58 research outputs found

    Code improvement and model validation for Asco-II Nuclear Power Plant model using a coupled 3D neutron kinetics/thermal-hydraulic code

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    This paper provides a Best Estimate validation calculation with a coupled thermal–hydraulic and 3D neutron kinetic model for Ascó-II Nuclear Power Plant. Common NRC codes have been used for its purpose. TRACE is the code used for the thermal–hydraulic system calculations; PARCS is the code used for the 3D neutron kinetics calculations. Cross section calculations were performed with the HELIOS lattice physics code, finally GenPMAXS was used to convert the cross section into the PARCS format. A simplified three dimensional 3D neutronics model of the Ascó II NPP is used as a core kinetics model. A 3D cylindrical thermal–hydraulic vessel plus 1D representation of the remainder of the full plant model is used as the thermal–hydraulic model. The transient selected to ensure the model validation is an actual 50% Loss of Load. This transient is characterized by space–time effects and was used to validate different thermal–hydraulic system models for the GET university group in the past. The scenario is also good to ensure the validation of a coupled 3D neutron kinetics code since it provides a transient situation between two stable regions at 100% and 50%. From the current code versions used, some source code modifications have been carried out in order to ensure the correct feedback between thermal–hydraulic and neutron kinetics code. In that sense, a dynamic control rod movement between TRACE and PARCS has been implemented. This is a complete control rod position feedback during transient scenarios. After all the work was performed, the important TH and NK time trend parameters were compared to the plant data and the comparison was reasonable with some discrepancy, thus the developed system models and the code modifications are robust enough to be used for future safety analysis. New coupled code capability has been tested and found as a required capability, when validating 3D NK–TH coupled calculations.Peer ReviewedPostprint (published version

    PVST, a tool to assess the power to volume scaling distortions associated to code simulations

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    System codes along with necessary nodalizations are valuable tools for thermal hydraulic safety analysis. In order to assess the safety of a particular power plant, in addition to the validation and veri cation of the code, the nodalization of the system needs to be quali ed. Since most existing experimental data come from tests performed on scaled-down facilities, any quali cation process must therefore address scale considerations. Along these lines, the Group of Thermal Hydraulic Studies at Technical University of Catalonia (GET) developed SCUP, a scaling-up methodology for qualifying full-scale nodalizations through a systematic procedure based on the extrapolation of post-test simulations of Integral Test Facilities (ITF) experiments. For that purpose, GET created thePostprint (author's final draft

    Kv-scaling in thermal hydraulics: Background, applications and forthcoming uses

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    Addressing the scaling issue refers to a rather complex process of demonstrating the applicability of activities devoted to predict the behaviour of actual nuclear power plants using the knowledge acquired in scaled-down test facilities. Such activities involve, among others, the evaluation of the capability of Best Estimate codes to scale-up processes from reduced scale test facilities to full scale Nuclear Power Plants (NPP) and the quantification of the effects of scale distortions. In this context, a scaled calculation is a system-code simulation in which, defined test conditions of an Integral Test Facility (ITF) are scaled-up to a NPP nodalization to reproduce the same scenario. The practical use of such kind of calculation is to permit a comparison of the behaviour of the plant and the ITF nodalizations under the same conditions. The comparison between the NPP -scaled results and those of the experiment post-test calculation will show unavoidable differences or distortions. Explaining such distortions is the key process in methods devoted to qualify plant nodalizations. The aim of this paper is to show the effectiveness of -scaled calculations and to outline the forthcoming use of hybrid nodalizations and scale-up nodalizations. The paper includes a thorough literature review of these type of approaches as well as the perspectives of future use of the scaling analysis. Such future uses include the feedback to experimentation. Despite the fact that the hybrid calculations presented here are related to existing ITFs and NPPs, feedback to experimentation intents to show the essentials of a future practice to be mainly implemented in modular ITFs.Peer ReviewedPostprint (published version

    Applying UPC scaling-up methodology to the LSTF-PKL counterpart test

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    In the framework of the nodalization qualification process and quality guarantee procedures and following the guidelines of Kv-scaled analysis and UMAE methodology, further development has been performed by UPC team resulting in a scaling-up methodology. Such methodology has been applied in this paper for analyzing discrepancies that appear between the simulations of two counterpart tests. It allows the analysis of scaling-down criterion used for the design of an ITF and also the investigation of the differences of configuration between an ITF and a particular NPP. For analyzing both, it applies two conceptsPostprint (published version

