing OKM1 (CD 11) antigens include acute leukemias which are unequivocally identifiable as being of either myeloid or myelomonocytic origin. However, further investigations, including immunophenotypic and cytoplasmic analysis, ultrastructural cytochemistry and gene analysis with molecular probes (tests applicable to normal myeloid cells), are necessary in order to determine the actual origin of blasts and to recognize the differentiation stages of the various types of leukemic cells from patients with undifferentiated forms of leukemia.

Antibodies, Monoclonal↗
PubMed1988

Aggressive natural killer cell leukemia/lymphoma with N901-positive surface phenotype: evidence for the existence of a third lineage in lymphoid cells.

The morphology, immunologic and functional properties of peripheral blood and bone marrow cells or cultured cells from 2 patients with clinically aggressive non-T, non-B lymphoma/leukemia are described. The leukemic cells possessed medium to large granules in the cytoplasm, antigens against CD38, CD2, CD25, OKIa1, CD16, TA-1, CD9, CD24 and NKH-1 (N901) monoclonal antibodies on their cell surface, and also showed a high natural killer (NK) activity. Phenotypically, the cells in these disorders were quite different from T gamma leukemia cells bearing Fc receptor or the traditionally reported NK leukemia cells possessing HNK-1 (Leu 7) antigens on their surface. In addition, these leukemias/lymphomas belonged to neither T- nor B-cell lineage, proved by studying clonal gene rearrangement for the T beta and T gamma receptor, and immunoglobulin. Hence, a quite interesting and important point, as suggested by our data, is that all our cases expressed an antigen for NKH-1 (N901), which is detectable on all NK cell surfaces and they lacked the antigen for Leu 7 (HNK-1), which is usually detected on the surface of leukemic NK cells. These facts indicate that we are dealing with a leukemic NK cell subset which is quite different from cells of all other reported cases of NK cell leukemias. We therefore concluded that such disorders with an aggressive clinical nature and a poor prognosis as in our cases belong to a new clinical entity originating from a portion of the NK cell subset.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