Literatura académica sobre el tema "Mousse PU"
Crea una cita precisa en los estilos APA, MLA, Chicago, Harvard y otros
Consulte las listas temáticas de artículos, libros, tesis, actas de conferencias y otras fuentes académicas sobre el tema "Mousse PU".
Junto a cada fuente en la lista de referencias hay un botón "Agregar a la bibliografía". Pulsa este botón, y generaremos automáticamente la referencia bibliográfica para la obra elegida en el estilo de cita que necesites: APA, MLA, Harvard, Vancouver, Chicago, etc.
También puede descargar el texto completo de la publicación académica en formato pdf y leer en línea su resumen siempre que esté disponible en los metadatos.
Artículos de revistas sobre el tema "Mousse PU"
1
Madrange, L., P. Ehabouryi, O. Ferrandon, M. Mazeti y J. Rodeaud. "Étude de la formation et de la stabilité des mousses chimiques de surface de la Vienne". Revue des sciences de l'eau 6, n.º 3 (12 de abril de 2005): 315–35. http://dx.doi.org/10.7202/705178ar.
Texto completoResumen
Le recensement de la charge polluante rejetée dans la rivière Vienne (France) par les usines et les stations d'épuration de Limoges à Confolens a été effectué. Des campagnes de prélèvement et d'observations visuelles ont permis de localiser les lieux d'apparition de mousses en aval d'usines de fabrication de pâte à papier et de cartons. L'étude du pouvoir moussant des mélanges des deux principaux rejets polluants (papeterie et cartonnerie) a permis de mettre en évidence des phénomènes de synergie entre certains mélanges se traduisant à la fois par une augmentation du pouvoir moussant et de la stabilité de la mousse dans le temps. L'étude par « HPLC » montre l'apparition de pics supplémentaires confirmant l'interaction entre les constituants des rejets; le principal effluent a pu être suivi à l'aide de ses caractéristiques chimiques dans la rivière et dans les mousses jusqu'à Confolens.
2
Christians, Jean-François. "Redécouverte de Schistostega pennata (Hedwig) F. Weber et D. Mohr (Schistostegaceae, Bryophyta) dans le massif du Pilat (Loire, France)". Bulletin mensuel de la Société linnéenne de Lyon 84, n.º 7 (2015): 215–25. http://dx.doi.org/10.3406/linly.2015.17768.
Texto completoResumen
La redécouverte d’anciennes localités de Schistostega pennata dans le Parc naturel régional du Pilat est consécutive à des prospections ciblées, menées dans le cadre d’une enquête participative initiée par Isabelle Charissou sur le site «Bryophytes de France », également relayée par la Société Botanique du Centre-Ouest et par l’Amicale Legendre des Botanistes du Limousin. À cette occasion, de nouvelles stations ont également pu être mises en évidence. La biologie et l’écologie de cette mousse sont présentées, puis seront précisées ses répartitions ancienne et actuelle pour le massif du Pilat.
3
Thomas, Marc, Emmanuel Discamps, Mathieu Lejay, Xavier Muth y Jean-Guillaume Bordes. "Os qui roule n’amasse pas mousse. Une expérimentation sur le tri différentiel des vestiges lithiques et osseux dans un écoulement turbulent". Paléo 33 (2023): 146–63. http://dx.doi.org/10.4000/1296o.
