[Allergic granulomatous angitis causing ureteral stenosis].
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Adult↗
Biomedical subjects
H Sano
Publications and source records attributed to H Sano.
Long-term mechanical properties of EDTA-demineralized dentin matrix.
PURPOSE: To determine the long-term ultimate tensile strength (UTS) and modulus of elasticity (E) of EDTA-demineralized human dentin after storage in PBS (phosphate buffered saline) for up to 48 months. MATERIALS AND METHODS: Dentin beams measuring 0.7 x 0.7 x 8.0 mm were prepared from the crowns of extracted human third molars. The ends of the beams were covered with resin composite and demineralized for 6 days in 0.5 mol/L EDTA (pH = 7.0). Demineralized control specimens were subjected to tensile testing at 0.5 mm/min after 24 hours of immersion in PBS solution. Experimental specimens were stored in PBS at room temperature (25 degrees C) and tested after 18 and 48 months. The maximum load at failure and the load/displacement curves were used to calculate the UTS as a function of the cross-sectional area and E, respectively. The results were analyzed by ANOVA and Student Neuman Keuls tests. TEM micrographs were obtained from the control specimens and from those that were stored and tested after 48 months. RESULTS: No significant changes in either UTS or E were observed in the specimens after long-term storage. The 48-month values were not statistically significantly different from the values obtained at 24 hours (p > 0.05). TEM images revealed a normal, intact structure of the collagen fibrils with no signs of degradation or denaturation. CONCLUSION: Long-term storage of EDTA-demineralized human dentin in PBS solution did not cause any significant reduction of its mechanical properties. The structure of the collagen fibrils as observed by TEM appeared normal and did not seem affected by long-term storage.
Analysis of Variance↗
Ability of adhesive systems to seal dentin surfaces: an in vitro study.
PURPOSE: The objective of this study was to evaluate the ability of three adhesive systems to seal dentin by measuring the permeability of dentin before and after bonding procedures. MATERIALS AND METHODS: Thirty-six flat dentin surfaces were prepared from human extracted teeth and connected to a fluid-filled system for permeability measurements. The hydraulic conductance of the flat occlusal surface of dentin was measured by the filtration technique, before and after application of ScotchBond MP Plus, Prime & Bond 2.0, and All-Bond 2. Bonding procedures were followed by P-50 resin composite application. The specimens were then perfused with silver nitrate to permit morphologic localization of microleakage pathways using SEM. RESULTS: The results showed that the best dentin seal was produced by All-Bond 2, followed by Prime & Bond 2.0, and ScotchBond MP Plus. However, none of the three bonding systems tested was able to totally prevent the passage of fluid across the dentin in every specimen. When observed with SEM, each adhesive system exhibited different patterns of leakage. CONCLUSION: The inability of all three materials to create a perfect seal in vitro raises concerns about the ability of these adhesive systems to provide completely sealed restorations in vivo. However, because the current study applied pressure 3 to 6 times higher than physiologically normal, it is likely that the leakage represents a worst-case scenario.
Adhesives↗
An ultrastructural study of the influence of acidity of self-etching primers and smear layer thickness on bonding to intact dentin.
PURPOSE: The objectives of this study were (1) to determine the depth of demineralization into intact dentin using several self-etching primer systems with different pH values, and (2) to evaluate whether hybridization of intact dentin in Clearfil SE Bond may be affected by variation in the thickness of the smear layers. MATERIALS AND METHODS: Dentin disks were created from mid-coronal dentin in extracted, human third molars. Three self-etching primer systems (Clearfil Liner Bond II, Liner Bond 2V, and SE Bond) were applied separately to these disks to evaluate how deep self-etching systems penetrate through smear layers into intact dentin. Dentin treated with All-Bond 2 using the "no-etch" technique was used as a control group. In the second part of the study, dentin disks with different smear-layer thicknesses were produced. The cryofractured control group was devoid of a smear layer. The experimental teeth were ground with 60-, 180-, or 600-grit SiC paper and bonded using SE Bond. Dentin disks were bonded together and examined with TEM. RESULTS: All-Bond 2 did not etch beyond the smear layer. The three self-etching primers etched beyond the smear layer to form true hybrid layers within intact dentin. This layer was thickest with Liner Bond 2 (ca 1.2 to 1.4 microns), but very thin (0.5 micron) using both Liner Bond 2V and SE Bond. Application of SE Bond to dentin of different surface roughness produced hybridized smear layers of variable thickness. However, the thickness of the underlying true hybrid remained consistent for the four groups (ca 0.4 to 0.5 micron). CONCLUSION: Self-etching primers create thin hybrid layers that incorporate the smear layer. The suspicion that thick smear layers may interfere with the diffusion of self-etching primers into the underlying intact dentin was not confirmed.
