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Biomedical subjects

T Fukuda

Publications and source records attributed to T Fukuda.

At least 1,027 records · Page 57Linked to original sources

Biochemical and membrane functional alterations in red cells during preparation and storage of leukocyte- and platelet-poor red cell suspensions prepared by warm-centrifuge method.

A simple technique for effective removal of leukocytes and platelets from red blood cells (RBC) was reported. In that technique whole blood was incubated at 37 degrees C. In the modified procedure phosphate buffer was added to the starting RBC. Changes in red cells during preparation and storage at 4 degrees C of RBC suspensions were evaluated. Reconstituted RBC were incubated at 37 degrees C for 1 hr. After centrifugation, the lower compartment was separated with a special apparatus and diluted with 0.9% saline, which contained 78% red cells and 3% leukocytes and platelets of the starting RBC. In the incubation and subsequent preparation steps, 2,3-diphosphoglycerate levels were decreased, but not adenosine triphosphate. One-day storage caused no serious metabolic changes in red cells. Red cell osmotic fragility was not changed throughout. Stored RBC maintained sterility. The in vitro data indicate that red cells in leukocyte- and platelet-poor RBC suspensions processed with the warm-centrifuge method retained high biochemical and membrane functional abilities for 1 day.

2,3-Diphosphoglycerate↗

Effects of dobutamine on the in vivo urethra in the female dog.

The effect of dobutamine on the proximal urethra was investigated in vivo in female dogs. Dobutamine administered intra-arterially at the bifurcation of the iliac artery produced a rise in pressure and shortening along the transverse axis in the urethra.

Animals↗

Visualization of the cerebrospinal fluid drainage into the Galen's vein.

Arachnoid granulations are not always present in lower mammals and primate newborns. In order to visualize the route for the cerebrospinal fluid (CSF) to drain into the venous system, horseradish peroxidase (HRP) was injected into the lateral ventricle or cisterna cerebellomedullaris of the mouse and rat. From 30 to 60 min after the commencing of a slow infusion for 15-30 min of 0.05-0.1 ml solution containing 10-20 mg HRP, the mouse, whose skull had been exposed, was dropped into cold acetone at dry ice temperature; other animals were fixed by perfusion with aldehyde solution. The frozen head was dissected in a cryostat kept at -18 degrees C to remove the skull, but leave the dura mater and the falx cerebri. The brain with meninges was cut into 30-45 microns sagittal sections in the cryostat, and processed for peroxidase reaction. The perfusion-fixed brains were used for scanning electron microscopy and for electron microscope observation of the tracer. The reaction product was found within fenestrated venous capillaries of the choroid plexus. The route for the HRP in the CSF to drain into the sinus rectus via the vena choroidea and vena cerebri magna was directly visualized in the mouse.

Animals↗

Effect of tricyclic drugs on mitochondrial membrane.

The effects of tricyclic drugs (clomipramine, imipramine, chlorpromazine and promethazine) on isolated liver mitochondria of rats were examined. All the drugs tested accelerated state 4 respiration. Their stimulative potency at concentrations below 100 microM was in the order of chlorpromazine greater than clomipramine greater than imipramine, promethazine. On state 3 respiration, the chlorine containing drugs had an inhibitive effect at high concentrations, while the other drugs seemed to have a slightly stimulative effect. These drugs stimulated latent ATPase activity of mitochondria. Clomipramine and chlorpromazine inhibited 2, 4-dinitrophenol-stimulated ATPase activity in a dose-dependent fashion. Imipramine also inhibited 2, 4-dinitrophenol-stimulated ATPase activity at high concentrations. Promethazine, however, had almost no effect. All the drugs induced potassium release from mitochondrial vesicles, and their potency was in the order of clomipramine greater than chlorpromazine greater than imipramine greater than promethazine. These results suggest that clomipramine, imipramine, chlorpromazine and promethazine cause impediments in both mitochondrial respiration and ion compartmentation, and that the chlorine containing drugs are more toxic than others on the functions of the mitochondrial membrane.

Adenosine Triphosphatases↗

Determination of the onset of beta-methyl-digoxin action by potentiation of the adenosine response in guinea pigs.

The onset of beta-methyl-digoxin action was investigated by the potentiation of the adenosine response in guinea pigs and rats, and compared with that of digoxin and dipyridamole. A number of i.v. infusions of adenosine were given to determine the mean control adenosine response and its 95% confidence limits. After oral administration of the drugs, successive infusions of adenosine were continued until a drug-induced potentiation of the adenosine response was observed. The time of appearance of the potentiated adenosine response was marked as the onset of action of the drugs. The onset of action in guinea pigs was 9 to 12 min for 0.2 to 0.4 mg/kg of beta-methyl-digoxin, 90 to 100 min for 0.2 mg/kg of digoxin and 25 min for 5 mg/kg of dipyridamole. The maximal potentiation was 48.8 to 53.8% at 18 to 21 min for beta-methyl-digoxin, 74.5% at 130 min for digoxin and 74.8% at 80 min for dipyridamole. Adenosine infused i.v. into rats produced heart block, as in guinea pigs. However, in rats, the adenosine response was not potentiated by beta-methyl-digoxin and digoxin. Dipyridamole at a dose as high as 200 mg/kg produced 25.8% potentiation at 36 min after oral administration to rats.

