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Biomedical subjects

M Yamazaki

Publications and source records attributed to M Yamazaki.

At least 271 records · Page 15Linked to original sources
PubMed1998

Stimulation of interleukin-6 production in human dental pulp cells by peptidoglycans from Lactobacillus casei.

Interleukin-6 (IL-6), which is a multifunctional cytokine, has an important role in acute and chronic inflammation. The peptidoglycan (PG) was purified from Lactobacillus casei, which was a Gram-positive bacteria frequently isolated from deep carious lesions and suspected to be a pathogen of pulpitis. In this study, the effects of PG on the production of IL-6 in human dental pulp cells were examined. PG stimulated IL-6 production in a time- and dose-dependent manner. Reverse transcriptase-polymerase chain reaction experiments showed that the increase was dependent on the enhancement of IL-6 mRNA levels. These findings suggest that Gram-positive bacteria, such as L. casei, from carious lesions, might be involved in developing pulpitis through the stimulation of IL-6 production.

Cells, Cultured↗
PubMed1998

Stimulatory effect of interleukin-6 on plasminogen activator activity from human dental pulp cells.

The plasminogen activator (PA)-plasmin proteolytic system has recently received considerable attention because of its participation in a wide variety of biological activities and in pathological conditions involving tissue destruction. We examined the effects of interleukin-6 (IL-6) on PA activity and the gene expressions of tissue type (t) PA and PA inhibitor-1 (PAI-1) in human dental pulp (HDP) cells. IL-6 treatment induced significantly high PA activity in the HDP cells in a time- and dose-dependent manner, compared with nontreated controls. Western-blot analysis showed that tPA protein in the conditioned medium was stimulated by IL-6, compared with the control. The tPA and PAI-1 mRNA levels were increased in HDP cells treated with IL-6, as shown by reverse transcriptase-polymerase chain reaction. These results suggest that IL-6 stimulated PA activity through an enhancement of tPA gene expression and may be involved in extracellular matrix degradation through the stimulation of the PA-plasmin system of HDP cells.

Blotting, Western↗
PubMed1998

Effect of the application of dentin primers and a dentin bonding agent on the adhesion between the resin-modified glass-ionomer cement and dentin.

OBJECTIVES: This study was designed to evaluate the influence of the application of dentin primer and/or dentin bonding agent on the adhesion of a resin-modified glass-ionomer cement to dentin. METHODS: Bovine dentin was pretreated with Dentin Conditioner or EDTA 3-2 solution, primed by an experimental dentin primer, and applied with a dentin bonding agent. A resin-modified glass-ionomer cement, Fuji II LC, was then adhered to the dentin. The tensile bond strength between the light-cured glass-ionomer cement and the pretreated dentin was measured. The components of the experimental dentin primers were 2-hydroxyethyl methacrylate (HEMA), glyceryl methacrylate (GM) and a water-soluble photo-polymerization initiator, 2-hydroxy-3-(3,4-dimethyl-9-oxo-9H-thioxanthen-2-yloxy)-N,N, N-trimethyl-1- propanaminium chloride (OTX). Significant differences in the data were examined by an analysis of variance and Scheffe's test for multiple comparisons between the means at p = 0.05. RESULTS: A significantly higher mean bond strength between the Fuji II LC and dentin was obtained by EDTA 3-2 pretreatment, QTX/GM priming, and LB Bond application. This value was comparable with that obtained with the resin composite system. Scanning electron microscopy observation showed the formation of a hybrid layer with a thickness of 1-1.5 microns. SIGNIFICANCE: The data obtained in this investigation suggest that the adhesion of Fuji II LC to dentin is closer to that provided by a resin composite system than to that of conventional glass-ionomer cements.

Adhesiveness↗
PubMed1998

The inhibitory effect of lycorine on tumor cell apoptosis induced by polymorphonuclear leukocyte-derived calprotectin.

