Magnetic Diagram of the High-Pressure Stabilized Multiferroic Perovskites of the BiFe1-yScyO3 Series

Magnetic properties of the high-pressure stabilized perovskite BiFe1-yScyO3 phases (0.1 ≤ y ≤ 0.9) have been studied by means of magnetization measurements and neutron diffraction. The metastable perovskites of this series undergo irreversible polymorphic transformations upon annealing, the phenomenon referred to as conversion polymorphism. It has been found that the solid solutions with y ≥ 0.70 exhibit no long-range magnetic ordering regardless of their polymorph modification, while those with y ≤ 0.60 are all antiferromagnets. Depending on the scandium content, temperature and structural distortions, three types of the antiferromagnetic orderings, involving collinear, canted and cycloidal spin arrangements, have been revealed in the phases obtained via conversion polymorphism and the corresponding magnetic phase diagram has been suggested

3D stochastic bicontinuous microstructures: Generation, topology and elasticity

Motivated by recent experimental investigations of the mechanical behavior of nanoporous metal we explore an efficient and robust method for generating 3D representative volume elements (RVEs) with strikingly similar behavior. Our approach adopts Cahn's method of generating a Gaussian random field by taking a superposition of standing sinusoidal waves of fixed wavelength but random in direction and phase. In its theory part, our study describes closed-form expressions for how the solid volume fraction affects the binarization level, mean structure size, specific surface area, averages of mean and Gaussian curvature, and the scaled topological genus. Based on numerical studies we report on criteria for achieving representative realizations of the structure by proper choice of the number of waves and element size. We also show that periodic structures are readily created. We analyze the mechanical properties considering linear and infinitesimal elasticity and evaluate the residual anisotropy (which can be made small) and the effective values of the Young's modulus and Poisson's ratio. The numerical results are in excellent agreement with experimental findings for the variation of stiffness with solid fraction of nanoporous gold made by dealloying. We propose scaling relations that achieve naturally a perfect agreement with the numerical and experimental data. The scaling relation for the stiffness accounts for a percolation-to-cluster transition in the random field microstructure at a finite solid fraction. We propose that this transition is the origin of the previously reported anomalous compliance of nanoporous gold

Internal delensing of cosmic microwave background polarization B-Modes with the POLARBEAR experiment

International audienceUsing only cosmic microwave background polarization data from the polarbear experiment, we measure B-mode polarization delensing on subdegree scales at more than 5σ significance. We achieve a 14% B-mode power variance reduction, the highest to date for internal delensing, and improve this result to 22% by applying for the first time an iterative maximum a posteriori delensing method. Our analysis demonstrates the capability of internal delensing as a means of improving constraints on inflationary models, paving the way for the optimal analysis of next-generation primordial B-mode experiments

Amelogenesis Imperfecta caused by N-Terminal Enamelin Point Mutations in Mice and Men is driven by Endoplasmic Reticulum Stress

‘Amelogenesis imperfecta’ (AI) describes a group of inherited diseases of dental enamel that have major clinical impact. Here, we identify the aetiology driving AI in mice carrying a p.S55I mutation in enamelin; one of the most commonly mutated proteins underlying AI in humans. Our data indicate that the mutation inhibits the ameloblast secretory pathway leading to ER stress and an activated unfolded protein response (UPR). Initially, with the support of the UPR acting in pro-survival mode, Enam(p.S55I) heterozygous mice secreted structurally normal enamel. However, enamel secreted thereafter was structurally abnormal; presumably due to the UPR modulating ameloblast behaviour and function in an attempt to relieve ER stress. Homozygous mutant mice failed to produce enamel. We also identified a novel heterozygous ENAM(p.L31R) mutation causing AI in humans. We hypothesize that ER stress is the aetiological factor in this case of human AI as it shared the characteristic phenotype described above for the Enam(p.S55I) mouse. We previously demonstrated that AI in mice carrying the Amelx(p.Y64H) mutation is a proteinopathy. The current data indicate that AI in Enam(p.S55I) mice is also a proteinopathy, and based on comparative phenotypic analysis, we suggest that human AI resulting from the ENAM(p.L31R) mutation is another proteinopathic disease. Identifying a common aetiology for AI resulting from mutations in two different genes opens the way for developing pharmaceutical interventions designed to relieve ER stress or modulate the UPR during enamel development to ameliorate the clinical phenotype

Human and Canine Echinococcosis Infection in Informal, Unlicensed Abattoirs in Lima, Peru

Echinococcus granulosus infections are a major public health problem in livestock-raising regions around the world. The life cycle of this tapeworm is sustained between dogs (definitive host, canine echinococcosis), and herbivores (intermediary host, cystic hydatid disease). Humans may also develop cystic hydatid disease. Echinococcosis is endemic in rural areas of Peru; nevertheless, its presence or the extension of the problem in urban areas is basically unknown. Migration into Lima, an 8-million habitant's metropolis, creates peripheral areas where animals brought from endemic areas are slaughtered without veterinary supervision. We identified eight informal, unlicensed abattoirs in a peripheral district of Lima and performed a cross-sectional study in to assess the prevalence of canine echinococcosis, evaluated by coproELISA followed by PCR evaluation and arecoline purge. Eight of 22 dogs (36%) were positive to coproELISA, and four (18%) were confirmed to be infected with E. granulosus tapeworms either by PCR or direct observation (purge). Later evaluation of the human population living in these abattoirs using abdominal ultrasound, chest X-rays and serology, found 3 out of 32 (9.3%) subjects with echinococcal cysts in the liver (two viable, one calcified), one of whom had also lung involvement and a strongly positive antibody response. Autochthonous transmission of E. granulosus is present in Lima. Informal, unlicensed abattoirs may be sources of infection to neighbouring people in this urban environment

Tissue Microenvironments Define and Get Reinforced by Macrophage Phenotypes in Homeostasis or during Inflammation, Repair and Fibrosis

Current macrophage phenotype classifications are based on distinct in vitro culture conditions that do not adequately mirror complex tissue environments. In vivo monocyte progenitors populate all tissues for immune surveillance which supports the maintenance of homeostasis as well as regaining homeostasis after injury. Here we propose to classify macrophage phenotypes according to prototypical tissue environments, e.g. as they occur during homeostasis as well as during the different phases of (dermal) wound healing. In tissue necrosis and/or infection, damage- and/or pathogen-associated molecular patterns induce proinflammatory macrophages by Toll-like receptors or inflammasomes. Such classically activated macrophages contribute to further tissue inflammation and damage. Apoptotic cells and antiinflammatory cytokines dominate in postinflammatory tissues which induce macrophages to produce more antiinflammatory mediators. Similarly, tumor-associated macrophages also confer immunosuppression in tumor stroma. Insufficient parenchymal healing despite abundant growth factors pushes macrophages to gain a profibrotic phenotype and promote fibrocyte recruitment which both enforce tissue scarring. Ischemic scars are largely devoid of cytokines and growth factors so that fibrolytic macrophages that predominantly secrete proteases digest the excess extracellular matrix. Together, macrophages stabilize their surrounding tissue microenvironments by adapting different phenotypes as feed-forward mechanisms to maintain tissue homeostasis or regain it following injury. Furthermore, macrophage heterogeneity in healthy or injured tissues mirrors spatial and temporal differences in microenvironments during the various stages of tissue injury and repair. Copyright (C) 2012 S. Karger AG, Base