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Biomedical subjects

Y Deguchi

Publications and source records attributed to Y Deguchi.

At least 109 records · Page 6Linked to original sources
PubMed1990

Enhanced expression of the heat shock protein gene in peripheral blood mononuclear cells of patients with active systemic lupus erythematosus.

The spontaneous increase in the transcription of the heat shock protein (hsp 70) gene in peripheral blood mononuclear cells of patients with active systemic lupus erythematosus (SLE) is shown by nuclear run on transcription assay. The transcription of hsp 70 gene in the peripheral blood mononuclear cells of five patients with active SLE was more than 10 times greater than that in five normal healthy subjects or three patients with bronchial asthma as controls. This suggests that heat shock proteins may be produced during an active immune response in patients with active SLE and play a part in a change related to lupus of the essential intracellular functions of peripheral blood mononuclear cells.

Female↗
PubMed1990

Enhancement of c-sis proto-oncogene transcription in bronchoalveolar mononuclear cells from patients with pulmonary sarcoidosis.

The expression of c-sis proto-oncogene in bronchoalveolar mononuclear cells was studied in seven patients with pulmonary sarcoidosis. By means of nuclear run on transcription assay, the transcriptional level of c-sis proto-oncogene in bronchoalveolar mononuclear cells was investigated. Expression of c-sis proto-oncogene in bronchoalveolar mononuclear cells was enhanced. Enhancement of c-sis transcription may be involved in the process of activation of bronchoalveolar mononuclear cells in patients with pulmonary sarcoidosis.

Actins↗
PubMed1990

Induction of differentiation of human leukemia cells by various combinations of cytokines and low-molecular-weight inducers.

To explore agents for differentiation therapy of leukemias, various combinations of cytokines and low-molecular-weight inducers were examined for differentiation-inducing activity toward three kinds of human leukemia-derived cell lines. The strongest differentiation inducing activity on promyelocytic HL60 cells and histiocytic U937 cells was obtained by combining recombinant tumor necrosis factor (rTNF), interferon-gamma (IFN-gamma), retinoic acid (RA), and 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3). For myeloblastic ML1 cells, the combination of rTNF, IFN-gamma, and RA had the strongest differentiation-inducing activity.

Biological Factors↗
PubMed1990

[Long-term arterial infusion chemotherapy to the cancer patients].

Arterial infusion chemotherapy is an effective method for unresectable and recurrent cancer patients. But this method had some problems, in terms of efficacy, side effect and safety. Thus, we studied these problems in 33 patients. We inserted the tube into the proper hepatic artery in 25 cases and into the aorta in 8 cases, and used anticancer drugs, such as MMC, ADM and CDDP. In this study, no serial or severe side effects were noted. On the other hand, the obstruction of catheter and artery was found in a few cases. We encountered 2 cases of CR and 11 cases of PR. The effectiveness of this method is approximately 46.4%. These results suggested that long term arterial infusion chemotherapy for outpatients was a safe and effective method from the view point of quality of life in cancer patients.

Adult↗
PubMed1989

Enhanced transcription of c-myc proto-oncogene in spleen lymphocytes from lupus-prone mice during the growing process.

The expression of c-myc proto-oncogene in spleen lymphocytes has been studied in lupus-prone mice (MRL/Mp-lpr/lpr), an animal model for the human autoimmune disease systemic lupus erythematosus, during the growing process, in comparison to control mice (MRL/Mp-+/+). By Northern blot assay and nuclear run on transcription assay, we demonstrated the enhancement of c-myc proto-oncogene expression in spleen lymphocytes from lupus-prone mice in comparison to control mice and the level of expression of c-myc proto-oncogene increased during the growing process and deterioration of lupus symptoms, such as production of autoantibodies and lymphoproliferation, in this study.

Animals↗
PubMed1989

Enhancement of c-sis protooncogene transcription in bronchoalveolar mononuclear cells from patients with autoimmune diseases with lung involvement.

