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Y Oda

Publications and source records attributed to Y Oda.

At least 487 records · Page 27Linked to original sources
PubMed1991

Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands.

The effect of the ionophore A23187 on a. the release of thyroid hormone from perifused mouse thyroid glands and b. the morphological changes in follicular epithelial cells was evaluated. A23187 at a concentration of 5 mumol/l significantly inhibited both the TSH- and the forskolin-stimulated release of T3 and T4. In the presence of 3-isobutyl-1-methylxanthine or (4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone) RO 20-1724, A23187 did not affect the forskolin-stimulated release of cAMP, but did inhibit the release of T3 and T4 stimulated by forskolin. Light and electron microscopic evaluation of the follicular epithelial cells of mouse thyroid tissues following 1-h stimulation with forskolin showed numerous pseudopods engulfing luminal colloid of various size and the presence of reabsorbed colloid droplets in the apical cytoplasm. Quantitative electron microscopic analysis revealed that the addition of the ionophore A23187 reduced the number of reabsorbed colloid droplets to one eighth in follicular epithelial cells. These observations suggest that the increase in intracellular Ca2+ induced by the ionophore A23187 inhibits the TSH-stimulated thyroid hormone release independently of the cAMP level, and that the suppression of thyroid hormone release may be due to an inhibition of colloid reabsorption.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Human recombinant interleukin 1 inhibits TSH-stimulated morphological changes in thyroid follicles cultured as semi-organs.

To study the effects of human recombinant interleukin-1 on thyrocytes, we cultured thyroid follicles as semi-organs, each consisting of approximately 10-20 follicles, in the presence or absence of IL-1 alpha or beta. Semi-organ culture reproduces the in vivo environment well. After culture for 2 or 4 days, the follicles were incubated with TSH (10 U/l) for 4 h and fixed for light and electron microscopical examinations. Regardless of the presence or absence of IL-1, follicular structure, polarity, and luminal colloid did not change during culture. In thyroid epithelial cells cultured without IL-1, TSH markedly induced elongation of microvilli and formation of reabsorbed colloid droplets. On the other hand, both IL-1 alpha and beta inhibited these TSH-stimulated changes. The degree of inhibition correlated with the concentration of exposure to IL-1. We conclude that IL-1 inhibits TSH-stimulated morphological changes in thyroid follicles cultured as semi-organs, depending on the concentration of IL-1.

Animals↗
PubMed1991

[A case report of condyloma acuminatum of the posterior urethra].

A case of urethral condyloma acuminatum is reported. A 77-year-old man was admitted to Konan Hospital to undergo surgery for benign prostatic hyperplasia. By urethrography and urethroscopy, a circumferential papillary lesion was disclosed in the posterior urethra extending from the membraneous urethra. Transurethral resection was performed on July 19, 1989. Pathohistological diagnosis was condyloma acuminatum/condyloma acuminatum in which the antigen of papilloma virus was detected by PAP stain.

Aged↗
PubMed1991

[Immunomodulatory effects of interferons on target human gliosarcoma cells in the tumor-specific CTL- and LAK-mediated cytolysis].

We compared the regulatory effects of interferon (IFN)-beta and IFN-gamma on the susceptibility of a human gliosarcoma line GI-1 to the attack of autologous cloned tumor-specific cytotoxic T-lymphocytes (CTL) and lymphokine-activated killer (LAK) cells. Preincubation of GI-1 cells with IFN-gamma caused augmented susceptibility to the cytotoxic attack of two autologous CTL clones, whereas IFN-beta exhibited no such marked effect. On the other hand, preincubation with either IFN-beta or IFN-gamma made the GI-1 cells resistant to the attack of autologous LAK cells. Both IFNs augmented the surface expression of HLA class-I molecules on GI-1 cells. A monoclonal anti-HLA class-I antibody blocked the cytolysis by one CTL clone, but not by the other one. These results suggest that IFN-gamma exerts some different effect (s) from that of IFN-beta on the target GI-1 cells in their susceptibility to the CTL-mediated cytolysis, and that recognition mechanisms of target cells by the CTL are different from those by LAK cells. This draws our attention to IFN administration in adoptive immunotherapy against brain tumors using CTLs and LAK cells.

