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Biomedical subjects

H Takada

Publications and source records attributed to H Takada.

At least 181 records · Page 10Linked to original sources
PubMed1996

Inheritance of acetohexamide reductase activities in liver microsomes and cytosol of rats.

The inheritance patterns of acetohexamide reductase activities in liver microsomes and cytosol of rats were determined by using the inbred Wistar-Imamichi and Fischer-344 strains as a model of low and high metabolizers, respectively. A simple Mendelian genetic analysis for the frequency distribution of acetohexamide reductase activity in liver microsomes of male rats led us to conclude that the phenotype is genetically regulated by an autosomal co-dominant fashion. Female rats, unlike male rats, did not exhibit microsomal enzyme activity in parental, first filial (F1) and second filial (F2) generations, indicating that the inheritance of the microsomal enzyme activity is sex-limited. On the other hand, the frequency distribution of acetohexamide reductase activities in liver cytosol of male and female rats was unimodal in all generations and there was no significant difference among these cytosolic enzyme activities.

Alcohol Oxidoreductases↗
PubMed1996

Interleukin-8 gene expression by human dental pulp fibroblast in cultures stimulated with Prevotella intermedia lipopolysaccharide.

Interleukin (IL)-8 mRNA expression was investigated in human dental pulp fibroblast cultures after stimulation with lipopolysaccharide (LPS) prepared from Prevotella intermedia and inflammatory cytokines. The expression of IL-8 mRNA and the release of IL-8 induced by P. intermedia LPS in pulpal fibroblast cultures were detected by Northern blot analysis and ELISA, respectively. The sufficient concentration of P. intermedia LPS on the IL-8 mRNA expression was 0.1 microgram/ml in pulpal fibroblast cultures. IL-8 mRNA levels began to increase after 2 h of exposure, reached a maximum at 4 to 8 h, and declined after 48 h, reaching the unstimulated level by 60 h. IL-8 production by the pulpal fibroblasts began to increase after 8 h of exposure upon stimulation with 10 microgram/ml of P. intermedia LPS. By contrast Salmonella LPS and synthetic lipid A did not increase IL-8 mRNA concentrations in pulpal fibroblast cultures. Recombinant human IL-1 alpha, beta, and tumor necrosis factor-alpha were capable of stimulating these cells to express IL-8 mRNA but natural human interferon-beta, gamma, and recombinant human IL-6 were incapable in our assay. These results suggest that pulpal fibroblasts are immunoresponsive cells and can elaborate IL-8 upon stimulation with P. intermedia LPS.

Adolescent↗
PubMed1996

Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells.

To clarify the role of intercellular communication in the liver during accumulation of neutrophils, the release of cytokine-induced neutrophil chemoattractant (CINC) (interleukin-8 [IL-8] related protein in rodents) by hepatocytes was investigated in the presence of Kupffer cell-conditioned medium in vitro. Kupffer cells were prepared by perfusion of rat liver with collagenase followed by centrifugation on a metrizamide gradient and were cultured in the presence or absence of lipopolysacharide (LPS). The conditioned medium was collected after 24 hours, and rat hepatocytes were cultured in the presence or absence of Kupffer cell-conditioned medium. An amount of CINC in the culture supernatant was measured by western blotting analysis and enzyme-linked immunosorbent assay (ELISA), and expression of its messenger RNA (mRNA) was assessed by the polymerase chain reaction. LPS-stimulated Kupffer cell-conditioned medium enhanced an expression of CINC mRNA in hepatocytes and increased the production of CINC by hepatocytes. Enhanced production of CINC was not shown when the Kupffer cell-conditioned medium was pretreated with heat (56 degrees C, 30 minutes). The production of CINC by hepatocytes in the presence of the LPS-stimulated Kupffer cell-conditioned medium was reduced by an antibody against interleukin 1 beta (IL-1 beta), but not by antibodies against tumor necrosis factor alpha (TNF-alpha) or LPS. These results suggest that production of CINC by hepatocytes could be regulated by IL-1 beta released from Kupffer cells, leading to neutrophil accumulation during liver injury, because this protein is a strong chemoattractant for neutrophils.

Animals↗
PubMed1996

Functional difference between Thy-1-positive and Thy-1-negative gamma delta T cells induced by Escherichia coli infection in mice.

