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Biomedical subjects

A Kuramoto

Publications and source records attributed to A Kuramoto.

At least 73 records · Page 4Linked to original sources
PubMed1993

Presence of a regulatory element within the first intron of the human platelet-derived growth factor-A chain gene.

We detected a suppressive element in the first intron of the human platelet-derived growth factor A chain (PDGF-A) gene. Two or more proteins, at least 110-kd and 90-kd proteins, were bound over a wide region of this fragment, and the fragment suppressed the expression of the PDGF-A chain via these proteins in vivo. Since the fragment also had suppressor activity on the promoter of the PDGF-B chain, it may be involved in a suppressive mechanism of gene expression common to PDGF-A and -B chains. Four tandem repeats of CCCCAT(CCCC) and three direct repeats of GGGGAG were observed in this region. The expression of the PDGF-A chain is considered to be regulated by a mechanism involving not only the 5' upstream region but also introns.

Base Sequence↗
PubMed1993

Expressions of DNA topoisomerase I and II gene and the genes possibly related to drug resistance in human myeloma cells.

In order to clarify the mechanism of drug resistance in human myeloma cells, we investigated the expressions of DNA topoisomerase I and topoisomerase II gene and the genes possibly related to drug resistance; multi-drug resistant gene 1 (MDR-1), glutathione S-transferase class pi gene (GST-pi), by Northern blotting. Myeloma cells in eight of 15 cases prior to chemotherapy expressed topoisomerase I mRNA considerably, while the expression of topoisomerase II mRNA was detected weakly in only one of 16 myeloma patients. There was not any correlation between expression of topoisomerase I mRNA and clinical drug resistance. Significant expression of MDR-1 mRNA and P-glycoprotein was not detected in 25 cases of multiple myeloma prior to chemotherapy and even after several courses of VAD (vincristine, adriamycin and dexamethasone) therapy by Northern blotting and immunostaining using monoclonal anti-P-glycoprotein antibody (MRK-16), respectively. On the other hand, 16 of 21 myeloma cases showed significant expression of GST-pi protein and GST-pi mRNA with the various strengths, but there was no apparent correlation between GST-pi mRNA expression and clinical response. Therefore these data suggest that expression of the genes we tested may not determine the level of drug resistance in multiple myeloma, but lower or no significant expression of topoisomerase II mRNA in most myeloma cells indicates the possibility that topoisomerase II inhibitors such as VP-16 and topoisomerase II-mediated cytotoxic drugs such as adriamycin, are not so effective for the treatment of multiple myeloma.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

CD4+, CD45RA+, CD29- T-cell lymphocytic leukemia functioning as T suppressor inducer for B-cell immunoglobulin synthesis.

We describe here a case of T-cell lymphocytic leukemia (T-CLL) which coexpressed CD4 and CD45RA cell-surface antigens and functioned as suppressor inducer cells. The patient, an 81 year-old man, had massive generalized lymphadenopathy. His hemoglobin was 9.4g/dl, the platelet count 94,000, and the WBC was 895,000/microliters with 98% abnormal lymphoid cells. He had massive hepatosplenomegaly. Serum LDH was elevated to 3,990 u/l. The T-CLL cells coexpressed antigens detected by MAbs CD2, CD3, CD4, CD5, Ti(TcR alpha/beta; WT31) CD45 and CD45RA, but did not express any other antigens including CD1, CD8, CD29, and TCR gamma/delta, Ti gamma A and TQ-1. The cell-surface phenotypes of the cultured cells established by utilizing recombinant interleukin 2 were basically the same as those of the uncultured peripheral blood lymphoid cells. Both the peripheral blood and cultured cells clearly showed gene rearrangement for T cell receptors, TcR beta and TcR gamma. No association with human T-cell leukemia virus-1 (HTLV-1) was found by means of electron microscopic studies or the application of MAbs to p19 and p24 of HTLV-1. No anti-HTLV-1 antibody was detected. By the means of two color fluorescence, it was clearly demonstrated that the leukemic cells possessing CD4 in the peripheral blood and cell cultures coexpressed CD45RA, but did not express either CD29 or TQ-1. In vitro immunoglobulin synthesis by normal T and B cells was remarkably reduced in the presence of CD8+ T and leukemic cells. This suggests suppressor inducer T cell activity for the leukemic cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Regulation of the human platelet-derived growth factor B-chain gene.

