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Artykuły w czasopismach na temat "Souris de laboratoire – Embryons"
HOUDEBINE, L. M. "Les manipulations génétiques : comment améliorer la croissance". INRAE Productions Animales 3, nr 3 (4.07.1990): 207–14. http://dx.doi.org/10.20870/productions-animales.1990.3.3.4377.
Pełny tekst źródłaRowe-Pirra, William. "Pseudo-embryons en laboratoire". Pour la Science N° 514 - août, nr 8 (4.05.2020): 13b. http://dx.doi.org/10.3917/pls.514.0013b.
Pełny tekst źródłaDiaite, Amadou, A. Gueye, Yaya Thiongane, Moustapha Lo, T. N. Dieye i Georges Vassiliades. "Observation dans les Niayes du Sénégal d'une souche de Trypanosoma (Duttonella) vivax transmissible d'un bovin à des souris par la seringue". Revue d’élevage et de médecine vétérinaire des pays tropicaux 51, nr 2 (1.02.1998): 127–29. http://dx.doi.org/10.19182/remvt.9638.
Pełny tekst źródłaByrom, B., Suman M. Mahan i Anthony F. Barbet. "Le développement d’anticorps contre Cowdria ruminantium chez la souris et leur rôle dans la cowdriose". Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, nr 1-2 (1.01.1993): 197–201. http://dx.doi.org/10.19182/remvt.9361.
Pełny tekst źródłaGOCKO, X., i C. PLOTTON. "Controverses et origine de Sars-CoV-2". EXERCER 32, nr 175 (1.09.2021): 316–19. http://dx.doi.org/10.56746/exercer.2021.175.316.
Pełny tekst źródłaMaurin-Blanchet, H. "A propos d’un cas de toxico-pathologie chez des souris de laboratoire". Bulletin de l'Académie Vétérinaire de France, nr 4 (1986): 443. http://dx.doi.org/10.4267/2042/64810.
Pełny tekst źródłaGuerin, B., J. P. Builly, P. Humblot, M. Nibart i M. Thibier. "Effets de la contamination expérimentale in vitro des embryons de souris et de brebis par Campylobacter fetus". Bulletin de l'Académie Vétérinaire de France, nr 1 (1988): 63. http://dx.doi.org/10.4267/2042/64519.
Pełny tekst źródłaGama, Andrea, Linamary Perea, Catalina Yepes, Jhon J. Betancur, Jorge Vargas, Jerôme Amiaud, Sylvie Babajko, Frédéric Lezot i Beatriz Castaneda. "Effets de l’inhibition post-natale de RANKL sur l’éruption et la formation radiculaire des molaires de souris C57BL/6". L'Orthodontie Française 90, nr 1 (marzec 2019): 55–63. http://dx.doi.org/10.1051/orthodfr/2019008.
Pełny tekst źródłaMilon, G. "Listeria monocytogenes : interaction avec le système immunitaire d'un hôte expérimental, la souris de laboratoire". Médecine et Maladies Infectieuses 25 (luty 1995): 219–24. http://dx.doi.org/10.1016/s0399-077x(05)81059-5.
Pełny tekst źródłade Mestre, Amanda M. "Causes génétiques d’avortement chez la jument". Le Nouveau Praticien Vétérinaire équine 17, nr 58 (2023): 40–47. http://dx.doi.org/10.1051/npvequi/2023033.
Pełny tekst źródłaRozprawy doktorskie na temat "Souris de laboratoire – Embryons"
Nowak, Victor. "Caractérisation de l'expression de facteurs potentiellement impliqués dans la spécification en épiblaste dans l'embryon de souris préimplantatoire". Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://theses.bu.uca.fr/nondiff/2023UCFA0033_NOWAK.pdf.