We recently demonstrated that calprotectin, an abundant calcium-binding protein complex in polymorphonuclear leukocytes (PMNs), has the capacity to induce growth inhibition and apoptotic cell death against a variety of tumor cell lines and normal cells such as fibroblasts. Therefore, calprotectin which is released to extracellular spaces, might cause tissue destruction in severe inflammatory conditions. In search of drugs to suppress the cytotoxic effects of calprotectin, we screened plant products that have been used as Chinese medicines. Using MM46 mouse mammary carcinoma cells as targets, we found that hot water extracts of Crinum asiaticum showed strong inhibition of calprotectin-induced cytotoxicity in vitro. By purification studies, we identified the alkaloid, lycorine, as the active inhibitory molecule. Lycorine inhibits not only induction of MM46 cell death by calprotectin but also inhibits the suppressive effect of calprotectin on target DNA synthesis at a half effective concentration of 0.1-0.5 microg/ml. Lycorine has been reported to posses inhibitory activity against protein translation. Since we previously showed that target protein synthesis is necessary for induction of cell death and that calprotectin actually upregulates the net protein synthesis of MM46 cells, we compared the dose-response relationship between the inhibitory effects of lycorine on calprotectin action and target protein synthesis. Although 1 microg/ml lycorine did not bring about marked inhibition of protein synthesis in MM46 cells without calprotectin, it attenuated the protein synthesis that was augmented by calprotectin to the level of protein synthesis in cells not treated with calprotectin. These results suggest that lycorine inhibition for calprotectin cytotoxicity is not solely due to its inhibitory effect on protein synthesis.

Amaryllidaceae Alkaloids↗
PubMed1998

Effect of nonsteroidal anti-inflammatory drugs on lipid peroxidation by hydroxyl radical.

1. Effects of acetaminophen and sodium salicylate on hydoxyl radical elimination were studied using an electron-spin-resonance spin-trapping method. The effects of these agents on lipid peroxidation of the human erythrocyte membrane were also investigated by the thiobarbituric acid method. 2. Acetaminophen and sodium salicylate depressed hydroxyl radical generated by Cu2+/H2O2. 3. Acetaminophen inhibited Cu2+/H2O2-dependent lipid peroxidation; however, sodium salicylate enhanced Cu2+/H2O2-dependent lipid peroxidation.

Acetaminophen↗
PubMed1998

Molecular characterization of plastidic phosphoserine aminotransferase in serine biosynthesis from Arabidopsis.

Serine biosynthesis in plants proceeds by two pathways; a photorespiratory pathway which is associated with photorespiration and a pathway from phosphoglycerate. A cDNA encoding plastidic phosphoserine aminotransferase (PSAT) which catalyzes the formation of phosphoserine from phosphohydroxypyruvate has been isolated from Arabidopsis thaliana. Genomic DNA blot analysis indicated that this enzyme is most probably encoded by a single gene and is mapped on the lower arm of chromosome 4. The deduced protein contains an N-terminal extension exhibiting the general features of a plastidic transit peptide, which was confirmed by subcellular organelle localization using GFP (green flourescence protein). Northern analysis indicated preferential expression of PSAT in roots of light-grown plants, supporting the idea that the phosphorylated pathway may play an important role in supplying the serine requirement of plants in non-green tissues. In situ hybridization analysis of PSAT revealed that the gene is generally expressed in all types of cells with a significantly higher amount in the meristem tissue of root tips.

Amino Acid Sequence↗
PubMed1998

A novel method to immobilize bioactive substances on hydrophobic surfaces using a polymerizable cationic lipid.

We have successfully developed a novel method to stably immobilize bioactive substances that have anionic groups, such as heparin and succinylated collagen (SC), on hydrophobic surfaces through ionic complexation using a polymerizable cationic lipid, diallyl(dioleyl)ammonium bromide (DADOA). It is composed of a hydrophobic part consisting of long hydrocarbon chains and a hydrophilic head with double bonds which render it polymerizable. Analysis of the modification with DADOA and heparin suggested that the modification formed a thin layer, roughly 60 nm in thickness, as a result of the spontaneous deposition of DADOA and heparin dissolved in water, through the hydrophobic interaction between DADOA and the surface and the ionic complexation between DADOA and heparin. The heparin deposition and its rate of release in plasma were 1.5 microg/cm2 and 0.0017 U/cm2/min, respectively. Cytotoxicity test results showed that the polymerization of the deposited DADOA rendered the modified surface stable and noncytotoxic. Further, antithrombogenicity and cell attachability test results demonstrated that heparin and SC were effectively immobilized on hydrophobic surfaces through ionic complexation. This method has proved useful for the modification of the hydrophobic surfaces of medical devices because the modification process can be performed under aqueous conditions without the use of organic solvents which induce crazing/cracking of plastic casings.

