Synthesis of geopolymer emulsions

The understanding of emulsion geopolymer synthesis is a major issue for several industrial applications such as the formation of hierarchically porous material for filtration, lightweight materials for civil engineering or even the conditioning of radioactive mineral oil. Emulsion stability (irreversible coarsening, creaming…) are mainly controlled by the interfacial properties (surface tension and nature of the surfactant) and the viscosity ratio between the dispersed (hd) and the continuous phase (hc). The aim of this paper is thus to study model emulsions (composed of hexadecane (C16) as dispersed phase and metakaolin based geopolymer as continuous phase) with the highest volume fraction of C16 as possible. Surfactant was added to the mixture to stabilize the C16 droplets and geopolymer emulsion was synthesis under shear stirring. The influence of the viscosity of the geopolymer paste controlled by the water content was studied and results show that emulsions are unstable for a viscosity ratio hd/hc lower than 0.01. Up to 70% in volume of C16 was incorporated within the geopolymer and hierarchical porous network was thus obtained. Indeed after removal the C16 phase, the porous network was characterized and a specific surface area of 90 m²/g, a mean mesopore diameter of 19 nm, a macropore size distribution ranged between 10-200 µm (fig 1.) and a compression strength of around 0.5 MPa were obtained. Please click Additional Files below to see the full abstract

HARD PHOTON PRODUCTION IN NUCLEUS-NUCLEUS COLLISIONS AT 30 MeV/u AND 44 MeV/u

Doubly differential cross-sections for Bremsstrahlung production have been measured in the reactions 40Ar + 197Au at 30 MeV/u and 86Kr +12C, AgNat and 197Au at 44 MeV/u. A qualitative analysis of the characteristics of the γ-ray emission suggests strongly that the initial proton-neutron collisions are the main source of nuclear Bremsstrahlung

Haploinsufficiency for Translation Elongation Factor eEF1A2 in Aged Mouse Muscle and Neurons Is Compatible with Normal Function

Translation elongation factor isoform eEF1A2 is expressed in muscle and neurons. Deletion of eEF1A2 in mice gives rise to the neurodegenerative phenotype "wasted" (wst). Mice homozygous for the wasted mutation die of muscle wasting and neurodegeneration at four weeks post-natal. Although the mutation is said to be recessive, aged heterozygous mice have never been examined in detail; a number of other mouse models of motor neuron degeneration have recently been shown to have similar, albeit less severe, phenotypic abnormalities in the heterozygous state. We therefore examined the effects of ageing on a cohort of heterozygous +/wst mice and control mice, in order to establish whether a presumed 50% reduction in eEF1A2 expression was compatible with normal function. We evaluated the grip strength assay as a way of distinguishing between wasted and wild-type mice at 3-4 weeks, and then performed the same assay in older +/wst and wild-type mice. We also used rotarod performance and immunohistochemistry of spinal cord sections to evaluate the phenotype of aged heterozygous mice. Heterozygous mutant mice showed no deficit in neuromuscular function or signs of spinal cord pathology, in spite of the low levels of eEF1A2

Optimised and Rapid Pre-clinical Screening in the SOD1G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis (ALS)

The human SOD1G93A transgenic mouse has been used extensively since its development in 1994 as a model for amyotrophic lateral sclerosis (ALS). In that time, a great many insights into the toxicity of mutant SOD1 have been gained using this and other mutant SOD transgenic mouse models. They all demonstrate a selective toxicity towards motor neurons and in some cases features of the pathology seen in the human disease. These models have two major drawbacks. Firstly the generation of robust preclinical data in these models has been highlighted as an area for concern. Secondly, the amount of time required for a single preclinical experiment in these models (3–4 months) is a hurdle to the development of new therapies. We have developed an inbred C57BL/6 mouse line from the original mixed background (SJLxC57BL/6) SOD1G93A transgenic line and show here that the disease course is remarkably consistent and much less prone to background noise, enabling reduced numbers of mice for testing of therapeutics. Secondly we have identified very early readouts showing a large decline in motor function compared to normal mice. This loss of motor function has allowed us to develop an early, sensitive and rapid screening protocol for the initial phases of denervation of muscle fibers, observed in this model. We describe multiple, quantitative readouts of motor function that can be used to interrogate this early mechanism. Such an approach will increase throughput for reduced costs, whilst reducing the severity of the experimental procedures involved

How accurate appraisal of behavioral costs and benefits guides adaptive pain coping

Coping with pain is a complex phenomenon encompassing a variety of behavioral responses and a large network of underlying neural circuits. Whether pain coping is adaptive or maladaptive depends on the type of pain (e.g., escapable or inescapable), personal factors (e.g., individual experiences with coping strategies in the past), and situational circumstances. Keeping these factors in mind, costs and benefits of different strategies have to be appraised and will guide behavioral decisions in the face of pain. In this review we present pain coping as an unconscious decision-making process during which accurately evaluated costs and benefits lead to adaptive pain coping behavior. We emphasize the importance of passive coping as an adaptive strategy when dealing with ongoing pain and thus go beyond the common view of passivity as a default state of helplessness. In combination with passive pain coping, we highlight the role of the reward system in reestablishing affective homeostasis and discuss existing evidence on a behavioral and neural level. We further present neural circuits involved in the decision-making process of pain coping when circumstances are ambiguous and, therefore, costs and benefits are difficult to anticipate. Finally, we address the wider implications of this topic by discussing its relevance for chronic pain patients

Parkin Deficiency Delays Motor Decline and Disease Manifestation in a Mouse Model of Synucleinopathy

In synucleinopathies, including Parkinson's disease, partially ubiquitylated α-synuclein species phosphorylated on serine 129 (PS129-α-synuclein) accumulate abnormally. Parkin, an ubiquitin-protein ligase that is dysfunctional in autosomal recessive parkinsonism, protects against α-synuclein-mediated toxicity in various models

Early Detection of Motor Dysfunction in the SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis (ALS) Using Home Cage Running Wheels

The SOD1G93A mouse has been used since 1994 for preclinical testing in amyotrophic lateral sclerosis (ALS). Despite recent genetic advances in our understanding of ALS, transgenic mice expressing mutant SOD1 remain the best available, and most widely used, vertebrate model of the disease. We previously described an optimised and rapid approach for preclinical studies in the SOD1G93A mouse. Here we describe improvements to this approach using home cage running wheels to obtain daily measurements of motor function, with minimal intervention. We show that home cage running wheels detect reductions in motor function at a similar time to the rotarod test, and that the data obtained are less variable allowing the use of smaller groups of animals to obtain satisfactory results. This approach refines use of the SOD1G93A model, and reduces the number of animals undergoing procedures of substantial severity, two central principles of the 3Rs (replacement, reduction and refinement of animal use in research). The small group sizes and rapid timescales enable affordable large-scale therapeutic pre-screening in the SOD1G93A mouse, as well as rapid validation of published positive effects in a second laboratory, one of the major stumbling blocks in ALS preclinical therapy development

La lateralisation cerebrale et les relations cerveau-immunite. Approches lesionnelle et comportementale

SIGLEINIST T 76448 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc