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K Tadokoro

Publications and source records attributed to K Tadokoro.

197 records · Page 11Linked to original sources
PubMed1982

Induction of choline kinase by polycyclic aromatic hydrocarbons in rat liver. I. A comparison of choline kinases from normal and 3-methylcholanthrene-induced rat liver cytosol.

Choline kinase in rat liver has been shown to be induced up to 2-fold by the administration of polycyclic aromatic hydrocarbon carcinogens such as 3-methylcholanthrene and 3,4-benzo[a]pyrene (Ishidate, K., Tsuruoka, M. and Nakazawa, Y., (1980) Biochem. Biophys. Res. Commun. 96, 946-952). In order to characterize the nature of choline kinase induction by these carcinogens, the 3-methylcholanthrene-induced form as well as the normal form of choline kinase were partially purified from rat liver cytosol through acid treatment, (NH4)2SO4 precipitation and DEAE-cellulose column chromatography with linear KCl-gradient elution, and the catalytic properties were compared between the two preparations. Both enzyme activities were purified about 17-fold with a yield of 50% through the purification steps and there appeared no detectable difference in the elution pattern from either DEAE-cellulose column or Sephadex G-200 gel filtration. On the other hand, some differences were observed in catalytic properties between the two enzyme preparations; (1) the induced form showed a higher apparent Km value for choline (0.19 mM) when compared to the normal form (0.11 mM) and (2) the addition of polyamines caused a considerable increase in the maximum reaction velocity for the normal form whereas no remarkable change for the induced form, when the activities were plotted as a function of choline concentration. The overall results suggest that the 3-methylcholanthrene-induced form of choline kinase in rat liver could be different from the normal form, or that there exist several isoenzymes of choline kinase in rat liver, and one or some of them are inducible by the administration of polycyclic aromatic hydrocarbons.

Adenosine Triphosphate↗
PubMed1980

Antigenicity of semisynthetic penicillin preparations to evoke systemic anaphylactic reactions in animal models.

Four commercially available penicillin preparations (benzylpenicillin, aminobenzylpenicillin, carbenicillin and sulbenicillin) and two kinds of the new semisynthetic penicillin preparations (mezlocillin and piperacillin) evoked systemic anaphylactic reactions in guinea pigs immunized with one of the following penicillin-Ascaris extract (As) conjugates in aluminum hydroxide gel (alum), i.e., benzylpenicilloyl (BPO)-As, aminobenzylpenicilloyl (ABPO)-As, carbenicilloyl (CBPO)-As, sulbenicilloyl (SBPO)-As, mezlocillin-As conjugate (MEZ-As) and piperacillin-As conjugate (PIP-As). The tracheal chains prepared from the tracheas of the guinea pigs immunized with BPO-As, MEZ-As, or PIP-As revealed anaphylactic contractions in vitro on addition of benzylpenicillin, mezlocillin, or piperacillin preparations. These results indicated that the semisynthetic penicillin preparations as well as benzylpenicillin preparation have enough antigenicity to evoke systemic anaphylactic reactions in guinea pigs immunized with penicillin-As conjugate. Such guinea pigs seem to be suitable animals for investigations of penicillin allergy.

Allergens↗
PubMed1980

IgE antibodies produced in mice instrumental in analyses of antigenicity of cephalothin preparation.

IgE antibodies to a cephalothin preparation were produced in mice which had been immunized with cephalothin-Ascaris extract conjugate mixed with Al(OH)3 gel plus Bordetella pertussis. Mice which had been irradiated just before receiving the booster injection wtih the conjugate showed higher IgE antibody levels against the preparation in comparison with unirradiated mice. The specificities of IgE antibodies against the preparation were examined with an inhibition test of passive cutaneous anaphylactic (PCA) reaction. The intensity of the PCA reaction evoked by the cephalothin preparation in the rats was substantially or partially reduced by a pretreatment of the animals with an injection of a cephalothin preparation from another source or a cephaloridine preparation. Meanwhile, a prior injection of a cefazolin, a 7-aminocephalosporanic acid, a benzylpenicillin (PcG) preparation, or an aminobenzylpenicillin preparation into the animals showed only weak or no influence on the PCA reaction. These results suggest that the acyl side chain of cephalothin plays an important role as eliciting antigenic determinant in the PCA reaction. The difference in the antigenic specificity between the cephalothin and PcG preparation is also discussed.

Animals↗
PubMed1978

Benzylpenicillin preparations can evoke a systemic anaphylactic reaction in guinea pigs.

All of the five commercially available benzylpenicillin preparations obtained from different sources and a PcG preparation prepared by filtration of a commercial PcG on Sephadex G10 elicited the systemic anaphylactic reactions in guinea pigs which had been immunized with benzylpenicilloyl (BPO)-Ascaris extract conjugate (BPO-As) mixed with aluminum bydroxide gel. These preparations could evoke no such reactions in guinea pigs immunized with BPO-bovine gamma globulin conjugate (BPO-BGG) emulsified with complete Freund's adjuvant. The severity of the systemic anaphylactic reactions correlated significantly with the titers of either 8-day passive cutaneous anaphylactic (8-day PCA) reactions or 4-hr PCA reactions evoked with the same benzylpenicillin preparations. In vitro benzylpenicillin preparation contracted the tracheas of the guinea pigs immunized with BPO-As. These results indicated that the commercially available benzylpenicillin preparations have enough antigenicity to evoke systemic anaphylactic reactions in guinea pigs immunized with BPO-As mixed with aluminum hydroxide gel. Such guinea pigs represent an animal model for investigation of penicillin allergy.