Adenosine↗

Production of a monoclonal antibody to a membrane antigen of human T-cell leukaemia virus (HTLV1/ATLV)-infected cell lines from a systemic lupus erythematosus (SLE) patient: serological analyses for HTLV1 infections in SLE patients.

Human T-cell leukaemia virus (HTLV1/ATLV), which causes adult T cell leukaemia (ATL), is an infectious, lymphotrophic retrovirus unique for humans. The present study was undertaken to determine whether HTLV1 had any pathogenetic role for systemic lupus erythematosus (SLE). The incidence of antibodies to ATL cell-associated antigens (ATLA) in sera from patients with SLE and other collagen diseases was investigated by an indirect immunofluorescent cytoplasmic staining of an HTLV1-infected cell line (MT-1). A radioimmunoassay was also performed to detect antibodies to HTLV1 protein and crude membrane fraction derived from an HTLV1-producing cell line MT-2. Furthermore, an Epstein-Barr virus (EBV)-transformed B cell line (ES-1) was constructed from an SLE patient, which produced a monoclonal antibody (IgG, lambda) reactive to an HTLV1-related cell-membrane antigen expressed on MT-1 and MT-2 cells. The specific reactivity of the monoclonal antibody was analysed by an indirect immunofluorescent cell-membrane staining and a microcytotoxicity test. The incidence of anti-ATLA antibodies was not different among SLE and other collagen diseases. The monoclonal antibody produced by ES-1 stained and killed HTLV1-infected cell lines specifically, but did not react with other human lymphoid cell lines. This monoclonal antibody failed to react with peripheral blood mononuclear cells (PBMC), mitogen-induced T cell blasts, and iododeoxyuridine-treated T cells from SLE patients. Thus, a possible role of HTLV1 in the aetiology of SLE was not established.

Antibodies, Monoclonal↗

[Changes in placental enzymatic activities in relation to estrogen production during pregnancy].

To study the mechanism of production of estrogen during pregnancy, the following in vitro and in vivo studies were undertaken; 1) Weight of human placenta and total estradiol (E2) levels in the maternal peripheral vein were measured at different weeks of gestation. 2) Changes in E2 levels after DHA-S 100mg loading were calculated at the 1st, 2nd and 3rd trimesters. 3) Steroid enzyme activities including sulfatase, 3 beta-HSD and aromatase in placenta obtained in the 1st, 2nd and 3rd trimesters were measured. Results were as follows; 1) The weight of the human placenta increased gradually as gestation progressed. Twofold placental weight was noticed from the 2nd to the 3rd trimester. 2) Total E2 in the maternal peripheral vein increased steadily, being 4.07 +/- 1.74 ng/ml at the 1st trimester, 27.72 +/- 11.67 ng/ml and 104.12 +/- 57.89 ng/ml at the 2nd and 3rd trimesters respectively. The increase in E2 from the 2nd to the 3rd trimester was greater than that of the placental weight. 3) Increases in E2 following DHA-S loading were 1.01 ng/ml at the 1st, 29.2 ng/ml at the 2nd and 98.2 ng/ml at the 3rd trimester. 4) No significant differences were observed between placental 3 beta-HSD and sulfatase activities in the placenta obtained at the three different stages of pregnancy, while aromatase activity was found to be significantly higher in the placenta of the 3rd trimester than that of 2nd trimester. These results indicate that the remarkable increase in estrogen production in the 3rd trimester may be explained partially by increased aromatizing enzyme activity in the placenta.

Dehydroepiandrosterone↗

Antitumor activity of the DNA fraction from Mycobacterium bovis BCG. II. Effects on various syngeneic mouse tumors.

MY-1, a fraction extracted from BCG and composed of 70.0% DNA and 28.0% RNA, was examined for its antitumor activity against 9 different syngeneic mouse tumors. Tumor regression was induced in almost all of the mice bearing any of five kinds of solid tumors by repeated intralesional injections of 100 micrograms MY-1. When cells of some tumors were inoculated intradermally together with MY-1, tumor growth was suppressed, lung metastases were inhibited, and the survival times of mice bearing 1 of 3 leukemic tumors were prolonged. Repeated sc injections with MY-1 in sites remote from tumor cell inoculation or repeated iv injections were more or less effective against three kinds of solid tumors. Mice inoculated with Lewis lung carcinoma cells in a hind footpad and whose legs were amputated 9 days later were given iv or sc injections of MY-1 every other day (8 times in total), resulting in substantial prolongation of survival. No direct cytotoxicity of MY-1 for these tumors could be shown in three kinds of experiments, which indicates that the antitumor mechanism of MY-1 is host mediated. MY-1 was equally effective in mice with or without presensitization with BCG, whereas BCG was much more effective in BCG-sensitized mice. This finding suggests that a delayed-type hypersensitivity reaction elicited by BCG protein is not required for the antitumor activity of MY-1.

Animals↗