The expression of c-sis protooncogene in bronchoalveolar mononuclear cells has been studied in patients with autoimmune diseases with lung involvement. By nuclear run on transcription assay, we examined the transcriptional level of c-sis protooncogene in bronchoalveolar mononuclear cells from the patients. We demonstrated the enhancement of c-sis protooncogene expression in bronchoalveolar mononuclear cells from patients with autoimmune diseases with lung involvement in this study. It could suggest that the enhancement of c-sis transcription, which we first demonstrated, is involved in the existence of activated steps of bronchoalveolar mononuclear cells from patients with autoimmune diseases with lung involvement.

Autoimmune Diseases↗
PubMed1989

Mutant fibronectin gene in skin fibroblasts of sclerotic lesions from patients with progressive systemic sclerosis.

A mutant fibronectin gene was identified in skin fibroblasts obtained from sclerotic lesions of 7 patients with progressive systemic sclerosis. We found 2 point mutations adjacent to the cell-attachment tetrapeptide DNA sequence in the cell-binding domain of the fibronectin gene. This observation suggests that the mutant fibronectin is related to an integral component of sclerotic pathogenesis through abnormal cellular interactions.

Amino Acid Sequence↗
PubMed1989

Molecular cloning of gltS and gltP, which encode glutamate carriers of Escherichia coli B.

Two genes encoding distinct glutamate carrier proteins of Escherichia coli B were cloned into an E. coli K-12 strain by using a cosmid vector, pHC79. One of them was the gltS gene coding for a glutamate carrier of an Na+-dependent, binding protein-independent, and glutamate-specific transport system. The content of the glutamate carrier was amplified about 25-fold in the cytoplasmic membranes from a gltS-amplified strain. The gltS gene was located in a 3.2-kilobase EcoRI-MluI fragment, and the gene product was identified as a membrane protein with an apparent Mr of 35,000 in a minicell system. A gene designated gltP was also cloned. The transport activity of the gltP system in cytoplasmic membrane vesicles from a gltP-amplified strain was driven by respiratory substrates and was independent of the concentrations of Na+, K+, and Li+. An uncoupler, carbonylcyanide m-chlorophenylhydrazone, completely inhibited the transport activities of both systems, whereas an ionophore, monensin, inhibited only that of the gltS system. The Kt value for glutamate was 11 microM in the gltP system and 3.5 microM in the gltS system. L-Aspartate inhibited the glutamate transport of the gltP system but not that of the gltS system. Aspartate was taken up actively by membrane vesicles from the gltP-amplified strain, although no aspartate uptake activity was detected in membrane vesicles from a wild-type E. coli strain. These results suggest that gltP is a structural gene for a carrier protein of an Na+-independent, binding protein-independent glutamate-aspartate transport system.

Blotting, Southern↗
PubMed1989

Nuclear phosphotyrosyl-protein with DNA-binding ability in peripheral blood mononuclear cells from systemic lupus erythematosus patients.

This study examined the phosphorylation of cytoplasmic and nuclear proteins in peripheral blood mononuclear cells (PBMC) of systemic lupus erythematosus (SLE) patients. The cytoplasmic and nuclear protein kinase activity in PBMC from SLE patients was at least five-fold higher than that of normal healthy subjects. PBMC of SLE patients produced different nuclear endogenous substrates on phosphorylation and also displayed distinct protein kinase activity. Nuclear phosphoproteins, with human PBMC DNA-binding ability, of 38 kD and 70 kD were detected from both SLE patients and normal healthy subjects, while the 40 kD phosphoprotein, with tyrosine as the main phosphorylation residue, was found only in SLE patients. Other nuclear phosphoproteins, and most of the detected cytoplasmic phosphoproteins, were present in higher levels in both normal PBMC with mitogen stimulation, such as PHA, and SLE PBMC. The expression level of the 40 kD nuclear phosphotyrosyl-protein showed a positive correlation with the clinical disease activity of SLE. These results suggest that PBMC from SLE patients had distinct tyrosine protein kinase (TPK) activity and/or a different endogenous substrate of nuclear DNA-binding proteins in tyrosine phosphorylation. The possible significance of tyrosine phosphorylation in PBMC of SLE patients in the pathogenesis, and its clinical meaning, are discussed.

