161 research outputs found

    Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review

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    Rabbit haemorrhagic disease virus (RHDV) is a calicivirus of the genus Lagovirus that causes rabbit haemorrhagic disease (RHD) in adult European rabbits (Oryctolagus cuniculus). First described in China in 1984, the virus rapidly spread worldwide and is nowadays considered as endemic in several countries. In Australia and New Zealand where rabbits are pests, RHDV was purposely introduced for rabbit biocontrol. Factors that may have precipitated RHD emergence remain unclear, but non-pathogenic strains seem to pre-date the appearance of the pathogenic strains suggesting a key role for the comprehension of the virus origins. All pathogenic strains are classified within one single serotype, but two subtypes are recognised, RHDV and RHDVa. RHD causes high mortality in both domestic and wild adult animals, with individuals succumbing between 48-72 h post-infection. No other species has been reported to be fatally susceptible to RHD. The disease is characterised by acute necrotising hepatitis, but haemorrhages may also be found in other organs, in particular the lungs, heart, and kidneys due to disseminated intravascular coagulation. Resistance to the disease might be explained in part by genetically determined absence or weak expression of attachment factors, but humoral immunity is also important. Disease control in rabbitries relies mainly on vaccination and biosecurity measures. Such measures are difficult to be implemented in wild populations. More recent research has indicated that RHDV might be used as a molecular tool for therapeutic applications. Although the study of RHDV and RHD has been hampered by the lack of an appropriate cell culture system for the virus, several aspects of the replication, epizootology, epidemiology and evolution have been disclosed. This review provides a broad coverage and description of the current knowledge on the disease and the virus

    Optimisation en fluage et fatigue-fluage d'aciers martensitiques à 9%Cr par traitement thermo-mécanique

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    National audienceL'utilisation des aciers martensitiques à 9-12%Cr est envisagée dans les futurs réacteurs nucléaires de génération IV. En service, ils seront soumis à du fluage à haute température ainsi qu'à des sollicitations de fatigue-fluage. Or de récents travaux sur l'acier commercial P91 ont montré que des sollicitations cycliques de fatigue combinées au fluage conduisent à un adoucissement rapide du matériau, lié à un grossissement de sa microstructure. Des traitements thermomécaniques ont donc été réalisés dans le but d'affiner et de stabiliser la microstructure de cet acier. Le traitement thermomécanique présenté ici conduit à une martensite plus fine, émaillée de nombreux et fins précipités de type MX. Le P91 optimisé montre un net gain en termes de propriétés mécaniques par rapport à l'acier P91 à réception : sa dureté est plus élevée de 100 Hv, sa limite d'élasticité conventionnelle est supérieure de 430 MPa à 20°C et de 220 MPa à 550°C, sa durée de vie en fluage à 650°C est 20 fois supérieure et son adoucissement à 650°C est légèrement moins rapide

    Influence de traitements thermo-mécaniques sur les performances en fluage et en fatigue d'aciers martensitiques à 9% Cr

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    National audienceLe développement des réacteurs nucléaires de génération IV et des réacteurs à fusion nucléaire requiert l'utilisation de matériaux possédant de bonnes propriétés mécaniques au-delà de 550 °C. En service, ces matériaux seront soumis à du fluage à haute température couplé à des sollicitations cycliques de fatigue. Les aciers martensitiques à 9-12 % Cr sont pressentis pour ces applications; cependant leur comportement en fatigue et fatigue-fluage à haute température est encore insuffisant : la microstructure martensitique grossit et l'acier s'adoucit rapidement. Afin de stabiliser sa microstructure, l'acier commercial P91 a subi un traitement thermo-mécanique incluant du laminage à 600 °C suivi d'un revenu d'une heure à 700 °C. Les observations microstructurales confirment que le traitement thermo-mécanique a conduit à une martensite plus fine, émaillée de nombreux et fins précipités de type MX. Les divers essais mécaniques réalisés prouvent que ces changements ont un effet positif sur les propriétés de l'acier : sa dureté est plus élevée de 100 Hv par rapport à l'acier P91 à réception, et sa limite d'élasticité conventionnelle est supérieure de 430 MPa à 20 °C et de 220 MPa à 550 °C. La durée de vie du P91 optimisé en fluage à 650 °C sous 120 MPa est plus de 14 fois supérieure à celle du P91; et l'essai de fatigue à 650 °C et 0,7 % de déformation totale montre un adoucissement légèrement moins rapide

    Relationship between microstructure and mechanical behaviour of thermomechanically optimised 9-12% Cr steels

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    International audienceThe development of Generation IV fission nuclear reactors and fusion nuclear reactorsrequires materials able to resist to high temperature (650°C) creep, but also to creep-fatigue.Martensitic 9-12%Cr steels are candidate materials for these applications.Recent studies on commercial P91 steel showed that cyclic loadings coupled to high temperature creep loadings lead to a strong softening effect, which affects the steelmechanical strength. This effect is due to the decrease of the dislocations density and thecoarsening of martensitic microstructure.Thermomechanical treatments, including warm-rolling in austenitic phase and tempering,have been applied to P91 in order to refine its microstructure and to improve its precipitationstate. The temperature of rolling was set at 600°C, and those of annealing at 650°C and700°C, thanks to MatCalc calculations.Microstructural observations proved that the warm-rolling and the following tempering lead toa finer martensite pinned with numerous small precipitates. In terms of mechanical propertiesimprovement, the hardness of thermomechanically treated P91 is higher than that of asreceivedP91. The yield strengths are higher than that of P91 (around 400 MPa at 20°C; andmore than 200 MPa at 550°C). Preliminary creep resu lts show that these treatments improvethe creep lifetime by at least a factor 8

    Carcinoma-associated fucosylated antigens are markers of the epithelial state and can contribute to cell adhesion through CLEC17A (Prolectin)

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    International audienceTerminal fucosylated motifs of glycoproteins and glycolipid chains are often altered in cancer cells. We investigated the link between fucosylation changes and critical steps in cancer progression: epithelial-to-mesenchymal transition (EMT) and lymph node metastasis. Using mammary cell lines, we demonstrate that during EMT, expression of some fucosylated antigens (e.g.: Lewis Y) is decreased as a result of repression of the fucosyltransferase genes FUT1 and FUT3. Moreover, we identify the fucose-binding bacterial lectin BC2L-C-Nt as a specific probe for the epithelial state. Prolectin (CLEC17A), a human lectin found on lymph node B cells, shares ligand specificities with BC2L-C-Nt. It binds preferentially to epithelial rather than to mesenchymal cells, and microfluidic experiments showed that prolectin behaves as a cell adhesion molecule for epithelial cells. Comparison of paired primary tumors/ lymph node metastases revealed an increase of prolectin staining in metastasis and high FUT1 and FUT3 mRNA expression was associated with poor prognosis. Our data suggest that tumor cells invading the lymph nodes and expressing fucosylated motifs associated with the epithelial state could use prolectin as a colonization factor
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