Texto completoResumen
Les vestiges lithiques et fauniques constituent les principaux témoins des occupations paléolithiques. Les proportions relatives de ces matériaux au sein des assemblages sont utilisées pour définir la fonction des sites ou parties de site. Or, de nombreux processus naturels sont susceptibles d’occasionner des tris sur les ensembles de vestiges, parmi lesquels les écoulements turbulents, intervenant dans de nombreux domaines (e.g. fluviatile, ruissellement concentré). Afin d’évaluer cet impact, de nombreuses expérimentations ont déjà été réalisées, mais peu d’entre elles ont concerné à la fois les vestiges fauniques et lithiques. Ainsi, l’impact comparé des écoulements de régime turbulent sur ces deux types de vestiges reste difficile à caractériser. De plus, la plupart des expérimentations connues concernent des ossements complets, parfois encore articulés, rendant toute comparaison difficile avec le référentiel fossile où les ossements sont fracturés et brûlés lors des activités de subsistance.Dans cet article, nous présentons les résultats d’une expérimentation dont l’objectif était d’évaluer l’impact relatif d’un écoulement turbulent sur différentes catégories (silex, vestiges osseux brûlés et non brûlés, tissu compact et spongieux) et classes de taille de vestiges.Le principal résultat de cette expérimentation est la mise en évidence d’une mobilité plus forte de toutes les catégories et classes de taille de vestiges fauniques par rapport aux vestiges lithiques, et ce quelle que soit leur taille.Le tri généré est corrélé à la densité des vestiges, soit, du plus mobile au moins mobile : l’os spongieux brûlé, l’os compact brûlé, l’os spongieux non brûlé, l’os compact non brûlé et le silex. Par ailleurs, nous avons pu mesurer qu’un tri dimensionnel même léger des vestiges lithiques implique un tri conséquent des ensembles de vestiges fauniques. Dans le cas inverse, lorsque l’analyse granulométrique des vestiges lithiques ne révèle pas de tri, nos expérimentations soulignent que ce résultat ne peut être avancé comme argument pour un bon degré d’intégrité des ensembles fauniques.Ainsi, lorsque des processus sédimentaires impliquant des écoulements concentrés sont mis en évidence par les études géoarchéologiques, des précautions doivent être prises concernant les interprétations d’ordre archéozoologique.
4
Hwang, Cheol Kyu, Chun Sung Kim, Hack Sun Choi, Scott R. McKercher y Horace H. Loh. "Transcriptional Regulation of Mouse μ Opioid Receptor Gene by PU.1". Journal of Biological Chemistry 279, n.º 19 (3 de marzo de 2004): 19764–74. http://dx.doi.org/10.1074/jbc.m400755200.
Texto completoResumen
We previously reported that the 34-bp cis-acting element of the mouse μ opioid receptor (MOR) gene represses transcription of the MOR gene from the distal promoter. Using a yeast one-hybrid screen to identify potential transcription factors of the MOR promoter, we have identified PU.1 as one of the candidate genes. PU.1 is a member of theetsfamily of transcription factors, expressed predominantly in hematopoietic cells and microglia of brain. PU.1 plays an essential role in the development of both lymphoid and myeloid lineages. Opioids exert neuromodulatory as well as immunomodulatory effects, which are transduced by MOR. Moreover, MOR-deficient mice exhibit increased proliferation of hematopoietic cells, suggesting a possible link between the opioid system and hematopoietic development. The PU.1 protein binds to the 34-bp element of the MOR gene in a sequence-specific manner confirmed by electrophoretic mobility shift assay and supershift assays. We have also determined endogenous PU.1 interactions with the 34-bp element of MOR promoter by chromatin immunoprecipitation assays. In co-transfection studies PU.1 represses MOR promoter reporter constructs through its PU.1 binding site. When the PU.1 gene is disrupted as in PU.1 knock-out mice and using small interfering RNA-based strategy in RAW264.7 cells, the transcription of the endogenous target MOR gene is increased significantly. This increase is probably mediated through modification of the chromatin structure, as suggested by the reversal of the PU.1-mediated repression of MOR promoter activity after trichostatin A treatment in neuroblastoma NMB cells. Our results suggest that PU.1 may be an important regulator of the MOR gene, particularly in brain and immune cells.
5
Gerasimo, P., C. Duserre y H. Metivier. "Biological Behaviour of Pu Administered to Animals as Pu-Standard LICAM(C) Complex: Therapeutical Attempts to Decrease Pu Kidney Burden". Human Toxicology 5, n.º 5 (septiembre de 1986): 309–18. http://dx.doi.org/10.1177/096032718600500503.
Texto completoResumen
The biological fate of plutonium (Pu) introduced as a Pu-standard LICAM(C) complex was investigated in male rats of two strains, in male and female mice and in the baboon. We observed that, whatever the animal species or the entry route, this complex was deposited rapidly in the kidney. In addition, more of the complex accumulated in the rat (16% of injected radioactivity) than in either the mouse (7%) or baboon (5%). This Pu deposit was cleared spontaneously with a half-life of 10 days in the rat and only 5 days in the mouse. We noted that the complex was deposited on bone during this period and that, 10 days after the introduction of Pu, the skeleton became the main organ of retention of Pu (7% of the dose in the rat, 4% in mice and 3% in the baboon). In spite of this, which would indicate that Pu-standard LICAM(C) resembles a weak complex, gut transfer was comparable with that of a strong complex 1.10-3 ( f1 = 1.10-3) . Pu deposit seemed to be pH dependent and could be modified be varying the pH balance of urine. Bicarbonate was among the most effective of the different drugs used to affect this balance, as 5 h of continuous perfusion decreased the kidney Pu burden by a factor of 4. Such efficacy was also observed with diethylenetriaminepenta-acetic acid (DTPA) perfusion. The pragmatic consequence of these experiments is the recommendation of mixed therapy: standard LICAM(C) plus bicarbonate or DTPA.
