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Biomedical subjects

Y Fujii

Publications and source records attributed to Y Fujii.

At least 1,045 records · Page 58Linked to original sources
PubMed1986

Cytoplasmic proteins, association with phospholipid vesicles and its dependency on cholesterol.

Since the plasticity of the plasma membrane is correlated with changes in its dynamic behavior and biological functions, the content of cholesterol in this membrane is thought to have an important role in the regulation of cell metabolism. The research reported here was done to clarify the role of cholesterol in the interaction of the innersurface of plasma membrane with cytoplasmic proteins in relation to the regulatory mechanism of signal transduction. Many cytoplasmic proteins of EATC or rat liver cells were found to associate with DPPC liposomes and they induced a transient increase in membrane permeability at the phase transition temperature of the liposomal lipid. The association and the permeability increase were inhibited by the introduction of cholesterol into DPPC liposomes, and the sensitivity of individual proteins to the action of cholesterol differed. F-actin, but not G-actin, associated selectively with the liposomes. Also, the main endothermic peak of the unilamellar DPPC liposomes was shifted from 37 degrees C to 43 degrees C by this protein association, evidence of transformation from a unito multilamellar structure. The introduction of cholesterol into the liposomal membrane caused a reduction in the energy content of the phase transition and in the inhibition of protein-membrane interaction. We concluded that the cholesterol in the plasma membrane contributes to the regulation of cell surface signal transduction.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1986

[Epinephrine uptake and release and presynaptic alpha 2-adrenoceptic regulation in the guinea pig hypothalamus].

The uptake and the release of [3H] epinephrine ([3H] E) and the release of endogenous E in slices of guinea pig hypothalamus were investigated. [3H]E rapidly accumulated in the slices incubated in Krebs-Ringer solution containing [3H]E. Kinetic analysis indicated two components of E accumulation, one representing a high (Km1, 7.7 X 10(-8) M and Vmax1, 0.13 pmoles/mg/10 min) and the other a low (Km2, 1.8 X 10(-6) M and Vmax2, 1.4 pmoles/mg/10 min) affinity uptake system. Endogenous E released in response to electrical stimulation was estimated using gas chromatography and mass spectrometry. The electrical stimulation produced a release of both [3H]norepinephrine ([3H]NE) and [3H]E from hypothalamic slices preloaded with [3H]NE. With electrical stimulation of the slices, there was an efflux of [3H]E from tissues preloaded with [3H]E, in a current- and frequency-dependent manner. Electrically stimulated release of [3H]E from the slices was inhibited by tetrodotoxin (10(-6) M) and by a calcium-free medium containing EGTA (10(-4) M), in cases of up to 1 mA of intensity of electrical stimulation. The release of [3H]E induced by electrical stimulation was enhanced by yohimbine, and this effect was suppressed by clonidine. These results provide strong evidence for the neurotransmitter role of this catecholamine in the hypothalamus and suggest the possible existence of a presynaptic regulatory mechanism of E release, through the presynaptic alpha 2 receptors on the E nerve terminals.

Animals↗
PubMed1986

[Effects of gomisin A, a lignan component of Schizandra fruits, on experimental liver injuries and liver microsomal drug-metabolizing enzymes].

Effects of oral administration of gomisin A, one of the components isolated from Schizandra fruits, on liver injuries induced by CCl4, d-galactosamine and dl-ethionine and on liver microsomal drug-metabolizing enzyme activities were investigated. Gomisin A suppressed the increase of serum transaminase activities and the appearances of histological changes such as degeneration and necrosis of hepatocyte, inflammatory cell infiltration and fatty deposition in each type of liver injury. The repeated administration of gomisin A (30 or 100 mg/kg, p.o., daily for 4 days) induced an apparent increase of liver weight in liver-injured and normal rats. Gomisin A decreased serum triglyceride and lipid contents of the liver in biochemical studies. Increases of microsomal cytochrome b5 and P-450, elevations of NADPH cytochrome C reductase, aminopyrine N-demethylase and 7-ethoxycoumarin O-deethylase activities and decrease of 3,4-benzo(a)pyrene hydroxylase activity per cytochrome P-450 were observed after the administration of gomisin A. In addition, gomisin A was found to enhance the incorporation of 14C-phenylalanine into liver protein and to shorten the hexobarbital-induced sleeping time. These changes caused by gomisin A were similar to those by phenobarbital. However, gomisin A is distinctly different from phenobarbital in the finding that phenobarbital lessened the survival ratio of CCl4-intoxicated mice, but gomisin A did not. Our observation suggest that gomisin A shows an antihepatotoxic action by oral application and also has hypolipidemic (mainly triglyceridemic) and liver protein synthesis-facilitating actions and that the enlargement of the liver seen with gomisin A is the adaptive hypertrophy which is due to the induction of drug-metabolizing enzymes.