There is an increase in number of gamma delta T cells in the peritoneal cavity after intraperitoneal (i.p.) inoculation with Escherichia coli. The E. coli-induced gamma delta T cells in C3H/He mice contain a large amount of Thy-1-negative population in addition to the Thy-1-positive population. We investigated the difference between the Thy-1-positive and the Thy-1-negative gamma delta T cells. Although it was found that only up to 4% of the gamma delta T cells on day 5 after infection were in cycling phase, and that the gamma delta T cells did not proliferate by immobilized anti-T-cell receptor (TCR) gamma delta monoclonal antibody stimulation, the gamma delta T cells proliferated in the presence of interleukin-2 (IL-2) and IL-7. The Thy-1-negative gamma delta T cells showed higher proliferative response compared with the Thy-1-positive gamma delta T cells. Furthermore, the Thy-1-negative gamma delta T cells showed lower IFN-gamma mRNA expression than the Thy-1-positive gamma delta T cells. On the other hand, both the Thy-1-positive and Thy-1-negative gamma delta T cells predominantly expressed V gamma 1, V gamma 4, V gamma 5, V gamma 6 and V delta 1, and no difference of V region usage was detected between them. These results suggest that functions of Thy-1-positive gamma delta T cells differ from Thy-1-negative gamma delta T cells although Thy-1-positive and Thy-1-negative gamma delta T cells may have similar V region repertoire and, possibly, similar antigen specificity.

Animals↗
PubMed1996

Structural characteristics of peptidoglycan fragments required to prime mice for induction of anaphylactoid reactions by lipopolysaccharides.

Structural characteristics of peptidoglycan fragments required to prime mice for the induction of anaphylactoid reactions by Salmonella abortusequi lipopolysaccharide were examined in endotoxin-resistant C3H/HeJ mice, with special focus on the disaccharide-pentapeptide [N-acetylglucosaminyl-beta(1-4)-N-acetylmuramyl-L-alanyl-D -isoglutaminyl-meso-2,6-diaminopimelyl (DAP)-D-alanyl-D -alanine] and its smaller partial derivatives. The bacterial and synthetic muramyl tripeptides (DAP- and lysine [Lys]-type, respectively) and synthetic muramyl dipeptide primed mice for induction of anaphylactoid reactions accompanied by death within 1 h. The disaccharide-tripeptide exhibited weaker activity, and the disaccharide-tetrapeptide and muramyl tetrapeptide exhibited marginal activity. In contrast, intact peptidoglycans of various bacteria and the disaccharide-pentapeptide lacked the priming activity, although they showed adjuvant activity similar to that of the above components.

Anaphylaxis↗
PubMed1996

Lipoteichoic acid and interleukin 1 stimulate synergistically production of hepatocyte growth factor (scatter factor) in human gingival fibroblasts in culture.

Lipoteichoic acids (LTA) from various gram-positive bacteria, including oral streptococci such as Streptococcus sanguis, enhanced the production of hepatocyte growth factor (HGF) (scatter factor) by human gingival fibroblasts in culture, whereas lipopolysaccharides (LPS) from various gram-negative bacteria did not. In contrast, LPS induced interleukin 1 activity in human gingival epithelial cells in culture, while LTA had little effect. LTA and recombinant human interleukin 1 alpha enhanced synergistically the production of HGF/SF in human gingival fibroblast cultures. Recombinant human HGF, in turn, enhanced the proliferation of human gingival epithelial cells in culture.

Cells, Cultured↗
PubMed1996

Plasma endothelin-1 levels during asphyxia in the fetal goat.

The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO2, PCO2 and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 +/- 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO2 (r = -0.41, p < 0.05) and pH (r = - 0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.

Animals↗
PubMed1996

Induction of lymphocytes cytotoxic to oral epithelial cells by Streptococcus mitis superantigen.

