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N Terada

Publications and source records attributed to N Terada.

At least 217 records · Page 12Linked to original sources
PubMed1995

IL-4 upregulates Fc epsilon RI alpha-chain messenger RNA in eosinophils.

By using the reverse transcription polymerase chain reaction and Southern blot hybridization, we demonstrated that Fc epsilon RI alpha-chain (Fc epsilon RI alpha) messenger RNA was expressed in eosinophils purified from the peripheral blood of patients with allergic rhinitis and that this expression was enhanced by IL-4. However, studies in which flow cytometry or immunostaining was used did not reveal the expression of Fc epsilon RI alpha protein on eosinophils from peripheral blood. Neither IL-4 alone nor the combination of IL-4 and other cytokines could induce detectable Fc epsilon RI alpha protein; nevertheless, they do express Fc epsilon RI alpha mRNA. Double-labeling immunostaining on cryostat sections of nasal mucosa clearly demonstrated that some Fc epsilon RI alpha-positive cells were eosinophil cationic protein-positive, which confirms their eosinophilic nature. Not all the eosinophil cationic protein-positive cells express on Fc epsilon RI alpha signal. Considering that Fc epsilon RI alpha mRNA was detectable in four of five samples of eosinophils from those patients with nasal allergy and that only one of five eosinophil samples from normal subjects expressed Fc epsilon RI alpha mRNA, the level of Fc epsilon RI expression may be correlated with the activation of eosinophils. It seems very likely that some other unidentified factors are required for the process from the expression of Fc epsilon RI alpha mRNA to that of Fc epsilon RI as a protein.

Adolescent↗
PubMed1995

No effect of RU 486 (mifepristone) on hepatocellular tumorigenesis in orchiectomized male mice induced by 3'-methyl-4-dimethylaminoazobenzene.

Effects of RU 486 (mifepristone) on hepatocellular tumorigenesis in orchiectomized male mice induced by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) were investigated. Male mice that had been treated with 3'-Me-DAB neonatally were orchiectomized at one month of age, and injected daily with vehicle only or RU 486 at 0.2 or 0.4 mg/day thereafter. In the liver of orchiectomized males injected with vehicle only, adenomatous nodules developed at incidences of 16.2 and 38.5% at 9 and 12 months of age, respectively, but no carcinomas developed at these ages. Injections of RU 486 at 0.2 or 0.4 mg/day neither affect incidences of adenomatous nodules in the liver, their numbers per mouse, and their areas, nor promote the development of carcinomas. The present results suggest that the long term administration of RU 486 has no effects on hepatocellular tumorigenesis.

Animals↗
PubMed1995

Correlation between serum prolactin levels and hepatocellular tumorigenesis induced by 3'-methyl-4-dimethylaminoazobenzene in mice.

Ovariectomy at 1 month of age promotes development of hepatocellular adenomatous nodules in female C57BL/6 x DS-F1 mice treated neonatally with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB). Implantation of oestradiol-17 beta (E2) pellets at 1 month of age suppresses nodule development. Since E2 increases serum levels of prolactin, high serum levels of prolactin in mice that have received implants of E2 pellets may play a role in the suppression of hepatocellular tumorigenesis. Therefore, to investigate the role of prolactin in hepatocellular tumorigenesis, we examined development of adenomatous nodules in female mice that had been treated neonatally with 3'-Me-DAB and had undergone ovariectomy at 1 month of age, under various serum levels of prolactin. Treatment of these mice with perphenazine (dopamine antagonist) from 6 months of age or transplantation of pituitary glands under the renal capsule at 6 months of age markedly increased serum levels of prolactin and significantly suppressed the incidence of adenomatous nodules at 12 months of age. Implantation of E2 pellets at 1 month of age increased serum levels of prolactin to a greater extent and further decreased the incidence of adenomatous nodules. Treatment of mice that had received implants of E2 pellets at 1 month of age with bromocriptine (dopamine agonist) from 6 months of age decreased serum levels of prolactin, and was accompanied by an increase in the incidence of nodules. The present results showed that an increase in serum levels of prolactin was accompanied by a decrease in incidence of liver tumours induced by 3'-Me-DAB in mice, suggesting a suppressive effect of prolactin on liver tumorigenesis in mice. Thus, it is possible that the suppressive effect of oestrogen on liver tumorigenesis in mice is mediated, at least in part, by prolactin.

