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Biomedical subjects

T Matsuyama

Publications and source records attributed to T Matsuyama.

At least 19 recordsLinked to original sources
PubMed1995

Efficacy of TNF-alpha gene-transduced tumor cells in treatment of established in vivo tumor.

The therapeutic effect of TNF gene-transduced mouse fibrosarcoma cells (Meth-A: C5) on pre-inoculated parental cells (Meth-A: M0) was studied. Subcutaneous (s.c.) transplantation of M0 cells into one flank of syngeneic BALB/c mice was followed by s.c. injection of irradiated MO or C5 into the opposite flank 1 week later. The initial M0 tumor (T-MO) completely regressed in C5-vaccinated mice, whereas in M0-vaccinated mice continuous growth of T-M0 was observed. When a similar experiment was carried out in SCID mice, no regression of T-MO was observed, suggesting that the tumor regression in BALB/c mice was not due to direct anti-tumor activity of TNF secreted from C5, but to systemic immunity. Regression of the rechallenged M0 tumor was observed in mice which had shown T-MO regression by C5 vaccination, but rechallenged Colon 26 cells (syngeneic to BALB/c mice) continued to grow, indicating a specific immunity to Meth-A cells). The systemic immunity evoked in C5-vaccinated mice was directly demonstrated by enhanced killer activities of LAK and CTL with a proliferation of T-cell population in their splenocytes. Abrogation of the therapeutic effect of C5 vaccination with anti-Thy 1 and anti-Lyt 2 also demonstrates the involvement of cellular immunity in tumor regression.

Animals↗
PubMed1995

An IRF-1-dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes.

Lymphocytes are particularly susceptible to DNA damage-induced apoptosis, a response which may serve as a form of 'altruistic suicide' to counter their intrinsic high potential for mutation and clonal expansion. The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes, but an as yet unknown, p53-independent pathway(s) appears to mediate the same event in mitogen-activated mature T lymphocytes. Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the antioncogenic transcription factor interferon regulatory factor (IRF)-1. Thus two different anti-onco-genic transcription factors, p53 and IRF-1, are required for distinct apoptotic pathways in T lymphocytes. We also show that mitogen induction of the interleukin-1 beta converting enzyme (ICE) gene, a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, is IRF-1-dependent. Ectopic overexpression of IRF-1 results in the activation of the endogenous gene for ICE and enhances the sensitivity of cells to radiation-induced apoptosis.

Animals↗
PubMed1995

Molecular cloning of LSIRF, a lymphoid-specific member of the interferon regulatory factor family that binds the interferon-stimulated response element (ISRE).

Interferon regulatory factor (IRF) genes encode a family of DNA-binding proteins that are involved in the transcriptional regulation of type-I interferon and/or interferon-inducible genes. We report here the characterization of LSIRF, a new member of the IRF gene family cloned from mouse spleen by the polymerase chain reaction using degenerate primers. LSIRF was found to encode a 51 kDa protein that shares a high degree of amino acid sequence homology in the DNA-binding domain with other IRF family members. LSIRF expression was detectable only in lymphoid cells. In contrast to other IRF genes, LSIRF expression was not induced by interferons, but rather by antigen-receptor mediated stimuli such as plant lectins, CD3 or IgM crosslinking. In in vitro DNA binding studies, LSIRF was able to bind to the interferon-stimulated response element (ISRE) of the MHC class I promoter. The expression pattern and DNA binding activities suggest that LSIRF plays a role in ISRE-targeted signal transduction mechanisms specific to lymphoid cells.

Amino Acid Sequence↗
PubMed1995

Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta.

In mice lacking the interleukin-2 receptor beta chain (IL-2R beta), T cells were shown to be spontaneously activated, resulting in exhaustive differentiation of B cells into plasma cells and the appearance of high serum concentrations of immunoglobulins G1 and E as well as autoantibodies that cause hemolytic anemia. Marked infiltrative granulocytopoiesis was also apparent, and the animals died after about 12 weeks. Depletion of CD4+ T cells in mutant mice rescued B cells without reversion of granulocyte abnormalities. T cells did not proliferate in response to polyclonal activators, nor could antigen-specific immune responses be elicited. Thus, IL-2R beta is required to keep the activation programs of T cells under control, to maintain homeostasis, and to prevent autoimmunity.

Animals↗
PubMed1995

Spontaneous resistance to acute T-cell leukaemias in TCRV gamma 1.1J gamma 4C gamma 4 transgenic mice.