Allyl Compounds↗
PubMed1998

Treatment of disseminated intravascular coagulation (DIC) with all-trans retinoic acid in an endotoxin-induced rat model.

Anticoagulant drugs such as heparin are often administered to patients with disseminated intravascular coagulation (DIC) who are also being treated for their underlying disease. The pathophysiology of DIC is so varied that treatment with medications other than anticoagulants may be useful. All-trans retinoic acid (ATRA), which is used for the treatment of acute promyelocytic leukemia (APL), improves DIC in APL. In vitro studies have reported that ATRA caused downregulation of tissue factor and upregulation of thrombomodulin (TM) on endothelial cells as well as APL cells. We examined the effect of ATRA in an endotoxin-induced rat DIC model. DIC was induced in male Wistar rats with a 4-h sustained infusion of endotoxin at a dose of 30 mg/kg. ATRA (20 mg/day) was given every day for 1 week before the injection of endotoxin. ATRA improved the increase in thrombin-antithrombin III (TAT) complex and D-dimer in this model. Fibrin deposition in renal glomeruli was inhibited by ATRA administration, with an increase in the intensity of immunohistochemical TM staining. These findings suggest that ATRA has beneficial effects in the endotoxin-induced rat DIC model. The mechanism may be an upregulation of TM expression on endothelial cells.

Animals↗
PubMed1998

Effects of dietary taurine on egg weight.

Two experiments were conducted to determine whether taurine supplementation to laying hens would influence laying performance. In Experiment 1, a total of 120 White Leghorn hens were fed diets supplemented with 0, 0.25, or 0.5% taurine for 5 wk. Egg weight was reduced significantly by supplementing 0.25 and 0.5% taurine; however, taurine did not affect other laying performance variables. In Experiment 2, a total of 240 White Leghorn hens were fed diets supplemented with 0 or 0.5% taurine and 0 or 0.1% methionine for 7 wk. Egg weight was decreased due to supplementing taurine in the diets; however, dietary methionine did not affect egg weight, and there was no interaction between dietary taurine and methionine. These results suggest that dietary taurine has the potential to decrease egg weight without affecting egg production, feed conversion, or body weight.

Animals↗
PubMed1998

Effects of volatile anesthetic agents on in situ vascular smooth muscle transmembrane potential in resistance- and capacitance-regulating blood vessels.

INTRODUCTION: This study was designed to compare the inhibitory effect of inhaled volatile anesthetic agents on in situ sympathetic neural versus nonneural regulation of vascular smooth muscle transmembrane potentials as correlates of vascular smooth muscle tone in resistance- and capacitance-regulating blood vessels. METHODS: Vascular smooth muscle transmembrane potentials were measured in situ with glass microelectrodes in neurally intact, small (200-300 m OD) mesenteric arteries and veins of rats before, during, and after inhaled halothane, isoflurane, or sevoflurane (0.5 or 1.0 minimum alveolar concentration [MAC]). Such transmembrane potentials and their anesthetically induced changes were compared, respectively, with those measured in similar vessel preparations after local sympathetic neural denervation with 6-hydroxydopamine. RESULTS: In neurally intact vessels, transmembrane potentials (in millivolts, mean +/- SD) before inhalation of the anesthetic agent were -39 +/- 2.8 (artery) and -43 +/- 4.6 (vein). At 1.0 MAC, halothane, isoflurane, and sevoflurane induced respective hyperpolarizations (in millivolts, mean +/- SD) of 9 +/- 3.1, 6 +/- 2.7, and 9 +/- 4.0 in arteries and 6 +/- 4.4, 2.8 +/- 3.0, and 8.7 +/- 5.6 in veins. Sympathetic denervation significantly attenuated these hyperpolarizations (except for venous response to isoflurane). At 0.5 MAC, transmembrane potential responses to all three volatile anesthetic agents were small and not consistently significant in either the intact or denervated vessels. CONCLUSIONS: In resistance-regulating arteries in situ, inhaled halothane, isoflurane, and sevoflurane (1.0 MAC) attenuate both sympathetic neural and nonneural regulation of vascular smooth muscle transmembrane potentials (and tone). In capacitance-regulating veins in situ, sevoflurane (1.0 MAC) also attenuates both regulatory mechanisms, whereas halothane and isoflurane primarily attenuate nonneural mechanisms. At 0.5 MAC, none of these agents significantly affected either mode of regulation of vascular smooth muscle transmembrane potentials in arteries or veins.