Pełny tekst źródłaAfter fertilization the mouse embryo performs two rounds of differentiation before implantation. The first allows the formation of outer cells which, that give the Trophectoderm (TE) and the inner cells which give the Inner Cell Mass (ICM). The second step takes place within the ICM by producing the Epiblast (Epi) and the Primitive Endoderm (PrE) cells positioning in a “salt and pepper” pattern in the ICM. Recent studies show that NANOG is necessary for Epi specification, but not sufficient, suggesting that other factors may be involved in the initiation of this differentiation.My goal was to identify other factors that could be involved, as NANOG, in the initiation of Epi specification. I focused on the Fgf4 gene, which is a known Epi marker and a target gene of NANOG, to identify in-silico several potentially implicated factors: TEAD4, SOX2, SOX21 and OCT4. Analysis of their expressions highlighted the heterogeneity of those factors at different stages and between, and also an inverted correlation between SOX2 and SOX21 expressions during the development. Those results and data from literature made me hypothesize that TEAD4 and SOX21 would be repressors while NANOG and SOX2 would be activators of FGF4 expression and Epi specification. There would be then a competition between those factors. But nowadays, my work on the analysis of SOX21 overexpression in the embryo didn't allow me to validate this hypothesis. In parallel, I started to develop embryonic stem cells allowing an overexpression of SOX21 or TEAD4. Thanks to these cells, we will be able to study the DNA binding mechanisms of those factors and the impact on the target genes, and also the putative competition between them
Koné, Maïmouna. "Nucléologenèse et régulation de l'expression de l'hétérochromatine péricentromérique dans l'embryon précoce de souris". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLA030.
Pełny tekst źródłaIn mice, the preimplantation period is characterized by several events, the most important is the activation of the embryonic genome (EGA) taking place between the late 1-cell (minor phase) and late 2-cell (major phase) stages. Among the genes expressed are the ribosomal DNAs required for the formation of the ribosomes and the pericentromeric heterochromatin (sense and antisense RNA) important for the formation of heterochromatin clusters. It is known that the ribosomal RNAs are synthesized in the nucleolus. In the embryo after fertilization, the nucleolus is replaced by nucleolus precursor bodies (NPBs). These NPBs then evolve during embryonic development to form nucleoli but the mechanisms involved in the formation of nucleoli remain mostly unknown. Moreover, there are very few data on the organization of ribosomal genes based on their transcriptional status (active or inactive) in embryos. I therefore focused during my PhD thesis on the nucleologenesis process and on the organization of ribosomal genes in the mouse preimplantation embryo. Furthermore, it is well known that the two parental pronuclei (paternal and maternal) progress asynchronously after fertilization, the pericentromeric heterochromatin organizing faster around NPBs in the maternal pronucleus. In the second part of my thesis, I therefore focused on the role NPBs may have in the organization of pericentromeric hetero-chromatin during development and on the contribution of each gamete
Guyot, Romain. "Organogenèse testiculaire chez la souris, implications des protéases et des antiprotéases : conséquences de l'expositions in utéro à des perturbateurs endocriniens". Lyon 1, 2004. http://www.theses.fr/2004LYO11002.
Pełny tekst źródłaAoidi, Rifdat. "Étude du rôle de la voie ERK/MAPK dans le développement embryonnaire chez la souris". Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27476.
