Synthesis and luminescence properties of Ca3Ga2Si3O12:RE3+ (RE = Eu/Tb) powder phosphors

Rare earth ions (Eu³⁺ or Tb³⁺)‐activated Ca₃ Ga₂ Si₃O₁₂ (CaGaSi) phosphors were synthesized by using a sol–gel method. Photoluminescence spectra of Eu³⁺:CaGaSi phosphors exhibited five emission bands at 578, 592, 612, 652 and 701 nm, which were assigned to the transitions (⁵D₀ → ⁷F₀, ⁷F_1, ⁷F₂, ⁷F₃ and ⁷F₄), respectively, with an excitation wavelength of λ_exci = 392 nm. Among these, the transition ⁵D₀ → ⁷F₂ (612 nm) displayed bright red emission. In the case of Tb³⁺:CaGaSi phosphors, four emission bands were observed at 488 (⁵D₄ → ⁷F₆), 543 (⁵D₄ → ⁷F₅), 584 (⁵D₄ → ⁷F₄) and 614 nm (⁵D₄ → ⁷F₃) from the measurement of PL spectra with λ_exci = 376 nm. Among these, the transition ⁵D₄ → ⁷F₅ at 543 nm displayed bright green emission. The structure and morphology of the phosphors were studied from the measurements of X‐ray diffraction (XRD), scanning electron microscopy (SEM) and energy‐dispersive X‐ray analysis (EDAX) results. Copyright © 2011 John Wiley & Sons, Ltd.     

The effect of osteoporosis on residual ridge resorption and masticatory performance in denture wearers

doi: 10.1111/j.1741‐2358.2011.00610.x The effect of osteoporosis on residual ridge resorption and masticatory performance in denture wearers Aim: To compare masticatory performance, masticatory efficiency and residual ridge resorption (RRR) in osteoporotic and non‐osteoporotic edentulous subjects after rehabilitation with complete dentures. Method: Thirty subjects fulfilling the inclusion criteria were enrolled from the patients visiting the Department of Prosthodontics for complete denture fabrication. Two groups consisting of control subjects (group I; N = 15) and osteoporotic subjects (group II; N = 15) were formed. Complete dentures satisfying certain criteria were fabricated for both groups. Masticatory performance and efficiency were measured 6 months after denture insertion. Areal measurements were taken on lateral cephalograms before and 6 months after denture fabrication. The data were then computed to analyse differences between groups I and II using SPSS statistical software version 15.0. Results: Six months after denture fabrication, the masticatory performance and efficiency were significantly higher (p < 0.001) for group I, with a significant decrease in maxillary and mandibular sagittal area seen in both groups. The rate of bone loss was more in group II compared with group I. Conclusion: Greater masticatory function was demonstrated by the non‐osteoporotic group, and the rate of RRR was more in the osteoporotic group compared with the normal group. In this pilot study, osteoporosis leads to greater RRR, decreased masticatory performance and efficiency in edentulous subjects 6 months after denture insertion. Screening for osteoporosis is suggested as a routine procedure for all edentulous subjects undergoing rehabilitation. Recall check‐ups for osteoporotic patients should be more frequent, and these patients may require more frequent denture remakes.     

Locus Heterogeneity for Waardenburg Syndrome is Predictive of Clinical Subtypes

Waardenburg syndrome (WS) is a dominantly inherited and clinically variable syndrome of deafness, pigmentary changes, and distinctive facial features. Clinically, WS type I (WS1) is differentiated from WS type II (WS2) by the high frequency of dystopia canthorum in the family. In some families, WS is caused by mutations in the PAX3 gene on chromosome 2q. We have typed microsatellite markers within and flanking PAX3 in 41 WS1 kindreds and 26 WS2 kindreds in order to estimate the proportion of families with probable mutations in PAX3 and to study the relationship between phenotypic and genotypic heterogeneity. Evaluation of heterogeneity in location scores obtained by multilocus analysis indicated that WS is linked to PAX3 in 60% of all WS families and in 100% of WS1 families. None of the WS2 families were linked. In those families in which equivocal lod scores (between −2 and +1) were found, PAX3 mutations have been identified in 5 of the 15 WS1 families but in none of the 4 WS2 families. Although preliminary studies do not suggest any association between the phenotype and the molecular pathology in 20 families with known PAX3 mutations and in four patients with chromosomal abnormalities in the vicinity of PAX3, the presence of dystopia in multiple family members is a reliable indicator for identifying families likely to have a defect in PAX3.     

Synthesis and biological evaluation of 1-substituted-3-(6-methylpyridin-2-yl)-4-([1,2,4]triazolo[1,5-a]pyridin-6-yl)pyrazoles as transforming growth factor-β type 1 receptor kinase inhibitors

A series of 1-substituted-3-(6-methylpyridin-2-yl)-4-([1,2,4]triazolo[1,5-a]pyridin-6-yl)pyrazoles 14a-ae, 16a, 16b, and 21a-c has been prepared and evaluated for their ALK5 inhibitory activity in an enzyme assay and in a cell-based luciferase reporter assay. The 4-([1,2,4]triazolo[1,5-a]pyridin-6-yl)-N-(4-methoxyphenyl)-3-(6-methylpyridin-2-yl)-1H-pyrazole-1-carbothioamide (14n) inhibited ALK5 phosphorylation with IC(50) value of 0.57 nM and showed 94% inhibition at 100 nM in a luciferase reporter assay using HaCaT cells permanently transfected with p3TP-luc reporter construct.     

Effect of leucine on enzymes of the tryptophan-niacin metabolic pathway in rat liver and kidney

Dietary excess of leucine affects tryptophan–niacin metabolism adversely and has thus been implicated in the etiology of pellagra. To understand the biochemical basis of leucine-induced changes in tryptophan–niacin metabolism the effect of leucine on enzymes of tryptophan–niacin metabolism was investigated. Excess of leucine in the diet had no effect on rat liver 3-hydroxyanthranilate oxygenase and nicotinate phosphoribosyltransferase but significantly decreased the activity of quinolinate phosphoribosyltransferase of rat liver and kidney. The activities of tryptophan oxygenase in liver and picolinate carboxylase in kidney were significantly higher in leucine-fed animals than in the controls. Also, oxidation of [U-¹⁴C]tryptophan in vivo was higher in leucine-fed animals. Increased picolinate carboxylase and decreased quinolinate phosphoribosyltransferase activities would result in a decrease in NAD formation from dietary tryptophan. Lowered NAD formation from tryptophan particularly when the niacin concentrations in the diet are marginal would result in a state of conditioned niacin deficiency.