Anaphylaxis↗
PubMed1978

Antibody formation to double-stranded DNA in nu/nu and nu/+ mice.

Antibody formation to double-stranded (ds-) DNA in nude mice (nu/nu) and normal littermates (nu/+) was studied using a Millipore filter method. The mean antibody titre to ds-DNA in the sera of nu/nu mice was generally higher than that in nu/+ mice raised in the same environment. However, in both genotypes, anti-ds-DNA titres varied according to the environmental condition in which the animals were raised. Mice maintained germ-free showed no significant antibody formation to ds-DNA. Nu/+ thymus and spleen cells passively transferred to nu/nu mice reduced the antibody titre to ds-DNA in the recipients. Immunochemical studies indicated that the antibodies to ds-DNA were IgM. It is suggested that T cell-mediated regulatory mechanisms control antibody formation to ds-DNA and that some infections trigger antibody formation to ds-DNA.

Animals↗
PubMedDate not supplied

Gene amplification and overexpression of epidermal growth factor receptor in squamous cell carcinoma of the head and neck.

The degree of gene amplification for epidermal growth factor receptor (EGFR) and its expression levels were examined in 4 cases of tumor lesions and their cell lines of human squamous cell carcinoma (SCC) of the oral cavity. The amplification was detected in 1 case (ZA), but not significantly in 3 other cases (HOC605, HOC815, and HOC927) in which the amplification did not occur during the cell line establishment. In those 3 cases, levels of EGFR synthesis and human EGF (hEGF) binding capacity were varied: HOC605 and HOC815 had slightly increased levels of hEGF binding capacity and EGFR synthesis, respectively. While HOC927 had the lowest levels of both, the hEGF binding capacity was elevated in the tumor lesion when compared with the normal counterpart of the same patient. These results suggest that the increased capacity for EGF binding plays a more important role than does gene amplification on the tumorigenesis of SCC of the head and neck.

Carcinoma, Squamous Cell↗
PubMedDate not supplied

Extensive proliferation of mature connective-tissue type mast cells in vitro.

There are two phenotypically distinct subpopulations of mast cells in rodents: connective tissue-type mast cells (CTMC) and mucosal mast cells (MMC). These populations differ in their location, cell size, staining characteristics, ultrastructure, mediator content and T-cell dependency. Several investigators recently reported a further subclass of mast cells which arise when normal mouse haematopoietic cells are cultured with interleukin-3 (IL-3); IL-3 is an activity similar or identical to mast-cell growth factor, histamine-producing factor, or P-cell stimulating factor. These cultured mast cells are in many ways similar to MMC; they stain with Alcian blue but not safranin, contain chondroitin sulphate E proteoglycan rather than heparin proteoglycan and have relatively low histamine content, as do MMC. Although proliferation of MMC is known to be T-cell dependent in vivo and thought to be IL-3-dependent in vitro, the factors on which CTMC proliferation depends remain elusive. Here we show that mature CTMC purified from mouse peritoneal cells can proliferate in vitro in methylcellulose culture and maintain the appearance and function of CTMC. We also present evidence that mature CTMC cannot proliferate in the presence of pure IL-3 alone.

Animals↗
PubMedDate not supplied

Restricted use of T-cell receptor V beta genes in posttransfusion graft-versus-host disease.

BACKGROUND: Posttransfusion graft-versus-host disease (PT-GVHD) is a pathophysiological process of the immune system. Mature donor T cells that have survived the host defense mechanisms recognize recipient allo-antigens through antigen-specific T-cell receptors and mount an immune attack against certain host antigens. STUDY DESIGN AND METHODS: To characterize the T cells involved in PT-GVHD, expression of the T-cell receptor V beta genes in peripheral blood T cells isolated from four PT-GVHD patients was analyzed. T-cell receptor beta chain cDNA derived from mRNA extracted from peripheral blood lymphocytes was amplified by an inverse polymerase chain reaction method, and the cDNA was subsequently cloned and sequenced. RESULTS: The cDNA clones derived from patients with PT-GVHD showed remarkable differences in the distribution of T-cell receptor V beta gene use from that in normal controls. Very restricted T-cell receptor V beta gene repertoires and preferential expression of certain V beta gene segments were revealed in the peripheral blood lymphocytes of each patients. Shared V beta gene use among the patients was not observed, probably because of HLA differences among the patient-donor combinations. CONCLUSION: This restricted use reflected in vivo expansion of a limited number of engrafted T-cell clones at the onset of PT-GVHD and suggested that those oligoclonal donor T cells may be involved in the induction of PT-GVHD.

Aged↗