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Biomedical subjects

H Ida

Publications and source records attributed to H Ida.

At least 127 records · Page 7Linked to original sources
PubMed1992

Bucillamine inhibits T cell adhesion to human endothelial cells.

We investigated the ability of bucillamine [N-(2-mercapto-2-methyl-propionyl)-L-cysteine] to prevent T cell adhesion to endothelial cells (EC) isolated from human umbilical vein. When EC were pretreated with bucillamine, T cell binding to the EC was suppressed in a dose dependent fashion. The T cells could bind preferentially to recombinant interferon-gamma (rIFN-gamma) treated EC compared with untreated EC. Bucillamine could also suppress T cell binding to rIFN-gamma treated EC as well as untreated EC. Addition of copper sulfate to bucillamine decreased significantly the percent T cell adhesion to the EC compared with bucillamine alone. The magnitude of inhibition by bucillamine and copper sulfate was similar in EC treated with rIFN-gamma as well as in untreated EC. H2O2 also inhibited the T cell binding to both untreated and rIFN-gamma treated EC. The inhibitory effects of bucillamine with or without copper sulfate on T cell binding to EC were abolished completely by catalase but not by superoxide dismutase. Our results suggest that hydrogen peroxide generated by bucillamine, with or without copper sulfate, inhibits T cell binding to EC. We believe, therefore, that bucillamine may suppress inflammation, such as that in rheumatoid synovitis, by reducing the emigration of chronic inflammatory cells from capillaries into tissue.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Effects of lobenzarit disodium on human endothelial cells. Lobenzarit disodium inhibits proliferative response, HLA-DR antigen expression, and T cell adherence toward endothelial cells.

The therapeutic action of lobenzarit disodium (CCA) on the function of endothelial cells (EC) isolated from human umbilical cord veins was investigated. CCA suppressed 3H-thymidine incorporation into EC in a dose-dependent manner. Significant inhibition was detected at a concentration of 50 micrograms/ml. The expression of HLA-DR antigen on the surface of EC was increased when EC were cultured with recombinant interferon-gamma (rIFN gamma). Treatment of EC with either IFN gamma or interleukin-1 enhanced the adhesion of T cells to EC. The kinetics of HLA-DR antigen expression by EC cultured with IFN gamma was different from the kinetics of T cell-EC adhesion, however. Neither anti-HLA-DR nor anti-HLA-ABC monoclonal antibody inhibited T cell binding to EC monolayers. CCA suppressed the expression of HLA-DR antigen by EC cultured with rIFN gamma. In an EC monolayer adhesion assay, CCA also inhibited T cell adhesion to EC in the presence of either IFN gamma or interleukin-1. Significant inhibition was observed at a CCA concentration of 10 micrograms/ml, a level that is easily attainable in serum. These results suggest that CCA may suppress rheumatoid synovitis by reducing the angiogenesis and emigration of chronic inflammatory cells from the blood into the synovium.

Cell Adhesion↗
PubMed1991

Different B-cell responses to human T-cell lymphotropic virus type I (HTLV-I) envelope synthetic peptides in HTLV-I-infected individuals.

HTLV-I (human T-cell lymphotropic virus type I) is the retrovirus related to two distinct diseases, adult T-cell leukemia/lymphoma (ATLL) and HTLV-I-associated myelopathy (HAM). We analyzed the difference in antibody activities against the viral protein and the difference in specificities of anti-HTLV-I envelope antibodies among HTLV-I-infected individuals from the same HTLV-I-endemic area using a HTLV-I-gag-env hybrid protein and HTLV-I-env-encoded synthetic peptides as antigens, respectively. The difference in the responses of IgG anti-HTLV-I envelope antibody production among HTLV-I-infected individuals was qualitative as well as quantitative. Sera from patients with HAM showed significantly higher activities of antibodies against HTLV-I-gag-env hybrid protein than sera from other HTLV-I-infected individuals including ATLL patients. The specificities of IgG anti-HTLV-I-envelope antibodies, tested on seven synthetic envelope peptides, were directed mainly against four sites, V1E7 (residues 97-111), V1E8 (191-209), and V1E9 (268-286) on gp46 and V1E1 (342-363) on gp21. Three of these sites were shown to be immunodominant T-cell sites in mice in our previous study. Whereas patients in all categories made antibodies specific for V1E1 and V1E8, only HAM patients made antibodies to the V1E7 and V1E9 epitopes, suggesting a qualitative difference in response. Whether this difference is of pathogenetic significance is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Synergistic effects of phorbol ester and interferon-alpha: target cell class I HLA antigen expression and resistance to natural killer and lymphokine-activated killer cell-mediated cytolysis.