Adenoma↗
PubMed1995

Anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome) causing hepatosplenomegaly due to the infiltration of hemoglobin-bearing blast cells: an autopsy case.

An autopsy case of a 42 year old man with the anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome) is reported. The patient was admitted because of a 1 month history of fatigue and fever. Physical examination showed hepatosplenomegaly. Laboratory data showed leukopenia, mild normocytic anemia, and high levels of serum lactate dehydrogenase and vitamin B12. Bone marrow aspirate revealed an elevated number of erythroblasts, with dyserythropoiesis (E/M = 3.7). After admission, thrombocytopenia progressed rapidly, but blast cells were not seen in the peripheral blood throughout the clinical course. On the 56th hospital day, the patient died of pneumonia. At autopsy, the spleen weighed 550 g and the liver 1800 g. Histologically, the white and red pulps of the spleen and the portal region and sinusoid of the liver were diffusely infiltrated by blast cells that were positive for anti-hemoglobin (Hb) antibody on immunoperoxidase staining. The bone marrow, the lymph nodes, the adrenal glands, the pancreas, and the heart were also infiltrated by the blast cells. This was thus considered to be a rare case of the anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome), the findings showing that Hb immunoperoxidase staining is useful for the diagnosis of this condition.

Adult↗
PubMed1995

Interleukin-5 upregulates intercellular adhesion molecule-1 gene expression in the nasal mucosa in nasal allergy but not in nonallergic rhinitis.

The effect of interleukin-5 (IL-5) on intercellular adhesion molecule-1 (ICAM-1) gene expression in human nasal mucosa was studied using the method of gene expression quantification. Recombinant human IL-5 was shown to induce ICAM-1 gene expression in the nasal mucosa of patients with nasal allergy, but not in the mucosa of non-allergic patients. The peak level of ICAM-1 gene expression was seen 6 h after IL-5 stimulation. In the nasal mucosa of patients with nasal allergy, IL-5 might act not only as an eosinophil chemotactic factor, but also as an enhancement factor for the expression of adhesion molecules, thereby accelerating eosinophil appearance. The results also suggest that the nasal mucosa of patients with nasal allergy somehow favors adhesion molecule induction by IL-5.

Adolescent↗
PubMed1995

Role of capsaicin-sensitive trigeminal nerves in development of hyperreactive nasal symptoms in guinea pig model of nasal allergy.

The effect of capsaicin pretreatment on frequency of sneezing, decrease of nasal patency, and increase of vascular dye leakage induced by antigen or histamine challenge on the guinea pig nasal mucosa was investigated. The animals were sensitized intraperitoneally with ovalbumin. Capsaicin pretreatment significantly inhibited sneezing induced by nasal challenge with histamine and antigen, indicating that capsaicin-sensitive sensory nerves constitute an afferent pathway of the sneezing reflex in nasal allergy. Although capsaicin pretreatment tended to inhibit the decrease of nasal patency and the increase of vascular dye leakage of the nasal mucosa induced by antigen challenge, this tendency was not statistically significant. The present study indicated that the participation of a local reflex via capsaicin-sensitive trigeminal nerves in nasal vascular responses observed after antigen challenge in the guinea pig model of nasal allergy is rather small compared to the large direct vascular effects of chemical mediators released from basophilic cells in the nasal mucosa.

Airway Resistance↗
PubMed1995

Suppressive effect of anti-alpha 1-antichymotrypsin serum on pulmonary fibrosis induced by phorbol myristate acetate in vivo.