Pełny tekst źródłaLes mammifères possèdent deux MAP kinases kinases (MEK1 et MEK2), impliquées dans l’activation de la voie ERK/MAPK essentielle pour la différenciation, la prolifération et la survie cellulaire. Le premier objectif de cette thèse était de déterminer si les fonctions des kinases MEK1 et MEK2 sont redondantes durant le développement embryonnaire. Les souris Mek1-/- meurent à mi-gestation d’une malformation du placenta. Les souris Mek2-/- ne présentent aucun phénotype majeur, suggérant que ces deux protéines ont des rôles différents. Cependant, la plupart des mutants Mek1+/-Mek2+/- meurent pendant la gestation d’un sous-développement du placenta, indiquant que Mek1 et Mek2 ont chacun un rôle dans le développement des tissus extraembryonnaires. À ce jour aucune évidence claire ne permet de statuer sur la redondance fonctionnelle de MEK1 et MEK2. Afin de vérifier la spécificité fonctionnelle de Mek1 et Mek2, nous avons généré au laboratoire un allèle « knockin », exprimant l’ADNc de Mek2 sous contrôle du locus Mek1 (Mek12). L’analyse de ces souris a révélé la redondance fonctionnelle entre MEK1 et MEK2. L’analyse de combinaisons alléliques de Mek a démontré qu’une expression minimale de protéines MEK est cruciale pour le développement embryonnaire et la survie. Le second objectif de cette thèse était de caractériser les mutants Mp1. Les protéines d’échafaudage permettent de moduler l’activité de la voie ERK/MAPK et facilitent la transmission rapide du signal. Parmi les protéines d’échafaudage connues, seule MP1 (Mek Partner 1) a été identifiée comme étant un partenaire spécifique de MEK1 et ERK1. Cette spécificité suggère que MP1 pourrait contribuer à la différence d’activation de MEK1 et MEK2 en spécifiant le signal qui passe par Mek1. Afin d’étudier le rôle de Mp1 au cours du développement chez la souris, nous avons généré des souris Mp1-/-. L’analyse de ces mutants indique que le gène Mp1 est essentiel pour la survie et que sa fonction est nécessaire suite à la post-implantation. La dérégulation de la voie ERK/MAPK dans le développement chez l’homme a aussi des conséquences phénotypiques. Au cours des dernières années, une classe de syndromes a été caractérisée : Les « Rasophaties ». Ces syndromes partagent des caractéristiques communes qui sont, une mutation dans des gènes de la voie ERK/MAPK, une dysmorphologie cranio-faciale, des malformations cardiaques et cutanées ainsi qu’un retard mental. Parmi les mutations de la voie ERK/MAPK qui ont été identifiées, une mutation ponctuelle dans le gène Mek1 (Mek1Y130C) cause le syndrome Cardio-Facio-Cutané (CFC). Le dernier objectif de cette thèse était de générer un modèle animal pour le CFC portant la mutation Mek1Y130C. Les souris portant l’allèle Mek1Y130C présentent les phénotypes associés au CFC (i.e sténose pulmonaire, dysmorphologie cranio-faciale et défauts neurologiques).
Mammals possess two MAP kinase kinase (MEK1 and MEK2), involved in ERK/MAPK pathway. This pathway is essential for proliferation, differentiation and cell survival. The first objective of my thesis was to determinate if MEK1 and MEK2 kinases are redundant during embryonic development. Mek1-/- mice die at embryonic day E10.5 due to placental defects, whereas Mek2-/- mice survive with a normal lifespan suggesting that MEK1 possesses functions not shared by MEK2. However, most Mek1+/-Mek2+/- embryos also die from placental defects, indicating that both Mek genes contribute to placental development. To date, no clear evidence on MEK1 and MEK2 redundancy has been provided. To assess the functional specificity of the Mek1 and Mek2 genes, we produced a Mek1-knockin allele in which the Mek2 coding sequences were placed under the control of Mek1 regulatory sequences. Analyzing these mice allowed us to demonstrate that MEK1 and MEK2 can substitute for each other and that a minimal amount of MEK is critical for placenta development and embryo survival. The second objective of my thesis was to characterize Mp1 mutants. Scaffold proteins modulate MAPK pathway by providing spatial and temporal specificity. Among known ERK/MAPK scaffold proteins, only MP1 (Mek Partner 1) is specific to MEK1 and ERK1, raising the question of the specificity of MP1 in the regulation of ERK/MAPK pathway via MEK1. In order to investigate Mp1 function in vivo, we generated Mp1 knock-out mice. Analyzing these mice enable us to suggest that Mp1 is required for embryonic development and is essential during post-implantation. Deregulation of Ras/MAPK pathway also causes developmental phenotypes in human. During the last decade, a new class of syndromes, which share common phenotypes such as mutations in Ras/MAPK pathway, cranio-facial dysmorphology, cardiac and cutaneous malformations and neurological delay has been described and named Rasophaties. Among the DNA mutations found in rasopathies, the Mek1 mutation, Mek1Y130C, causes cardio-facio-cutaneous syndrome (CFC). The last objective of my thesis was to generate a mouse model of CFC, with the Mek1Y130C mutation. I found that mice carrying the Mek1Y130C mutation partially recapitulate CFC syndrome (i.e pulmonary stenosis, crani-facial dysmophia and neurological defects).