The concept of tumour surveillance implies that specific and non-specific components of the immune system eliminate tumours in the early phase of malignancy. The immunological mechanisms that control growth of preneoplastic cells are, however, not known. T cells expressing gamma delta T-cell receptors (TCR) were first described as lymphocytes with reactivity against various tumour cells, which suggests that gamma delta T cells could mediate tumour surveillance. Here we show that TCRV gamma 1.1J gamma 4C gamma 4 transgenic mice are spontaneously resistant to acute T-cell leukaemias but cannot reject non-haematopoietic tumours. TCRV gamma 1.1J gamma 4C gamma 4+ hybridomas isolated from these mice react in vitro against almost all haematopoietic tumour cell lines tested. Recognition of tumour cells depends on the gamma delta TCR but is independent of major histocompatibility complex (MHC) class I, MHC class II, or TAP-2 peptide transporter expression. Ligand recognition is influenced by the murine Nromp gene, which confers resistance or susceptibility to tuberculosis, lepra and leishmaniasis. These data indicate that TCRV gamma 1.1+ T cells confer spontaneous immunity against haematopoietic tumours in vivo and link innate resistance to bacterial infections with tissue-specific tumour surveillance by gamma delta+ T cells.

3T3 Cells↗
PubMed1995

Immunocytochemical demonstration of developmental distribution of muscarinic acetylcholine receptors in rat parietal cortex.

The present investigation reveals many cortical neurons immunopositive for M35, the monoclonal antibody raised against purified muscarinic acetylcholine receptor (mAChR) proteins, in the early postnatal rat brain. The ontogeny of mAChR expression, exemplified on the parietal neocortex, was studied in a series of rat pups from postnatal days (PD) 1, 3, 7, 14 and 21. Immunoprecipitation in the parietal somatosensory cortex was manifest in the population of pyramidal neurons during postnatal development. In particular during the early postnatal ages, until 2 weeks after birth, M35 immunoreactivity (M35-ir) was present in all neuronal compartments, indicating transportation of mAChR protein in axonal and dendritic processes as observed in light and electron microscopic analysis. The immunoprecipitation in the apical dendrites yielded dense labeling in layer 1 where the distal processes of the pyramidal dendrites branched extensively forming a plexus that intermingled with horizontal fibers in this superficial layer. At PD21, immunolabeling in layer 1 and in axons of pyramidal cells was reduced compared to earlier ages suggesting a transient expression of mAChRs in these neuronal structures. The development of M35-ir in the cortex appeared to antedate that of its cholinergic afferentation as indicated by AChE histochemical study.

Acetylcholinesterase↗
PubMed1995

Characterization of nodules induced by bioactive glass on cultured periodontal-ligament fibroblasts.

We previously reported that materials leached from bioactive glass (BG) and vitamin D3 induced the formation of nodules on cultured periodontal-ligament fibroblasts (PLF). In this study, we have investigated the relationship between the conditions of the materials and nodule formation, analyzed morphologically, and also studied whether the production of nodules was specific to cultured PLF. PLF and skin fibroblasts were cultured in the presence or absence of BG. The amounts of calcium, phosphate, sodium and silicon in the culture medium and the number of nodules were measured at the 55th day. The nodules were observed microscopically and analyzed using an X-ray microanalyzer. In PLF, nodules were formed regardless of the presence or absence of BG; however, they were more numerous in the presence of BG. In skin fibroblasts, nodules were not observed. The amounts of calcium and silicon were higher in the presence of BG, while the amount of phosphate was lower. The nodules appeared crystalline with a spongy structure and contained calcium and phosphorus. Our results show that the nodules were associated with PLF and precipitated by the materials (higher concentrations of calcium and silicon), and they were spongy crystal composed of calcium and phosphorus.

Biocompatible Materials↗
PubMed1995

Phenytoin and fluoride act in concert to stimulate bone formation and to increase bone volume in adult male rats.

