21 research outputs found
Analyses of the phébus FPT3 experiment using the severe accident codes ATHLET-CD, ICARE/CATHARE, and MELCOR
The aim of the Phébus Fission Product (FP) experimental program is to study the degradation phenomena and the behavior of the FPs released in the reactor coolant system and the containment building. The program consists of four in-pile bundle tests (FPTO, FPT1, FPT2, and FPT3), performed under different conditions concerning the thermal hydraulics and the environment of fuel rods, in particular, the amount of steam (strongly or weakly oxidizing atmosphere). The last test of this program, FPT3, was performed in November 2004 in Cadarache. During the FPT3 experiment, for the first time, boron carbide (B4C) was used as the absorber material instead of Ag-In-Cd, which was used in all the previous tests. Boron carbide is used in western-type pressurized water reactors, the EPR, boiling water reactors, and the WER; consequently, assessing the effects Of B4C on the main degradation phenomena and on gas release, as well as its impact on FP behavior is very important. This paper describes results from the Phébus FPT3 experiment, summarizes the test code modeling used in the different code applications, and reports the code results comparing some important experimental parameters, in particular regarding B4C control rod behavior. The severe accident codes used in these studies are Analysis of Thermal-Hydraulics of LEaks and Transients with Core Degradation (ATHLETCD), ICARE/CATHARE, and MELCOR. The first part is an overview of the experimental results (boundary conditions, temperature evolutions, hydrogen and carbon compound releases coming from the oxidation of the Zircaloy claddings and the B4C absorber, and bundle degradation). The second part summarizes the code modeling used in the different code applications, in particular, those regarding absorber rod degradation and the oxidation process. The third part summarizes the code results comparing some important experimental parameters [thermal behavior, gas releases (H 2, CO, CO2), and bundle degradation]. The conclusion focuses on the capabilities of the severe accident codes to simulate control rod behavior in a fuel rod assembly during the course of a severe accident transient
Identification of cardiac myosin peptides capable of inducing autoimmune myocarditis in BALB/c mice.
Immunization with cardiac myosin induces T cell-mediated myocarditis in genetically predisposed mice and serves as a model for autoimmune heart disease. This study was undertaken to identify pathogenic epitopes on the myosin molecule. Our approach was based on the comparison of the pathogenicity between cardiac (alpha-)myosin and soleus muscle (beta-)myosin. We show that alpha-myosin is the immunodominant isoform and induces myocarditis at high severity and prevalence whereas beta-myosin induces little disease. Therefore the immunodominant epitopes of alpha-myosin must reside in regions of different amino acid sequence between alpha- and beta-myosin isoforms. Cardiac myosin peptides corresponding to these regions of difference were synthesized and tested for their ability to induce inflammatory heart disease. Three pathogenic peptides were identified. One peptide that is located in the head portion of the molecule induced severe myocarditis, whereas two others that reside in the rod portion possessed only minor pathogenicity. The identification of pathogenic epitopes on the cardiac myosin molecule will allow detailed studies on the recognition of this antigen by the immune system and might be used to downmodulate ongoing heart disease
Identification of cardiac myosin peptides capable of inducing autoimmune myocarditis in BALB/c mice.
Child and Environmental Predictors for Pre-Kindergarten Language and Emergent Literary Skills
B4C oxidation modelling in severe accident codes: Applications to PHEBUS and QUENCH experiments
Boron carbide is used in many nuclear power plants like BWR, VVER, some PWR, and EPR as a neutron absorber material. Consequently, it is important to assess its role in the core degradation phenomena during a severe accident (SA), as well as that of the carbon gas released from its degradation on the fission products behaviour. This paper describes the progresses achieved in the frame of the Network of Excellence SARNET concerning the B4C control rod degradation modelling in Severe Accident codes, such as ATHLET-CD, ICARE2, ASTEC MELCOR and MAAP. These new developments complete improvements made during the European Union 5th Framework COLOSS project. Starting from basic modelling derived from available tests reported in the literature, large improvements of the kinetic correlation for B4C oxidation were obtained from analytical experiments performed at FzK (Germany) and IRSN (France), mostly in the temperature range above 1400 K. The new modelling was considered in the analysis of experiments involving a B4C control rod in small fuel rod assemblies, such as Phebus FPT3 in-pile experiment, as well as out of pile experiments Quench 07 and 09, aimed at studying the course of severe accidents. Regarding the hydrogen generation, the results given by different code simulations are consistent with the experimental values. Concerning the control rod degradation, SA codes such as ICARE2 and ATHLET-CD, using suitable modelling of B4C oxidation, predicted rather well the total carbon release. The results of the MELCOR code, involving initially a B4C oxidation model designed to be used for BWR control blades, have been largely improved in the most recently released version, with a model extended for PWR B4C control rods. Codes still have some difficulties to reproduce the final degradation of fuel bundles involving B4C rods. Spreading of molten materials from the control rods onto fuel rods of the bundle is suspected, suggesting that the main effect of the B4C control rod materials on the bundle behaviour during degradation is connected with B4C-Stainless Steel (SS) eutectics formation and B4C-SS-Zry liquid mixture relocation. These phenomena are not accounted for in the SA codes. The need for further code developments of the early phase of core degradation is recognized, involving the absorber rod material behaviour. The BECARRE experiments, on-going in the framework of the International Source Term Program, are designed to provide in-depth understanding of these phenomena and help improving their modelling. © 2009 Elsevier Ltd. All rights reserved
Predicting Expressive Language From Early Vocalizations in Young Children With Autism Spectrum Disorder: Which Vocal Measure Is Best?
Advantage of Recombinant Technology for the Identification of Cardiac Myosin Epitope of Severe Autoimmune Myocarditis in Lewis Rats.
Caspase-9 regulates apoptosis/proliferation balance during metamorphic brain remodeling in Xenopus
During anuran metamorphosis, the tadpole brain is transformed producing the sensorial and motor systems required for the frog's predatory lifestyle. Nervous system remodeling simultaneously implicates apoptosis, cell division, and differentiation. The molecular mechanisms underlying this remodeling have yet to be characterized. Starting from the observation that active caspase-9 and the Bcl-XL homologue, XR11 are highly expressed in tadpole brain during metamorphosis, we determined their implication in regulating the balance of apoptosis and proliferation in the developing tadpole brain. In situ hybridization showed caspase-9 mRNA to be expressed mainly in the ventricular area, a site of neuroblast proliferation. To test the functional role of caspase-9 in equilibrating neuroblast production and elimination, we overexpressed a dominant-negative caspase-9 protein, DN9, in the tadpole brain using somatic gene transfer and germinal transgenesis. In both cases, abrogating caspase-9 activity significantly decreased brain apoptosis and increased numbers of actively proliferating cells in the ventricular zone. Moreover, overexpression of XR11 with or without DN9 was also effective in decreasing apoptosis and increasing cell division in the tadpole brain. We conclude that XR11 and caspase-9, two key members of the mitochondrial death pathway, are implicated in controlling the proliferative status of neuroblasts in the metamorphosing Xenopus brain. Modification of their expression during the critical period of metamorphosis alters the outcome of metamorphic neurogenesis, resulting in a modified brain phenotype in juvenile Xenopus