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Biomedical subjects

S Tajima

Publications and source records attributed to S Tajima.

At least 397 records · Page 22Linked to original sources
PubMed1985

High susceptibility to ADP-induced thrombus formation in mast cell-deficient W/Wv mice.

We used mast cell-deficient W/Wv mice to clarify whether mast cell-derived heparin may play a role in inhibiting thrombus formation in the living organism. Small veins in the mesentery of W/Wv or congenic +/+ mice were stretched over an inverted microscope; a micropipette filled with varying concentrations of ADP was set close to the outside of a vein by using a micromanipulator. Thrombus formation was directly examined under the microscope. The concentration of ADP necessary for thrombus formation was significantly lower in the W/Wv mice than in the congenic +/+ mice. Furthermore, the concentration of ADP necessary for aggregation of platelets in platelet-rich plasma (PRP) was significantly lower in W/Wv mice than in +/+ mice. The higher sensitivity of PRP of W/Wv mice is not attributed to the platelets, but to the plasma, since platelets of +/+ mice suspended in platelet-poor plasma (PPP) of W/Wv mice were more sensitive to ADP than platelets of W/Wv mice suspended in PPP of +/+ mice. The present results suggest that plasma of W/Wv mice may lack any inhibitory factor(s) or contain promoting factor(s) for platelet aggregation.

Adenosine Diphosphate↗
PubMed1985

Cells of a human monocytic leukemia cell line (THP-1) synthesize and secrete apolipoprotein E and lipoprotein lipase.

A human cell line established from a patient of an acute monocytic leukemia (THP-1) retained an ability to synthesize and secrete plasma apolipoprotein E like protein. The protein was identified with monospecific antibody raised against human plasma apolipoprotein E. The cells also secreted lipoprotein lipase (EC 3.1.1.34). The enzyme was characterized as lipoprotein lipase on the basis of the requirement of apolipoprotein C-II as an activator and the inhibition of its activity by sodium chloride. The secretion of both apolipoprotein E and lipoprotein lipase was markedly enhanced in the process of differentiation into macrophage-like cells by the addition of 4 beta-phorbol 12 beta-myristate 13 alpha-acetate.

Apolipoprotein C-II↗
PubMed1985

A 38 base pair insertion in the pro alpha 2(I) collagen gene of a patient with Marfan syndrome.

Abnormalities in type I collagen have been recognized in a number of connective tissue disorders. In the Marfan syndrome, an autosomal dominant condition producing a generalized abnormality in connective tissue, no consistent abnormality has been identified, although one individual has been found to have an elongated pro alpha 2(I) collagen chain [Byers et al, Proc Natl Acad Sci USA 78:7745, 1981]. To determine the nature of the alteration in the gene that produced this abnormality, we studied the pro alpha 2(I) gene from this individual by genomic blotting and gene cloning. Genomic mapping studies detected no abnormalities. However, analysis of the cloned segment of the pro alpha 2(I) collagen gene from the Marfan individual indicates that the gene contains a 38 base pair insertion in an intron near the collagenase cleavage site. Although the relationship of this insertion to the protein abnormality is unclear, it may be a useful marker for the diagnosis of the Marfan syndrome.

Base Sequence↗
PubMed1985

A paradoxical effect of hydralazine on prolyl and lysyl hydroxylase activities in cultured human skin fibroblasts.

The effect of hydralazine on several parameters of collagen biosynthesis has been studied in cultured human skin fibroblasts. Cells treated with hydralazine synthesized procollagen which was severely deficient in hydroxyproline and hydroxylysine, indicating inhibition of prolyl and lysyl hydroxylase reactions in the cell. Assays of prolyl and lysyl hydroxylase activities, however, revealed markedly increased levels in hydralazine-treated cells. The stimulatory effect of hydralazine could not be simulated in cell extracts, demonstrating its requirement for intact cells. The effect occurred slowly over a period of 96 h and was dependent on hydralazine concentration between 10 and 100 microM. This phenomenon was also observed in lysyl hydroxylase-deficient mutants. In both normal and mutant cells the relative magnitude of the hydralazine effect could be modified by ascorbic acid in the culture medium. Ascorbic acid increased the response of prolyl hydroxylase to hydralazine from 1.5- to 2-fold to 3- to 7-fold, whereas it decreased the response of lysyl hydroxylase to hydralazine from 4- to 8-fold to 2- to 3-fold. Total collagen synthesis was substantially reduced in hydralazine-treated cells; the time course and the dose-response relationship were similar to those observed for the hydroxylases. alpha, alpha'-Dipyridyl, an iron chelator, mimicked these effects of hydralazine. The studies suggest the existence in cultured cells of a compensatory mechanism for overproduction of these crucial enzymes in collagen biosynthesis, a mechanism which remains functional in cells derived from patients afflicted with hydroxylysine-deficient collagen disease.