We have recently demonstrated that phenytoin is an osteogenic agent at low doses. The present paper describes observations that a mitogenic dose (i.e., 20 microM in BGJb medium) of fluoride significantly augments the phenytoin-dependent stimulation of normal human bone cell proliferation and alkaline phosphatase (ALP) activity in cell culture. Additionally, the present study was designed to investigate whether fluoride and phenytoin would interact to increase bone formation in rats in vivo. Four groups of weight-matched adult male rats received daily I.P. injection of (1) vehicle (10% DMSO), (2) 5 mg/kg/day phenytoin, (3) 5 mg/kg/day phenytoin and 50 ppm NaF, and (4) 50 ppm NaF and vehicle, respectively, for 36 days. Sodium fluoride (NaF) was delivered in drinking water. Blood samples were drawn weekly and analyzed for serum osteocalcin, ALP, calcium, phosphorus, and 25(OH)D3. Rats were labeled with tetracycline at day 21 and 30 and histomorphometric analysis was carried out on the tibia at the end of the experiment. Neither agent by itself or together affected the serum calcium, phosphorus, or 25(OH)D3 levels. All measures of bone formation, i.e., serum osteocalcin level and ALP activity, bone ALP specific activity, mineral apposition rate, bone formation rate, and % bone formation surface, were increased by each agent. Fluoride and phenytoin together produced bigger increases in each parameter than did each agent alone. Trabecular bone volume was increased in the tibial metaphysis by fluoride or phenytoin alone; and when administered together, the two agents produced a greater increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1995

Morphological differences in the skull of ascorbic acid-deficient ODS rats.

The physiological importance of ascorbic acid (AsA) in bone formation has been thought to be due mainly to its effects on collagen production and, consequently, matrix formation. However, effects of AsA deficiency on growing animals are poorly understood. The purpose of this experiment was to find how AsA deficiency affects craniofacial growth cephalometrically, and the periodontal ligament and the bone density of alveolar septum histologically. Five-week-old growing male rats with hereditary defects in AsA synthesis (ODS rats) placed on an AsA-deficient or minimally supplemented diet for 4 weeks showed a marked reduction in plasma AsA level and a negative or slight increment in body weight. Cephalometric evaluation revealed that craniofacial growth was influenced by AsA deficiency. Histological observations of periodontal structure and bone density in AsA-deficient animals showed no difference from controls, whereas the periodontal ligament of the upper first molar in the deficient animals was narrower than that of controls. These observations indicate that AsA deficiency reduces craniofacial size and the width of the periodontal ligament significantly in growing rats, whereas bone density is not affected. Thus, AsA, through collagen production, may be important to the increase in size of the craniofacial structures in growing animals.

Alveolar Bone Loss↗
PubMed1995

Therapeutic effect of bifemelane on unilateral cerebral ischemia in gerbils.

To examine the therapeutic effect of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane) on neuronal ischemia-reperfusion injury, we evaluated the neurological score in gerbils subjected to unilateral common carotid occlusion. Using the neurological score method, we selected animals which showed stroke symptoms without seizures, because seizure activity can modify the neurological outcome. Just after the clip removal following 30 min of ischemia, 0.2 ml of either vehicle (0.9% saline, n = 10) or bifemelane (25 mg/kg, n = 10) was administered intraperitoneally. Then, the neurological score and the maximum inclination at which the gerbil could maintain its equilibrium were recorded at 5, 10, and 30 min, and 1, 2, 3, 6, and 24 hr after the insult. Animals were then decapitated and their brains were processed for immunohistochemical investigation. Treatment with bifemelane after reperfusion significantly improved the neurological score and motor function. Immunohistochemistry using an antibody for microtubule-associated protein 2 clearly demonstrated preservation of staining especially in the caudate-putamen in the animals treated with bifemelane. The present findings suggest a beneficial effect of bifemelane on neuronal ischemia-reperfusion injury, which may be common after cerebral ischemia.

Animals↗
PubMed1995

Increased F1/GAP-43 mRNA accumulation in gerbil hippocampus after brain ischemia.

To assess whether ischemia could induce GAP-43 mRNA expression, we performed in situ hybridization in gerbil brains that had been subjected to 5 min of global ischemia. In control dentate granule cells, little hybridization was detected in contrast to the intense signal generated by pyramidal neurons of the adult hippocampal formation. After ischemia, we detected a robust GAP-43 signal over hippocampal granule cells at 3 h of reperfusion, persisting through 7 days, and disappearing by 14 days. This demonstrated GAP-43 gene induction after ischemia, and suggests that GAP-43 may be involved in reactive events, including fiber sprouting and synaptic reorganization, that follow ischemia.

Animals↗
PubMed1995

PUVA suppresses the expression of cell adhesion molecules of lymphocytes.