The preparation of a superantigenic fraction F-2 from the culture supernatant of Streptococcus mitis 108, a fresh isolate from human tooth surfaces, was reported previously. Now, to determine the possible pathogenic role of the superantigen in oral mucosal diseases, we examined the cytotoxic effects of human peripheral blood T-cells activated with F-2 on human oral epithelial cells. T-cells activated with F-2 were cytotoxic to the human squamous carcinoma HO-1-N-1 cells derived from the oral mucosa, similar to those activated with Staphylococcus aureus enterotoxin B (SEB). This cytotoxic effect was increased in a dose-dependent manner by the addition of the respective stimulant, F-2 or SEB, to the cytotoxic assay system. F-2 endowed mainly CD8+ T-cells with cytotoxic activity. Pretreatment with human interferon gamma increased the sensitivity of the HO-1-N-1 cells to the cytotoxic effects of F-2-activated T-cells. The F-2-activated T-cells were also cytotoxic to human keratinocytes derived from gingiva. There was no correlation between the degree of cytotoxicity and the levels of tumor necrosis factor alpha in co-cultures of F-2-activated T-cells and HO-1-N-1 cells. A double-chamber plate experiment revealed no cytotoxic effects when the F-2-activated T-cells were separated from the HO-1-N-1 cells. Supernatants of the co-cultures of target and effector cells were not cytotoxic to HO-1-N-1 cells. These findings suggest that the cytotoxic effects of the F-2-activated T-cells on HO-1-N-1 cells were mediated not by soluble factors but by the direct interaction between the activated T-cells and the target cells. The cytotoxicity of the F-2-activated T-cells against HO-1-N-1 cells was markedly inhibited by monoclonal antibodies (MAbs) against CD11a and CD54, but was only slightly inhibited by MAbs against human leukocyte antigen (HLA)-DR and CD2. Thus, the interaction between lymphocyte-function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) was crucial for the F-2-dependent T-cell-mediated cytotoxicity against oral epithelial cells, while HLA-DR and CD2 molecules are not necessarily involved in the cytotoxicity observed.

Antigens, Bacterial↗
PubMed1996

Central conduction in somatosensory evoked potentials: comparison of ulnar and median data and evaluation of onset versus peak methods.

To compare central conduction in ulnar and median nerve somatosensory evoked potentials (SEPs), we recorded SEPs from the neck and scalp elicited by median and ulnar nerve stimulation in 46 normal young adults. We determined the central conduction time (CCT) in each subject from peak-to-peak and onset-to-onset measurements. The mean value of the onset CCT for the ulnar nerve SEP was 6.2 +/- 0.3 msec, and for the median nerve SEP, 5.9 +/- 0.3 msec. Onset CCT was significantly longer for the ulnar nerve SEP, and there was a significant correlation between onset CCT in both median and ulnar nerve SEPs and subject height. In contrast, the mean value of the "conventional" peak CCT for the ulnar nerve SEP was 5.6 +/- 0.6 msec, and for the median nerve SEP, 5.8 +/- 0.5 msec, with no significant difference between them. In addition, the peak CCT was not correlated with subject height in the ulnar or median nerve SEPs. Our findings suggest that onset CCT measurement is superior to the conventional peak CCT measurement for ulnar as well as median nerve SEPs, and confirm that the central conduction pathway for the ulnar nerve SEP is slightly longer than that for the median nerve SEP.

Adolescent↗
PubMed1996

Microstructure of etched "IPS Empress" heat-pressed ceramics observed by SEM.

A valuable characteristic of the "IPS Empress" used for producing all ceramic dental restorations is that it is a prefired ceramic ingot. The ingot is heated, softened and press-injected into the cavity, and ceramic restorations are fabricated by the lost wax casting method. The leucite crystal present in the ingot are scattered and distributed into the glassy phase in a more homogeneous manner through this pressing procedure, and the resulting ceramics are of higher flexural strength than conventional ones. The present study was carried out to clarify the microstructure of Empress ceramics by etching, and to observe the etched surface by scanning electron microscopy, in comparison with several other conventional ceramics. It was shown that the form and distribution of the leucite crystals in Empress ceramics are quite different before and after pressing, and that the staining and layering ceramics are also different from conventional ceramics. The method of surface treatment of ceramics prior to etching, such as fracturing or grinding, the kind of etching material used, the concentration and the etching time are important factors for revealing, observing and evaluating the microstructure of ceramics containing leucite crystals.

Aluminum Oxide↗
PubMed1996

Acetohexamide reductase activities in liver microsomes and cytosol of cisplatin-treated male rats: cisplatin indirectly modulates the microsomal enzyme activity.

Treatment with cisplatin, at a dose of 7.2 mg/kg body weight, caused a significant decrease of acetohexamide reductase activity in liver microsomes of male rats at 4 and 7 days after its treatment; this dose of cisplatin has been reported to decrease testosterone levels in serum of male rats. However, the treatment with cisplatin could not decrease acetohexamide reductase activity in liver cytosol of male rats at the days tested. Although acetohexamide reductase activity in liver microsomes of male rats, as described above, was decreased by the treatment with cisplatin, the decreased microsomal enzyme activity was nearly restored when testosterone propionate was given once daily for 7 days after cisplatin treatment. Based on these results, it is reasonable to postulate that cisplatin indirectly decreases the microsomal enzyme activity which is regulated by androgens, by causing a significant decrease of the testosterone level in serum of male rats.

