A perovskite oxide with high conductivities in both air and reducing atmosphere for use as electrode for solid oxide fuel cells

Electrode materials which exhibit high conductivities in both oxidising and reducing atmospheres are in high demand for solid oxide fuel cells (SOFCs) and solid oxide electrolytic cells (SOECs). In this paper, we investigated Cu-doped SrFe0.9Nb0.1O3−δ finding that the primitive perovskite oxide SrFe0.8Cu0.1Nb0.1O3−δ (SFCN) exhibits a conductivity of 63 Scm−1and 60 Scm−1 at 415 °C in air and 5%H2/Ar respectively. It is believed that the high conductivity in 5%H2/Ar is related to the exsolved Fe (or FeCu alloy) on exposure to a reducing atmosphere. To the best of our knowledge, the conductivity of SrFe0.8Cu0.1Nb0.1O3−δ in a reducing atmosphere is the highest of all reported oxides which also exhibit a high conductivity in air. Fuel cell performance using SrFe0.8Cu0.1Nb0.1O3−δ as the anode, (Y2O3)0.08(ZrO2)0.92 as the electrolyte and La0.8Sr0.2FeO3−δ as the cathode achieved a power density of 423 mWcm−2 at 700 °C indicating that SFCN is a promising anode for SOFCs

Conductivity and redox stability of new double perovskite oxide Sr 1.6 K 0.4 Fe 1+ x Mo 1− x O 6− δ (x= 0.2, 0.4, 0.6)

A series of new perovskite oxides Sr1.6K0.4Fe1+xMo1−xO6−δ (x = 0.2, 0.4, 0.6) were synthesised by solid state reaction method. Synthesis of Sr1.6K0.4Fe1+xMo1−xO6−δ (x = 0.2, 0.4, 0.6) was achieved above 700 °C in 5 % H2/Ar, albeit with the formation of impurity phases. Phase stability upon redox cycling was only observed for sample Sr1.6K0.4Fe1.4Mo0.6O6−δ. Redox cycling of Sr1.6K0.4Fe1+xMo1−xO6−δ (x = 0.2, 0.4, 0.6) demonstrates a strong dependence on high temperature reduction to achieve high conductivities. After the initial reduction at 1200 °C in 5 %H2/Ar, then re-oxidation in air at 700 °C and further reduction at 700 °C in 5 %H2/Ar, the attained conductivities were between 0.1 and 58.4 % of the initial conductivity after reduction 1200 °C in 5 %H2/Ar depending on the composition. In the investigated new oxides, sample Sr1.6K0.4Fe1.4Mo0.6O6−δ is most redox stable also retains reasonably high electrical conductivity, ~70 S/cm after reduction at 1200 °C and 2–3 S/cm after redox cycling at 700 °C, indicating it is a potential anode for SOFCs

Single-neutron transfer from 11Be gs via the (p,d) reaction with a radioactive beam

The 11Be(p,d)10Be reaction has been performed in inverse kinematics with a radioactive 11Be beam of E/A = 35.3 MeV. Angular distributions for the 0+ ground state, the 2+, 3.37 MeV state and the multiplet of states around 6 MeV in 10Be were measured at angles up to 16 deg CM by detecting the 10Be in a dispersion-matched spectrometer and the coincident deuterons in a silicon array. Distorted wave and coupled-channels calculations have been performed to investigate the amount of 2+ core excitation in 11Be gs. The use of "realistic" 11Be wave functions is emphasised and bound state form factors have been obtained by solving the particle-vibration coupling equations. This calculation gives a dominant 2s component in the 11Be gs wave function with a 16% [2+ x 1d] core excitation admixture. Cross sections calculated with these form factors are in good agreement with the present data. The Separation Energy prescription for the bound state wave function also gives satisfactory fits to the data, but leads to a significantly larger [2 x 1d] component in 11Be gs.Comment: 39 pages, 12 figures. Accepted for publication in Nuclear Physics A. Added minor corrections made in proof to pages 26 and 3

MSH3 polymorphisms and protein levels affect CAG repeat instability in huntington's disease mice

Expansions of trinucleotide CAG/CTG repeats in somatic tissues are thought to contribute to ongoing disease progression through an affected individual's life with Huntington's disease or myotonic dystrophy. Broad ranges of repeat instability arise between individuals with expanded repeats, suggesting the existence of modifiers of repeat instability. Mice with expanded CAG/CTG repeats show variable levels of instability depending upon mouse strain. However, to date the genetic modifiers underlying these differences have not been identified. We show that in liver and striatum the R6/1 Huntington's disease (HD) (CAG)~100 transgene, when present in a congenic C57BL/6J (B6) background, incurred expansion-biased repeat mutations, whereas the repeat was stable in a congenic BALB/cByJ (CBy) background. Reciprocal congenic mice revealed the Msh3 gene as the determinant for the differences in repeat instability. Expansion bias was observed in congenic mice homozygous for the B6 Msh3 gene on a CBy background, while the CAG tract was stabilized in congenics homozygous for the CBy Msh3 gene on a B6 background. The CAG stabilization was as dramatic as genetic deficiency of Msh2. The B6 and CBy Msh3 genes had identical promoters but differed in coding regions and showed strikingly different protein levels. B6 MSH3 variant protein is highly expressed and associated with CAG expansions, while the CBy MSH3 variant protein is expressed at barely detectable levels, associating with CAG stability. The DHFR protein, which is divergently transcribed from a promoter shared by the Msh3 gene, did not show varied levels between mouse strains. Thus, naturally occurring MSH3 protein polymorphisms are modifiers of CAG repeat instability, likely through variable MSH3 protein stability. Since evidence supports that somatic CAG instability is a modifier and predictor of disease, our data are consistent with the hypothesis that variable levels of CAG instability associated with polymorphisms of DNA repair genes may have prognostic implications for various repeat-associated diseases