This study was undertaken to investigate whether target cell class I HLA antigen expression induced by phorbol ester and interferon-alpha (IFN-alpha) was associated with resistance to natural killer (NK) cells and lymphokine-activated killer (LAK) cell-mediated cytotoxicity. Class I antigen expression on the surface of the K562 erythroleukemia cell line was enhanced by either IFN-alpha or phorbol ester (PDBu). Addition of PDBu together with IFN-alpha had a synergistic effect on class I antigen expression on the cells. Furthermore, synergism between IFN-alpha and PDBu was also found in class I antigen expression by MOLT-3 cells. This synergistic effect on class I antigen expression was blocked by the protein synthesis inhibitor (cycloheximide). Pretreatment of K562 cells with PDBu and IFN-alpha made them more resistant to lysis by NK and LAK cells than did either PDBu or IFN-alpha. In contrast to PDBu, 4 alpha PDD, a biologically inactive phorbol analogue, alone or combination with IFN-alpha, had no effect on class I antigen expression and susceptibility to lysis by NK and LAK cells. Kinetic experiments showed an inverse relationship between the expression of class I antigens and susceptibility to NK cell-mediated cytolysis. Using cold target competition analysis, target cells pretreated with PDBu and IFN-alpha clearly competed less effectively than did untreated cells for lysis of untreated target cells. These results demonstrate that target cells pretreated with PDBu and IFN-alpha decrease their sensitivity to natural killer and lymphokine-activated killer cells inversely with target cell class I HLA antigen expression.

Cell Line↗
PubMed1991

Endothelial cells stimulate proliferation of human thyroid epithelial cells.

The present study was undertaken to investigate cellular interactions between human thyroid epithelial cells (thyrocytes) and endothelial cells. Normal thyrocytes were cultured with either mitomycin C-treated endothelial cells or mitomycin C-treated human foreskin fibroblasts. The proliferative responses of thyrocytes were markedly stimulated by endothelial cells, but not by skin fibroblasts. The proliferative response of the thyrocytes obtained from patients with Graves' disease were similar to that of normal thyrocytes. Furthermore, the cell number of thyrocytes in endothelial cell-thyrocyte co-culture was markedly increased as compared with that in thyrocytes alone. The culture medium of endothelial cells only partly had any effect in the endothelial cell-thyrocyte co-culture experiment. Indomethacin, a cyclooxygenase inhibitor, did not increase the endothelial cells-induced thyrocyte proliferation. Furthermore, the increased proliferative response of thyrocytes stimulated by endothelial cells was not suppressed by heparin. These results suggest that endothelial cells increase thyrocyte proliferation, and that cell contact or extracellular matrix production by endothelial cells may play an important role in the proliferation of thyrocytes.

Cell Count↗
PubMed1991

Detection of Leu-19 (CD56) antigen on human thyroid epithelial cells by an immunohistochemical method.

The Leu-19 (CD56) antigen, which is recognized by anti-Leu-19 and NKH-1 monoclonal antibody, is a 200,000-220,000 molecular weight (MW) glycoprotein that is expressed predominantly on human natural killer (NK) cells that mediate major histocompatibility complex (MHC)-unrestricted cytotoxicity. However, cross-reactivity of this antibody has been observed in lung cancer, and in muscle and neural tissues. In the present study, we used the immunoperoxidase technique to examine the expression of Leu-19 antigen in human thyroid epithelial cells. In normal thyroid tissues (n = 4), thyroid tissues from Graves' patients (n = 7) and benign thyroid tumours (n = 7), thyroid epithelial cells expressed Leu-19 antigen in all cases. In thyroid papillary carcinoma (n = 6) there was no expression in four cases. This staining pattern of anti-Leu-19 antibody is similar to that of anti-thyroid peroxidase antibody. These findings implicate that the expression of Leu-19 antigen is closely related to the differentiation of thyroid epithelial cells.