Acid Etching, Dental↗
Effect of smear layers on the bonding of a self-etching primer to dentin.
PURPOSE: The objective of this work was to evaluate the effect of the absence and presence of smear layers on bonds made to dentin using a self-etching primer system, Clearfil SE Bond. MATERIALS AND METHODS: Dentin surfaces with different smear layer thickness were created from mid-coronal sound dentin in extracted, human third molars. The control group was cryofractured to create a bonding surface that was devoid of a smear layer. The experimental teeth were ground with wet 60-, 180- or 600-grit SiC paper. They were bonded using SE Bond, followed by resin composite buildups. After 1 day, bonded specimens were sectioned into multiple 1- x 1-mm beams. Microtensile bond strengths were determined and the results analyzed with ANOVA and the Student Neuman Keuls test. Fractographic study of cross sections of failed interfaces from the dentin side of representative beams was performed using both SEM and TEM. RESULTS: SE Bond produced high bond strengths (ca 50 MPa) to both smear layer-free and smear layer-covered dentin. SEM examination was inadequate to define the exact nature of interfacial failures. TEM observations demonstrated a thin (ca 400 to 500 nm) hybrid layer in the fractured dentin and thicker (ca 1 to 4 microns) hybrid layers on smear layer-covered dentin. This included a thick, hybridized smear layer and a thin, underlying true hybrid layer in the intact dentin. Separation of the two hybrid layers was not evident in interfacial failures. CONCLUSION: Self-etching primers create thin hybrid layers that incorporate the smear layer. This study shows that formation of true hybrid layers occurs irrespective of smear layer thickness and that both hybrid layers may function as a unit during loading without separation. identification of secondary cracks from TEM fractographic analysis exemplifies the complex reaction to tensile stresses in multilayered joint systems that comprise materials of variable compliance.
Acid Etching, Dental↗
Physical properties of the dentin-enamel junction region.
PURPOSE: To determine the physical properties between enamel and dentin at the dentin-enamel junction (DEJ) region of natural tooth structure. MATERIALS AND METHODS: Ultimate tensile cohesive strengths of the DEJ region of human and bovine teeth were measured using a microtensile test, and the nanohardness and Young's modulus from deep enamel to superficial dentin of human teeth were measured using a nanoindentation tester. RESULTS: The mean ultimate tensile cohesive strengths of bovine and human DEJ region were 47.7 MPa and 51.5 MPa, respectively. The nanohardness, dynamic hardness and Young's modulus of the DEJ region showed moderate values between those of enamel and dentin. Comparison of the cohesive strength of the human DEJ region with previous results of the bond strength of resin bonding systems indicate that current resin bonding systems might reproduce the biological adhesion of enamel to dentin in terms of the tensile strength. Moreover, the indentation properties of the DEJ region showed higher values than those of the underlying dentin or of resin impregnated dentin.
Acid Etching, Dental↗
Microtensile bond strength to dentin and cavity adaptation of Cerec 2 inlay restoration.