Truchet, Sandrine. "Voies de signalisation de l'interféron-gamma dans les ovocytes et les embryons pré-implantatoires de souris". Paris, Muséum national d'histoire naturelle, 2003. http://www.theses.fr/2003MNHN0003.
Pełny tekst źródłaInterferon-gamma (IFNg) is a cytokine which is best known for its role in the immune system and exerts pleitropic biological activities such as antiviral, antitumoral and antiproliferative effects. Upon binding of IFNg on its specific cellular receptor (IFNGR), intracellular signal transduction relies on two protein families, namely the Janus Kinases (JAKs) which are associated to each receptor's subunits, and the transcription factor STAT1 (Signal Transducer and Activator of Transcription 1). Interaction between IFNg and its receptor triggers a cascade of phosphorylations which leads to the phosphorylation of cytoplasmic STAT1, its dimerization and nuclear translocation. Once in the nucleus, activated STAT1 binds to specific DNA elements named GAS (Gamma Activated Sequence/Site) located in the promoters of IFNg inducible genes and activates their transcription. Nevertheless, some publications suggest that the IFNg/IFNGR complexe may play a role in intracellular trafficking of STAT1 and even in its nuclear translocation which could be mediated by the nuclear localization sequence (NLS) of IFNg. Indeed, no NLS has been identified in STAT proteins. The aim of this study was to use mouse ovocytes and preimplantation embryos as models to explore the signal transduction induced by IFNg in these cells and the mechanisms underlying the intracellular trafficking of its receptor eventually leading the nuclear localization of IFNg and/or its receptor. It was first shown, both by indirect immunofluorescence and RT-PCR, that the two subunits (IFNGR1 and IFNGR2) of the IFNg receptor are naturally expressed in mouse ovocytes and preimplantation embryos. However, despite the apparent binding of IFNg to its receptor, no massive nuclear accumulation of STAT1 is observed in mouse ovocytes and preimplantation embryos upon IFNg stimulation, whatever the doses or the stimulation times tested. Conversely, STAT1 as well as other members of this transcription factors family appear to be permanently phosphorylated and reside in the nuclear compartment, associated with interchromatin granules clusters (IGCs) or "speckles". On the other hand, anti-IFNGR1 antibody recognizes systematically an epitope associated with the nucleolar compartment, in mouse ovocytes and preimplantation embryos, as well as in several somatic cell lines. This epitope was purified from nucleoli preparations and immunoprecipitated from total nuclear extracts. In both cases, a single peptide with an apparent molecular weight of about 31 kDa was detected by Western blot analysis. This epitope is now being identified by mass spectrometry
Escuin, Sarah. "Fonctions de la kinase NIK dans la migration neuronale radiale au cours du développement du cortex cérébral chez la souris". Université Louis Pasteur (Strasbourg) (1971-2008), 2007. http://www.theses.fr/2007STR13141.
Pełny tekst źródłaMenard, Claudine. "Ontogénèse des canaux calciques de type L. Influence de l'acide rétinoi͏̈que". Montpellier 2, 1999. http://www.theses.fr/1999MON20098.
Pełny tekst źródłaMiladinović, Olivera. "Molecular profiling of the embryonic hematopoietic stem cell niche". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS025.pdf.