Administration, Inhalation↗
PubMed1998

Kinetical analysis of tumor cell death-inducing mechanism by polymorphonuclear leukocyte-derived calprotectin: involvement of protein synthesis and generation of reactive oxygen species in target cells.

We have previously shown that calprotectin, the most abundant cytosolic protein existing in polymorphonuclear leukocytes (PMNs), induces apoptotic cell death in various tumor cells, suggesting that calprotectin is an effector molecule against tumor cells in PMNs. To explore the cell death-inducing mechanism of the factor, we examined the involvement of target protein synthesis and generation of reactive oxygen species (ROS) in the reaction. Calprotectin induced cell death in MM46 mouse mammary carcinoma cells after a 14-16 hr lag time. When the factor was removed from the medium up to about 12 hr after culturing, the effect was diminished. The induction of cell death by calprotectin was markedly inhibited by the presence of the RNA synthesis inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide. However, the addition of these inhibitors after 12 hr of culturing was unable to inhibit the reaction. Up to 12 hr of culturing, the net protein synthesis of MM46 cells was augmented by the presence of calprotectin, but thereafter was impaired. The induction of cell death was also inhibited by the antioxidative reagents N-acetyl-L-cysteine (NAC) or propyl gallate. The addition of NAC even 15 hr later significantly attenuated the calprotectin effect. Flow cytometry analysis showed that calprotectin began to increase the ROS content in MM46 cells after 8-12 hr of culturing, and that the increase was abrogated by the antioxidants. Thus, protein synthesis and ROS generation may be essential elements in the early or later phases of the cell death-inducing reaction of calprotectin, respectively.

Animals↗
PubMed1998

Anti-Candida activity of calprotectin in combination with neutrophils or lactoferrin.

The effect of an anti-microbial protein, calprotectin, in combination with neutrophils on the growth of Candida albicans was investigated. The growth inhibition of C. albicans by murine neutrophils was augmented by the addition of a low concentration of calprotectin prepared from rat peritoneal exudate cells. The concentrations of calprotectin causing 50% inhibition of growth of C. albicans in the absence or presence of neutrophils at an effector-to-target (E/T) ratio of 30 and 60 were estimated to be 0.45, 0.34 and 0.28 U/ml, respectively. The anti-Candida activity of calprotectin was completely inhibited by 2 microM of zinc ion, while it only partially lowered the activity of the combination of calprotectin and neutrophils. Lactoferrin, which is an anti-microbial protein released from neutrophils, strongly inhibited the growth of C. albicans in combination with calprotectin. These results suggest that calprotectin and lactoferrin released from neutrophils may cooperate to inhibit the growth of C. albicans at a local lesion of the infection where there is an accumulation of neutrophils.

Animals↗
PubMed1998

Assignment of biochemical functions to glycosyl transferase genes which are essential for biosynthesis of exopolysaccharides in Sphingomonas strain S88 and Rhizobium leguminosarum.

Glycosyl transferases which recognize identical substrates (nucleotide-sugars and lipid-linked carbohydrates) can substitute for one another in bacterial polysaccharide biosynthesis, even if the enzymes originate in different genera of bacteria. This substitution can be used to identify the substrate specificities of uncharacterized transferase genes. The spsK gene of Sphingomonas strain S88 and the pssDE genes of Rhizobium leguminosarum were identified as encoding glucuronosyl-(B1-->4)-glucosyl transferases based on reciprocal genetic complementation of mutations in the spsK gene and the pssDE genes by segments of cloned DNA and by the SpsK-dependent incorporation of radioactive glucose (Glc) and glucuronic acid (GlcA) into lipid-linked disaccharides in EDTA-permeabilized cells. By contrast, glycosyl transferases which form alternative sugar linkages to the same substrate caused inhibition of polysaccharide synthesis or were deleterious or lethal in a foreign host. The negative effects also suggested specific substrate requirements: we propose that spsL codes for a glucosyl-(beta1-->4)-glucuronosyl transferase in Sphingomonas and that pssC codes for a glucuronosyl-(beta1-->4)-glucuronosyl transferase in R. leguminosarum. Finally, the complementation results indicate the order of attachment of sphingan main-chain sugars to the C55-isoprenylphosphate carrier as -Glc-GlcA-Glc-isoprenylpyrophosphate.