PURPOSE: To examine the bond strength of Cerec 2 inlays both to dentin surface by microtensile testing and to cavity walls by cavity adaptation in Class II restorations, using three luting materials. MATERIAL AND METHODS: VitaMark II disc was bonded to the coronal dentin surface with Clapearl DC (Clearfil DC)/Linerbond IIsigma (Linerbond 2V), AP-X/Linerbond IIsigma or Fluorocement (Panavia F)/ED Primer. After 24-hr storage in water, microtensile bond strengths (MTB) were measured. Additionally, Cerec inlays were luted to the MO cavities prepared in molars with the same materials. After thermocycling (x2000), the restorations were sectioned mesio-distally. Gap formation was microscopically examined along the cavity walls. RESULTS: There was no significant difference in MTB among the materials (Clapearl DC: 20.89 +/- 4.58 MPa, AP-X: 24.22 +/- 5.97 MPa, Fluorocement: 19.82 +/- 6.43 MPa, Scheffé, P > 0.05). The frequency of gap formation was higher in AP-X than in Clapearl DC and Fluorocement (chi2-test, P < 0.05). Debonding occurred more often at the luting material/dentin interface than at the inlay/luting material interface (Sign test, P < 0.05).
Analysis of Variance↗
[Case of recurrent subglottic stenosis later followed by the development of Wegener's granulomatosis].
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Adult↗
HPLC analysis of dental resin composites components.
Five uncured commercial dental resin composites (two bis-glycidyl methacrylate based products and three non-bis-glycidyl methacrylate based products) were examined for contamination with bisphenol A, which is a known xenobiotic. After the samples were processed with acetonitrile for extraction of their components, high performance liquid chromatography analysis was performed and the eluted peaks were fractionated for comparison using UV spectra. The results suggested that all the resin composites tested were contaminated with bisphenol A or its derivatives. Theoretically, bisphenol A is not a component of dental resin composite, but it could remain as an impurity of the composite during the synthesis of Bis-GMA. The results suggest that it is necessary to investigate the ability of this impurity and its derivatives in dental resin composites to cause estrogenic effects, as well as to evaluate the release of the impurity from cured resin composites.
Benzhydryl Compounds↗
Auranofin inhibits interleukin-1beta-induced transcript of cyclooxygenase-2 on cultured human synoviocytes.
The aim of this study was to characterize the effects of auranofin (2,3,4,6-tetra-O-acetyl-l-thio-beta-D-gluco-pyranosato-S) on cyclooxygenase expression and prostaglandin E(2) synthesis on cultured human synovial fibroblast-like cells (synoviocytes). Synoviocytes were treated with auranofin in the presence or absence of interleukin-1beta. Cultured supernatants were harvested for prostaglandin E(2) synthesis. Cyclooxygenase-1 and -2 expression was analyzed with Western and Northern blotting. Translocation of nuclear factor-kappa B p65 was determined by immunostaining. Cytotoxicity was measured with 51Cr release assay. Auranofin attenuated interleukin-1beta-induced prostaglandin E(2) production of the cells in a dose-dependent fashion. Auranofin selectively suppressed interleukin-1beta-induced cyclooxygenase-2 mRNA and protein expression of the cells without alteration of cyclooxygenase-1 expression. Also, auranofin interfered with interleukin-1beta-induced translocation of nuclear factor-kappa B. These inhibitory effects did not originate in the cytotoxicity of the agent. Our data indicate that auranofin inhibits interleukin-1beta-induced prostaglandin E(2) synthesis and cyclooxygenase-2 expression via suppression of nuclear factor-kappa B activation on synoviocytes.
Auranofin↗
Advanced glycation end product-induced peroxisome proliferator-activated receptor gamma gene expression in the cultured mesangial cells.
