An in vitro comparison of nickel and chromium release from brackets

This study aimed at comparing amounts of nickel (Ni) and chromium (Cr) released from brackets from different manufacturers in simulated oral environments. 280 brackets were equally divided into 7 groups according to manufacturer. 6 groups of brackets were stainless steel, and 1 group of brackets was made of a cobalt-chromium alloy with low Ni content (0.5%). International standard ISO 10271/2001 was applied to provide test methods. Each bracket was immersed in 0.5 ml of synthetic saliva (SS) or artificial plaque fluid (PF) over a period of 28 days at 37ºC. Solutions were replaced every 7 days, and were analyzed by spectrometry. The Kruskal-Wallis test was applied. Amounts of Ni release in SS (µg L-1 per week) varied between groups from "bellow detection limits" to 694, and from 49 to 5,948.5 in PF. The group of brackets made of cobalt-chromium alloy, with the least nickel content, did not release the least amounts of Ni. Amounts of Cr detected in SS and in PF (µg L-1 per week) were from 1 to 10.4 and from 50.5 to 8,225, respectively. It was therefore concluded that brackets from different manufacturers present different corrosion behavior. Further studies are necessary to determine clinical implications of the findings.

Sublattice magnetism in sigma-phase Fe(100-x)Vx (x=34.4, 39.9, and 47.9) studied via zero-field (51)V NMR

The successful measurements of a sublattice magnetism with (51)V NMR techniques in the sigma-phase Fe(100-x)V(x) alloys with x=34.4, 39.9, and 47.9 are reported. Vanadium atoms, which were revealed to be present on all five crystallographic sites, are found to be under the action of the hyperfine magnetic fields produced by the neighboring Fe atoms, which allow the observation of (51)V NMR signals. Their nuclear magnetic properties are characteristic of a given site, which strongly depend on the composition. Site A exhibits the strongest magnetism while site D is the weakest. The estimated average magnetic moment per V atom decreases from 0.36 mu(B) for x=34.4 to 0.20 mu(B) for x=47.9. The magnetism revealed at V atoms is linearly correlated with the magnetic moment of Fe atoms, which implies that the former is induced by the latter.

Microstructural characterization of as-cast Cr-Si alloys

This work presents results of microstructural characterization of as-cast Cr-Si alloys. The alloys were prepared by arc melting pure Cr (min. 99.996%) and Si (min. 99.998%) powder mixtures under argon atmosphere in a water-cooled copper crucible with nonconsumable tungsten electrode and titanium getter. The phases were identified by scanning electron microscopy (SEM), using the back-scattered electron (BSE) image mode and X-ray diffraction (XRD). The results confirm the currently accepted Cr-Si phase diagram in terms of the invariant reactions and solid phases present in this system. Small corrections are proposed for the compositions of the liquid phase in the following reactions: (i) L double left right arrow Cr-ss+Cr3Si, from 15 to 16 at.% Si; (ii) L+alpha Cr5Si3 double left right arrow CrSi, from 51 at.% Si to slightly above 53 at.% Si; (iii) L double left right arrow CrSi+CrSi2, from 56 to slightly above 57 at.% Si; (iv) L double left right arrow CrSi2+Si, from 82 to slightly above 85 at.% Si. (c) 2006 Elsevier Inc. All rights reserved.

Contribution of TIR domain-containing adapter inducing IFN-beta-mediated IL-18 release to LPS-induced liver injury in mice.

BACKGROUND/AIMS: After treatment with heat-killed Propionibacterium acnes mice show dense hepatic granuloma formation. Such mice develop liver injury in an interleukin (IL)-18-dependent manner after challenge with a sublethal dose LPS. As previously shown, LPS-stimulated Kupffer cells secrete IL-18 depending on caspase-1 and Toll-like receptor (TLR)-4 but independently of its signal adaptor myeloid differentiation factor 88 (MyD88), suggesting importance of another signal adaptor TIR domain-containing adapter inducing IFN-beta (TRIF). Nalp3 inflammasome reportedly controls caspase-1 activation. Here we investigated the roles of MyD88 and TRIF in P. acnes-induced hepatic granuloma formation and LPS-induced caspase-1 activation for IL-18 release. METHODS: Mice were sequentially treated with P. acnes and LPS, and their serum IL-18 levels and liver injuries were determined by ELISA and ALT/AST measurement, respectively. Active caspase-1 in LPS-stimulated Kupffer cells was determined by Western blotting. RESULTS: Macrophage-ablated mice lacked P. acnes-induced hepatic granuloma formation and LPS-induced serum IL-18 elevation and liver injury. Myd88(-/-) Kupffer cells, but not Trif(-/-) cells, exhibited normal caspase-1 activation upon TLR4 engagement in vitro. Myd88(-/-) mice failed to develop hepatic granulomas after P. acnes treatment and liver injury induced by LPS challenge. In contrast, Trif(-/-) mice normally formed the hepatic granulomas, but could not release IL-18 or develop the liver injury. Nalp3(-/-) mice showed the same phenotypes of Trif(-/-) mice. CONCLUSIONS: Propionibacterium acnes treatment MyD88-dependently induced hepatic granuloma formation. Subsequent LPS TRIF-dependently activated caspase-1 via Nalp3 inflammasome and induced IL-18 release, eventually leading to the liver injury.