Pełny tekst źródłaHematopoietic stem cells (HSCs) constitute a rare population of cells at the foundation of the adult hematopoietic system. During mouse ontogeny, the first adult-type HSCs are autonomously generated in the Aorta-Gonad-Mesonephros (AGM) region at mid-gestation. More precisely, HSCs emerge from aortic endothelial cells through an endothelial to hematopoietic transition. The AGM hematopoietic microenvironment is composed of diverse cell types including mesenchymal stromal cells, sympathetic nerve cells, macrophages and vascular smooth muscle cells. Although the subaortic mesenchyme is known to play a key role in AGM hematopoiesis, its molecular identity still remains elusive. To address this critical issue, we designed a laser capture strategy to isolate in the mouse embryo the dorsal and ventral aortic tissues at three developmental stages. By combining bulk and single cell transcriptomics and lineage tracing, I contributed to reveal the existence of a unique mesenchymal cell population expressing both neuronal and mesenchymal genes in the subaortic tissue at embryonic day 11.5. Using loss-of-function experiments and genetic tools in the zebrafish model that I implemented in the team, I showed that Decorin, encoding an extracellular matrix protein, is necessary for HSC development in vivo. Taken together, my PhD project provides new insights on the molecular identity of the AGM hematopoietic microenvironment and leads to the identification of potential novel HSC regulators in the embryo
Boeri, Juliette. "Propriétés d’excitabilité des cellules de Renshaw au cours du développement embryonnaire de la moelle épinière, chez la souris". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS381.
Pełny tekst źródłaAs many developing neuronal networks, embryonic spinal cord spontaneously generates recurrent synchronized neural activity, which is involved in multiple aspects of motor circuit maturation. During an initial embryonic period (E12.5 to E14.5 in mice), this activity is mainly under the control of acetylcholine, GABA and glycine release. In motoneurons, this activity is characterized by giant depolarizing potentials (GDPs), mainly evoked by a release of GABA, the latter being regulated by the activation of cholinergic receptors, suggesting a recurrent loop between motoneurons and GABAergic interneurons. The mechanisms of this neurotransmitters release and the identification of the first functional GABAergic interneurons interacting with motoneurons are unknown. On this basis, we show that at E12.5, Renshaw cells (RCs) express GABA and also generate GDPs that can evoke multiple action potentials or "plateau potentials". Distinct firing patterns of RCs, in response of injected current, were observed and classified as single-spiking, repetitive-firing or sodium plateau potentials. Between E12.5 and E14.5, while motoneurons intrinsic excitability classically increases, RCs intrinsic excitability surprisingly transitory regresses. We show that the ratios of persistent sodium and potassium voltage-dependent conductances play a major role in determining firing patterns and account for the regression of RCs intrinsic excitability
Jachowicz, Joanna Weronika. "Molecular mechanisms underlying heterochromatin formation in the mouse embryo". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ094/document.
Pełny tekst źródłaTo study the formation of heterochromatin in mouse preimplantation embryo, I focused on two different genetic regions – pericentric repeats and L1 transposable elements - in order to investigate the mechanisms that lead to their repression and the distinct role that these regions can play during the process of development and cell division. My experiments show that the specific spatial organization of pericentric domains is essential for their repression and for their correct organization. Moreover, my findings suggest that defects in organization of heterochromatin lead to improper cell division and proliferation. The second part of my thesis shows that the tight regulation of L1 transposable elements is required for the preimplantation development of mouse embryos. Additionally, it is the first attempt to elucidate the biology of L1 elements in the early mouse embryo through the use of targeted transcription modifiers
Książki na temat "Souris de laboratoire – Embryons"
1952-, Costantini Frank, i Lacy Elizabeth, red. Manipulating the mouse embryo: A laboratory manual. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1986.
Znajdź pełny tekst źródłaHogan, Brigid. Manipulating the mouse embryo: A laboratory manual. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1986.
Znajdź pełny tekst źródłaMichael, Potter, red. The BALB/C mouse: Genetics and immunology. Berlin: Springer-Verlag, 1985.
Znajdź pełny tekst źródła(Editor), Andras Nagy, red. Manipulating the Mouse Embryo: A Laboratory Manual. Wyd. 3. Cold Spring Harbor Laboratory Press, 2002.