BACKGROUND: PMA induces pulmonary fibrosis in the rabbit (1). Pulmonary fibrosis induced by PMA occurs in the alveolar wall and has the same pattern as idiopathic pulmonary fibrosis (IPF)(2), so this system can be used as an animal model for IPF. PMA also increases the content of alpha-1-antichymotrypsin (ACT) in cultured alveolar macrophages of bronchoalveolar lavages (BAL), and dexamethasone inhibits this PMA-induced increase (3). Here we investigated the role of ACT in pulmonary fibrosis induced by PMA. EXPERIMENTAL DESIGN: Rabbits were treated intratracheally for 6 days with saline, dimethyl sulphoxide (DMSO) used as a solvent of PMA, PMA dissolved in DMSO or PMA plus anti-ACT rabbit serum. BAL samples were obtained. ACT in cell pellet and cell-free fluid of BAL were assayed by radioimmunoassay. Sections of the lung were examined histologically by a point count method. The ratio of fibrosis to elastosis (fibrotic ratio) was evaluated for each rabbit by the ratio of total points of collagen stained by the Azan-Mallory method to those of elastic fiber stained by the Elastica van Gieson method. Hydroxyproline (HP) was assayed biochemically, and the amount of HP in the alveolar wall for each rabbit was calculated using the assayed values of HP and the ratio of histologic collagen points in the alveolar wall to those in the lung tissue by a point count method. RESULTS: The fibrotic ratio of the PMA group increased fourfold compared with that of the saline group. The ratio of the PMA plus anti-ACT group decreased and was similar to that of the saline group. The ratio of the DMSO group was about two times as much as that of the saline or the PMA plus anti-ACT groups. The calculated amount of hydroxyproline in the alveolar wall of the PMA group increased and was approximately 1.5-fold compared with that of the saline group. The amount of HP of the PMA plus anti-ACT group decreased and was similar to that of the saline group. In the BAL, the amount and the percentage of ACT in cell pellet per macrophage of the PMA group increased more than those of the saline and DMSO groups. The amount and percentage of the PMA plus anti-ACT group were significantly less than those of the PMA group. Those of the DMSO group were similar to those of the saline group. CONCLUSIONS: These findings suggest that anti-ACT has a suppressive effect on pulmonary fibrosis induced by PMA and that ACT is important in the PMA model of pulmonary fibrosis.

Animals↗
PubMed1995

[An experimental study on recovery of lacerated skeletal muscle: correlation between separation gap and the potential for recovery].

Skeletal muscle has a potential for recovery with muscle tissue when the lacerated stumps are maintained in contact. However, when there is no contact, this potential for recovery is unknown. Here we report our studies on the correlation between the recovery and the separation distance between the stumps in partially lacerated muscles in Wistar rat. The gastrocnemius muscle was subjected to a partial wedge-shaped laceration which allowed the surrounding tissue to hold a constant separation distance between the stumps throughout the duration of the study. Groups each of 7 rats were examined at 1, 2, and at 4 days, and at 1, 2, 2, and at 6 weeks after the laceration was performed. In each group, 5 rats underwent histological and immunohistological examinations, while the other 2 underwent electronmicroscopic examination. The muscle stumps initially degenerated, and then began to regenerate at 4 days after the laceration. During this period, local basement membranes remained intact allowing regeneration of muscle fibers. However, the absence of basement membrane between the stumps led to a random regeneration pattern of myotubes growing into the granulation tissue in the wedge-shaped gap. The electronmicroscopic findings showed that these growing myotubes had no basement membrane. The maximum growth of these myotubes was found to be 1.20 +/- 0.31 mm reached at 3 weeks after the laceration, suggesting that the maximum gap was approximately 1.0 mm across which there is a potential for recovery through regeneration.

Animals↗
PubMed1994

Activation of MAP2-kinase in B lymphocytes by calcium ionophores.

The role of increases in intracellular calcium levels on tyrosine phosphorylation in human B lymphocytes was studied. Stimulation of normal, resting B lymphocytes or B lymphoblastoid cells with the calcium ionophores ionomycin or A23187 induced the tyrosine phosphorylation and the enzymatic activation of microtubule-associated protein-2 kinase (MAP2-K). Treatment of these cells with PMA induced tyrosine phosphorylation of a protein with the identical mobility, as well as the enzymatic activation of MAP2-K. Stimulation of these cells with ionomycin also resulted in increased ribosomal S6 kinase activity. Activation of MAP2-K in B lymphocytes by calcium ionophore was rapid (detectable within 1 min), transient (returning to background levels by 45 min), and dependent on extracellular calcium. These results demonstrate that transmembrane calcium flux induced by calcium ionophore results in the tyrosine phosphorylation and enzymatic activation of MAP2-K in human B cells.