    Master’s degree in Nuclear Engineering UPC-ENDESA. A consolidated international program

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    The Master’s degree in Nuclear Engineering (MNE) UPC-ENDESA offers a unique and practical oriented training, with the aim to prepare competent engineers so that they can assume managerial positions within the Nuclear Industry. The program combines science, technology and management in the nuclear energy field, including the elements of the safety culture. MNE is embedded in EMINE, the European Master in Nuclear Energy (KIC InnoEnergy) and is completely taught in English. Its 90 credits (each credit implies 25 hours of student’s work) are divided into one year of subjects (60 credits), and one semester of internship plus final project (30 credits). MNE has a strong industrial implication: lecturers from companies, research institutes and the Spanish Regulatory Authority (cover about one half of the lectures; companies accept students in internships and organize technical visits. The participation of professionals external to the University in the definition and revision of the Program is one of MNE’s assets. A large portion of the contents of the MNE are organized in the form of Problem and Project Based Learning: real industrial problems are brought into the classroom to be solved by students, most of the time assisted by experts from the nuclear industry. MNE is in continuous evolution, seeking for a continuous improvement of the contents and learning methods. Starting the sixth edition, the master is firmly consolidated and the alumni value it positively.Postprint (published version

    Characterization of the molecular changes associated with the overexpression of a novel epithelial cadherin splice variant mRNA in a breast cancer model using proteomics and bioinformatics approaches: identification of changes in cell metabolism and an increased expression of lactate dehydrogenase B

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    Breast cancer (BC) is the most common female cancer and the leading cause of cancer death in women worldwide. Alterations in epithelial cadherin (E-cadherin) expression and functions are associated to BC, but the underlying molecular mechanisms have not been fully elucidated. We have previously reported a novel human E-cadherin splice variant (E-cadherin variant) mRNA. Stable transfectants in MCF-7 human BC cells (MCF7Ecadvar) depicted fibroblast-like cell morphology, E-cadherin wild-type downregulation, and other molecular changes characteristic of the epithelial-to-mesenchymal transition process, reduced cell-cell adhesion, and increased cell migration and invasion. In this study, a two-dimensional differential gel electrophoresis (2D-DIGE) combined with mass spectrometry (MS) protein identification and bioinformatics analyses were Results: By 2D-DIGE and MS analysis, 50 proteins were found differentially expressed (≥ Δ1.5) in MCF7Ecadvar compared to control cells. Validation of transcript expression was done in the ten most overexpressed and underexpressed proteins. Bioinformatics analyses revealed that 39 of the 50 proteins identified had been previously associated to BC. Moreover, metabolic processes were the most affected, and glycolysis the canonical pathway most altered. The lactate dehydrogenase B (LDHB) was the highest overexpressed protein, and transcript levels were higher in MCF7Ecadvar than in control cells. In agreement with these findings, MCF7Ecadvar conditioned media had lower glucose and higher lactate levels than control cells. MCF7Ecadvar cell treatment with 5 mM of the glycolytic inhibitor 2-deoxy-glucose led to decreased cell viability, and modulation of LDHB expression in MCF7Ecadvar cells with a specific small interfering RNA resulted in decreased cell proliferation. Finally, a positive association between expression levels of the E-cadherin variant and LDHB transcripts was demonstrated in 21 human breast tumor tissues, and breast tumor samples with higher Ki67 expression showed higher LDHB mRNA levels. Conclusions: Results from this investigation contributed to further characterize molecular changes associated to the novel E-cadherin splice variant expression in BC cells. They also revealed an association between expression of the novel variant and changes related to BC progression and aggressiveness, in particular those associated to cell metabolism. Keywords: Breast cancer, Epithelial cadherin, Alternative splicing, Epithelial to mesenchymal transition, Proteomic analysis, 2D-DIGE, Mass spectrometry, Glycolysis, Lactate dehydrogenase

    ETV5 i RUNX1, nous factors de transcripció implicats en la invasió miometrial del carcinoma endometrial

