791 research outputs found

    Effect of three surface conditioning methods to improve bond strength of particulate filler resin composites

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    The use of resin-based composite materials in operative dentistry is increasing, including applications in stress-bearing areas. However, composite restorations, in common with all restorations, suffer from deterioration and degradation in clinical service. Durable repair alternatives by layering a new composite onto such failed composite restorations, will eliminate unnecessary loss of tooth tissue and repeated insults to the pulp. The objective of this study was to evaluate the effect of three surface conditioning methods on the repair bond strength of a particulate filler resin-composite (PFC) to 5 PFC substrates. The specimens were randomly assigned to one of the following surface conditioning methods: (1) Hydrofluoric (HF) acid gel (9.5%) etching, (2) Air-borne particle abrasion (50 mum Al2O3), (3) Silica coating (30 mum SiOx, CoJet(R)-Sand). After each conditioning method, a silane coupling agent was applied. Adhesive resin was then applied in a thin layer and light polymerized. The low-viscosity diacrylate resin composite was bonded to the conditioned substrates in polyethylene molds. All specimens were tested in dry and thermocycled (6.000, 5-55 degreesC, 30 s) conditions. One-way ANOVA showed significant influence of the surface conditioning methods (p &lt;0.001), and the PFC types (p &lt;0.0001) on the shear bond strength values. Significant differences were observed in bond strength values between the acid etched specimens (5.7-14.3 MPa) and those treated with either air-borne particle abrasion (13.0-22.5 MPa) or silica coating (25.5-41.8 MPa) in dry conditions (ANOVA, p &lt;0.001). After thermocycling, the silica coating process resulted in the highest bond values in all material groups (17.2-30.3 MPa). (C) 2005 Springer Science + Business Media, Inc.</p

    The Association Between Smartphone Addiction and Sleep: A UK Cross-Sectional Study of Young Adults

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    Background: In a large UK study we investigated the relationship between smartphone addiction and sleep quality in a young adult population. Methods: We undertook a large UK cross-sectional observational study of 1,043 participants aged 18 to 30 between January 21st and February 30th 2019. Participants completed the Smartphone Addiction Scale Short Version, an adapted Pittsburgh Sleep Quality Score Index and reported smartphone use reduction strategies using both in-person (n = 968) and online (n = 75) questionnaires. A crude and adjusted logistic regression was fitted to assess risk factors for smartphone addiction, and the association between smartphone addiction and poor sleep. Results: One thousand seventy one questionnaires were returned, of which 1,043 participants were included, with median age 21.1 [interquartile range (IQR) 19–22]. Seven hundred and sixty three (73.2%) were female, and 406 reported smartphone addiction (38.9%). A large proportion of participants disclosed poor sleep (61.6%), and in those with smartphone addiction, 68.7% had poor sleep quality, compared to 57.1% of those without. Smartphone addiction was associated with poor sleep (aOR = 1.41, 95%CI: 1.06–1.87, p = 0.018). Conclusions: Using a validated instrument, 39% young adults reported smartphone addiction. Smartphone addiction was associated with poor sleep, independent of duration of usage, indicating that length of time should not be used as a proxy for harmful usage

    Kinetic Characterization and X-ray Structure of a Mutant of Haloalkane Dehalogenase with Higher Catalytic Activity and Modified Substrate Range

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    Conversion of halogenated aliphatics by haloalkane dehalogenase proceeds via the formation of a covalent alkyl-enzyme intermediate which is subsequently hydrolyzed by water. In the wild type enzyme, the slowest step for both 1,2-dichloroethane and 1,2-dibromoethane conversion is a unimolecular enzyme isomerization preceding rapid halide dissociation. Phenylalanine 172 is located in a helix-loop-helix structure that covers the active site cavity of the enzyme, interacts with the Clβ of 1,2-dichloroethane during catalysis, and could be involved in stabilization of this helix-loop-helix region of the cap domain of the enzyme. To obtain more information about the role of this residue in dehalogenase function, we performed a mutational analysis of position 172 and studied the kinetics and X-ray structure of the Phe172Trp enzyme. The Phe172Trp mutant had a 10-fold higher kcat/Km for 1-chlorohexane and a 2-fold higher kcat for 1,2-dibromoethane than the wild-type enzyme. The X-ray structure of the Phe172Trp enzyme showed a local conformational change in the helix-loop-helix region that covers the active site. This could explain the elevated activity for 1-chlorohexane of the Phe172Trp enzyme, since it allows this large substrate to bind more easily in the active site cavity. Pre-steady-state kinetic analysis showed that the increase in kcat found for 1,2-dibromoethane conversion could be attributed to an increase in the rate of an enzyme isomerization step that preceeds halide release. The observed conformational difference between the helix-loop-helix structures of the wild-type enzyme and the faster mutant suggests that the isomerization required for halide release could be a conformational change that takes place in this region of the cap domain of the dehalogenase. It is proposed that Phe172 is involved in stabilization of the helix-loop-helix structure that covers the active site of the enzyme and creates a rigid hydrophobic cavity for small apolar halogenated alkanes.

    Dual endothelin-converting enzyme/neutral endopeptidase blockade in rats with D-galactosamine-induced liver failure

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    Secondary activation of the endothelin system is thought to be involved in toxic liver injury. This study tested the hypothesis that dual endothelin-converting enzyme / neutral endopeptidase blockade might be able to attenuate acute toxic liver injury

    Renal phenotype of Et-1 transgenic mice is modulated by androgens

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    <p>Abstract</p> <p>Introduction</p> <p>Activation of the endothelin (ET) system promotes inflammation and fibrosis in various tissues including the kidney. Male ET-1 transgenic mice are characterized by chronic kidney inflammation and renal scarring. We hypothesized that this renal phenotype might be modulated by androgens. Thus the aim of our study was to elucidate the impact of gonadectomy in ET-1 transgenic mice on kidney function and morphology.</p> <p>Methods</p> <p>Male ET-1 transgenic mice at the age of 10 weeks were randomly allocated to the following groups: normal ET transgenic mice (ET; n = 17) and ET transgenic mice that underwent castration (ET+cas; n = 12). Study duration was 9 months. Creatinine clearance and protein excretion was monitored. At study end animals were sacrificed and kidneys were harvested for histology/immunhistochemistry.</p> <p>Results</p> <p>Castration significantly ameliorated glomerulosclerosis in ET-1 transgenic mice (ET glomerulosclerosis-score: 3.0 ± 0.17 vs ET+cas: 2.4 ± 0.17; p < 0.05) as well as renal perivascular fibrosis (ET fibrosis-score: 3.0 ± 0.14 vs ET+cas: 2.2 ± 0.14; p < 0.05). However, interstitial fibrosis and media/lumenratio of renal arteries remained unaffected by castration. Regarding inflammation, castration significantly reduced the number of CD4-positive cells in renal tissue of ET-1 transgenic mice (ET CD4-positive cells/10000 cells: 355 ± 72 vs ET+cas: 147 ± 28; p < 0.05). Renal tissue contents of CD8 positive cells as well as of macrophages were not affected by castration. Regarding kidney function castration significantly reduced proteinuria in ET-1 transgenic mice whereas creatinine clearance did not differ between study groups.</p> <p>Conclusion</p> <p>Our study demonstrates that the renal histopathological phenotype in male ET-1 transgenic mice with regard to glomerulosclerosis, proteinuria, perivascular fibrosis and immune cell immigration is ameliorated by castration. We thus conclude that the effects of ET-1 overexpression on renal tissue injury are modulated by androgens.</p
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