Human platelet-derived growth factor (PDGF) B chain is a cellular homologue of v-sis, closely involved in cell growth and oncogenicity. Analysis in this study showed the importance of not only the region near the TATAA box but also the fragment -355 bases or more upstream in the expression of the PDGF-B chain gene. However, tissue specificity was not clear in the 5' upstream region alone, and regulation by gene methylation or by elements other than in the 5' region seemed to be necessary. In A172 cells, the half-life of mRNA was much shorter in the PDGF-B chain (< 2 hours) than in the PDGF-A chain (7 hours). Regulation of the PDGF-B chain gene may markedly differ from that of the PDGF-A chain gene not only at the transcriptional level but also at the post-transcriptional level.

Chloramphenicol O-Acetyltransferase↗
PubMed1993

Cytogenetic abnormalities of hematopoietic tissue in retired workers of the Ohkunojima poison gas factory.

A high incidence of cancer of the respiratory tract has been reported among former workers in a poison gas manufacturing plant which operated on Ohkunojima from 1927 to 1945. This report provides evidence of a high incidence of chromosome abnormality and sister chromatid exchange (SCE) rate among the former workers, as well as cytogenetic changes in two patients among the former workers with chronic myelocytic leukemia (CML). A chromosome study of seven former workers with chronic bronchitis revealed a stable type of aberration, the average abnormality being 10.9 +/- 4.4 percent, which is equivalent to those of atomic bomb survivors exposed at 1.2 km from the hypocenter. The SCE rate observed in 16 former workers ranged from 4.9 +/- 2.1 to 17.8 +/- 3.9, which was significantly higher than in the control group (p < 0.03). One of the CML patients showed an extremely high percentage of missing Y chromosomes along with t(9;22) translocation which is a specific chromosome aberration for the disease. Furthermore, the patient had almost a 3 times higher SCE rate compared to the control group and a high incidence of chromosome abnormality (12.1%) of the peripheral lymphocytes. These results suggest that the development of leukemia in this patient was strongly related to poison gas exposure.

Aged↗
PubMed1993

A possible mechanism of inability of immunoglobulin heavy-chain production in Bence-Jones type myeloma cells.

To clarify the mechanism of the inability of immunoglobulin heavy (IgH) chain production in Bence-Jones (BJ) type myeloma cells, we examined the rearrangement of the IgH gene, the expression of IgH mRNA and the presence of functional nuclear factors that bind to the IgH gene enhancer in myeloma cells from 6 cases of BJ-type myelomas, and three myeloma cell lines and one Epstein-Barr virus-transformed B cell line having no IgH chain production. All BJ-type myeloma cells we examined showed rearranged bands by Southern blotting using the JH probe, and the rearrangement of VDJ segments in these cells was confirmed by PCR amplification of VDJ segments with consensus VH and JH primers. However, the expressions of IgH mRNA were not detected by Northern blotting in any of the BJ-type myeloma cells or the three non-producer myeloma cell lines. These findings suggested that the transcription of the IgH gene ceased in these cells, and alteration of this transcriptional apparatus may explain this inability. The functional nuclear factors that bind to IgH gene enhancers (HE2 and HE3) were absent in the myeloma cells from one case of BJ-type myelomas among these BJ-type myeloma cells and myeloma cell lines. This suggests that alteration of the enhancer binding factors may be one of the reasons why BJ-type myeloma cells are unable to produce the IgH chain.