To determine the therapeutic mechanism of PUVA in psoriasis vulgaris, the effects of PUVA on activated T lymphocytes were investigated in vitro. Peripheral blood mononuclear cells (PBMC) obtained from healthy volunteers were activated with Con A stimulation (Con A blasts). Both untreated PBMC and Con A blasts were irradiated with UVA light in the presence of 8-methoxypsoralen (8-MOP). The expressions of CD4, CD8, VLA-4 and LFA-1 of PBMC and Con A blasts were stained with each monoclonal antibody and the intensity of fluorescence was analyzed by FACScan. PUVA-treated PBMC showed decreased response to both Con A and PHA stimulation. PUVA treatment also suppressed the IL-2 production of Con A blasts and IL-2 response of PBMC with increasing UVA fluence. The expressions of LFA-1, VLA-4, CD4, CD8 and CD25 (IL-2R) molecules were decreased in PUVA-treated Con A blasts. Con A blasts were more sensitive than untreated PBMC to PUVA treatment. These results suggest that the therapeutic effects of PUVA on psoriasis vulgaris can be induced by suppression of the expression of cell surface molecules of activated T lymphocytes.

Cell Adhesion Molecules↗
PubMed1995

Mutational analysis of flagellum-independent surface spreading of Serratia marcescens 274 on a low-agar medium.

In a previous study (J. O'Rear, L. Alberti, and R. M. Harshey, J. Bacteriol. 174:6125-6137, 1992) we reported the isolation of several transposon mutants of Serratia marcescens 274 that were defective either in swarming alone or in both swimming and swarming motility. All the nonflagellate (Fla-) mutants, while defective in both types of motility, were able to spread rapidly on the surface of low-agar (0.35%) media. We show here that some of the swarming-defective mutants are defective in the production of serrawettin W1, an extracellular cyclic lipopeptide produced by S. marcescens 274. When combined with a Fla defect, the serrawettin (Swt) mutants are deficient in spreading on low-agar media. The spreading deficiency can be overcome by serrawettin supplied extracellularly. Introduction of Fla defects into chemotaxis mutants does not affect this mode of surface translocation. These results suggest that spreading may be a passive form of translocation. We also report that swarming defects in all mutants showing a Dps phenotype (able to swarm within the inoculated area but unable to move outward) in the earlier study can be overcome by changing the commercial source of agar.

Agar↗
PubMed1995

Circulating erythropoietin in patients with acquired aplastic anaemia.

The plasma erythropoietin (Epo) concentration was measured by radioimmunoassay in 75 patients with acquired aplastic anaemia. Overall there was an inverse relationship between the concentration of plasma Epo and the degree of anaemia. Plasma Epo concentrations were lower in patients who were sampled soon after diagnosis as opposed to those studied at later times. Although a decrease in the plasma Epo concentration was noted in all erythroid responders following immunosuppressive (IS) therapy or bone marrow transplantation (BMT), it was lower in patients undergoing BMT than in those receiving IS therapy for any given degree of anaemia.

Adolescent↗
PubMed1995

Suppression of plasma-activated factor VII levels by warfarin therapy.

To investigate the effect of warfarin treatment on the early phase of tissue factor-induced coagulation, we measured plasma-activated factor VII (factor VIIa) levels by a direct fluorogenic assay in 74 cardiovascular disease patients on long-term oral anticoagulation. We divided the patients into three groups based on the international normalized ratio (INR). In the patients with INR ranges of < 1.7 and 1.7 to 2.5, factor VIIa levels were 42% and 61% lower, respectively, than in age- and sex-matched controls. Factor VII coagulant activity (factor VIIc), factor VII antigen (factor VIIag), protein C, and factor X levels were also reduced to a similar extent in both groups. However, in patients with an INR > 2.5, the factor VIIa level was not decreased compared with that at an INR of 1.7 to 2.5, although the factor VIIc, factor VIIag, factor X, and protein C levels were all decreased further. Although the precise relation between the reduction of factor VIIa levels and the increase of INR requires appropriately designed long-term clinical trials, our data suggest that an INR range of 1.7 to 2.5 is sufficient for the suppression of factor VIIa. During the long-term follow-up of three patients with congenital antithrombin III or protein C deficiency, the factor VIIa level was more responsive to changes in the warfarin dose than the INR, and there were generally no corresponding changes of the thrombin-antithrombin III complex (TAT) level. However, one patient showed a transient marked increase of factor VIIa during the discontinuation of warfarin that was accompanied by an increase in TAT. Based on these findings, factor VIIa could be useful for monitoring both hypercoagulable and hypocoagulable states.

Adult↗