Ascorbic Acid↗
PubMed1985

Suppression of delayed-type hypersensitivity mediated by macrophage-like cells in mice with experimental liver injury.

The intensity of picryl chloride-induced delayed-type hypersensitivity (PCl-DTH) was significantly lowered in mice with experimental liver injury induced by the injection of carbon tetrachloride (CCl4) or 1-naphthylisothiocyanate (ANIT). Adherent spleen cells prepared from mice with liver injury suppressed the PCl-DTH in normal syngeneic mice by adoptive transfer at the time of immunization with picryl chloride (PCl). Cianidanol, administered orally to recipient mice immediately after the transfer of adherent spleen cells, caused total prevention of the PCl-DTH from suppression by the transferred adherent spleen cells. In in vitro studies, the adherent spleen cells from both CCl4-treated and ANIT-treated mice produced higher amounts of prostaglandin E2 (PGE2) than those from normal mice. The addition of cianidanol at the beginning of incubation caused an inhibition of PGE2 production of the adherent spleen cells. Furthermore, the spleen cell suspensions from CCl4-treated mice gave a marked increase in generation of superoxide anions (O2-), also inhibited by the addition of cianidanol. Gathered results support the adherent spleen cell as being the cell causing the suppression of DTH in mice with experimental liver injury; the important role of PGE2 and O2- in the suppression of DTH mediated by the adherent spleen cells was demonstrated. Cianidanol eliminated the suppression of DTH, owing principally to the inhibitory effect on the production of PGE2 and O2- from the adherent spleen cells.

1-Naphthylisothiocyanate↗
PubMed1984

Association of apolipoprotein A-II with egg phosphatidylcholine unilamellar vesicles.

Interaction of human apolipoprotein A-II (apoA-II) with egg yolk phosphatidylcholine unilamellar vesicles (diameter, 20-26 nm) was studied. ApoA-II bound to the vesicles in a saturable manner and was displaced by apolipoprotein C-III1 (apoC-III1) while bound apoC-III1 was displaced by apoA-II, with apparent deformation of the vesicles, as observed in electronmicrographs. Free apoA-II that had been displaced from the lipid surface was readsorbed to vesicles successively added to the medium. Disruption of the vesicular structure occurred in less than 3% of the vesicles under the experimental conditions. Isothermal binding data were analyzed according to a reversible equilibrium binding model. The dissociation constant, Kd, was 5.8 X 10(-7) M, and the maximum binding level, N, was 1.46 amino acid residues per phospholipid for apoA-II assuming that 70% of the phospholipid is in the outer leaflet of the vesicles, while for apoC-III1 the Kd and N values were 7.8 X 10(-7) M and 1.34 amino acid residues per phospholipid in the outer leaflet, respectively. All these parameters show good agreement with those for triglyceride-phospholipid particles of approximately the same diameter as that of the vesicles (J. Biol. Chem. (1983) 258, 10073-10082). Thus the parameters represent the equilibrium binding of apoA-II to the surface of phosphatidylcholine unilamellar vesicles.

Apolipoprotein A-II↗
PubMed1984

Mechanism of action of lipoprotein lipase on triolein particles: effect of apolipoprotein C-II.

Triolein particles stabilized by a phosphatidylcholine monolayer were used to study the lipoprotein lipase (LpL) reaction. They were prepared in two different sizes and with triolein and phosphatidylcholine in the molar ratios of 0.9-1.2 : 1 (small particles) and 8-17 : 1 (large particles). The rate of hydrolysis by LpL of phosphatidylcholine on the surface of both lipid particles was only 1/20 as much as that of triolein, even if it was activated to the maximum by apolipoprotein C-II (apoC-II). Thus, the phospholipase activity of LpL was low enough to measure the initial rate of hydrolysis of triolein without causing a gross change of the surface of the lipid particle. When the hydrolysis of triolein by LpL was monitored, fatty acid was released at a constant rate until all of the triolein molecules were hydrolyzed. The enzyme required 220 +/- 17 and 66 +/- 9 nM apoC-II for its half-maximal activity (Km (apoC-II] with small and large particles as a substrate (1.15 mM triolein for small and 2.13 mM triolein for large particles), respectively, using various concentrations of LpL. The Km(apoC-II) values for these two substrates became similar when LpL activity was analyzed with respect to the density of apoC-II on the phosphatidylcholine monolayer at the surface of the particles (bound apoC-II/phosphatidylcholine). The concentration of substrate particles did not affect the Km(apoC-II) values. The presence of an adequate amount of apoC-II increased the maximal activity of LpL (Vmax(triolein)) from 0.48 +/- 0.21 to 6.81 +/- 0.45 and from 0.32 +/- 0.04 to 7.13 +/- 0.64 mmol/h/mg with a slight decrease in the apparent Michaelis constant (Km(triolein)) for small (from 90 to 54 microM triolein) and large (from 1.00 to 0.65 mM triolein) particles, respectively. Although the apparent Km for triolein in large particles was about ten times greater than that in small particles, the values became similar when they were corrected for the concentration of phosphatidylcholine (50-100 microM phosphatidylcholine), which corresponded to the surface area of the substrate particles. It was suggested that bound apoC-II molecules were transferred relatively slowly to other lipid particles while LpL molecules moved rapidly among the lipid particles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Isolation and characterization of a human pro alpha 2(I) collagen gene segment.