We identified the AGEs-induced expression of peroxisome proliferator-activated gamma (PPAR gamma) in the cultured mesangial cells using reverse transcription-polymerase chain reaction, electrophoretic mobility shift assay (EMSA), and Western immunoblotting. Administration of AGEs-BSA into the cultured mesangial cells resulted in an increase in the levels of mRNA and proteins for PPAR gamma in a dose-dependent manner. Specific bands which indicate the protein binding to PPAR gamma responsive element (PPRE) in the nuclear extracts were also detected in AGEs-BSA-treated mesangial cells, but not found in BSA-treated cells by EMSA. Antioxidants, NAC, PDTC, and aminoguanidine, attenuated the gene expression and activity of PPAR gamma induced by AGEs. These results indicate that PPAR gamma was induced and activated by the oxidative signal(s) evoked by AGEs-ligand-receptor interactions. AGEs-induced gene expression of PPAR gamma and the signal intensity of PPAR gamma and PPRE complex were attenuated furthermore by protein kinase C inhibitors, calphostin C and staurospolin, but not abolished completely, indicating that both signal transduction pathways through the induction of PKC activation and independent of PKC activation were involved in the AGEs-mediated expression and activation process of PPAR gamma. AGEs also increased the gene expression of smooth muscle alpha-actin, which is a marker for phenotypic change in mesangial cells. It is suggested therefore that AGEs-induced transcription factor as the oxidative stress may have a role in the differentiation of mesangial cells.
Actins↗
Cytosolic phospholipase A2 activation is essential for beta 1 and beta 2 integrin-dependent adhesion of human eosinophils.
We examined the role of cytosolic phospholipase A2 (cPLA2) during human eosinophil adherence to ICAM-1- or VCAM-1-coated plates. IL-5-stimulated eosinophils adhered to ICAM-1 through the beta 2 integrin CD11b/CD18, while nonstimulated eosinophils did not. By contrast, nonstimulated eosinophils adhered to VCAM-1 through the beta 1-integrin VLA-4/CD29. Both IL-5-induced adhesion to ICAM-1 and spontaneous adhesion to VCAM-1 corresponded temporally to cPLA2 phosphorylation, which accompanied enhanced catalytic activity of cPLA2. The structurally unrelated cPLA2 inhibitors, arachidonyl trifluoromethylketone and surfactin, significantly inhibited eosinophil adhesion to ICAM-1 and VCAM-1 in a concentration-dependent manner. Inhibition of secretory PLA2, 5-lipoxygenase, or cyclooxygenase did not affect eosinophil adhesion. Addition of arachidonic acid to eosinophils after cPLA2 inhibition with arachidonyl trifluoromethylketone or surfactin did not reverse the blockade of adhesion to ICAM-1 or VCAM-1. However, CV-6209, a receptor-specific antagonist of platelet-activating factor, inhibited all integrin-mediated adhesion. The activated conformation of CD11b as identified by the mAb, CBRM1/5, as well as quantitative surface CD11b expression were up-regulated after IL-5 stimulation. However, cPLA2 inhibition neither prevented CBRM1/5 expression nor blocked surface Mac-1 up-regulation caused by IL-5. Our data suggest that cPLA2 activation and its catalytic product platelet-activating factor play an essential role in regulating beta 1 and beta 2 integrin-dependent adhesion of eosinophils. This blockade occurs even in the presence of up-regulated eosinophil surface integrin.
Arachidonic Acids↗
Purification, molecular cloning, and catalytic activity of Schizosaccharomyces pombe pyridoxal reductase. A possible additional family in the aldo-keto reductase superfamily.
Pyridoxal reductase (PL reductase), which catalyzes reduction of PL by NADPH to form pyridoxine and NADP(+), was purified from Schizosaccharomyces pombe. The purified enzyme was very unstable but was stabilized by low concentrations of various detergents such as Tween 40. The enzyme was a monomeric protein with the native molecular weight of 41,000 +/- 1,600. The enzyme showed a single absorption peak at 280 nm (E(1%) = 10.0). PL and 2-nitrobenzaldehyde were excellent substrates, and no measurable activity was observed with short chain aliphatic aldehydes; substrate specificity of PL reductase was obviously different from those of yeast aldo-keto reductases (AKRs) so far purified. The peptide sequences of PL reductase were identical with those in a hypothetical 333-amino acid protein from S. pombe (the DDBJ/EMBL/GenBank(TM) accession number D89205). The gene corresponding to this protein was expressed in Escherichia coli, and the purified protein was found to have PL reductase activity. The recombinant PL reductase showed the same properties as those of native PL reductase. PL reductase showed only low sequence identities with members of AKR superfamily established to date; it shows the highest identity (18.5%) with human Shaker-related voltage-gated K(+) channel beta2 subunit. The elements of secondary structure of PL reductase, however, distributed similarly to those demonstrated in the three-dimensional structure of human aldose reductase except that loop A region is lost, and loop B region is extended. Amino acid residues involved in substrate binding or catalysis are also conserved. Conservation of these features, together with the major modifications, establish PL reductase as the first member of a new AKR family, AKR8.