Carbohydrate Sequence↗
PubMed1998

Four new immunosuppressive components, kobiin and kobifuranones A, B, and C, from an ascomycete, Gelasinospora kobi.

A new sesterterpenetriol named kobiin and three new 2-furanones named kobifuranones A, B, and C were isolated from an Ascomycete, Gelasinospora kobi. Kobiin, the main immunosuppressive principle of this fungus, possesses a bicyclic skeleton of five- and fifteen-membered rings. Kobifuranones A, B, and C were supposed to be metabolites formed from a common intermediate biosynthesized through the acetate-malonate pathway. The immunosuppressive activity of kobiin and kobifuranones A, B, and C was evaluated in a system of mouse spleen lymphocytes stimulated to proliferate with concanavalin A and lipopolysaccharide.

Animals↗
PubMed1998

Immunosuppressive components from an Ascomycete, Diplogelasinospora grovesii.

Two known fungal metabolites, macrophin and colletodiol, and a new stereoisomer of colletodiol named 10-epi-colletodiol, were isolated as immunosuppressive principles from an Ascomycete, Diplogelasinospora grovesii. The IC50 values of the major active component among them, macrophin, were calculated to be 0.4 and 0.3 microgram/ml against concanavalin A- and lipopolysaccharide-induced proliferations of mouse spleen lymphocytes, respectively. A new natural product, 4,8-dimethyl-1,5-dioxacyclooctane-2,6-dione, and a known fungal metabolite, isosclerone, which showed no immunosuppressive activity, were also isolated from this fungus.

Animals↗
PubMed1998

Pharmacologically active components of viticis fructus (Vitex rotundifolia). II. The components having analgesic effects.

The extract of Viticis Fructus appeared to have an analgesic effect, and was subjected to activity-guided separation using acetic acid-induced writhing in mice. The active fraction gave new compounds, vitexfolin A (1A), B and C, 10-O-vanilloylaucubin (3), dihydrodehydrodiconiferylalcohol-beta-D- (2'-O-p-hydroxybenzoyl)glucoside (4), and vanilloyl-beta-D-(2'O-p-hydroxybenzoyl)glucoside, together with agnuside (2) and erythro- and threoguaiacylglycerols. Compounds 1A and 2-4 showed significant writhing inhibition following oral administration at doses of 15, 50, 25, and 50 mg/kg, respectively. The effect on pressure pain threshold was tested using compounds 1A and 2 at a dose of 50 mg/kg, and only the former produced the analgesia. The analgesic effect of some related iridoid glucosides is also discussed.

Administration, Oral↗
PubMed1998

[Biological response modifier activity of Lactococcus lactis 332].

The biological response modifier (BRM) activity of a preparation of heat killed cells of Lactococcus lactis 332 which can produce large amount of lactate in culture, was investigated in C3H/He and ICR mice. Intraperitoneal injection of Lactococcus lactis 332 caused an accumulation of neutrophils and macrophages in the peritoneal cavity of the mice, similarly to BRMs used clinically. As a parameter of the activation of macrophages, the effect of the Lactococcus lactis 332 preparation on the production of tumor necrosis factor (TNF) was examined. The Lactococcus lactis 332 preparation was revealed to have both priming and triggering activities for the production of TNF. The TNF level in the sera reached about 1000 IU/ml in mice 2 h after the triggering injection. This preparation also stimulated peritoneal macrophages to produce TNF in vitro. Intratumoral injection of the Lactococcus lactis 332 preparation regressed MM46 tumor cells in C3H/He mice. These results suggest that the Lactococcus lactis 332 preparation is a biological response modifier (BRM) with various activities on phagocytes similarly to a streptococcal antitumor agent, OK432, used clinically.

Animals↗