Resistance to maxillary premolar fractures after restoration of class II preparations with resin composite or ceromer.

OBJECTIVE: The aim of this study was to evaluate the resistance to fracture of intact and restored human maxillary premolars. METHOD AND MATERIALS: Thirty noncarious human maxillary premolars, divided into three groups of 10, were submitted to mechanical tests to evaluate their resistance to fracture. Group 1 consisted of intact teeth. Teeth in group 2 received mesio-occlusodistal cavity preparations and were restored with direct resin composite restorations. Teeth in group 3 received mesio-occlusodistal cavity preparations and were restored with ceromer inlays placed with the indirect technique. After restoration, teeth were stored at 37 degrees C for 24 hours and then thermocycled for 500 cycles at temperatures of 5 degrees C and 55 degrees C. RESULTS: Statistical analysis revealed that group 3 (178.765 kgf) had a significantly greater maximum rupture load than did group 1 (120.040 kgf). There was no statistically significant difference between groups 1 and 2 or between groups 2 and 3. CONCLUSION: Class II cavity preparations restored with indirect ceromer inlays offered greater resistance to fracture than did intact teeth. The fracture resistance of teeth restored with resin composite was not significantly different from that of either the ceromer or intact teeth.     

Achieving primary closure and enhancing aesthetics with periodontal microsurgery.

The continuous search for improved surgical procedures to address gingival deformities is a consequence of an increasing demand for aesthetics in the periodontal clinical practice. Innovative techniques have been reported to help clinicians achieve predictability in root coverage. Significant progress can be attributed to the inclusion of the operative microscope in periodontal therapy, particularly in regards to obtaining primary closure. This article describes a microsurgical technique used to treat gingival recessions, showing its potential for obtaining optimal aesthetic results.     

Licensed human natural killer cells aid dendritic cell maturation via TNFSF14/LIGHT

Interactions between natural killer (NK) cells and dendritic cells (DCs) aid DC maturation and promote T-cell responses. Here, we have analyzed the response of human NK cells to tumor cells, and we identify a pathway by which NK–DC interactions occur. Gene expression profiling of tumor-responsive NK cells identified the very rapid induction of TNF superfamily member 14 [TNFSF14; also known as homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes (LIGHT)], a cytokine implicated in the enhancement of antitumor responses. TNFSF14 protein expression was induced by three primary mechanisms of NK cell activation, namely, via the engagement of CD16, by the synergistic activity of multiple target cell-sensing NK-cell activation receptors, and by the cytokines IL-2 and IL-15. For antitumor responses, TNFSF14 was preferentially produced by the licensed NK-cell population, defined by the expression of inhibitory receptors specific for self-MHC class I molecules. In contrast, IL-2 and IL-15 treatment induced TNFSF14 production by both licensed and unlicensed NK cells, reflecting the ability of proinflammatory conditions to override the licensing mechanism. Importantly, both tumor- and cytokine-activated NK cells induced DC maturation in a TNFSF14-dependent manner. The coupling of TNFSF14 production to tumor-sensing NK-cell activation receptors links the tumor immune surveillance function of NK cells to DC maturation and adaptive immunity. Furthermore, regulation by NK cell licensing helps to safeguard against TNFSF14 production in response to healthy tissues.Natural killer (NK) cells play an important role in protecting the host against viral infection and cancer. As well as having potent cytotoxic activity, NK cells are endowed with immunoregulatory activity (1, 2). For example, NK cell activation induces the production of chemokines, such as macrophage inflammatory protein-1α (MIP-1α) and IL-8, and proinflammatory cytokines, such as IFN-γ, GM-CSF, and TNF-α. These molecules regulate the recruitment and activity of numerous immune cell types (1, 2). Importantly, NK cells can promote development of T-cell responses via NK–dendritic cell (DC) interactions that favor both DC maturation and NK-cell activation (3–5), with NK cell-derived IFN-γ skewing T-cell differentiation toward the Th1 phenotype (6, 7).Cytotoxic activity and cytokine production are coupled to signaling pathways downstream of a repertoire of activating and inhibitory receptors; signals from activating receptors (including NKG2D, DNAM-1, and 2B4, as well as the natural cytotoxicity receptors NKp30, NKp44, and NKp46) compete with signals from inhibitory receptors such as the killer cell immunoglobulin-like receptors (KIRs) and CD94/NKG2A heterodimers to regulate activation. In addition, NK cells express CD16, the low-affinity receptor for IgG, conferring antibody-dependent cellular cytotoxicity (8–10). Activation thus coordinates the killing of target cells, the induction of inflammation, and the promotion of adaptive immunity. This potent cytotoxicity and proinflammatory activity must be strictly controlled to minimize damage to healthy tissue. Functional competency of unstimulated NK cells is achieved via a process termed “licensing” or “education” (11–14). Licensing ensures that only those NK cells expressing inhibitory receptors for self-MHC class I can respond to target cells and NK cells that lack inhibitory receptors for self-MHC class I molecules are rendered hyporesponsive, preventing them from attacking healthy cells expressing normal levels of MHC class I molecules.We have analyzed the consequences of human NK cell activation by tumor cells. Our results reveal induction of the TNF superfamily member 14 (TNFSF14), also known as homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes (LIGHT) (15). We show that activated NK cells produce TNFSF14 in response to different stimuli, that tumor cells induce TNFSF14 production by licensed NK cells, and that TNFSF14-producing NK cells aid DC maturation during NK–DC cross-talk.     