DNA↗
PubMed1989

Changes in inducible nuclear factors with specific binding ability to c-myc gene fragments in peripheral blood mononuclear cells from systemic lupus erythematosus patients.

Using a gel retardation assay, we found new nuclear proteins of peripheral blood mononuclear cells (PBMC) from systemic lupus erythematosus (SLE) patients specifically binding to c-myc gene fragments. A different pattern could be detected between SLE patients and healthy controls for the c-myc exon I fragment, but both groups had similar patterns for the c-myc 5'-upper region fragment. For the c-myc exon I fragment, one DNA-protein complex was induced only in SLE patients and the other DNA-protein complex was amplified in SLE and normal PBMC with mitogen stimulation. It is suggested that abnormal c-myc protooncogene transcription in PBMC from SLE patients could be related to differences in nuclear specific binding proteins. These differences apparently play a key role in abnormal lymphocyte function in changes in gene regulation.

DNA↗
PubMed1989

C-myc gene binding factors in peripheral blood mononuclear cells from patients with systemic lupus erythematosus (SLE).

We characterized the nuclear proteins with specific binding ability against c-myc gene by gel-shift assay in cell extracts of peripheral blood mononuclear cells (PBMC) from SLE patients and SLE-prone mice with use of distinct c-myc fragments. With the fragment named Fmyc in our experiments, two kinds of complexes which we call C1 and C2 respectively were found in PBMC from SLE patients and SLE-prone mice. The C1 was shown to be inducible in PBMC from healthy persons without nascent protein synthesis after lectin binding to the cell and found to be elevated in the SLE patients and in all of the established cell lines we examined. The C2 seemed to be peculiar to SLE subjects. The binding site of the C1 factor (C1F) and C2 factor (C2F) which forms C1 and C2 respectively with Fmyc appeared to be common and were found to reside at 51 kbp sequence (from XhoI to Sau3A) of exon I of c-myc gene. Interestingly, XhoI site of the binding site was highly demethylated in PBMC of SLE patients as compared with healthy persons. The roles of these binding factors for the pathogenesis of SLE are discussed.

DNA-Binding Proteins↗
PubMed1989

[The characteristic changes of immune function with aging].

It is well-known that the most prominent age-related immunological abnormalities were reduced immune response against foreign antigens and increased auto-antibody production against intrinsic antigens. To explain these immunological abnormalities, we examined the various functions of human lymphocytes from aged and young groups at cellular, molecular and genetic levels. The results indicate: The first, T cells from the aged showed significantly reduced proliferative response not only to specific antigen TAP but also to mitogen PHA or combined stimulation of PMA and ionomycin. The second, the number of IL-2 receptor, particularly high affinity ones, on aged T cells were significantly reduced in the aged after TAP and PHA stimulation. The third, the ability to express Tac (p55) and p70/75 of IL-2R and to internalize the rIL-2 bound to the receptor were reduced in aged T cells. The fourth, although the ability to proliferate in response to SAC stimulation was two folds less in the aged B cells than that in the young ones, the capacity to differentiate into IgG and IgA class ISC after the combined stimulation with SAC and partially purified BCDF were rather increased on the basis of the number of viable cells recovered. The fifth, the amount of IL-2 activity produced by aged T cells was ten fold less than that by young ones, but the amount of BCDF activity produced by aged T cells was three folds higher than that by young ones after PHA stimulation. An inverse correlation between IL-2 activity and BCDF activity was found when the both activities were determined in the same sample. The sixth, the combined stimulation with PMA and ionomycin could induce proliferative response to highly purified T cells, T cell subsets and B cells. The degree of age-related decline of the proliferative response of CD-8 positive T cells was most significant, that of CD-4 positive ones was next and that of B cells was least. The seventh, although the maximum of c-myc mRNA level was attained at 2 hr after the stimulation and similar amount between the both age groups, the amount of mRNA at 8 or 24 hr was rather higher in the aged T cells than in the young ones. The reduction of the degradation rate of c-myc mRNA seemed to be the cause. We found no difference of the maximum amount and kinetics of c-myb mRNA between both age groups in T cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Age-related changes of heat shock protein gene transcription in human peripheral blood mononuclear cells.