B-Lymphocytes↗
PubMed1994

Effects of NG-nitro-L-arginine and/or L-arginine on experimental pulmonary metastasis in mice.

Effects of NG-nitro-L-arginine methyl ester (L-NAME; an inhibitor of nitric oxide (NO) synthase) and/or L-arginine (substrate of NO synthase) on pulmonary metastasis of murine melanoma and Lewis lung carcinoma cells were investigated. L-NAME, L-arginine or both L-NAME and L-arginine was injected i.p. into mice 5, 3, and 1 h before and 1, 3, 5, and 7 h after the injection of tumor cells into mice via a tail vein. The administration of L-NAME (9.3 mumol/mouse) alone or L-arginine alone (46.5 or 186 mumol/mouse) potentiated pulmonary metastasis of highly and poorly metastatic B16 melanoma cells. L-NAME alone also increased the number of pulmonary metastasis of Lewis lung carcinoma cells, but L-arginine (185 mumol/mouse) did not. However, the combination of L-NAME and L-arginine increased the number of pulmonary metastasis of both the melanoma and Lewis lung carcinoma cells synergistically. L-NAME or L-arginine administration enhanced the retention of B16 melanoma cells in the lungs examined 24 h after the tumor cell injection. Synergistic effect of L-NAME and L-arginine was also seen in the tumor cell retention. The present results suggest that the metastatic potentials of the tumor cells do not simply correlate to NO production in vivo.

Animals↗
PubMed1994

Rapamycin selectively inhibits translation of mRNAs encoding elongation factors and ribosomal proteins.

The immunosuppressant rapamycin (RAP) has been demonstrated to specifically inhibit the activity of p70 S6 kinase (p70s6k) and subsequent phosphorylation of ribosomal S6 protein in mammalian cells. Addition of RAP to proliferating lymphoid cells resulted in inhibition of protein synthesis before any changes in the rate of cell proliferation. When the cellular composition of proteins was examined by gel electrophoresis, RAP dramatically inhibited synthesis of selective proteins, particularly elongation factor 2 (eEF-2). The inhibition of eEF-2 synthesis by RAP was at the translational level. Further, RAP inhibited the polysomal association of mRNAs encoding not only eEF-2 but also elongation factor 1-alpha and ribosomal proteins without affecting mRNA translation of any of a number of nonribosomal proteins. Since levels of activity of p70s6k are correlated with the rate of biosynthesis of eEF-2, p70s6k might be involved in coordinate translational regulation of ribosomal protein mRNAs in higher eukaryotes, which have a conserved sequence at their 5' end. Specific inhibition of ribosomal protein synthesis likely explains the differential antiproliferative effect of RAP on proliferating and mitogen-activated quiescent cells.

Base Sequence↗
PubMed1994

Differential activation of p21ras in CD45RA+ and CD45RO+ human T lymphocytes.

CD45RA+ and CD45RO+ human T cells differ in their functional responses to different forms of mitogenic stimulation. However, little is known about the intracellular signaling events related to the functional differences in these two subsets. In the present study, we examined the ability of different Abs to the TCR/CD3 complex to activate the p21ras proto-oncogene product in CD45RA+ and CD45RO+ T cells. Stimulation with soluble OKT3 anti-CD3 mAb induced activation of p21ras in CD45RA+ cells but not in CD45RO+ cells, although soluble anti-CD3 was able to induce both activation of CD3-associated kinases and IL-2 responsiveness in CD45RO+ cells. Similar results were obtained by using UCHT1, a different anti-CD3 Ab. In contrast, cross-linked anti-CD3 or the combination of phorbol ester and ionomycin were found to activate p21ras equally in both T cell subsets. Our results demonstrate a selective inability of CD45RO+ human T cells to activate p21ras in response to soluble anti-CD3 mAb.

Antibodies, Monoclonal↗
PubMed1994

Angiostatic activities of medroxyprogesterone acetate and its analogues.