Properties of slow-release phosphorus fertilizers with special references to their use on drained peatland forests : A review

Tiivistelmä: Hidasliukoisten fosforilannoitteiden ominaisuudet ja käyttökelpoisuus suometsien lannoituksessa. Kirjallisuuteen perustuva tarkastelu

Comparaison des performances des systèmes CR à aiguilles et à poudre en mammographie.

Objectifs: Comparaison des performances en qualité d'image des deux types de systèmes CR. Matériels et méthodes: Les performances ont été mesurées au moyen de la fonction de transfert de modulation (FTM), du spectre de bruit, de l'efficacité quantique de détection (DQE),le seuil de détection du contraste en épaisseur d'or et la dose glandulaire moyenne. Les systèmes CR à aiguilles Agfa HM5.0 et Carestream SNP-M1 ont étécomparés aux systèmes à poudre Agfa MM3.0, Fuji ProfectCS et Carestream EHR-M3. Résultats: La FTM à 5mm-1 de Agfa HM5,0 et Carestream SNP-M1 est 0,21 et 0,27, et entre 0,14 et 0,16 pour les systèmes à poudre. Un DQE maximal de 0,51 et 0,5 a étéobtenu pour Agfa HM5,0 et Carestream SNP-M1, et 0,35, 0,50 et 0,34 pour Agfa MM3,0, Fuji Profect et Carestream EHR-M3. Des valeurs de DQE à 5mm-1 de0,18 et 0,13 ont été obtenues pour Agfa HM5,0 et Carestream SNP-M1, et entre 0,04 et 0,065 pour les systèmes à poudre. Les seuils de détection du contrastede Agfa HM5,0 et Carestream SNP-M1 étaient 1,33im et 1,29im, et 1,45im et 1,63im pour Agfa MM3,0 et Fuji Profect. Conclusion: Les systèmes à aiguilles offrent des meilleures FTM et DQE et un seuil de visibilité du contraste plus bas que les systèmes à poudre .

Defective tumor necrosis factor-alpha-dependent control of astrocyte glutamate release in a transgenic mouse model of Alzheimer disease.

The cytokine tumor necrosis factor-alpha (TNFalpha) induces Ca2+-dependent glutamate release from astrocytes via the downstream action of prostaglandin (PG) E2. By this process, astrocytes may participate in intercellular communication and neuromodulation. Acute inflammation in vitro, induced by adding reactive microglia to astrocyte cultures, enhances TNFalpha production and amplifies glutamate release, switching the pathway into a neurodamaging cascade (Bezzi, P., Domercq, M., Brambilla, L., Galli, R., Schols, D., De Clercq, E., Vescovi, A., Bagetta, G., Kollias, G., Meldolesi, J., and Volterra, A. (2001) Nat. Neurosci. 4, 702-710). Because glial inflammation is a component of Alzheimer disease (AD) and TNFalpha is overexpressed in AD brains, we investigated possible alterations of the cytokine-dependent pathway in PDAPP mice, a transgenic model of AD. Glutamate release was measured in acute hippocampal and cerebellar slices from mice at early (4-month-old) and late (12-month-old) disease stages in comparison with age-matched controls. Surprisingly, TNFalpha-evoked glutamate release, normal in 4-month-old PDAPP mice, was dramatically reduced in the hippocampus of 12-month-old animals. This defect correlated with the presence of numerous beta-amyloid deposits and hypertrophic astrocytes. In contrast, release was normal in cerebellum, a region devoid of beta-amyloid deposition and astrocytosis. The Ca2+-dependent process by which TNFalpha evokes glutamate release in acute slices is distinct from synaptic release and displays properties identical to those observed in cultured astrocytes, notably PG dependence. However, prostaglandin E2 induced normal glutamate release responses in 12-month-old PDAPP mice, suggesting that the pathology-associated defect involves the TNFalpha-dependent control of secretion rather than the secretory process itself. Reduced expression of DENN/MADD, a mediator of TNFalpha-PG coupling, might account for the defect. Alteration of this neuromodulatory astrocytic pathway is described here for the first time in relation to Alzheimer disease.