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Biomedical subjects

R Takimoto

Publications and source records attributed to R Takimoto.

35 records · Page 2Linked to original sources
PubMed1997

[Hemolytic anemia and thrombocytopenia induced by cimetidine: recurrence with ranitidine administration].

A 69-year-old woman was admitted with apoplexy after operation of mitral valve stenosis and gastrectomy due to a gastric ulcer. In June 1994, her condition gradually worsened after acute pneumoniae in her right lung. Intravenous hyperalimentation with cimetidine administration was started to improve her undernourishment, because she had a history of gastric ulcer. However, after 10 days from the start of cimetidine therapy, anemia progressed rapidly. Biochemical examinations revealed that the serum indirect bilirubin and LDH levels were elevated and no serum haptoglobin was detected. These results indicated the development of hemolytic anemia, but at that time we could not clarify the reason. In October 1994, thrombocytopenia gradually progressed, and we halted the administration of cimetidine to ranitidine. Both hemolytic anemia and thrombocytopenia was dramatically improved after cessation of cimetidine administration. We then changed the drug from cimetidine, however the same phenomena have appeared again. The patient was in stable condition, after cessation of H2-blockers administration. The complication of hemolytic anemia and thrombocytopenia associated with H2-blocker administration in Japan.

Aged↗
PubMed1997

[Thrombocytopenia associated with sodium polystyrene sulfonate].

A 84-year-old man was admitted with diabetes mellitus, hypertension and chronic renal failure in September 1994. In October 1995, his renal function gradually worsened with hyperkalemia. Sodium polystyrene sulfonate (Kayexalate) was administered orally for the treatment of hyperkalemia. However, after 7 days from the start of Kayexalate therapy, thrombocytopenia progressed gradually, and 12 days later the initial platelet count of 20.7 x 10(4)/microliter decreased to 8.6 x 10(4)/microliter. This thrombocytopenia rapidly improved after cessation of Kayexalate administration. In December 1995, readministration of Kayexalate for the treatment of hyperkalemia induced thrombocytopenia again. Bone marrow aspiration biopsy revealed normal counts of nucleated cells and megakaryocytes with no increase in blasts. No other disorders which cause thrombocytopenia were seen in this patient. The complication of thrombocytopenia associated with Kayexalate has not been reported. This is the first reported case of thrombocytopenia caused by Kayexalate administration.

Aged↗
PubMed1996

Successful treatment of vitiligo with PUVA-pigmented autologous epidermal grafting.

BACKGROUND: The methoxypsoralen-ultraviolet A-light (PUVA)-induced pigmented epidermal grafting procedure appears to be a more effective treatment for vitiligo than similar treatments presently available. This finding was based on: 1) a more vigorous and completely homogeneous repigmentation was observed in the vitiliginous area and 2) that the treatment was safe, easy, inexpensive, and not time-consuming (approximately 3-4 hours), thus making it a suitable outpatient clinic treatment procedure for vitiligo patients. PATIENTS AND METHODS: Twenty-eight patients with amelanotic depigmented lesions that had been refractory to conventional therapy were treated using suction blisters from autologous epidermal sheets. These had 8-methoxypsoralen (8-MOP) solution applied and had been exposed to ultraviolet A light (topical PUVA) in order to stimulate melanogenesis. RESULTS: Successful repigmentation was obtained after transplantation in all patients with segmental and localized vitiligo. The most homogeneous repigmentation was obtained within 3 months after grafting. CONCLUSIONS: This novel procedure is an excellent tool by which to treat segmental and localized vitiligo lesions that have failed to respond to other therapies.

Adolescent↗
PubMed1995

Identification of a transforming growth factor beta-1 activator derived from a human gastric cancer cell line.

It has been shown that some types of tumour cells produce activated transforming growth factor beta-1 (TGF-beta 1). However, the mechanism for the activation of TGF-beta 1 derived from tumour cells has not been fully elucidated. The present study was undertaken to characterise an activator of latent TGF-beta 1 secreted from a human gastric cancer cell line, KATO-III. Western blot analyses using antibodies for TGF-beta 1, latency associated peptide (LAP) and latent TGF-beta 1-binding protein (LTBP) revealed that, in the cell lysate of KATO-III, TGF-beta 1 protein was expressed as a small latent complex of TGF-beta 1 and LAP. This was also confirmed by a gel chromatographic analysis of the cell lysate obtained from KATO-III. A 2.5 kb transcript of TGF-beta 1 mRNA was detected in KATO-III cells by Northern blot analysis. A gel chromatographic analysis of the conditioned medium from KATO-III cells revealed, in addition to the active form of TGF-beta 1, a factor which activated latent TGF-beta 1 from NRK-49F cells at fractions near a molecular size of 65,000. This factor was inactivated by heat (100 degrees C), acidification, trypsin and serine protease inhibitors. TGF-beta 1 activity in KATO-III cell lysate was not detected in the untreated state, but potent TGF-beta 1 activity was detected after acid treatment. These results suggest that KATO-III releases not only a latent TGF-beta 1 complex but also a type of serine protease, different from plasmin, plasminogen activator, cathepsin D, endoglycosidase F or sialidase, which activates the latent TGF-beta 1 complex as effectively as acid treatment.

Blotting, Northern↗
PubMed1994

Transforming growth factor beta 1 secreted from scirrhous gastric cancer cells is associated with excess collagen deposition in the tissue.