Antigens, CD↗
PubMed1991

Phenotypic characteristics of T cells interacted with synovial cells.

We demonstrated the phenotypic characteristics of T cells interacted with synovial fibroblast-like cells. A small percentage of peripheral blood T cells adhered to synovial fibroblast-like cells. When synovial cells were treated with interferon-gamma or interleukin-1 beta, the percentage of T cells that adhered to the treated cells markedly increased in comparison with the value for untreated synovial cells. The kinesis of T cell adherence to treated synovial cells differed from that of HLA-DR antigen expression on synovial cells. T cell adherence was not blocked by mouse monoclonal anti-HLA-DR and anti-HLA-ABC antibodies. The phenotypes of the adherent and nonadherent T cells were investigated with a flow cytometer. The CD29 + subset was more adhesive than the CD45RA + subset to IL-1 beta-stimulated synovial cells. The proportions of high density lymphocyte function associated antigen (LFA)-1 alpha and LFA-1 beta were greater in the adherent than in the nonadherent T cells, and the mean fluorescence intensities of LFA-1 alpha, LFA-1 beta and CD2 molecules on adherent T cells were significantly higher than those on nonadherent T cells. Our results support the concept that an interaction between infiltrating lymphocytes and synovial cells occurs in the synovium, resulting in the initiation and perpetuation of immune responses in synovial tissue in rheumatoid arthritis.

Adult↗
PubMed1991

Phase II evaluation of combined cisplatin and vindesine in advanced squamous cell carcinoma of the esophagus: Japanese Esophageal Oncology Group Trial.

In the present phase II study, 31 patients with advanced measurable esophageal carcinomas were treated with a combination of 30 mg vindesine/m2 and 70 mg cisplatin/m2. The overall response rate was 16.1% (95% confidence limits, 7.1-32.6%). Responses were seen in metastatic sites, including the liver in two patients, a lung in one, neck or mediastinal lymph nodes in two and primary sites in two. The response durations were between one and two months for patients achieving partial response. The average survival time after first administration was 5.5 months for patients who responded to treatment, whereas, for those who did not, it was 7.3 months. The major form of toxicity was myelosuppression, 14 patients developed grade 2-3 toxicity and one sepsis which led to death. No superiority of the combined chemotherapy over either cisplatin or vindesine therapy alone was suggested for cases of advanced squamous cell carcinoma of the esophagus by the present study.

Aged↗
PubMed1990

Galactosylceramide and galactosylsphingosine loading studies in cultured skin fibroblasts in human and murine globoid cell leukodystrophy.

Cell level studies of 3H-galactosylceramide(GalCer) and 3H-galactosyl sphingosine (GalSph) have been carried out in cultured skin fibroblasts from human and murine globoid cell leukodystrophy (GLD). GalCer loading studies disclosed that the hydrolysis rates of GalCer in human control and GLD were 72% and 45%, respectively, and those from the murine control and GLD cells were 77% and 21%, respectively, on the 5th day of culture. On the other hand, GalSph loading studies showed that the hydrolysis rate of GalSph in the human control and GLD were 40% and 10%, respectively, and those from murine control and GLD cells were 38% and 10% on the 12th day of culture. These data suggest that both GalCer and GalSph degradations were impaired in cell level in human and murine GLD. Furthermore, when radioactive 3H-GalSph was loaded into cultured fibroblasts from murine and human GLD, 3H-GalCer band was formed via GalSph. These data strongly suggest that GalCer could be synthesized through the GalSph route as a minor pathway at least in cultured skin fibroblasts, although the major pathway to synthesize GalCer should be via ceramide.

Animals↗
PubMed1990

Abnormality in cultured oligodendrocytes and Schwann cells isolated from the twitcher mouse.

