34 research outputs found

    Post-weld heat treatment stress relaxation in Zircaloy 4 plasma welds

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    We have studied the effect of a post-weld heat treatment on plasma arc welds on Zircaloy 4 plates. The samples consist of two 100 mm long, 50 mm wide, and 6.25 mm thick plates, welded along the rolling (longitudinal) direction. The heat-treatment consisted of a steady increase in temperature from room temperature to 450 degrees C over a period of 4.5 hours; followed by cooling with an equivalent cooling rate. Residual strains and stresses along the longitudinal, transverse and normal directions on an as-welded and a heat-treated specimen were measured by neutron diffraction on the ENGIN-X beamline at the Isis Facility, Rutherford Laboratory, UK. Peak tensile stresses of (105 +/- 25) MPa were found in the as-welded specimen, which were reduced to (70 20) MPa after the heat-treatment. Thermal compressive stresses of (-80 +/- 20) MPa were found along the normal direction, which were not affected by the heat treatment. The use of a full-pattern Rietveld refinement for the determination of bulk strains in Zircaloy specimens is also discussed

    Interferon induction in rabbits after intraduodenal administration of a phosphorylated glucomannan-protein fraction of the cell wall of Candida albicans

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    The aim of this work was to demonstrate whether a glucomannan protein fraction (GMP) of Candida albicans cell wall could induce interferon after intraduodenal administration in normal rabbits and rabbits immunized against C. albicans. For this purpose we collected simultaneously plasma and abdominal lymph for 10 h after the administration of the inducer. We observed a peak of antiviral activity in the lymph 4 h after intraduodenal administration of 20 mg GMP dissolved in saline to 6 normal rabbits. Immunized rabbits (anti-GMP titres greater than 1024) responded earlier (peak after 2 h) and more intensely; analysis of the values of the areas under the curve indicated that the IFN response in the lymph of immunized rabbits was significantly higher (P less than 0.0025) than in normal rabbits. Antiviral activity was absent in plasma in all cases. Preliminary characterization of the IFN activity has shown it to be trypsin-sensitive, acid and heat stable, and species-specific

    THE SECRETION OF ASPARTYL PROTEINASE, A VIRULENCE ENZYME, BY ISOLATES OF CANDIDA-ALBICANS FROM THE ORAL CAVITY OF HIV-INFECTED SUBJECTS

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    Prevalence, serotype and in vitro secretion of aspartyl proteinase, a virulence enzyme, were studied in Candida isolates from the oral cavity of 337 HIV-infected subjects. Controls were 95 age-sex-matched HIV- (seronegative) subjects, belonging to either HIV-risk categories (47) or to the normal, general population (48). Fungi were isolated from 155 HIV+ subjects. C. albicans was the most prevalent species (85.8% of all isolates). 94.6% of C. albicans isolates were serotype A and all were agglutinated by a monoclonal antibody (AF1) directed against a major mannoprotein immunogen of the candidal cell wall, confirming previous results with C. albicans isolates from non-immunodeficient subjects. With regard to the stage of HIV infection, there were no statistically significant differences in the incidence of oral Candida carriage between asymptomatic (stage II) HIV+ and HIV- subjects, and between stage II and lymphadenopathic (stage III) individuals. Also, the low (3.8%) incidence of oral candidiasis in the subjects of the latter stage was insignificant with respect to stage II subjects. However, the incidence of C. albicans in stage IV (AIDS) subjects (46.8%) was significantly higher than in all other subjects, and in almost all cases, fungal isolation was accompanied by oral thrush and lower CD4+ lymphocyte counts (less than 400 x 10(6)/L). All isolates of C. albicans were proteolytic in vitro, as assessed by scoring the proteinase activity on BSA agar and monitoring the secreted proteinase antigen by a highly sensitive (1 ng) and specific immunoenzymatic assa

    Post-weld heat treatment stress relaxation in Zircaloy 4 plasma welds

    No full text
    We have studied the effect of a post-weld heat treatment on plasma arc welds on Zircaloy 4 plates. The samples consist of two 100 mm long, 50 mm wide, and 6.25 mm thick plates, welded along the rolling (longitudinal) direction. The heat-treatment consisted of a steady increase in temperature from room temperature to 450 degrees C over a period of 4.5 hours; followed by cooling with an equivalent cooling rate. Residual strains and stresses along the longitudinal, transverse and normal directions on an as-welded and a heat-treated specimen were measured by neutron diffraction on the ENGIN-X beamline at the Isis Facility, Rutherford Laboratory, UK. Peak tensile stresses of (105 +/- 25) MPa were found in the as-welded specimen, which were reduced to (70 20) MPa after the heat-treatment. Thermal compressive stresses of (-80 +/- 20) MPa were found along the normal direction, which were not affected by the heat treatment. The use of a full-pattern Rietveld refinement for the determination of bulk strains in Zircaloy specimens is also discussed

    N-acetylcysteine inhibits the induction of an antigen-specific antibody response down-regulating CD40 and CD27 co-stimulatory molecules

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    We investigated the effect of N-acetylcysteine (NAC) on normal human B cell functions. We found that NAC significantly inhibited both the induction of the specific antibody response to the T-dependent antigen Candida albicans and T-dependent pokeweed mitogen (PWM)-induced polyclonal Ig production. NAC did not induce either cell death due to a non-specific toxicity or apoptosis. The NAC-induced inhibitory effect might be a functional consequence of: (i) a down-regulation of the expression on the B cell surface of CD40 and CD27 co-stimulatory molecules and (ii) a down-regulation of interleukin (IL-4) production. In contrast, NAC up-regulated interferon-γ (IFN-γ) production. NAC did not induce any effect on the T cell-independent B cell polyclonal activation system. These results indicate that NAC down-regulates T dependent B cell activation and leads to T helper cell type 1 (Th1) polarization
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