To explore the mechanism of increased collagen deposition in scirrhous carcinoma of the stomach, an attempt was made to define the role of transforming growth factor beta 1 (TGF-beta 1), secreted from tumour cells, as a possible humoral factor which functions in a paracrine manner to stimulate the production of collagen in regional fibroblasts. Immunohistochemical staining revealed that tumour cells in scirrhous carcinomas were generally stained more intensively than those in other types of carcinomas. On Northern blot analysis the tumour cells established from scirrhous carcinoma (KATO-III, OCUM-1 and HSC-39) exhibited relatively strong signals compared with those from non-scirrhous carcinoma (MKN-28 and MKN-45). In the culture media of scirrhous carcinoma cells, the active form of TGF-beta 1 was detected, while in those of the non-scirrhous carcinoma cells the latent form was demonstrated by both colony and radioreceptor assays. The culture medium from KATO-III showed strong stimulating activity of collagen synthesis in fibroblasts, and this activity was partially neutralised by an anti-TGF-beta 1 antibody. These results suggest that tumour cells in scirrhous carcinoma produce more active-form TGF-beta 1 than does non-scirrhous carcinoma and thus is partially responsible for the observed enhanced collagen deposition in the region.

Adenocarcinoma, Scirrhous↗
PubMed1994

Close correlation between the dephosphorylation of p53 and growth suppression by transforming growth factor-beta 1 in nasopharyngeal carcinoma cells transduced with adenovirus early region genes.

The mechanism of growth inhibition by transforming growth factor (TGF)-beta 1 was investigated. We examined the growth inhibitory effects of TGF-beta 1 on human nasopharyngeal carcinoma (KB) cells which constitutively expressed p53. TGF-beta 1 suppressed the DNA synthesis of KB cells in a dose-dependent manner. It had minimal effect on adenovirus-2-transduced KB cells expressing either adenovirus early region 1B (E1B) or 1A (E1A) product, which respectively binds to p53 or Rb product and inhibits its function, and no growth inhibition at all was observed with KB cells expressing both E1B and E1A products. Dephosphorylation of the p53 was promoted by TGF-beta 1 stimulation in KB cells, but not in E1B-producing KB cells, which sequestrate the function of p53. The growth inhibition of KB cells by TGF-beta 1 was significantly reduced by treatment with okadaic acid. These results suggest that p53 transduces the antiproliferative signal of TGF-beta 1 possibly through its dephosphorylation.

Adenovirus E1A Proteins↗
PubMed1994

[TGF-beta and platelet].

In the present paper, we investigated the pathophysiological implication of TGF-beta from megakaryocytes or megakaryoblasts in the development of myelofibrosis. In the bone marrow of myelofibrosis, proliferation of megakaryocytes is often noticed. We therefore investigated the TGF-beta expression in the bone marrow megakaryocytes from 12 chronic myeloproliferative disorder patients with myelofibrosis by immunohistochemical analysis. About all the specimen showed strong positivity for TGF-beta. In order to examine whether megakaryoblasts produce TGF-beta, we then measured TGF-beta activity in the conditioned medium (CM) of megakaryoblasts from a patient with acute megakaryoblastic leukemia who had profound myelofibrosis. The CM showed strong collagen synthesis stimulating activity which was nullified by addition of anti TGF-beta antibody. Since TGF-beta exists as latent form in platelets, TGF-beta was considered to be altered from active to latent form during megakaryocytes differentiation. In this context, MEG-01, a megakaryoblastic cell line which produces active TGF-beta was underwent differentiation to produce platelet-like bleb with TPA treatment. During the differentiation, MEG-01 showed the decrease of active TGF-beta production and increase of latent TGF-beta together with the production of LTBP. These results suggest that megakaryoblasts produce active TGF-beta and may may cause myelofibrosis, while more differentiated megakaryocytes produce latent TGF-beta. Mechanism by which megakaryoblast escape from negative autocrine of active TGF-beta was also investigated. MEG-01 was found to express mutated p53 which is considered to be responsible for impaired signal transduction of TGF-beta.

Blood Platelets↗
PubMed1993

[NEO-MACOP-B chemotherapy for the treatment of advanced-stage aggressive non-Hodgkin's lymphoma].

We conducted a new chemotherapy, NEO-MAC OP-B (addition of etoposide and mitoxantrone to MACOP-B with half dose of methotrexate and half administration of doxorubicin), to reduce severe mucositis, which is a major toxic effect of MACOP-B, and to increase its effect with etoposide and mitoxantrone as new non-cross resistant drugs. Between Jan. 1989 and Mar. 1993, 12 patients with previously untreated advanced aggressive non-Hodgkin's lymphoma (NHL), 2 patients with adult T cell lymphoma, and 3 patients with relapsed NHL, were treated with NEO-MACOP-B. After termination of NEO-MACOP-B therapy, 83.3% of 12 patients with previously untreated NHL were in complete remission (CR). After median follow-up of 22 months, Kaplan-Meier estimates showed that overall survival of 12 previously untreated patients was 71.4%, and relapse-free survival of complete responder was 83.3%. Toxic effects on all 17 patients were moderate with a lower incidence of severe mucositis (only one patient with relatively severe stomatitis, WHO Grade 3). No treatment related deaths were observed. Thus, NEO-MACOP-B is an effective and safe treatment for advanced stage aggressive NHL.

Adult↗
PubMed1992

[Successful treatment of prolonged anemia after major ABO incompatible bone marrow transplantation for a case of myelodysplastic syndrome with recombinant erythropoietin].

A delay in red cell recovery after ABO-incompatible bone marrow transplantation (BMT) is often observed. The authors experienced a case of prolonged anemia after a major ABO incompatible BMT for myelodysplastic syndrome which was successfully treated with recombinant human erythropoietin (Epo). Effects of Epo were confirmed by the recurrence of anemia after withdrawal of Epo as well as the rapid reincrease in reticulocytes on readministration. The patient received a dose of Epo which was similar to the amount used for renal anemia, however serum concentration of Epo after administration exceeded endogenous Epo levels. Epo may have a beneficial role in the treatment of prolonged anemia after BMT.

Anemia↗