Base Sequence↗
PubMed1993

Clinical and cytogenetic findings of myelodysplastic syndromes showing hypocellular bone marrow or minimal dysplasia, in comparison with typical myelodysplastic syndromes.

Hematologic and cytogenetic data were collected on 401 myelodysplastic syndromes (MDS) patients in Japan and their clinical relevance was analyzed. More than 50% of the MDS patients with hypocellular bone marrow had > 5% marrow blasts at the time of MDS diagnosis and frequently had complex aberrations (chromosome changes at three or more regions). They showed peripheral blood findings resembling those of aplastic anemia, but progression into leukemic phase and the prognosis tended to mimic typical MDS. In MDS patients with minimal dysplasia, hematologic parameters were different from those of aplastic anemia. However, the low incidence of leukemic transformation and the favorable prognosis was similar to that of aplastic anemia. More than 90% of the patients in this group had refractory anemia and had normal karyotypes. Thus differential diagnosis from a low grade aplastic anemia is important, since this type of MDS might have a clonal nature as well. In conclusion, although some hematologic and clinical deviations are noticed in MDS with hypocellular marrow or minimal dysplasia, these MDS subtypes might constitute marginal forms of MDS.

Adult↗
PubMed1993

1 alpha-Hydroxyvitamin D3 in the treatment of primary myelofibrosis: in vitro effect of vitamin D3 metabolites on the bone marrow fibroblasts.

Thrombocytopenia and splenomegaly improved in one of the four patients receiving 1 alpha-hydroxyvitamin D3 (1 alpha(OH)D3) for treatment of primary myelofibrosis (PMF). We compared the clinical results with the in vitro effects of vitamin D3 metabolites on the growth and collagen synthesis of bone marrow fibroblasts. The effects of vitamin D3 metabolites on control human bone marrow fibroblasts were first studied in vitro. On the growth, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) inhibited the platelet derived growth factor (PDGF) or human serum-induced proliferation at the concentrations of more than 10(-10) M, while in the presence of transforming growth factor-beta (TGF-beta) the inhibitory effects were mild or non-inhibitory. Both vitamin D3 metabolites inhibited procollagen synthesis at a concentration of more than 10(-8) M. The effect of 1,25(OH)2D3 on the PMF patients was examined. In two of the four patients, the human serum-induced growth inhibitory effect was observed at the concentration of 10(-8) M, in one patient no inhibition was observed and in one patient inhibition was observed at 10(-10) M, as was observed in the control donors. During the treatment with 1 alpha(OH)D3 the serum level of 1,25(OH)2D3 was 1-2 x 10(-10) M. These findings suggest that a minority of PMF patients have marrow fibroblasts with growth sensitivity to a pharmacological level of vitamin D3 and could be treated with 1 alpha(OH)D3 with some clinical improvements.

Aged↗
PubMed1993

[Vascular endothelial cell injury as the initial event in thrombotic thrombocytopenic purpura].

It is an important argument whether vascular endothelial injury is the initial event or not in TTP. There is many possible triggers to vascular endothelial injury: Endotoxins, immune complex, and drugs et al. In these conditions, some cytokines (TNF, IL-1 etc.) induce the activation of endothelial cell. Then, neutrophil can adhere to endothelial cells through adhesion molecules. Endothelial cells were injured, by the activation and the adhesion of neutrophil. The injury of the endothelial cells causes the exposure of subendothelial tissues, and then induce the platelet adhesion on these surface for the initial event of platelet aggregates. Although heterogenous triggers and pathophisiological events are recognized in TTP, endothelial cell injury is the initial event or the essential event.

Antigen-Antibody Complex↗
PubMed1993

Monoclonal gammopathy in atomic bomb survivors.