Alcohol Oxidoreductases↗
PubMed1995

Therapy with immunoglobulin suppresses myocarditis in a murine coxsackievirus B3 model. Antiviral and anti-inflammatory effects.

BACKGROUND: The treatment of some inflammatory diseases (eg, Kawasaki disease) with immunoglobulin has been demonstrated to be effective. Accordingly, to elucidate the mechanism underlying such actions of immunoglobulin, we examined its effects on murine coxsackievirus B3 (CB3) myocarditis. METHODS AND RESULTS: An in vitro study showed dose-dependent suppression of CB3 by immunoglobulin. Immunoglobulin 1 g.kg-1.d-1 IP was administered to CB3-infected C3H/He mice daily for 2 weeks, beginning simultaneously with virus inoculation in experiment 1 and on day 14 after virus inoculation in experiment 2. In both experiments, survival was higher in treated than in control mice; at the time of death, inflammatory also were reduced. Notably, in experiment 1, immunoglobulin administration completely suppressed the development of myocarditis. Serum-neutralizing antibody titers in the treated mice were significantly higher than those in untreated mice in experiment 1 but not in experiment 2. The circulating antibodies of the treated mice were primarily of exogenous origin in experiment 1 and of exogenous and endogenous origins in experiment 2. The analysis of splenic lymphocyte subsets revealed a marked decrease of the B cell population in the treated mice. CONCLUSIONS: Immunoglobulin therapy completely suppressed acute CB3 myocarditis by transferring the neutralizing antibody into the host in the acute viremic stage and induced an anti-inflammatory effect in the subsequent aviremic stage; the reduction of the splenic B-cell population may be closely associated with an anti-inflammatory effect.

Animals↗
PubMed1995

(+/-)-(Z)-2-(aminomethyl)-1-phenylcyclopropanecarboxamide derivatives as a new prototype of NMDA receptor antagonists.

(+/-)-(Z)-2-(Aminomethyl)-1-phenylcyclopropane-N,N-diethylcarbo xamide (milnacipran, 1), a clinically useful antidepressant, and its derivatives were prepared by an improved method and were evaluated as NMDA receptor antagonists. Of these, milnacipran (1), its N-methyl and N,N-dimethyl derivatives, 7 and 8, respectively, and its homologue 12 at the aminomethyl moiety had binding affinity for the receptor in vitro (IC50: 1, 6.3 +/- 0.3 microM; 7, 13 +/- 2.1 microM; 8, 88 +/- 1.4 microM; 12, 10 +/- 1.2 microM). These also protected mice from NMDA-induced lethality. These compounds would be important as anovel prototype for designing potent NMDA-receptor antagonists because of their characteristic structure, which clearly differentiated them from known competitive and noncompetitive antagonists to the receptor.

Animals↗
PubMed1995

An analogue of lipid A and LPS from Rhodobacter sphaeroides inhibits neutrophil responses to LPS by blocking receptor recognition of LPS and by depleting LPS-binding protein in plasma.

When incubated with lipopolysaccharide (LPS) in the presence of plasma, neutrophils become primed for enhanced release of superoxide in response to triggering by formyl-Met-Leu-Phe (fMLP). The effect of LPS on phagocytes is inhibited by a synthetic lipid A precursor, LA-14-PP (lipid IVa) or by LPS from Rhodobacter sphaeroides (Rs). We studied the mechanisms by which LA-14-PP or Rs-LPS inhibited LPS-induced responses. When neutrophils were exposed to LA-14-PP or Rs-LPS for 3 min and then to Escherichia coli-LPS, the antagonists inhibited priming for superoxide release, and also blocked up-regulation of CD11b and adherence. This inhibition was dependent on plasma, was not overcome by higher amounts of E. coli-LPS or plasma, and was not observed at 0 degrees C, suggesting that E. coli-LPS was not able to interact with its receptor or other cellular recognition molecule in neutrophils that had been exposed to the antagonists. The alternative possibility that LA-14-PP or Rs-LPS depleted a plasma cofactor, resulting in inhibition of priming, was investigated by using LPS from Porphyromonas gingivalis (Pg) and Bordetella pertussis (Bp). These LPS primed neutrophils in a plasma-dependent and CD14-dependent manner, but were not blocked by LA-14-PP or Rs-LPS. When sub-optimal concentrations of plasma were exposed to LA-14-PP or Rs-LPS, and then mixed with Pg-LPS or Bp-LPS, followed by incubation with neutrophils, priming and up-regulation of CD11b were inhibited, and this inhibition was overcome by increasing the concentration of plasma. Binding of LPS-binding protein (LBP) in plasma to immobilized E. coli-LPS was inhibited by pre-incubation of plasma with LA-14-PP or Rs-LPS. Together with the result that treatment of plasma with anti-LBP antibody abolished the cofactor activity of plasma, these results indicated that LA-14-PP and Rs-LPS depleted LBP from plasma, resulting in inability of LPS to act on neutrophils. Thus LA-14-PP and Rs-LPS inhibited the action of LPS on neutrophils by at least two mechanisms, blocking of LPS receptor recognition and depletion of the cofactor LBP.