Oligodendrocytes and Schwann cells were isolated from the brain and dorsal root ganglia of the twitcher mouse, a murine model of Krabbe's disease (globoid cell leukodystrophy), and grown in tissue culture. Oligodendrocytes were cultured for up to 22 d in vitro and were immunostained with a galactocerebroside antibody, a specific marker for oligodendrocytes. The control oligodendrocytes developed well-branched processes and membrane sheets, whereas the twitcher oligodendrocyte had wirelike processes with no membrane expansion and progressive degeneration. Schwann cells from the twitcher could not extend their processes as long as normal counterparts. The amounts of psychosine in the enriched population of oligodendrocytes and Schwann cells from the twitcher mouse are about 50-fold and 70-fold higher, respectively, than those in the control cells. These data suggest that psychosine may play an important role in the progression of abnormal features of oligodendroglial membrane formation and in the absence of process elongation in Schwann cells in the twitcher mutant.

Animals↗
PubMed1990

Biochemical and morphological studies of dorsal root ganglion and its cultured cells from twitcher mouse (murine globoid cell leukodystrophy).

The biochemical pathogenesis of globoid cell leukodystrophy (GLD) (Krabbe disease) was investigated in vitro using the cultured neural cells obtained from dorsal root ganglion (DRG) of twitcher mouse (murine Krabbe disease). Electron microscopic examination of twitcher DRG of 30 days old showed the demyelination and abnormal inclusion bodies, whereas mitochondrial structure appeared to be intact. Cultured neural cells from control mice were well proliferated to form the network processes, while those from twitcher were decreased in cell numbers and showed the vacuolation of cell body, degeneration of processes, and finally died after three weeks. There was no apparent difference of lipid composition between control and twitcher DRG, and the galactocerebroside levels from control were similar to those of twitcher. However, marked accumulation of psychosine was found in the 30-day-old-twitcher DRG. The level of psychosine from twitcher DRG was elevated approximately 70 to 80-fold compared with those of control. These data suggest that neural cells from twitcher mice degenerative with age also in vitro and accumulation of psychosine in twitcher DRG may play an important role for the demyelination in GLD.

Animals↗
PubMed1990

Biochemical pathogenesis of demyelination in globoid cell leukodystrophy (Krabbe's disease): the effects of psychosine upon oligodendroglial cell culture.

The effects of psychosine on the metabolism of myelin associated glycolipids such as galactocerebroside and sulfatide in mouse brain cell cultures were investigated in order to clarify the mechanism of demyelination in globoid cell leukodystrophy (Krabbe's disease). The incorporation of 3H-galactose into cerebroside and sulfatide was studied in the presence of psychosine (1-3 micrograms/ml medium). These data indicated that psychosine inhibited the incorporation of 3H-galactose into cerebroside and sulfatide not in astroglial cell culture but in oligodendroglial cell culture. Oligodendrocytes produce myelin in the central nervous system, and cerebroside and sulfatide are major components of myelin. These results suggest that psychosine influences the lipid metabolisms of myelin and subsequently leads to the demyelination in Krabbe's disease.

Animals↗
PubMed1990

Psychosine cytotoxicity in rat neural cell cultures and protection by phorbol ester and dimethyl sulfoxide.

In Krabbe's disease (globoid cell leukodystrophy), galactosylsphingosine (psychosine) is considered to be a causative agent of the pathology found in the nervous system of the patients. In our study, we examined the cytotoxic effect of psychosine in neural cell cultures derived from the rat nervous system. The concentration of toxic thresholds varied from cell type to cell type. The 50% of toxic doses for oligodendrocytes, astrocytes, and the sensory neurons of the dorsal root ganglia were 8, 20, and 30 micrograms/mL, respectively. Oligodendrocytes, therefore, appeared to show a higher sensitivity to psychosine than did astrocytes or neurons. When phorbol ester or DMSO was applied simultaneously with psychosine as protective agents in enriched cultures of rat oligodendrocytes, the total number of live cells and galactocerebroside-positive cells and the 2'3'-cyclic nucleotide 3'-phosphohydrolase activity in these cultures were considerably higher as compared with their levels in the experimental cultures treated with psychosine alone. These results indicate that phorbol ester and DMSO could serve as protective agents for psychosine neurotoxicity.

