145 research outputs found

    Er:YAG Laser and Fractured Incisor Restorations: An In Vitro

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    Introduction. The aim of this study was to analyse the effects of an Er:YAG laser on enamel and dentine in cases of dental restorations involving fractured teeth, utilizing the dental fragment. Materials and Methods. Seventy-two freshly extracted bovine incisors were fractured at the coronal level by using a hammer applied with a standardized method, and the fragment was reattached by using three different methods: Er:YAG laser, orthophosphoric acid, and laser plus acid. The different groups were evaluated by a test realized with the dynamometer to know the force required to successfully detach the reattached fragment and by a microinfiltration test by using a 0.5% methylene blue solution followed by the optic microscope observation. Results. The compression test showed only a slight difference between the three groups, without any statistical significance. The infiltration test used to evaluate the marginal seal between the fracture fragment and the tooth demonstrated that etching with Er:YAG laser alone or in combination with orthophosphoric acid gives better results than orthophosphoric acid alone, with a highly significant statistical result. Discussion. Reattaching a tooth fragment represents a clinically proven methodology, in terms of achieving resistance to detachment, and the aim of this work was to demonstrate the advantages of Er:YAG laser on this procedure. Conclusion. This “in vitro” study confirms that Er:YAG laser can be employed in dental traumatology to restore frontal teeth after coronal fracture

    Dominant-negative mutations in human IL6ST underlie hyper-IgE syndrome

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    Autosomal dominant hyper-IgE syndrome (AD-HIES) is typically caused by dominant-negative (DN) STAT3 mutations. Patients suffer from cold staphylococcal lesions and mucocutaneous candidiasis, severe allergy, and skeletal abnormalities. We report 12 patients from 8 unrelated kindreds with AD-HIES due to DN IL6ST mutations. We identified seven different truncating mutations, one of which was recurrent. The mutant alleles encode GP130 receptors bearing the transmembrane domain but lacking both the recycling motif and all four STAT3-recruiting tyrosine residues. Upon overexpression, the mutant proteins accumulate at the cell surface and are loss of function and DN for cellular responses to IL-6, IL-11, LIF, and OSM. Moreover, the patients’ heterozygous leukocytes and fibroblasts respond poorly to IL-6 and IL-11. Consistently, patients with STAT3 and IL6ST mutations display infectious and allergic manifestations of IL-6R deficiency, and some of the skeletal abnormalities of IL-11R deficiency. DN STAT3 and IL6ST mutations thus appear to underlie clinical phenocopies through impairment of the IL-6 and IL-11 response pathways

    Micromechanical Properties of Injection-Molded Starch–Wood Particle Composites

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    The micromechanical properties of injection molded starch–wood particle composites were investigated as a function of particle content and humidity conditions. The composite materials were characterized by scanning electron microscopy and X-ray diffraction methods. The microhardness of the composites was shown to increase notably with the concentration of the wood particles. In addition,creep behavior under the indenter and temperature dependence were evaluated in terms of the independent contribution of the starch matrix and the wood microparticles to the hardness value. The influence of drying time on the density and weight uptake of the injection-molded composites was highlighted. The results revealed the role of the mechanism of water evaporation, showing that the dependence of water uptake and temperature was greater for the starch–wood composites than for the pure starch sample. Experiments performed during the drying process at 70°C indicated that the wood in the starch composites did not prevent water loss from the samples.Peer reviewe

    Dominant-negative mutations in human IL6ST underlie hyper-IgE syndrome

    Get PDF
    Autosomal dominant hyper-IgE syndrome (AD-HIES) is typically caused by dominant-negative (DN) STAT3 mutations. Patients suffer from cold staphylococcal lesions and mucocutaneous candidiasis, severe allergy, and skeletal abnormalities. We report 12 patients from 8 unrelated kindreds with AD-HIES due to DN IL6ST mutations. We identified seven different truncating mutations, one of which was recurrent. The mutant alleles encode GP130 receptors bearing the transmembrane domain but lacking both the recycling motif and all four STAT3-recruiting tyrosine residues. Upon overexpression, the mutant proteins accumulate at the cell surface and are loss of function and DN for cellular responses to IL-6, IL-11, LIF, and OSM. Moreover, the patients’ heterozygous leukocytes and fibroblasts respond poorly to IL-6 and IL-11. Consistently, patients with STAT3 and IL6ST mutations display infectious and allergic manifestations of IL-6R deficiency, and some of the skeletal abnormalities of IL-11R deficiency. DN STAT3 and IL6ST mutations thus appear to underlie clinical phenocopies through impairment of the IL-6 and IL-11 response pathways
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