Acute-Phase Proteins↗
PubMed1995

Immunohistochemically demonstrated expression of HLA-DR antigen in colorectal adenocarcinomas and its relation to clinicopathological features.

We studied 148 colorectal adenocarcinomas to clarify any correlation between HLA-DR antigen expression on tumor cells and histopathological features. Paraffin sections of formalin-fixed tissues were stained with HLA-DR antigen using the indirect immunoperoxidase technique. All the tumor tissues were divided into two groups, depending on the incidence of HLA-DR-positive cells (greater and lesser than 50%). Carcinoma tissues with a higher incidence showed less mural invasion, lymphoductal invasion, venous invasion, lymphonodular metastasis, and peritoneal metastasis. Tissues with a high HLA-DR reactivity were more often observed for Dukes' A and B stages, whereas those with a low HLA-DR positivity were frequently Dukes' C and D stages. As for the cumulative survival rate, the group with high HLA-DR expression demonstrated significantly better survival. We speculate that HLA-DR expression by colorectal cancer cells exerts a favorable influence on clinical course.

Adenocarcinoma↗
PubMed1995

Chemotactic factors released from hepatocytes exposed to acetaminophen.

To clarify the mechanism of neutrophil infiltration in the liver of acetaminophen-induced hepatic injury, chemotactic factor released from hepatocytes exposed to acetaminophen has been investigated. Hepatocytes exposed to acetaminophen release nondialyzable chemotactic factor, although acetaminophen in itself inhibits chemotaxis of neutrophils. Chemotactic activity of the nondialyzable chemotactic factor was reduced after treatment with heat (56 degrees C, 30 min) or trypsin. Chemotactic activity was demonstrated at the molecular weights of around 25 and 55 kDa. Chemotactic activity of the conditioned medium was not significantly reduced in the presence of antibody against rat KC/gro protein (interleukin-8-related cytokine in rodent). Chemotactic activity of a 25-kDa factor was reduced by the antibody against the antibody against KC/gro protein, but that of a 55-kDa factor was not reduced. Immunoblot analysis revealed that the peptide reacted with antibody against rat KC/gro protein was demonstrated at a molecular weight of around 20-25 kDa, but not around 55kDa, when the conditioned medium of acetaminophen-treated hepatocytes was electrophoresed. These results suggest that hepatocytes exposed to acetaminophen release two types of chemotactic factors for neutrophils and that a major part of the chemotactic factor could be different from a member of interleukin-8 family.

Acetaminophen↗
PubMed1995

Colony-stimulating factors and coxackievirus B3 myocarditis in mice: macrophage colony-stimulating factor suppresses acute myocarditis with increasing interferon-alpha.

The effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) on murine coxsackievirus B3 myocarditis were investigated. A total of 4 x 10(6) U/kg/day M-CSF and 20 micrograms/kg/day G-CSF were injected subcutaneously every day on day 0 to day 14 starting simultaneously with virus inoculation. Serum interferon-alpha was measured periodically. The survival rate of the M-CSF group was higher than that of the untreated control group (p < 0.05). On days 7 and 14 cardiac disease was significantly lower in the M-CSF group than in the untreated control group. Myocardial virus titers on day 7 in the M-CSF group were lower compared with those of the untreated control group. No significant difference was seen in the survival, cardiac disease, or myocardial virus titers between the G-CSF and the control groups. Monocyte counts on days 7 and 14 in the M-CSF group were increased compared with those in the control group. Serum interferon-alpha titers in the M-CSF and G-CSF groups on day 4 and those in the M-CSF group on day 7 were significantly increased in comparison with those of the untreated control group. We conclude that M-CSF but not G-CSF has the potency to limit myocardial virus titers and to reduce cardiac disease in the acute coxsackievirus B3 myocarditis. This ability is associated with an elevated interferon-alpha. Thus macrophages may play a defensive role in this model.

Acute Disease↗