Animals↗
PubMed1986

Fluorescence and electron microscopic study of intracellular F-actin in concanavalin A-treated and cytochalasin B-treated Ehrlich ascites tumor cells.

To investigate the involvement of actin filaments in concanavalin A (Con A)-induced cap formation and cytochalasin B (CB)-induced zeiotic knob migration, the distribution of F-actin was studied in Con A-treated and CB-treated Ehrlich ascites tumor cells (EATC) by fluorescence microscopy using heavy meromyosin conjugated with a fluorescent dye, N-(7-dimethylamino-4-methylcoumarinyl) maleimide, (DACM-HMM). In non-treated cells, the diffuse fluorescence of DACM-HMM was observed in the cytoplasm, particularly intensely under the plasma membrane and around the nucleus. In Con A- and CB-treated cells, the fluorescence was seen at Con A-induced-capped and CB-induced-knob-accumulated regions. This fluorescence was more intense in CB-treated cells. To study the actin filaments in these fluorescent regions more clearly, the soluble components of the cells were eliminated by treatment with Triton X-100 or saponin solution containing a low concentration of glutaraldehyde, and the detergent-treated and saponin-treated cells were observed under a transmission electron microscope. Concentrated actin filaments were observed directly beneath the Con A-induced capping area and CB-induced zeiotic knob-accumulation area. The area of concentrated actin filaments appeared to correspond to the electron dense area observed in the identical region in the cells fixed without detergent treatment. More actin filaments were observed in CB-treated cells than in Con A-treated ones.

Actins↗
PubMed1986

Mechanisms of in vivo generation of cytotoxic effector cells against tumor in tumor-bearing mice.

Our previous study showed that spleen cells from BALB/c mice bearing RL male 1 lymphoma inhibited the growth of RL male 1 lymphoma by the Winn-type adoptive transfer assay. Although this antitumor activity was mediated by the T-cell subset manifesting the surface phenotype of cytotoxic T-lymphocytes (CTLs), this antitumor activity of spleen cells was not detected by the in vitro cell-mediated cytotoxicity assay (4-h 51Cr release assay). The present study is concerned with the hypothesis that the maturation of the CTLs directed against RL male 1 may be arrested in spleens of the RL male 1-bearing mice and the differentiation into mature CTLs may occur at the tumor site; i.e., the immature CTLs (activated precytotoxic T-cells) may acquire the killing activity when they contact tumor cells at the tumor site. This report shows that BALB/c mice bearing the progressive RL male 1 lymphoma were able to generate CTLs against RL male 1 in the peritoneal cavities when the mice were inoculated i.p. with the irradiated RL male 1 cells. The cytotoxic activity of the peritoneal exudate cells of the RL male 1-bearing mice appeared 3 to 5 days after i.p. inoculation of the irradiated RL male 1 cells and rapidly decreased on day 7 after inoculation. In addition, spleen cells from the RL male 1-bearing mice after i.p. inoculation of the irradiated RL male 1 cells were not cytotoxic, suggesting a highly localized response. The cytotoxic effector cells induced in the peritoneal cavities consisted of T-lymphocytes and natural killer cells. Both cell types were simultaneously induced in the peritoneal cavities of the RL male 1-bearing mice. The T-cell subset mediating cytolytic activity against RL male 1 was shown to consist of Lyt-1+2+ T-cells which were defined by cytolysis with anti-Lyt-1 or anti-Lyt-2 antibody and complement. On the other hand, the normal BALB/c mice inoculated i.p. with the irradiated RL male 1 cells generated natural killer cells in the peritoneal cavities and spleens but the CTLs were not induced. The results from the present and previous studies suggest that precytotoxic or immature cytotoxic T-cells in spleens of the tumor-bearing mice migrate into the circulation and then mature CTLs develop at the tumor site.