In this study, we show the age-related retardation of heat shock 70 kD protein (hsp 70) gene transcription in peripheral blood mononuclear cells (PBMC). The amount of maximum transcription of the hsp 70 gene is decreased in PBMC from aged subjects, compared with PBMC from young control subjects. It might mean that the ability for homeostasis against heat shock stress decreases in PBMC from aged subjects. Our observation might be at least correlative and consistent with the age-related change of a possible essential function in PBMC.

Actins↗
PubMed1988

Age-related changes of expression of IL-2 receptor subunits and kinetics of IL-2 internalization in T cells after mitogenic stimulation.

The age-associated changes of the expression of IL-2 binding molecules p55/Tac(alpha chain) and p70/75(beta chain) were examined after phytohemagglutinin (PHA) stimulation. The expressions of both p55/Tac molecules and p70/75 molecules were significantly reduced in the aged compared with those in the young persons. The amounts of p55/Tac and p70/75 molecules on T cells from the aged were 55% and 59% of those on young ones, respectively. The ratio of the amount of p70/75 to that of p55/Tac in aged T cells was 0.28 and that in young ones was 0.26. The ratio was somewhat higher in the aged but not significantly. We also examined the kinetics of IL-2 internalization mediated by its receptor. The calculated t1/2 of receptor-mediated IL-2 internalization was 17 min in the aged and 16 min in the young, respectively. There was no kinetic difference between the 2 groups. The percentage of the internalized IL-2 to the sum total was 58.2% in the aged and 73.4% in the young (P less than 0.02). the amount of internalized IL-2 in T cells from the aged was 48.6% of that from the young (P less than 0.01).

Adult↗
PubMed1988

Lupus-related transcript homologous to Abelson-murine leukemia virus.

In the present study, we found the expression of transcripts homologous to Abelson murine leukemia virus (A-MuLV) in lupus-prone mice and nonautoimmune mice. One of them, as the lupus-related transcript, is expressed in only lupus-prone mice and induced by bacterial lipopolysaccharide (LSP). We could not induce the transcript by LSP in nonautoimmune mice that we examined. The significance of the transcript autoimmune events in lupus-prone mice is discussed.

Abelson murine leukemia virus↗
PubMed1988

5-Azacytidine induced inhibition of mitogenic response by agents that activate or augment activation of human peripheral blood T lymphocytes.

Previous work from our laboratory demonstrated the mitogenic response of human peripheral blood T lymphocytes by phytohemagglutinin (PHA), phorbol myristate acetate (PMA) and ionomycin, or interleukin 2 (IL-2). Increasing levels of incorporated 5-azacytosine inhibited the action of the methyltransferase suggesting that incorporation of 5-azacytosine into DNA could be responsible for the inhibiting effect of 5-azacytidine (5-aza-CR) on DNA methylation. In this study, we first demonstrated the inhibition of mitogenic response by agents, such as PHA, PMA and ionomycin, or IL-2, that activate or augment activation of human peripheral blood T cells by treatment of the analog 5-azacytidine. Over 1 microM of 5-azacytidine, we detected significant inhibition of proliferative response and over 5 microM of 5-azacytidine toxic effect of cell viability. We found no significant change of T cell subsets after treatment of 5-azacytidine.

Adult↗