Alcohol Oxidoreductases↗
Characterization of the Ca2+-dependent binding of annexin IV to surfactant protein A.
We have shown previously that surfactant protein A (SP-A) binds to annexin IV in a Ca2+-dependent manner [Sohma, Matsushima, Watanabe, Hattori, Kuroki and Akino (1995) Biochem. J. 312, 175-181]. Annexin IV is a member of the annexin family having four consensus repeats of about 70 amino acids and a unique N-terminal tail. In the present study, the functional site of both annexin IV and SP-A for the Ca2+-dependent binding was investigated using mutant proteins. SP-A bound in a Ca2+-dependent manner to an annexin-IV truncation mutant consisting of the N-terminal domain and the first three domains (T(N-1-2-3)). SP-A also bound to T3-4, but this interaction was not Ca2+-dependent. SP-A bound weakly to the other truncation mutants (T(N-1-2), T(2-3) and T(2-3-4)). Each consensus repeat of annexin IV possesses a conserved acidic amino acid residue (Glu70, Asp142, Glu226 and Asp301) that putatively ligates Ca2+. Using annexin-IV DE mutants in which one, two or three residues out of the four Asp/Glu were altered to Ala by site-directed mutagenesis [Nelson and Creutz (1995) Biochemistry 34, 3121-3132], it was revealed that Ca2+ binding in the third domain is more important than in the other Ca2+-binding sites. SP-A is a member of the animal lectin group homologous with mannose-binding protein A. The substitution of Arg197 of rat SP-A with Asp or Asn eliminated binding to annexin IV, whereas the substitution of Glu195 with Gln was silent. These results suggest that the Ca2+ binding to domain 3 of annexin IV is required for the Ca2+-dependent binding by SP-A and that Arg197 of SP-A is important in this binding.
Animals↗
Pulmonary surfactant protein A modulates the cellular response to smooth and rough lipopolysaccharides by interaction with CD14.
Pulmonary surfactant protein A (SP-A) plays an important part in Ab-independent host defense mechanisms of the lung. In this study we investigated how SP-A interacts with distinct serotypes of bacterial LPS and modulates LPS-elicited cellular responses. SP-A bound to rough forms but not to smooth forms of LPS. In the macrophage-like cell line U937, SP-A inhibited mRNA expression and secretion of TNF-alpha induced by smooth LPS, but rough LPS-induced TNF-alpha expression was unaffected by SP-A. When U937 cells and rat alveolar macrophages were preincubated with SP-A, smooth LPS failed to induce TNF-alpha secretion, whereas rough LPS-induced TNF-alpha secretion was modestly increased. To clarify the mechanism by which SP-A modulates LPS-elicited cellular responses, we further examined the interaction of SP-A with CD14, which is known as a major LPS receptor. Western blot analysis revealed that CD14 was one of the SP-A binding proteins isolated from solubilized U937 cells. In addition, SP-A directly bound to recombinant soluble CD14 (rsCD14). When rsCD14 was preincubated with SP-A, the binding of rsCD14 to smooth LPS was significantly reduced but the association of rsCD14 with rough LPS was augmented. These results demonstrate the different actions of SP-A upon distinct serotypes of LPS and indicate that the direct interaction of SP-A with CD14 constitutes a likely mechanism by which SP-A modulates LPS-elicited cellular responses.
Animals↗
Introduction of mannose binding protein-type phosphatidylinositol recognition into pulmonary surfactant protein A.
