Addition of antibacterial agents to MMA-TBB dentin bonding systems--influence on tensile bond strength and antibacterial effect.
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To produce a bonding system which has both high bond strength and antibacterial properties, an antibacterial agent (vancomycin: VCM or metronidazol: MN) was added to the PMMA powder of 4-META/MMA-TBB resin (CB). The influence of the addition of an antibacterial agent on tensile bond strength to dentin and the antibacterial effect were investigated in this study. Forty-seven freshly extracted bovine first or second incisors were used to measure the tensile bond strength to dentin. The bond strengths to bovine dentin were not significantly decreased by addition of VCM (1%, 2%, 5%), or MN (1%) to CB (p < 0.05). The antibacterial effect of CB containing antibacterial agent on six strains of bacteria was investigated by the agar plate diffusion method, analyzing the appearance of the inhibition zone around a resin disk following anaerobic culturing. The resin disks containing VCM showed antibacterial effects on all of the strains examined; the widths of the inhibition zones were 4-15 mm. The resin disks containing MN showed antibacterial effects on three strains; the widths of the inhibition zones were 0-4 mm. It was thus possible to produce a bonding system with both antibacterial effect and high tensile bond strength by addition of VCM to PMMA powder. (+info)
Effect of the adhesive layer thickness on the fracture toughness of dental adhesive resins.
(50/933)
We investigated how the thickness of an adhesive layer between two Co-Cr alloy plates affected the mode I fracture toughness of dental adhesive resin by varying the type of resin using a double cantilever beam (DCB) test. Two typical adhesive resins (PV and SB) were used. The adhesive layers of the DCB test specimens were 20, 100 and 200 microns thick. The fracture modes of PV differed with the thickness of the adhesive layer, such as interface fracture at 20 microns thickness, and similar cohesive fracture at 100 and 200 microns thickness. In the case of SB, crack-propagating areas were observed as cohesive fractures in all test specimens with different adhesive layer thickness, and the surfaces of these areas became remarkably rougher as the thickness of the adhesive layer increased. The fracture toughness of PV was not affected by the differences in thickness between the 100 and 200 microns adhesive layers, but there was a notable decrease in fracture toughness when the adhesive layer decreased to a thickness of 20 microns. That of SB showed a tendency to increase as the adhesive layer became thicker. (+info)
Optical anisotropy in lipid bilayer membranes: coupled plasmon-waveguide resonance measurements of molecular orientation, polarizability, and shape.
(51/933)
The birefringence and linear dichroism of anisotropic thin films such as proteolipid membranes are related to molecular properties such as polarizability, shape, and orientation. Coupled plasmon-waveguide resonance (CPWR) spectroscopy is shown in the present work to provide a convenient means of evaluating these parameters in a single lipid bilayer. This is illustrated by using 1-10 mol % of an acyl chain chromophore-labeled phosphatidylcholine (PC) incorporated into a solid-supported PC bilayer deposited onto a hydrated silica surface. CPWR measurements were made of refractive index and extinction coefficient anisotropies with two exciting light wavelengths, one of which is absorbed by the chromophore and one of which is not. These results were used to calculate longitudinal and transverse molecular polarizabilities, the orientational order parameter and average angle between the longitudinal axis of the lipid molecule and the membrane normal, and the molecular shape factors of the lipid molecules. The values thereby obtained are in excellent agreement with parameters determined by other techniques, and provide a powerful tool for analyzing lipid-protein, protein-protein, and protein-ligand interactions in proteolipid films. (+info)
Fluorescent quenching-based quantitative detection of specific DNA/RNA using a BODIPY((R)) FL-labeled probe or primer.
(52/933)
We have developed a simple method for the quantitative detection of specific DNA or RNA molecules based on the finding that BODIPY((R)) FL fluorescence was quenched by its interaction with a uniquely positioned guanine. This approach makes use of an oligonucleotide probe or primer containing a BODIPY((R)) FL-modified cytosine at its 5'-end. When such a probe was hybridized with a target DNA, its fluorescence was quenched by the guanine in the target, complementary to the modified cytosine, and the quench rate was proportional to the amount of target DNA. This widely applicable technique will be used directly with larger samples or in conjunction with the polymerase chain reaction to quantify small DNA samples. (+info)
Lipopolysaccharide internalization activates endotoxin-dependent signal transduction in cardiomyocytes.
(53/933)
We tested the hypothesis that bacterial lipopolysaccharide (LPS) must be internalized to facilitate endotoxin-dependent signal activation in cardiac myocytes. Fluorescently labeled LPS was used to treat primary cardiomyocyte cultures, perfused heart preparations, and the RAW264.7 macrophage cell line. Using confocal microscopy and spectrofluorometry, we found that LPS was rapidly internalized in cardiomyocyte cultures and Langendorff-perfused hearts. Although LPS uptake was also observed in macrophages, only a fraction of these cells were found to internalize endotoxin to the extent seen in cardiomyocytes. Colocalization experiments with organelle or structure-specific fluorophores showed that LPS was concentrated in the Golgi apparatus, lysosomes, and sarcomeres. Similar intracellular localization was demonstrated in cardiomyocytes by transmission electron microscopy using gold-labeled LPS. The internalization of LPS was dependent on endosomal trafficking, because an inhibitor of microfilament reorganization prevented uptake in both cardiomyocytes and whole hearts. Inhibition of endocytosis specifically restricted early activation of extracellular signal-regulated kinase proteins and nuclear factor-kappaB as well as later tumor necrosis factor-alpha production and inducible nitric oxide synthase expression. In conclusion, we have demonstrated that bacterial endotoxin is internalized and transported to specific intracellular sites in heart cells and that these events are obligatory for activation of LPS-dependent signal transduction. (+info)
Restoration of endodontically treated teeth with carbon fibre posts--a prospective study.