An analysis of monoclonal gammopathy in relation to radiation exposure was conducted on atomic bomb survivors examined between October 1979 and September 1981 and between June 1985 and May 1987. There was no overall increase in the relative risk of monoclonal gammopathy and only a suggestive increase in benign monoclonal gammopathy in the second survey which did not achieve statistical significance (P = 0.17). Thirty-one cases were detected among 8796 individuals studied in the first survey, whereas 68 cases were found among 7350 people in the second survey. Among the 31 cases found in the first survey, 9 individuals (29%) died before the second survey: 4 of cancer, 4 of vascular disease, and 1 of infection. Among the 8 individuals with benign monoclonal gammopathy examined in both surveys, 4 developed suppression of residual immunoglobulin(s), suggesting the progression of monoclonal gammopathy. The overall relative risks of monoclonal gammopathy in atomic bomb survivors in the two surveys were not significantly increased with increasing radiation dose. Only benign monoclonal gammopathy in 1985-1987 showed a suggestive increase with radiation exposure. The relative risk of benign monoclonal gammopathy in 1985-1987 was 2.64 in the group exposed to 0.01-0.49 Gy and 2.14 in the > or = 0.50-Gy group (95% confidence intervals = 0.90-8.82 and 0.69-7.31, respectively).

Female↗
PubMed1993

Clinical implications of chromosomal abnormalities in 401 patients with myelodysplastic syndromes: a multicentric study in Japan.

It is well known that cytogenetic analysis in patients with myelodysplastic syndrome (MDS) provides information useful in determining their prognosis. Based on the chromosomal results obtained from 401 MDS patients by a multicentric study in Japan, we studied correlations between chromosomal findings and prognosis or leukemic transformation in MDS patients. Patients with complex aberrations (cytogenetic abnormalities at more than three chromosomes), of any subtype, had a poor prognosis; for example, > 60% of patients with refractory anemia (RA) showing complex aberrations died within one year, but only 11% of them developed leukemia. In patients with RA with ringed sideroblasts (RARS), > 70% of those with complex aberrations evolved into the leukemic phase and survived for less than one year, suggesting a biologic heterogeneity in RARS patients. By contrast, about 5% of patients with RA or RARS exhibiting chromosomal findings other than -7/7q-, +8, two aberrations, and complex aberrations, developed leukemia and had a favorable prognosis. Therefore, the presence of chromosome abnormalities alone in patients with RA or RARS is not a factor in predicting leukemic transformation or poor prognosis. In patients with refractory anemia with an excess of blasts (RAEB), the presence of chromosome aberrations at MDS diagnosis affected the occurrence of leukemic transformation (24% versus 43%), however, no particular difference was noted in patients with RAEB in transformation with regard to whether they had chromosome changes or not, and about 60% of them evolved into leukemia. The poor prognosis related to complex aberrations was consistently noted in all MDS subtypes or age-matched groups, indicating that this cytogenetic anomaly is an independent risk factor for a poor prognosis in MDS patients. The duration between MDS diagnosis and development of the leukemic phase and that between the latter and death were significantly shorter in patients with complex aberrations than those without this change. Although the clinical significance of certain chromosomal abnormalities differs among subtypes of MDS, a new scoring system for predicting prognosis by cytogenetic changes, in combination with hematologic parameters, was proposed.

Adolescent↗
PubMed1992

Expression of the heparin-binding growth factor receptor genes in human megakaryocytic leukemia cells.

K-sam/bek, N-sam/flg and FGFR3/sam3 establish gene family of the receptors for heparin-binding growth factors (HBGFs) or FGFs. These mRNAs were detected in human leukemia cells, CMK, K562 and HEL, which have megakaryocytic phenotype or the potency to differentiate into megakaryocytic lineage. In CMK cells N-sam/flg transcript level was enhanced by the culture with 12-O-tetradecanoylphorbol-13-acetate (TPA). cDNA-polymerase chain reaction identified K-sam/bek mRNA in human platelets, suggesting the involvement of HBGFs in megakaryocytopoiesis and functions of platelets.

Base Sequence↗