Pulmonary surfactant protein A (SP-A) and mannose-binding protein A (MBP-A) are collectins in the C-type lectin superfamily. These collectins exhibit unique lipid binding properties. SP-A binds to dipalmitoyl phosphatidylcholine (DPPC) and galactosylceramide (GalCer) and MBP-A binds to phosphatidylinositol (PI). SP-A also interacts with alveolar type II cells. Monoclonal antibodies (mAbs PE10 and PC6) that recognize human SP-A inhibit the interactions of SP-A with lipids and alveolar type II cells. We mapped the epitopes for anti-human SP-A mAbs by a phage display peptide library. Phage selected by mAbs displayed the consensus peptide sequences that are nearly identical to 184TPVNYTNWYRG194 of human SP-A. The synthetic peptide GTPVNYTNWYRG completely blocked the binding of mAbs to human SP-A. Chimeric proteins were generated in which the rat SP-A region Thr174-Gly194 or the human SP-A region Ser174-Gly194 was replaced with the MBP-A region Thr164-Asp184 (rat ama4 or hu ama4, respectively). The mAbs failed to bind hu ama4. Rat ama4 bound to an affinity matrix on mannose-sepharose but lost all of the SP-A functions except carbohydrate binding and Ca2+-independent GalCer binding. Strikingly, the rat ama4 chimera acquired the PI binding property that MBP-A exhibits. This study demonstrates that the amino acid residues 174-194 of SP-A and the corresponding region of MBP-A are critical for SP-A-type II cell interaction and Ca2+-dependent lipid binding of collectins.
Animals↗
Intraperitoneal administration of anti-c-fms monoclonal antibody prevents initial events of atherogenesis but does not reduce the size of advanced lesions in apolipoprotein E-deficient mice.
BACKGROUND: Atherosclerosis results from complex inflammatory-fibroproliferative responses. To elucidate the central role of macrophage and macrophage-colony stimulating factor (M-CSF) during atherogenesis, we used a new strategy to administer to adult apolipoprotein E (apoE)-deficient mice a monoclonal antibody (AFS98) raised against c-fms, the receptor of M-CSF. METHODS AND RESULTS: When 6-week-old apoE-deficient mice were fed a high-fat diet and injected with 2 mg of AFS98 intraperitoneally on alternate days for 6 weeks, accumulation of macrophage-derived foam cells in the aortic root was suppressed by 70% compared with that in controls. This preventive effect was associated with neither remarkable decrease of the number of circulating monocytes nor systemic growth retardation. In contrast, when apoE-deficient mice that had been fed a high-fat diet from 6 weeks of age were given AFS98 from 12 to 18 weeks of age, a minimal protective effect on lesion size was observed. CONCLUSIONS: These results suggest that (1) macrophage and M-CSF/c-fms play an essential role in the arterial wall during development of the fatty streak lesion and (2) blockade of the M-CSF/c-fms pathway could act as protection from at least early atherogenesis but could have a less preventive effect on maintenance of the advanced lesions.
Animals↗
Four rice genes encoding cysteine synthase: isolation and differential responses to sulfur, nitrogen and light.
Four cDNA clones, rcs1, rcs2, rcs3 and rcs4, encoding cysteine synthase [O-acetylserine(thiol)lyase] were isolated from rice. The predicted amino acid sequences contain the conserved PXXSVKDR region characteristic of cysteine synthase, which includes the lysine residue that binds the cofactor, pyridoxal 5'-phosphate. Molecular phylogenic analysis suggests that, whereas rcs1 and rcs3 belong to the cytosolic isoform family, rcs2 and rcs4 form a new family of cysteine synthase. Transcript accumulation of each gene was examined for organ specificity, and also for response to sulfur, nitrogen and light. The rcs1 transcript accumulated in all organs examined, and was induced in shoots and roots upon sulfur starvation under non-limiting nitrogen conditions. The rcs2 transcript accumulated in shoots grown in the light, but disappeared almost completely by dark treatment. The rcs3 transcript was found more abundantly in roots than in shoots, and was reduced in the dark, as well as under sulfur and nitrogen deprivation. The rcs4 transcript was scarce in all organs examined. These observations indicate that cysteine synthase genes encode functionally distinct cysteine synthase isoforms, and that they are coordinately regulated by the availability of sulfur, nitrogen, and light.
Amino Acid Sequence↗