Brain Neoplasms↗
PubMed1990

Structure of chicken 16-kDa beta-galactoside-binding lectin. Complete amino acid sequence, cloning of cDNA, and production of recombinant lectin.

The complete primary structure of chicken 16-kDa beta-galactoside-binding lectin (C-16) was determined. It was composed of 134 amino acid residues and has an acetylated NH2 terminus. A cDNA was also cloned, but no signal sequence was found in the initiator region. The initiator methionine remained as the NH2 terminus of the mature lectin. Although C-16 is distinct from chicken 14-kDa beta-galactoside-binding lectin (C-14), it proved to be a member of the vertebrate 14-kDa-type lectin family. Comparison of the primary structures between the vertebrate 14-kDa-type lectins suggests that C-14 and C-16 were produced by gene duplication of an ancestral lectin gene at a time close to the divergence of birds and mammals. Northern and Southern blot analysis indicated that these isolectins are encoded by individual genes which are differently regulated during the development of the embryo. A recombinant C-16 lectin was produced in Escherichia coli. The product was indistinguishable from the authentic C-16 lectin except that the NH2 terminus of the former was found to begin with free methionine.

Amino Acid Sequence↗
PubMed1990

Amino acid sequence and characterization of a heparin-binding neurite-promoting factor (p18) from bovine brain.

A neurite-promoting factor (p18) was isolated from bovine brain using ammonium sulfate fractionation, sulfated Sephadex G-50 chromatography, heparin-Sepharose gel chromatography, and reverse phase high performance liquid chromatography. The complete amino acid sequence of p18 was determined by automated Edman degradation of S-pyridylethylated p18, and its peptide fragments produced by cyanogen bromide cleavage and by digestion with specific endoproteinases. Alignment of the amino acid sequences of these peptides revealed that p18 consists of 119 amino acid residues with a calculated molecular weight of 14,200. p18 appears to possess five disulfide bonds per molecule. A region of amino acid sequence at the C terminus of p18 shows a structural feature homologous to that around the reactive sites of Kazal-type protease inhibitors. However, p18 did not exhibit anti-trypsin activity. p18 showed very little, if any, mitogenic activity toward NIH 3T3 cells and Swiss mouse 3T3 cells. p18 was found to bind to a specific receptor with an apparent Kd of approximately 8 nM and receptor numbers 1.7 x 10(5) and 1.0 x 10(4) for NIH 3T3 cells and PC12 cells (rat pheochromocytoma cells), respectively.

Amino Acid Sequence↗
PubMed1990

Studies on the structure and stabilizing factor of the CUUCGG hairpin RNA using chemically synthesized oligonucleotides.

A tridecaribonucleotide, r-UGAGCUUCGGCUC, and two analogues r(UGAGC)d(UUCG)r(GCUC) and r-UGAGCUUCIGCUC, which form a hairpin structure with a four-base-paired stem and a UUCG loop, were synthesized by the solid-phase phosphoramidite method. Properties of these three oligomers and d-TGAGCTTCGGCTC, the DNA analogue, were studied by UV, CD and NMR spectroscopy. The melting temperature (Tm) data suggest that the 2'-hydroxy1 groups and the 2-amino group of guanosine in the loop (9G) stabilize the CUUCGG hairpin which is known to have an unusually high Tm. NMR studies show that this 9G takes a syn conformation and the phosphodiester backbone has a turn at 9G-10G which is a junction of the stem and loop.

Base Sequence↗
PubMed1990

Infiltrative and cytolytic activities of lymphokine-activated killer cells against a human glioma spheroid model.