(54/933)
BACKGROUND: A prospective study was started in 1995 to evaluate the success of carbon fibre reinforced epoxy resin (CFRR) posts used to restore endodontically treated teeth. All the teeth in the study had lost more than 50% of their coronal structure. METHODS: Fifty-nine carbon fibre Composiposts cemented with Metabond and built up with Core Paste cores were placed into the teeth of 47 patients. Each tooth received a full-coverage restoration (porcelain fused to metal crown) and was followed for 6.7-45.4 months (average = 28.0 months, standard deviation = 10.7). RESULTS: Results for 52 teeth in 42 patients were analyzed. There were no fractures. The overall failure rate was 7.7% and the cumulative survival rate was 89.6% at the end of the follow-up period. The only statistically significant finding (p = 0.04) was that posts in lower premolars were at higher risk of failure. CONCLUSION: CFRR posts are among the most predictable systems available today. CFRR posts in the upper anterior teeth are associated with a higher success rate and longer life than those placed in premolars, especially lower premolars. This study contributes to the growing body of evidence that supports the use of CFRR posts in the restoration of endodontically treated teeth. (+info)
Assessment of the role of the inositol 1,4,5-trisphosphate receptor in the activation of transient receptor potential channels and store-operated Ca2+ entry channels.
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The mechanism for coupling between Ca(2+) stores and store-operated channels (SOCs) is an important but unresolved question. Although SOCs have not been molecularly identified, transient receptor potential (TRP) channels share a number of operational parameters with SOCs. The question of whether activation of SOCs and TRP channels is mediated by the inositol 1,4,5-trisphosphate receptor (InsP(3)R) was examined using the permeant InsP(3)R antagonist, 2-aminoethoxydiphenyl borate (2-APB) in both mammalian and invertebrate systems. In HEK293 cells stably transfected with human TRPC3 channels, the actions of 2-APB to block carbachol-induced InsP(3)R-mediated store release and carbachol-induced Sr(2+) entry through TRPC3 channels were both reversed at high agonist levels, suggesting InsP(3)Rs mediate TRPC3 activation. However, electroretinogram recordings of the light-induced current in Drosophila revealed that the TRP channel-mediated responses in wild-type as well as trp and trpl mutant flies were all inhibited by 2-APB. This action of 2-APB is likely InsP(3)R-independent since InsP(3)Rs are dispensable for the light response. We used triple InsP(3)R knockout DT40 chicken B-cells to further assess the role of InsP(3)Rs in SOC activation. (45)Ca(2+) flux analysis revealed that although DT40 wild-type cells retained normal InsP(3)Rs mediating 2-APB-sensitive Ca(2+) release, the DT40InsP(3)R-k/o cells were devoid of functional InsP(3)Rs. Using intact cells, all parameters of Ca(2+) store function and SOC activation were identical in DT40wt and DT40InsP(3)R-k/o cells. Moreover, in both cell lines SOC activation was completely blocked by 2-APB, and the kinetics of action of 2-APB on SOCs (time dependence and IC(50)) were identical. The results indicate that (a) the action of 2-APB on Ca(2+) entry is not mediated by the InsP(3)R and (b) the effects of 2-APB provide evidence for an important similarity in the function of invertebrate TRP channels, mammalian TRP channels, and mammalian store-operated channels. (+info)
Role of the phospholipase C-inositol 1,4,5-trisphosphate pathway in calcium release-activated calcium current and capacitative calcium entry.
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We investigated the putative roles of phospholipase C, polyphosphoinositides, and inositol 1,4,5-trisphosphate (IP(3)) in capacitative calcium entry and calcium release-activated calcium current (I(crac)) in lacrimal acinar cells, rat basophilic leukemia cells, and DT40 B-lymphocytes. Inhibition of phospholipase C with blocked calcium entry and I(crac) activation whether in response to a phospholipase C-coupled agonist or to calcium store depletion with thapsigargin. Run-down of cellular polyphosphoinositides by concentrations of wortmannin that block phosphatidylinositol 4-kinase completely blocked calcium entry and I(crac). The membrane-permeant IP(3) receptor inhibitor, 2-aminoethoxydiphenyl borane, blocked both capacitative calcium entry and I(crac). However, it is likely that 2-aminoethoxydiphenyl borane does not inhibit through an action on the IP(3) receptor because the drug was equally effective in wild-type DT40 B-cells and in DT40 B-cells whose genes for all three IP(3) receptors had been disrupted. Intracellular application of another potent IP(3) receptor antagonist, heparin, failed to inhibit activation of I(crac). Finally, the inhibition of I(crac) activation by or wortmannin was not reversed or prevented by direct intracellular application of IP(3). These findings indicate a requirement for phospholipase C and for polyphosphoinositides for activation of capacitative calcium entry. However, the results call into question the previously suggested roles of IP(3) and IP(3) receptor in this mechanism, at least in these particular cell types. (+info)