30 research outputs found
Comparison of the Push-Out Bond Strength of 5th, 6th, 7th and 8th Generation Bonding Agents to Intracanal Dentin of Primary Anterior Teeth
Background and Objective: Due to the importance of primary anterior teeth in chewing, pronunciation of words, self-confidence, facial appearance of children, efforts to preserve these teeth continue. The aim of the present study was to evaluate the push-out bond strength of 5th, 6th, 7th, and 8th generation bonding agents to intracanal dentin of primary anterior teeth which are reconstructed with the composite posts.
Methods: The present experimental in vitro study was conducted on 60 extracted primary anterior teeth with at least two-thirds of the root length remaining. The teeth were randomly divided into five groups: 5th generation (3M Adper single bond 2 Adhesive-USA), 6th generation (clearfil SE bond, Japan), 7th generation (kerr-optibond all in one Adhesive-Italy), and 8th generation total-etch and 8th generation self-etch (GC-G permio bond-Japan) bonding agents. After root canal preparation, prepared canals were filled with Metapex. The coronal 3mm of the canals was etched and impregnated with the dentin bonding agents. Then, they were restored with composite. The push-out test was performed to evaluate the bond strength of adhesives. Accordingly, by a light microscope the failure modes were determined.
Findings: The mean bond strength of 5th, 6th, 7th, and 8th generation (self-etch, total-etch) bonding agents was 4.36Β±2.15, 3.88Β±1.55, 4.29Β±2.02, 12.84Β±3.62, and 7.77Β±3.81 MPa, respectively. The push-out bond strength of the 8th generation bonding agent using both self-etch (p=0.000) and total-etch techniques was higher than the 5th, 6th, and 7th generation bonding agents (p=0.032, 0.01, 0.027, respectively). No significant difference was found between the bond strength of the 5th, 6th, and 7th generation bonding agents.
Conclusion: The push-out bond strength of the 8th generation bonding system was higher than the other groups. Therefore, the 8th generation bonding agents can be used to bond composite posts to intracanal dentin of primary anterior teeth. Also, self-etch (8th generation) has higher bond strength compared to the total-etch technique
Signaling pathways downstream of P2 receptors in human neutrophils
Extracellular nucleotides stimulate human neutrophils by activating the purinergic P2Y2 receptor. However, it is not completely understood which types of G proteins are activated downstream of this P2 receptor subtype. We investigated the G-protein coupling to P2Y2 receptors and several subsequent signaling events. Treatment of neutrophils with pertussis toxin (PTX), a Gi protein inhibitor, caused only βΌ75% loss of nucleotide-induced Ca2+ mobilization indicating that nucleotides cause Ca2+ mobilization both through Gi-dependent and Gi-independent pathways. However, the PLC inhibitor U73122 almost completely inhibited Ca2+ mobilization in both nucleotide- and fMLP-stimulated neutrophils, strongly supporting the view that both the PTX-sensitive and the PTX-insensitive mechanism of Ca2+ increase require activation of PLC. We investigated the dependence of ERK phosphorylation on the Gi pathway. Treatment of neutrophils with PTX caused almost complete inhibition of ERK phosphorylation in nucleotide or fMLP activated neutrophils. U73122 caused inhibition of nucleotide- or fMLP-stimulated ERK phosphorylation, suggesting that although pertussis toxin-insensitive pathways cause measurable Ca2+ mobilization, they are not sufficient for causing ERK phosphorylation. Since PLC activation leads to intracellular Ca2+ increase and PKC activation, we investigated if these intracellular events are necessary for ERK phosphorylation. Exposure of cells to the Ca2+ chelator BAPTA had no effect on nucleotide- or fMLP-induced ERK phosphorylation. However, the PKC inhibitor GF109203X was able to almost completely inhibit nucleotide- or fMLP-induced ERK phosphorylation. We conclude that the P2Y2 receptor can cause Ca2+ mobilization through a PTX-insensitive but PLC-dependent pathway and ERK phosphorylation is highly dependent on activation of the Gi proteins
The priming effect of extracellular UTP on human neutrophils: Role of calcium released from thapsigargin-sensitive intracellular stores
P2Y2 receptors, which are equally responsive to ATP and UTP, can trigger intracellular signaling events, such as intracellular calcium mobilization and mitogen-activated protein (MAP) kinase phosphorylation in polymorphonuclear leukocytes (PMN). Moreover, extracellular nucleotides have been shown to prime chemoattractant-induced superoxide production. The aim of our study was to investigate the mechanism responsible for the priming effect of extracellular nucleotides on reactive oxygen species (ROS) production induced in human neutrophils by two different chemoattractants: formyl-methionyl-leucyl-phenylalanine (fMLP) and interleukin-8 (IL-8). Nucleotide-induced priming of ROS production was concentration- and time-dependent. When UTP was added to neutrophil suspensions prior to chemoattractant, the increase of the response reached the maximum at 1Β min of pre-incubation with the nucleotide. UTP potentiated the phosphorylation of p44/42 and p38 MAP kinases induced by chemoattractants, however the P2 receptor-mediated potentiation of ROS production was still detectable in the presence of a SB203580 or U0126, supporting the view that MAP kinases do not play a major role in regulating the nucleotide-induced effect. In the presence of thapsigargin, an inhibitor of the ubiquitous sarco-endoplasmic reticulum Ca2+-ATPases in mammalian cells, the effect of fMLP was not affected, but UTP-induced priming was abolished, suggesting that the release of calcium from thapsigargin-sensitive intracellular stores is essential for nucleotide-induced priming in human neutrophils
Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks
The role of nucleotides in intracellular energy provision and nucleic acid synthesis has been known for a long time. In the past decade, evidence has been presented that, in addition to these functions, nucleotides are also autocrine and paracrine messenger molecules that initiate and regulate a large number of biological processes. The actions of extracellular nucleotides are mediated by ionotropic P2X and metabotropic P2Y receptors, while hydrolysis by ecto-enzymes modulates the initial signal. An increasing number of studies have been performed to obtain information on the signal transduction pathways activated by nucleotide receptors. The development of specific and stable purinergic receptor agonists and antagonists with therapeutical potential largely contributed to the identification of receptors responsible for nucleotide-activated pathways. This article reviews the signal transduction pathways activated by P2Y receptors, the involved second messenger systems, GTPases and protein kinases, as well as recent findings concerning P2Y receptor signalling in C6 glioma cells. Besides vertical signal transduction, lateral cross-talks with pathways activated by other G protein-coupled receptors and growth factor receptors are discussed
The Fatigue Behavior of Restorations Used Under the Rest of Removable Partial Denture
Statement of Problem: The question about resistance of resin composites under
rest in removable partial denture (RPD) is still unanswered. It is important to find
the strongest material that withstands the applied stresses when used under RPD
components.
Objectives: To evaluate and compare the fatigue behavior of amalgam and composite
restorations used under the rest of the removable partial denture.
Materials and Methods: Forty-five permanent human upper premolars were
prepared with standard class II DO cavities and divided into 3 groups of specimens
(n=15 for each group). Group I was filled with amalgam (Dispersalloy), group II and
III were filled with resin composite (Flitek Z250 and Tetric ceram, respectively). The
teeth were stored in distilled water for 14 days before testing. After thermocycling,
the βstaircaseβ approach was used to determine the flexural fatigue limits (FFL). The
mean differences were evaluated using One-Way ANOVA and post hoc test.
Results: A strong significant differences of flexural fatigue strength have been
found between amalgam and composite groups (P<0.001). There was no significant
difference between two groups of resin composite (P=0.1).
Conclusions: To achieve more flexural fatigue strength in the rest seats, the use of
resin composite in comparison with amalgam is recommended
The "Cooperative-Supportiveββ Intervention for Improving Mental Health Status among Pregnant Women
Paravertebral anesthesia: how substance P and the NK-1 receptor could be involved in regional block and breast cancer recurrence
Activation of human neutrophils by oleic acid involves the production of reactive oxygen species and a rise in cytosolic calcium concentration: a comparison with N-6 polyunsaturated fatty acids
Contains fulltext :
95617.pdf (publisher's version ) (Open Access)BACKGROUND: There is a growing body of evidence showing that dietary constituents and lipids in particular, influence the function of the human immune system. However, although the beneficial effects of oleic acid (OA) are clear, its mechanism of action at the molecular level is poorly understood. AIMS: To evaluate neutrophil activation under the influence of OA and compare this with several n-6 PUFAs. METHODS: Two key aspects of neutrophil activation were investigated: oxygen radical (ROS) production and intracellular Ca(2+) signaling. RESULTS: OA and the n-6 PUFA arachidonic acid (AA) both induced ROS production in a dose-dependent manner, although AA was the more potent stimulus. When looking for the mechanisms behind these effects, we found that both FA induce increases in cytosolic calcium concentration [Ca(2+)](i)), but whereas OA-induced ROS production is totally mediated through Ca2+ signaling, this is not the case for AA since ROS generation by AA is only partly inhibited in BAPTA-treated cells. We also found evidence for the involvement of protein kinase C (PKC) in the OA-induced ROS generation; by contrast, other enzymes apart from PKC seem to be implicated in n-6 PUFA-induced ROS production. In addition, our results argue against the involvement of a pertussis toxin-sensitive receptor activated by OA. CONCLUSIONS: OA differs from the n-6 PUFA AA in the activation of human neutrophils and these differences may be related to their distinct inmunomodulatory properties