In the present study, we investigated not only the cytotoxic effects of lymphokine-activated killer (LAK) cells on a tumor mass but also the ultrastructural cell-to-cell interaction between LAK effector cells and tumor cells during the cytolytic process within a three-dimensional solid tumor. A multicellular tumor spheroid of a human glioma cell line (U-251MG) was utilized as a solid tumor model. LAK cells were generated from peripheral blood lymphocytes of a healthy donor after stimulation by interleukin 2. Multicellular tumor spheroids with diameters of 500 microns were cocultivated with either LAK cells or nonactivated peripheral blood lymphocytes at the effector:target cell ratio of 20:1, and then time-sequential kinetic, morphological, and ultrastructural analyses were carried out. Morphological and kinetic studies showed that LAK cells directly infiltrated toward the inner areas of multicellular tumor spheroids and caused a progressive tumor destruction. In contrast, peripheral blood lymphocytes hardly exhibited such activities. Ultrastructurally, it was found that the infiltrating LAK effector cells were composed of heterogeneous subpopulations, T-like cells, and large granular lymphocyte-like cells. Both types of lymphocytes tightly adhered to the tumor cells and showed typical morphological features of killing them.

Cell Line↗
PubMed1990

Decreased susceptibility of lined human gliosarcoma cells to lymphokine-activated killer cell cytolysis by gamma-interferon treatment.

The susceptibility of the established cultured gliosarcoma line GI-1 to lymphokine-activated killer (LAK) cells was analyzed with and without interferon (IFN)-gamma treatment of target GI-1 cells. IFN-gamma treatment decreased the susceptibility of GI-1 cells to LAK cell cytolysis in a dose-dependent manner. Acid treatment of GI-1 cells increased their susceptibility to cytolysis compared with untreated cells. IFN-gamma treatment and acid treatment of GI-1 cells respectively increased and decreased the expression of class I HLA antigens on GI-1 cells. The susceptibility of GI-1 cells to LAK cell cytolysis and their expression of HLA class I molecules were inversely correlated. Subpopulation depletion experiments on the LAK cells with monoclonal antibodies and complement revealed that phenotypically natural killer type (CD16+) cells had a high cytotoxic activity against untreated GI-1 cells but a relatively low activity against IFN-gamma-treated GI-1 cells in both the precursor and effector phases. On the other hand, phenotypically T-type (CD3+) cells did not show these tendencies at all in both the precursor and the effector phases.

Antigens, Differentiation↗
PubMed1990

Pulmonary surfactant secretion in the type II pneumocytes in inflamed condition.

Basal PC secretion in the type II pneumocytes from bronchitic rats was the same as that in the type II pneumocytes from normal rats. Neutrophils activated by opsonized zymosan or PMA, stimulated PC secretion in type II pneumocytes without causing any cell damage. The stimulation required close accession or attachment of neutrophils and type II pneumocytes and was not affected by the pretreatment with either SOD, catalase, AA861 or alpha 1-antitrypsin.

Animals↗
PubMed1990

Left ventriculotomy of the heart: tissue repair and localization of collagen types I, II, III, IV, V, VI and fibronectin.

The reparative process following left ventriculotomy was investigated immunohistochemically using anti-type I, II, III, IV, V and VI collagen antibodies, and anti-fibronectin antibody. Wound healing began with proliferation of young fibroblasts positive for type I, III and V collagens at the wound margin; vascular granulation tissue then grew into the injured myocardium followed by deposition of fibrous components immunoreactive with type I and III. At 30 days after operation when almost the entire thickness of the myocardium at the wound was replaced by fibrosing granulation tissue, a small cluster of adipocytes appeared around capillaries at the wound margin. The granulation tissue was gradually replaced by the adipose tissue with establishment of a fibrous union at the subendocardium by 90 days. In addition to type I and III collagens, type VI collagen was detected in a fine fibrillary pattern along thick collagen fibre bundles in the fibrous tissue and around the adipocytes. Fibronectin was distributed diffusely in the granulation tissue and gradually decreased with increase of the fibrous components. These results indicate that the ventriculotomy was finally repaired in the form of a fibrous scar, particularly in the endocardium. There was marked infiltration of adipose tissue in the damaged myocardium. Presumably type VI collagen, as well as type I and type III collagens, plays an important role in wound union.

Animals↗
PubMed1990

Immunohistological study on collagenous proteins of benign and malignant human cartilaginous tumours of bone.