Znajdź pełny tekst źródłaManipulating the Mouse Embryo: A Laboratory Manual, Fourth Edition. Cold Spring Harbor Laboratory Press, 2013.
Znajdź pełny tekst źródłaJ, Hedrich Hans, i Bullock Gillian R, red. The laboratory mouse. Amsterdam: Elsevier Academic Press, 2004.
Znajdź pełny tekst źródłaLaboratory Mouse. Elsevier Science & Technology Books, 2012.
Znajdź pełny tekst źródłaLaboratory Mouse Handbook. American Association for Laboratory Animal Science, 2006.
Znajdź pełny tekst źródła(US), National Research Council. Microbial and Phenotypic Definition of Rats and Mice: Proceedings of the 1998 US/Japan Conference (The Compass Series). National Academies Press, 1999.
Znajdź pełny tekst źródła(US), National Research Council. A Scientific Rationale for Mobility in Solar System Exploration (Compass Series). Natl Academy Pr, 1999.
Znajdź pełny tekst źródłaCzęści książek na temat "Souris de laboratoire – Embryons"
Laimer, Margit, Rashmi Boro, Veronika Hanzer, Emmanuel Ogwok i Eduviges G. Borroto Fernandez. "Protocol on Mutation Induction in Coffee Using In Vitro Tissue Cultures". W Mutation Breeding in Coffee with Special Reference to Leaf Rust, 61–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-67273-0_5.
Pełny tekst źródłaGamage, Nadisha, Harish Cheruvara, Peter J. Harrison, James Birch, Charlie J. Hitchman, Monika Olejnik, Raymond J. Owens i Andrew Quigley. "High-Throughput Production and Optimization of Membrane Proteins After Expression in Mammalian Cells". W Methods in Molecular Biology, 79–118. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3147-8_5.
Pełny tekst źródłaUslu, Bahar. "Perspective Chapter: What about Embryo’s Rights?" W Embryology Update [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106781.
Pełny tekst źródłaTorres, Raul M., i Ralf Kühn. "Blastocyst transfer". W Laboratory Protocols for Conditional Gene Targeting, 123–26. Oxford University PressOxford, 1997. http://dx.doi.org/10.1093/oso/9780199636778.003.0027.
Pełny tekst źródłaFagan, Melinda Bonnie. "Stem cells". W Routledge Encyclopedia of Philosophy. London: Routledge, 2023. http://dx.doi.org/10.4324/9780415249126-q152-1.
Pełny tekst źródłaDupin, Elisabeth, i Nicole M. Le Dou Arin. "Culture of Avian Neural Crest Cells". W Essential Developmental Biology, 153–66. Oxford University PressOxford, 1993. http://dx.doi.org/10.1093/oso/9780199634231.003.0018.
Pełny tekst źródłaMorse, Ruth, i Saeed Kabrah. "Haematopoietic Stem Cell Transplantation and Stem Cell Plasticity". W Transfusion and Transplantation Science. Oxford University Press, 2018. http://dx.doi.org/10.1093/hesc/9780198735731.003.0010.
Pełny tekst źródła"Hudson River Fishes and their Environment". W Hudson River Fishes and their Environment, redaktorzy Isaac Wirgin i R. Christopher Chambers. American Fisheries Society, 2006. http://dx.doi.org/10.47886/9781888569827.ch19.
Pełny tekst źródła"Hudson River Fishes and their Environment". W Hudson River Fishes and their Environment, redaktorzy Isaac Wirgin i R. Christopher Chambers. American Fisheries Society, 2006. http://dx.doi.org/10.47886/9781888569827.ch19.
Pełny tekst źródłaStreszczenia konferencji na temat "Souris de laboratoire – Embryons"
Catlow, F., i G. M. Reeves. "Education in Nuclear Decommissioning in the North of Scotland". W The 11th International Conference on Environmental Remediation and Radioactive Waste Management. ASMEDC, 2007. http://dx.doi.org/10.1115/icem2007-7209.
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