The effects of medroxyprogesterone acetate (MPA) (I) and related compounds (II-VI) upon angiogenesis induced by basic fibroblast growth factor (bFGF) or transforming growth factor-alpha (TGF-alpha) were investigated using a rabbit corneal system for assay of angiogenesis. Dexamethasone (Dex) was used as a positive control. The MPA analogues tested were 6,6'-dehydro-MPA (II), megestrol acetate (III), 1-dehydromegestrol acetate (IV), melengestrol acetate (V), and 1-dehydromelengestrol acetate (VI). The inhibitory activities of these steroids using bFGF were in the order: Dex = MPA = (VI) = (V) > (IV) > (III). Steroid (II) was inactive. 5 alpha-dihydrotestosterone was weakly active, while estradiol-17 beta and progesterone were inactive. The angiostatic activity of MPA was completely abolished by mefipristone (RU 486) which showed no anti-angiogenic activity in this assay. With TGF-alpha, the order of angiostatic activities was Dex = (VI) > (IV) > (III) > (V). Steroid (II) was again inactive. Dex, MPA, and all the MPA analogues except steroid (II) markedly inhibited the activity of plasminogen activator secreted by cultured calf pulmonary artery endothelial cells, but did not inhibit growth of these cells. The binding affinities of MPA and its analogues to glucocorticoid, progesterone and androgen receptors were determined, but were found not to be correlated with their angiostatic activities.

Animals↗
PubMed1994

Regulation of B-cell immune responses: predominant role of interleukin-4 in triggering cell proliferation and Ig production in competent B cells.

We established a system for induction of competence in B cells following brief (45 min) exposure to either the combination of phorbol 12,13-dibutyrate (PDB) and ionomycin (I) (PDB/I) or PDB/anti-IgM. B cells, rendered competent in this fashion, were able to respond to PDB in the second or progression phase of culture but did not proliferate on their own. In addition, competent B cells were IL-2- or IL-4-responsive, due to up-regulation of their respective receptors following competence induction. IL-4 was found to have the most effective role in the progression phase to promote DNA synthesis and was able to enhance both IL-2 and IL-4 receptor expression. Whereas provision of IL-4 could induce IgM, IgG, and IgA in the absence of T cells, it did not result in IgE production. IgE production was only achieved in the presence of activated T cells (competent) together with competent B cells. These results indicate that IL-4 has a major role in B-cell immune responses following initial activation and trigger the cells, in the absence of T cells or other factors, to proliferate and differentiate into Ig-secreting cells. For IgE production in competent B cells, however, IL-4 alone could not overcome the requirement for activated T cells.

Antibodies, Anti-Idiotypic↗
PubMed1994

Inhibitory effect of sialoadenectomy on hepatocellular tumourigenesis in male mice induced by 3'-methyl-4-dimethylaminoazobenzene.

Male C57BL/6xDS-F1 mice that had been treated with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) neonatally were subjected to sialoadenectomy (removal of the submandibular salivary glands) 60 days after birth. The development of adenomatous nodules and carcinomas in the livers of these mice was compared with the livers of males without sialoadenectomy. The incidence of adenomatous nodules in sialoadenectomized males at 6, 8, 10, and 12 months was significantly lower than that in sham-operated animals. Carcinomas were found in the livers of both sham-operated and sialoadenectomized males that were 10 and 12 months old and were less frequent in sialoadenectomized males although the difference was significant only at the age of 12 months. Sialoadenectomy decreased the serum concentration of epidermal growth factor (EGF) by about 40%. The present results indicate that sialoadenectomy inhibits the development of hepatocellular tumours induced by 3'-Me-DAB in male mice, an effect which may be caused by decrease in the serum level of EGF.

Adenoma↗
PubMed1994

Biochemical properties of eosinophils and their preferential accumulation mechanism in nasal allergy.

Recent information intensely suggests that eosinophils are pivotal proinflammatory cells in a variety of allergic inflammatory diseases including bronchial asthma, nasal allergy, hypereosinophilic syndrome, and various cutaneous diseases. Eosinophils, via their release of basic proteins and lipid mediators, are strongly implicated in the onset of allergic symptoms of the nose. They play an important role particularly in nasal swelling and hyperreactivity. Despite the current multitude of research investigating eosinophils in vitro, the mechanism that mediates and controls the accumulation of eosinophils in vivo is incompletely understood. In this article the following issues will be addressed: (1) How do eosinophils migrate into the nasal mucosa? (2) What factors contribute to preferential eosinophil accumulation and their degranulation in nasal mucosa? (3) How can we inhibit the eosinophil accumulation and activation?

Animals↗