Search PubMed⌕ Search

Biomedical subjects

S Furusawa

Publications and source records attributed to S Furusawa.

At least 181 records · Page 10Linked to original sources
PubMed1985

[The disorder of vitamin D metabolism in patients with liver cirrhosis].

Liver cirrhosis (LC) is often associated with osteomalacia and osteoporosis. Since it has been shown that serum levels of 25 hydroxy vitamin D (25-OH-D) are reduced in LC, defective hepatic hydroxylation of vitamin D has been postulated to be responsible for the low serum 25-OH-D levels and skeletal demineralization. This study was designed, therefore, to determine serum 25-OH-D and 1 alpha, 25-(OH)2-D levels in patients with LC. Further, the response of serum 1 alpha, 25-(OH)2-D to a single oral dose of 1 alpha-OH-D3 (2 micrograms) was investigated. In 5 patients with severe decompensated LC and 3 patients with compensated LC, serum 25-OH-D and 1 alpha, 25-(OH)2-D levels were respectively measured by the modified method of Belsey and by that of Eisman. Serum 25-OH-D in patients with compensated and decompensated LC was significantly higher than that in normals. Serum levels of 1 alpha, 25-(OH)2-D in patients with decompensated LC were significantly lower than those in patients with compensated LC and normals. After a single oral administration of 1 alpha-OH-D3 at a dose of 2 micrograms, the 1 alpha, 25-(OH)2-D rose in each patient within 6h, reaching the maximum levels at 12h. The percent increase over the basal value in decompensated LC was similar to that in compensated LC.(ABSTRACT TRUNCATED AT 250 WORDS)

Dihydroxycholecalciferols↗
PubMed1985

Influence of ranitidine on hepatic blood flow assessed by organ-reflectance spectrophotometer and pulse-Doppler ultrasonic flowmeter.

The influence of the intravenous injection of ranitidine (50 mg) on hepatic hemodynamics was investigated in normal subjects and patients with chronic liver disease. Using the organ-reflectance spectrophotometer, the regional hepatic blood hemoglobin concentration (delta Er569-650), an indicator of the regional hepatic blood flow, and the oxygen saturation of hemoglobin in the regional hepatic tissue (So2) were measured in patients with chronic liver disease after ranitidine injection under peritoneoscopy. With the pulse-Doppler ultrasonic flowmeter, the portal blood flow was measured in patients with chronic liver disease and normal subjects. There were no significant changes in the regional hepatic blood flow, the oxygen saturation of hemoglobin, and the portal blood flow after the intravenous injection of ranitidine. Thus, it is concluded that usual dose of ranitidine has no significant influence on the hepatic blood flow and that it can be prescribed without reducing the hepatic blood flow.

Adult↗
PubMed1985

Inhibitory effect of PWM-stimulated OKT4+ subsets on erythro-, granulo- and megakaryocytopoiesis in vitro.

Normal human peripheral blood T cells and T-cell subsets defined by monoclonal antibodies of the OKT series were pretreated with pokeweed mitogen (PWM). Their effects on the haematopoietic precursors, erythroid (BFU-E, CFU-E), granulocyte-macrophage (CFU-GM) and megakaryocyte (CFU-M) colony forming cells were evaluated by coculture. While unstimulated T cells and T-cell subsets enhanced growth of autologous blood BFU-E, PWM-stimulated T and OKT4+ cells suppressed it, also inhibiting proliferation of both autologous and allogeneic bone marrow BFU-E, CFU-E, CFU-GM and CFU-M. PWM-stimulated OKT8+ cells had little effect on the growth of any of the precursors at the cell concentration at which growth was completely inhibited by PWM-stimulated OKT4+ cells. Irradiation of T or OKT4+ cells with 3000 rad before PWM stimulation completely abrogated the inhibition. These observations might be related to the mechanism of pancytopenia in some cases of immune-mediated aplastic anaemia.

Antibodies, Monoclonal↗
PubMed1985

Specific production of eosinophil colony stimulating factor from sensitized T cells from a patient with allergic eosinophilia.

To explore the possibility that an eosinophil colony stimulating factor (EO-CSF) is elaborated independently of neutrophil CSF (N-CSF), we compared the effect on the production of EO-CSF and N-CSF of adding a specific antigen, an aspergillus extract, to peripheral blood leucocytes of an eosinophilic patient with allergic bronchopulmonary aspergillosis. Conditioned media prepared from the patient's mononuclear (MN) and T cells were assayed for EO-CSF and N-CSF activities by agar culture technique, using normal human nonphagocytic MN bone marrow cells as target cells. The addition of the specific antigen to the cultures of the patient's MN or T cells significantly stimulated the production of EO-CSF, but not that of N-CSF, while the patient's non-T cells and normal MN or T cells were not stimulated by the antigen challenge to produce either CSF. These results suggest that EO-CSF is a factor distinct from N-CSF, that its production is dependent on the presence of sensitized T cells with antigen-specific stimulation, and that it might be one of the causes of blood eosinophilia in this patient.

Antigens, Fungal↗
PubMed1985

Anticancer activity of a natural product, viva-natural, extracted from Undaria pinnantifida on intraperitoneally implanted Lewis lung carcinoma.