Low-level laser therapy improves the VO<Subscript>2</Subscript> kinetics in competitive cyclists

Some evidence supports that low-level laser therapy (LLLT) reduces neuromuscular fatigue, so incrementing sports performance. A previous randomized controlled trial of our group showed increased exercise tolerance in male competitive cyclists treated with three different LLLT doses (3, 6, and 9 J/diode; or 135, 270, and 405 J/thigh) before time-to-exhaustion cycling tests. Now, the present study was designed to evaluate the effects of these LLLT doses on the VO₂ kinetics of athletes during cycling tests. Twenty male competitive cyclists (29 years) participated in a crossover, randomized, double-blind, and placebo-controlled trial. On the first day, the participants performed an incremental cycling test to exhaustion to determine maximal oxygen uptake (VO_2MAX) and maximal power output (PO_MAX), as well as a familiarization with the time-to-exhaustion test. In the following days (2 to 5), all participants performed time-to-exhaustion tests at PO_MAX. Before the exhaustion test, different doses of LLLT (3, 6, and 9 J/diode; or 135, 270, and 405 J/thigh, respectively) or placebo were applied bilaterally to the quadriceps muscle. All exhaustion tests were monitored online by an open-circuit spirometry system in order to analyze the VO₂ amplitude, VO₂ delay time, time constant (tau), and O₂ deficit. Tau and O₂ deficit were decreased with LLLT applications compared to the placebo condition (p < 0.05). No differences (p > 0.05) were found between the experimental conditions for VO₂ amplitude and VO₂ delay time. In conclusion, LLLT decreases tau and O₂ deficit during time-to-exhaustion tests in competitive cyclists, and these changes in VO₂ kinetics response can be one of the possible mechanisms to explain the ergogenic effect induced by LLLT.     

Fostering Children's Participation in Disaster Risk Reduction Through Play:A Case Study of LEGO and Minecraft

This article focuses on children's participation in disaster risk reduction.It draws on a 2018 study done in New Zealand with 33 school children who conducted p...     

Catalysis by cytochrome P-450 of an oxidative reaction in xenobiotic aldehyde metabolism: deformylation with olefin formation.

As we have briefly described elsewhere, cytochrome P-450 catalyzes the oxidative deformylation of cyclohexane carboxaldehyde to yield cyclohexene and formic acid in a reaction believed to involve a peroxyhemiacetal-like adduct formed between the substrate and molecular oxygen-derived hydrogen peroxide. This reaction is a useful model for the demethylation reactions catalyzed by the steroidogenic P-450s, aromatase, and lanosterol demethylase. In the present study, the cytochrome P-450-catalyzed formation of olefinic products from a series of xenobiotic aldehydes has been demonstrated. Isobutyraldehyde and trimethylacetaldehyde, but not propionaldehyde, are converted to the predicted olefinic products, suggesting a requirement for branching at the alpha carbon. In addition, the four C5 aldehydes of similar hydrophobicity were compared for their ability to undergo the reaction. The straight-chain valeraldehyde gave no olefinic products with five different rabbit liver microsomal P-450 isozymes. However, increasing activity was seen with the other isomers in the order of isovaleraldehyde, 2-methylbutyraldehyde, and trimethylacetaldehyde, with all of the P-450 cytochromes. The catalytic rate with trimethylacetaldehyde is highest with antibiotic-inducible P-450 form 3A6, followed by phenobarbital-inducible form 2B4 and ethanol-inducible form 2E1. Citronellal, a beta-branched aldehyde that is found in many essential oils and is widely used as an odorant and a flavorant, was found to undergo the oxidative deformylation reaction to yield 2,6-dimethyl-1,5-heptadiene, but only with P-450 2B4. The oxidative cleavage reaction with olefin formation appears to be widespread, as judged by the variety of aldehydes that serve as substrates and of P-450 cytochromes that serve as catalysts.