Over 20 kilobase pairs of the human pro alpha 2(I) collagen gene have been isolated and characterized by restriction endonuclease mapping, cell-free translation of hybrid-selected RNA, and DNA sequence analysis. We have sequenced an exon and determined its length to be 108 base pairs (bp). This is consistent with the organization of chick and sheep collagen genes in that exons are multiples of 9 bp in length, frequently being 54 and 108 bp. The sequenced exon was bordered by a GT (guanine-thymine) at its 3' end and an AT (adenine-thymine) at its 5' end. This pattern has been found at all normal intron-exon junctions in eukaryotic cells. The amino acid sequence derived from DNA sequencing of this 108 bp exon revealed 88% homology compared to the amino acid sequence of bovine pro alpha 2(I). The bases encoded 12 Gly-X-Y triplets characteristic of the helical portion of collagen. A unique sequence Gly-Gly-Lys-Gly-Glu-Lys identified this fragment as alpha 2(I) collagen.

Amino Acid Sequence↗
PubMed1984

Effect of cianidanol (KB-53) on the activity of mouse cytotoxic-T-lymphocytes.

The effect of cianidanol (KB-53) on the mouse cytotoxic-T-lymphocyte (CTL) activity of the splenic cells was investigated. The CTL activity of the splenic cells prepared from C3H/He, DBA/2 and CBA strain mice which had been sensitized with EL-4 cells were recognized markedly 11 d after the sensitization. The CTL activity showed an antigen specificity. KB-53, in a dose range of 125-1000 mg/kg, augmented the mouse CTL activity in a dose-dependent manner by oral administration once daily for 5 d beginning immediately after the sensitization. This CTL activity disappeared with treatment of the splenic cell with anti-thy-l serum and normal guinea pig serum, therefore, it was confirmed that the cytotoxic activity of the splenic cells which were prepared from the mice sensitized with EL-4 cells depended on the T-cell activity.

Animals↗
PubMed1984

Effect of cianidanol (KB-53) on the activity of mouse natural killer cells.

The effect of cianidanol (KB-53) on the mouse natural killer (NK) cell activity of the splenic cells was investigated using YAC-1 cells as target cells. The oral administration of KB-53 at a dose of 500 mg/kg augmented significantly the NK cell activity. The activity was observed maximally 3 d after the administration, and significant difference from the control was observed even at 7 d after the administration of KB-53. The oral administration of KB-53, at a dose range of 125-500 mg/kg, augmented the NK cell activity in a dose-dependent manner at 3 d after the administration.

Animals↗
PubMed1984

Antiallergic effect of 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidaz ole difumarate (KB-2413).

Antiallergic effects of 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidazol e difumarate (KB-2413) were investigated in immediate type hypersensitivities. KB-2413 (0.005-0.04 mg/kg p.o.) showed a marked inhibition on lethal anaphylaxis in guinea pigs induced by anti-egg albumin rabbit serum, and it was 30 and 1.6 times more potent than chlorpheniramine and ketotifen, respectively. KB-2413 (0.003-0.1 mg/kg p.o.) showed a dose-dependent inhibition on vascular permeability increase induced by 48 h homologous passive cutaneous anaphylaxis (PCA) and histamine in guinea pigs, being about 10-30 times and 3 times more potent than chlorpheniramine and ketotifen, respectively. All drugs did not completely inhibit 4 h heterologous PCA in guinea pigs induced by the anti-egg albumin rabbit serum in the doses used here, but KB-2413 was more effective than chlorpheniramine and ketotifen. No difference in inhibitory effect on the vascular permeability increase between the single and daily oral administration for 4 weeks of KB-2413 could be found. KB-2413, as well as chlorpheniramine and ketotifen, showed a dose-dependent inhibition on 48 h homologous PCA in rats at doses of 1-10 mg/kg p.o., and showed a concentration-dependent inhibition on Schultz-Dale reaction at 10(-8) - 10(-7) mol/l. KB-2413 (10(-5) - 10(-3) mol/l) showed a concentration-dependent inhibition of anaphylactic histamine release from isolated rat peritoneal mast cells which were passively sensitized by rat IgE. KB-2413 also inhibited compound 48/80-induced histamine release from rat peritoneal mast cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