Animals↗
PubMed1989

Fetal GM1-gangliosidosis: morphological and biochemical studies.

A 23-week fetus with GM1-gangliosidosis type 1 was studied morphologically and biochemically. The GM1-ganglioside content in the brain was approximately twice that of a control. A GM1-ganglioside comprised about 25% of the total ganglioside NANA (N-acetyl-neuraminic acid), whereas in control fetus brain the proportion was 14.3%. The storage of GM1-ganglioside in fetal GM1-ganglioside brain was confirmed by a thin-layer chromatogram immunostained with anti-GM1-ganglioside antibody. The accumulation of GM1-ganglioside in visceral organs (liver, spleen and kidney) was not detected with biochemical and immunochemical methods. However, in hepatocytes, Kupffer cells, renal tubular cells and spleen cells from the affected fetus, there were many vacuoles which could contain oligosaccharides as storage materials. These data suggest that pathochemical changes in the brain and visceral organs of an affected fetus are already evident in the second trimester of the pregnancy. Tissue specific accumulation of glycolipids or oligosaccharides in fetal GM1-gangliosidosis suggests that the biosynthesis or degradation of these compounds occurs at different periods.

Adult↗
PubMed1989

Studies on sialic acids. XIII. Isolation of 3-deoxy-D-glycero-D-galacto-2-nonulopyranosonic acid (KDN) from chum salmon, Oncorhynchus keta.

A method for analysis of 3-deoxy-D-glycero-D-galacto-2-nonulopyranosonic acid (KDN) by high-performance liquid chromatography (HPLC) with a strongly basic anion-exchange resin was developed. The method was applied to detect free KDN in water used to rinse of fertilized eggs of chum salmon, Oncorhynchus keta. Furthermore, KDN was isolated from the water as a fully protected derivative.

Animals↗
PubMed1989

[Evaluation of the degree of restoration of function with fixed molar bridges].

The purpose of this study was to determine the degree of restoration of masticatory function with fixed molar bridges. Evaluations were made of the deep temperature of the masseter muscle, masticatory performance and occlusal contacts (duration, force distribution, area and number of contacts). Criteria were established for the parameters above mention in 30 normal subjects. Fixed bridges were placed in 10 patients with missing only the mandibular first molar. Measurements were carried out both prior to and after placement of the prosthesis. The following results were obtained. 1. The deep temperature of the masseter muscle patients recovered in 30 days after prosthesis. 2. The total number of contact points and contact area increased after placement by 30 days. 3. The duration of occlusal contacts increased up to 30 days after placement. 4. The force distribution of occlusal contacts decreased for a time but recovered as the normal subjects after 30 days. 5. The masticatory performance was restored immediately after the placement and showed no change by 45 days.

Body Temperature↗
PubMed1989

[Application of neuronal cell culture in human degenerative brain disorders].

Neuronal cell culture system has been used for the study of pathochemical evaluations in human degenerative brain disorders, particularly for Krabbe's disease and neuronal ceroid lipofuscinosis. To understand the pathochemistry of Krabbe's disease, we added psychosine into neuronal cell cultures and psychosine treated cells showed the destruction of cytoskeleton and pathy intracellular changes. Electron microscopic finding showed the swelling of the mitochondria. Oligodendrocytes and Schwann cells were isolated from the brains and sciatic nerve of twitcher mouse as an authentic murine model of globoid cell leukodystrophy. Oligodendroglial cells cultured for 22 days were stained by anti-galactocerebroside antibodies. In twitcher oligodendrocyte processes were wirelike and progressively degenerated and there were few membranous expansion. Schwann cells from twitcher could not elongated their processes. These data suggest that psychosine might be important factor to result in these pathological conditions. Furthermore, we studied the effect of protease inhibitors, E-64 on dissociated primary cultures from fetal rat brain. After treated with E-64 in a concentration from 0.1-50 micrograms/ml, numerous cytoplasmic accumulations appeared in neuronal cells. These morphological pictures resemble with those of neuronal ceroid lipofuscinosis, Batten disease. We will discuss the relationship between the deficiency of catepsin H in Batten disease and inclusion bodies found in E-64.

Age Factors↗