Animals↗
PubMed1986

[A case of retroperitoneal alveolar soft part sarcoma].

We present the first case of retroperitoneal alveolar soft part sarcoma (ASPS) to be reported in Japan. The patient was a 27-years-old woman. After the retroperitoneal (tumors were) removed, bilateral lung metastasis was found and removed. Shortly thereafter, a recurrent retroperitoneal tumor arose, but because removal of the tumor was impossible, injection of 100 mg of cisplatin and 100 mg of adriamycin into the feeding artery was performed, and radiotherapy was also undertaken. However, the treatments were not effective, and the patient is now being followed on an outpatient basis.

Adult↗
PubMed1986

Effect of cerulenin, an inhibitor of fatty acid synthesis, on the immune cytolysis of tumor cells.

Effect of cerulenin, an inhibitor of biosynthesis of fatty acids and sterols on the immune cytolysis of tumor cells was investigated. In cytotoxicity experiment, MH134 cells pretreated with cerulenin in a range of concentrations causing minor cellular injuries were lysed by xenogeneic antiserum and complement in a significantly higher degree than non-treated MH134 cells. C3H/He mice inoculated ip with 1 X 10(5) syngeneic MH134 cells, received cerulenin on days 3 and 6, and then the antiserum against MH134 cells on days 4 and 7. Such mice survived markedly longer than 3 control groups of mice carrying MH134 tumor cells; one without treatments, one treated only with cerulenin and the other only with the antiserum. Inhibition of biosynthesis of cell membrane fatty acid and sterols, that was indicated by inhibition of 14C-acetate incorporation, is thought to enhance the susceptibility of the tumor cells to killing by antibodies and complement. Such an inhibitor of fatty acids and sterols might be a beneficial adjuvant to the adoptive cancer immunotherapy.

Acetates↗
PubMed1985

Epinephrine release and presynaptic alpha 2-adrenoceptic regulation in the guinea pig hypothalamus.

The release of epinephrine (E) and its regulation system were investigated in the slices of guinea pig hypothalamus. Electrical stimulation produced an efflux of [3H]E from tissues preloaded with [3H]E, in a current- and frequency-dependent manner. Stimulated [3H]E release was inhibited by tetrodotoxin and by a calcium-free medium containing ethylene glycol bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA). Stimulated [3H]E release was enhanced by yohimbine and this effect was suppressed by clonidine. These results provide strong evidence for the neurotransmitter role of E in the hypothalamus, and suggest the possible existence of regulatory mechanism of E release via presynaptic alpha 2-receptors.

Animals↗
PubMed1985

Quantitative radioautographic study of intracellular localization of calmodulin antagonist, W-7, in Chinese-hamster ovary cells.

The purpose of the present study was to analyse quantitatively the localization of calmodulin antagonist, n-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7) in CHO-Kl cells. The cultured CHO-Kl cells were labelled with 1 (16.7 microM), 2 (33.4 microM), 5 (83.5 microM) and 10 microCi/ml (167 microM) tritiated W-7. Some cells were preincubated in 10, 50 and 100 microM unlabelled W-7 for 30 min and then labelled with 2 or 5 microCi/ml tritiated W-7 for 1 h. The cells were doubly fixed in glutaraldehyde and osmium-tetroxide solution, and embedded in Epon. For light-microscopic radioautography, 2 micron-thick sections were wet mounted with radioautographic emulsion and exposed for 1 month. The radioautograms showed that large numbers of silver grains were mainly localized in the cytoplasm as well as in the nucleus. Quantitative analysis demonstrated that, in both the cytoplasm and nucleus, the number of silver grains was dependent on the concentration of the administered tritiated W-7 and the number was dramatically decreased by the pretreatment of unlabelled W-7. These results show that, in CHO-Kl cells, the W-7 binding sites are saturable. It is concluded that W-7 may get into CHO-Kl cells and be bound to a specific protein that may be calmodulin protein.

Animals↗