A natural product, named Viva-Natural, extracted from a dietary seaweed Undaria pinnantifida has been found to be therapeutically active against Lewis lung carcinoma (LLC). Viva-Natural also demonstrated moderate prophylactic activity against LLC in allogeneic mice. The active principle(s) which was concentrated in the water-insoluble fraction of Viva-Natural was essentially noncytotoxic in KB cell cultures, and probably a polysaccharide. Viva-Natural was found to be significantly effective in enhancing the natural cytolytic activity of peritoneal macrophages against KB cells as targets in in vitro assay, suggesting that the antitumor action of Viva-Natural might be indirect through the activation of nonspecific immune systems. A combination therapy of Viva-Natural and standard anticancer drugs was additively or synergistically effective.

Animals↗
PubMed1985

Adverse effect of cyclophosphamide at moderate dose in combination with standard drugs on intraperitoneally implanted Lewis lung carcinoma in mice.

Adverse (tumor-enhancing) effects of cyclophosphamide at moderate dose (50 mg/kg) given therapeutically were confirmed on the intraperitoneally implanted Lewis lung carcinoma (LLC) in allogeneic DBA/2 and BALB/c mice. It was recently demonstrated that antitumor effects of five standard drugs (actinomycin D, adriamycin, BCNU, 5-fluorouracil and methotrexate) were abolished or diminished when cyclophosphamide (50 mg/kg) was therapeutically combined with such drugs against intraperitoneally implanted LLC both in syngeneic C56BL/6 and allogeneic DBA/2 and BALB/c mice, while the effects of three drugs (cis-diamminedichloroplatinum, 5-thioguanine and vincristine) were not affected by the cyclophosphamide therapy. It is suggested that cyclophosphamide therapy at adjusted lower doses in man might not only be effective but also have a risk to enhance tumor growth and diminish the beneficial effects of other drugs in combination chemotherapy.

Animals↗
PubMed1983

Analysis of T cell hybridomas. IV. Characterization of inducible suppressor cell hybridomas.

The Ts3 subset of suppressor cells is generated after antigen priming, but, in order to express suppressor activity these cells require an additional activation step involving triggering with specific suppressor factors (TsF2). This report characterizes two cloned hybridoma cell lines (pTs3 hybridomas) that represent this stage of Ts3 cell differentiation. These hybridoma cells could be specifically activated with TsF2 to release another antigen-specific suppressor factor (TsF3) within 6 h. The inducible feature of these cells permitted analysis of the signals necessary for Ts3 activation. Antigen was not required for activation. Only TsF2 factors derived from antiidiotypic second-order suppressor cells could activate pTs3 hybridoma cells. There were stringent genetic restrictions on the ability of Ts2 to activate pTs3 cells. Triggering of pTs3 required corecognition of two determinants on the TsF2 molecular complex, i.e., the I-J and Igh-related idiotypic determinants. Thus, although pTs3 cells could absorb TsF2 from an I-J-mismatched source, these pTs3 were not activated by the allogeneic TsF2. For activation to occur, the H-2 (I-J) and Igh complexes of the TsF2 donor had to match those of the strain from which the pTs3 cells were derived. Mixing two distinct TsF2, one derived from an H-2-matched source and the other from an Igh-matched source, failed to activate pTs3 cells. Once activated, the pTs3 cells released a suppressive material that was indistinguishable from the TsF3 factors previously characterized in this system. Finally, the activation of the pTs3 cells apparently does not induce the de novo synthesis of TsF3 since the suppressive activity could be extracted from nonactivated pTs3 cells. Thus, the inducible pTs3 hybridomas represent a mature stage in the differentiation cycle of Ts3 cells and provide a means for studying the nature of the specific signals required for Ts3 activation.

Animals↗
PubMed1983

Effects of chlordiazepoxide, diazepam and oxazepam on the antitumor activity, the lethality and the blood level of active metabolites of cyclophosphamide and cyclophosphamide oxidase activity in mice.

Effects of chlordiazepoxide, diazepam and oxazepam on the antitumor activity and acute toxicity of cyclophosphamide and the level of its active metabolites in the plasma were investigated in mice. Cyclophosphamide was administered 24 h after the final injection of chlordiazepoxide, diazepam or oxazepam (100 mg/kg/d for 3 d, i.p.). Pretreatment with these drugs increased the acute toxicity of cyclophosphamide (300 or 450 mg/kg, i.p.), whereas drugs had no effect on the antitumor activity of cyclophosphamide (100 mg/kg, i.p.) against Ehrlich solid carcinoma. A high level of active metabolites of cyclophosphamide in the plasma after the administration of cyclophosphamide (300 or 450 mg/kg, i.p.) was observed in chlordiazepoxide-, diazepam- or oxazepam-treated mice. On the other hand, chlordiazepoxide, diazepam or oxazepam enhanced significantly the activity of cyclophosphamide oxidase in hepatic microsomes. It is concluded that potentiation of the acute toxicity at a high dose of cyclophosphamide by chlordiazepoxide, diazepam and oxazepam is due to an induction of microsomal drug-metabolizing enzyme which are responsible for the in vivo activation of cyclophosphamide.

Animals↗