The immunohistological distribution of collagen types I, II, III, V and VI in human benign and malignant cartilaginous tumours of bone was examined with regard to their aggressiveness. The matrix of enchondromas consisted of type II collagen distributed diffusely, and type VI predominantly localized in the immediate surroundings of the cells. Types I, III and V collagen were not found. These findings were similar to the distribution of collagenous proteins in normal hyaline cartilage where each lobule was consistently rimmed by types I and V collagen. In grade 1 chondrosarcomas, the main collagenous components of matrix were also types II and VI collagen. Type II was sometimes found in the cytoplasm of tumour cells and type VI tended to lose territorial localization. In addition, type I collagen was demonstrated consistently and type V in some cases. In grade 2 chondrosarcomas, type II collagen was demonstrated not only in the matrix but occasionally in the cytoplasm of tumour cells. Type VI was dispersed in the intercellular areas. The other collagenous proteins such as types I, III and V were also present in the matrix. In grade 3 chondrosarcomas, type II collagen was localized predominantly in the cytoplasm of tumour cells and in the adjacent matrix. Type VI was markedly decreased with complete loss of pericellular distribution, whereas types I, III and V were constantly present in the matrix. Those alterations in the distribution of collagen types correlated well with the aggressive behaviour of the tumours. The findings suggest that distribution of different collagen types in cartilaginous tumours reflects the immaturity of the tumour cells and is a useful indicator of their aggressiveness.

Adolescent↗
PubMed1990

Clonal analysis in the ultrastructure of cell-to-cell interaction between a human glioma cell line and autologous tumor-specific cytotoxic T lymphocytes.

The clonal analysis in the ultrastructure of tumor-lymphocyte interaction was carried out in order to investigate the precise mechanism responsible for CTL-mediated cytolysis of tumor cells. A glioma-derived cell line (GI-1) and autologous tumor-specific cytotoxic T lymphocyte (CTL) clones were established. The CTL lines were composed of the morphologically homogeneous lymphocytes with intracytoplasmic electron-dense secretory granules. After the stimulation by GI-1, the size of the CTLs increased, and the intracytoplasmic organellas were developed. It was noted that the intracytoplasmic secretory granules markedly increased in number and size, and many of them exhibited an "immature" appearance. On the other hand, the tumor cells underwent a progressive degeneration. In contrast, the stimulation by other antigens caused only small morphological changes in the CTLs. It is suggested, therefore, that the secretory function of tumor-specific CTLs is activated by the stimulation of the specific antigen, and that soluble factors in the secretory granules in the CTLs may be closely associated with the mechanism of target cell lysis.

Cell Communication↗
PubMed1990

Induction of umu gene expression in Salmonella typhimurium TA1535/pSK1002 by dimethyl sulfoxide (DMSO).

The genotoxicity of dimethyl sulfoxide (DMSO) was demonstrated by the umu test using Salmonella typhimurium TA1535/pSK1002 carrying the umuC-lacZ fusion gene. The level of beta-galactosidase activity which shows umu gene expression in the test system was dependent on the concentration of DMSO in the culture medium. The maximum beta-galactosidase activity was approximately 3.5 times as high as the background level with 10% of DMSO in the culture medium. The lowest concentration of DMSO required for a response of over twice the background level was approximately 5%. Four structurally related chemicals (acetone, di-n-butylsulfoxide, dimethylsulfide, methylphenylsulfoxide) did not show umu gene expression at their non-toxic doses.

Cloning, Molecular↗
PubMed1990

Complementary DNAs for choline acetyltransferase from spinal cords of rat and mouse: nucleotide sequences, expression in mammalian cells, and in situ hybridization.

Complementary DNA clones containing the entire coding region of choline acetyltransferase (ChAT) were isolated from the spinal cords of rat and mouse. The cDNAs of rat and mouse coded for 640 and 641 amino acids, respectively, and showed 95% mutual homology and 80% homology with the cDNA of porcine ChAT. Northern blot analysis revealed a single band of 4.4 kb in the spinal cord and brain in each species. Introduction of the cDNAs into Chinese hamster ovary cells and neuron-derived cell lines, N1E115 and NG108-15, expressed a high ChAT activity, which was inhibited by a specific ChAT inhibitor. In situ hybridization using the rat cRNA probe revealed specific labeling of the motoneurons in the spinal cord and neurons in various forebrain nuclei of the rat where the existence of cholinergic neurons has been demonstrated immunohistochemically.

Amino Acid Sequence↗