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    Actualment, en càncer d'endometri, està àmpliament acceptat el model dualístic que, atenent a bases morfològiques, diferencia tumors de tipus i o endometrioides dels de tipus ii o no endometrioides. La genètica molecular ha aportat dades que donen suport a aquest model dualístic de la tumorigènesi endometrial i algunes claus per a poder especular sobre la seqüència temporal de les alteracions moleculars que defineixen les rutes tumorigèniques. En els càncers endometrials endometrioides, o de tipus i, es coneixen alteracions majors, com poden ser el silenciament del gen PTEN, la inestabilitat de microsatèll. its associada a defectes en els gens reparadors de DNA, o mutacions al gen K-ras. Aquestes alteracions defineixen la progressió de l'endometri normal cap a la hiperplàsia i posteriorment cap al carcinoma. Recentment, l'ús de la tecnologia de microxips de cDNA per a identificar les diferències en els patrons d'expressió gènica entre els diferents tipus histològics de càncer d'endometri han permès la identificació de gens expressats diferencialment que podrien ajudar-nos a entendre les diferències en la biologia i el pronòstic clínic dels diferents histiotips tumorals. En el nostre laboratori hem aïllat i caracteritzat dos nous factors de transcripció, ETV5 i RUNX1, que estan associats amb els passos inicials de la infiltració miometrial en el càncer d'endometri endometrioide. Aquests estudis, i els d'altres gens implicats en el control de la mitosi com a mecanisme major de carcinogènesi en els càncers d'endometri no endometrioides, representen exemples de la utilitat dels estudis genètics amplis per a comprendre el procés de tumorigènesi i les rutes implicades en la patogènesi molecular del càncer d'endometri.A dualistic model, which has been established on a morphological basis and that differentiates type i endometrioid from type ii non-endometrioid endometrial cancer, is widely accepted. Molecular genetics have provided us with data supporting the dualistic model of endometrial tumorigenesis and with some clues to speculate about the sequence of the molecular alterations defining the tumorigenesis pathways. In type i endometrioid endometrial cancer, PTEN gene silencing, microsatellite instability associated with defects in DNA mismatch repair genes, or mutations in the K-ras gene are the known major alterations defining the progression from normal endometrium to hyperplasia and then on to carcinoma. Recently, cDNA microarray technology for identifying the differences in gene expression patterns between the histological types of endometrial cancer have permitted the identification of differentially expressed genes that could help us to understand differences in the biology and the clinical outcome between histiotypes. In our laboratory, we have recently isolated and characterized two new transcription factors, ETV5 and RUNX1, which expression appears to be associated with initial steps of myometrial infiltration in endometrioid endometrial carcinoma. These studies, as well as those on other genes involved in the mitotic checkpoint as a major mechanism of carcinogenesis in non-endometrioid endometrial cancer, represent examples of how useful large genetic screenings can be for understanding the tumorigenesis process and the future directions in the molecular pathogenesis of endometrial cancer

    The EMT signaling pathways in endometrial carcinoma

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    Endometrial cancer (EC) is the most common gynecologic malignancy of the female genital tract and the fourth most common neoplasia in women. In EC, myometrial invasion is considered one of the most important prognostic factors. For this process to occur, epithelial tumor cells need to undergo an epithelial to mesenchymal transition (EMT), either transiently or stably, and to differing degrees. This process has been extensively described in other types of cancer but has been poorly studied in EC. In this review, several features of EMT and the main molecular pathways responsible for triggering this process are investigated in relation to EC. The most common hallmarks of EMT have been found in EC, either at the level of E-cadherin loss or at the induction of its repressors, as well as other molecular alterations consistent with the mesenchymal phenotype-like L1CAM and BMI-1 up-regulation. Pathways including progesterone receptor, TGFβ, ETV5 and microRNAs are deeply related to the EMT process in EC

    Biological properties of extracellular vesicles and their physiological functions

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    In the past decade, extracellular vesicles (EVs) have been recognized as potent vehicles of intercellular communication, both in prokaryotes and eukaryotes. This is due to their capacity to transfer proteins, lipids and nucleic acids, thereby influencing various physiological and pathological functions of both recipient and parent cells. While intensive investigation has targeted the role of EVs in different pathological processes, for example, in cancer and autoimmune diseases, the EV-mediated maintenance of homeostasis and the regulation of physiological functions have remained less explored. Here, we provide a comprehensive overview of the current understanding of the physiological roles of EVs, which has been written by crowd-sourcing, drawing on the unique EV expertise of academia-based scientists, clinicians and industry based in 27 European countries, the United States and Australia. This review is intended to be of relevance to both researchers already working on EV biology and to newcomers who will encounter this universal cell biological system. Therefore, here we address the molecular contents and functions of EVs in various tissues and body fluids from cell systems to organs. We also review the physiological mechanisms of EVs in bacteria, lower eukaryotes and plants to highlight the functional uniformity of this emerging communication system
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