Homogenized stiffness matrices for mineralized collagen fibrils and lamellar bone using unit cell finite element models

Mineralized collagen fibrils have been usually analyzed like a two phase composite material where crystals are considered as platelets that constitute the reinforcement phase. Different models have been used to describe the elastic behavior of the material. In this work, it is shown that, when Halpin-Tsai equations are applied to estimate elastic constants from typical constituent properties, not all crystal dimensions yield a model that satisfy thermodynamic restrictions. We provide the ranges of platelet dimensions that lead to positive definite stiffness matrices. On the other hand, a finite element model of a mineralized collagen fibril unit cell under periodic boundary conditions is analyzed. By applying six canonical load cases, homogenized stiffness matrices are numerically calculated. Results show a monoclinic behavior of the mineralized collagen fibril. In addition, a 5-layer lamellar structure is also considered where crystals rotate in adjacent layers of a lamella. The stiffness matrix of each layer is calculated applying Lekhnitskii transformations and a new finite lement model under periodic boundary conditions is analyzed to calculate the homogenized 3D anisotropic stiffness matrix of a unit cell of lamellar bone. Results are compared with the rule-of-mixtures showing in general good agreement.The authors acknowledge the Ministerio de Economia y Competitividad the financial support given through the project DPI2010-20990 and the Generalitat Valenciana through the Programme Prometeo 2012/023. The authors thank Ms. Carla Gonzalez Carrillo by her help in the development of some of the numerical models.Vercher Martínez, A.; Giner Maravilla, E.; Arango Villegas, C.; Tarancón Caro, JE.; Fuenmayor Fernández, FJ. (2014). Homogenized stiffness matrices for mineralized collagen fibrils and lamellar bone using unit cell finite element models. 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MMTV-Wnt1 and -ΔN89β-Catenin Induce Canonical Signaling in Distinct Progenitors and Differentially Activate Hedgehog Signaling within Mammary Tumors

Canonical Wnt/β-catenin signaling regulates stem/progenitor cells and, when perturbed, induces many human cancers. A significant proportion of human breast cancer is associated with loss of secreted Wnt antagonists and mice expressing MMTV-Wnt1 and MMTV-ΔN89β-catenin develop mammary adenocarcinomas. Many studies have assumed these mouse models of breast cancer to be equivalent. Here we show that MMTV-Wnt1 and MMTV-ΔN89β-catenin transgenes induce tumors with different phenotypes. Using axin2/conductin reporter genes we show that MMTV-Wnt1 and MMTV-ΔN89β-catenin activate canonical Wnt signaling within distinct cell-types. ΔN89β-catenin activated signaling within a luminal subpopulation scattered along ducts that exhibited a K18+ER−PR−CD24highCD49flow profile and progenitor properties. In contrast, MMTV-Wnt1 induced canonical signaling in K14+ basal cells with CD24/CD49f profiles characteristic of two distinct stem/progenitor cell-types. MMTV-Wnt1 produced additional profound effects on multiple cell-types that correlated with focal activation of the Hedgehog pathway. We document that large melanocytic nevi are a hitherto unreported hallmark of early hyperplastic Wnt1 glands. These nevi formed along the primary mammary ducts and were associated with Hedgehog pathway activity within a subset of melanocytes and surrounding stroma. Hh pathway activity also occurred within tumor-associated stromal and K14+/p63+ subpopulations in a manner correlated with Wnt1 tumor onset. These data show MMTV-Wnt1 and MMTV-ΔN89β-catenin induce canonical signaling in distinct progenitors and that Hedgehog pathway activation is linked to melanocytic nevi and mammary tumor onset arising from excess Wnt1 ligand. They further suggest that Hedgehog pathway activation maybe a critical component and useful indicator of breast tumors arising from unopposed Wnt1 ligand

New Suggestions for the Mechanical Control of Bone Remodeling

Bone is constantly renewed over our lifetime through the process of bone (re)modeling. This process is important for bone to allow it to adapt to its mechanical environment and to repair damage from everyday life. Adaptation is thought to occur through the mechanosensitive response controlling the bone-forming and -resorbing cells. This report shows a way to extract quantitative information about the way remodeling is controlled using computer simulations. Bone resorption and deposition are described as two separate stochastic processes, during which a discrete bone packet is removed or deposited from the bone surface. The responses of the bone-forming and -resorbing cells to local mechanical stimuli are described by phenomenological remodeling rules. Our strategy was to test different remodeling rules and to evaluate the time evolution of the trabecular architecture in comparison to what is known from μ-CT measurements of real bone. In particular, we tested the reaction of virtual bone to standard therapeutic strategies for the prevention of bone deterioration, i.e., physical activity and medications to reduce bone resorption. Insensitivity of the bone volume fraction to reductions in bone resorption was observed in the simulations only for a remodeling rule including an activation barrier for the mechanical stimulus above which bone deposition is switched on. This is in disagreement with the commonly used rules having a so-called lazy zone