6
Zhou, Jing, Bo Li, Jun Wu, Fuhong He, Qiang Li, Xiaomei Yan, Yue Zhang et al. "Essential Role for PU.1 in MEIS1 Activation and MLL Fusion Leukemia",. Blood 118, n.º 21 (18 de noviembre de 2011): 3466. http://dx.doi.org/10.1182/blood.v118.21.3466.3466.
Texto completoResumen
Abstract Abstract 3466 Down-regulation of transcription factor PU.1, a key regulator of hematopoiesis, induces myeloid leukemia in mice, demonstrating a role of PU.1 as tumor suppressor. Recent studies, however, have also suggested that PU.1 is required for repopulation/self-renewal capacity of normal hematopoietic stem cells (HSCs), and presence of PU.1 activity may be necessary to favor growth of myeloid leukemia stem cells. To explore whether PU.1 could possibly act as an oncogene in the development of certain type of myeloid leukemia, we set to look for differential up-regulation of PU.1 among AML patients with distinct cytogenetic and genetic alterations in public databases. Consistent with recent molecular studies showing suppression of PU.1 expression by AML1-ETO and PML-RARa fusion proteins, PU.1 expresses at a significant lower level in AML patients with t(8;21) and t(15;17) translocations. In contrast, PU.1 expression level in MLL leukemia patients is significantly higher than that of other subgroups of AML. In addition, we found that a set of PU.1 direct target genes, as defined by genome wide location analysis of this factor, expresses at higher level in MLL leukemia patients comparing with those with t(8;21) and t(15;17) translocations, supporting an increased PU.1 activity in this subgroup of leukemia. In our effort to characterize the functional consequence of high expression of PU.1 in AML, we found that PU.1 plays an essential role in activation of MEIS1, an oncogene essential for MLL leukemia stem cell potential, and in development of MLL fusion leukemia. MEIS1, as PU.1, is differentially up-regulated in MLL leukemia patients, and expresses at a significant lower level in AML patients with t(8;21) and t(15;17) translocations. Among AML patients with higher level MEIS1 expression, a positive correlation was observed between expression of PU.1 and that of MEIS1. Using promoter reporter assay, electro mobility shift assay (EMSA) and chromatin immunoprecipiation (ChIP) analysis, we found that PU.1 directly binds to and activates MEIS1 promoter in vitro and in vivo. Analysis of a hypomorphic PU.1 mouse model indicated that PU.1 is required to maintain Meis1 expression in murine HSCs and progenitors, and knockdown of PU.1 in patient-derived MLL leukemia cell lines resulted in lower enrichment of PU.1 protein at MEIS1 promoter, accompanied by down-regulation of MEIS1 expression and decreased proliferation and survival of these cells. We are now examining whether the ability of MLL-AF9 fusion protein to drive leukemia is compromised in PU.1-deficient mouse HSC/HPCs, and whether introduction of exogenous Meis1 can compensate for the loss of PU.1 in the development of MLL-AF9 leukemia in mouse bone marrow transplantation model. Finally, we are also testing knock-down of PU.1 as a therapeutic approach to primary AMLs isolated from MLL leukemia patients. Collectively, our data indicate that PU.1 is required for the pathogenesis of MLL associated leukemia, at least partially, through direct activation of MEIS1. In veiw of the dependency of MEIS1 in MLL leukemic transformation, targeting PU.1 mediated MEIS1 gene activation could be an alternative or synergistic approach for MLL leukemia therapies aimed at inhibition of DOT1L and HOXA9. Disclosures: No relevant conflicts of interest to declare.
7
Staber, Philipp B., Pu Zhang, Min Ye, Gang Huang, Boris Bartholdy, Annalisa DiRuscio, Alexander K. Ebralidze y Daniel G. Tenen. "Autoregulation of the Transcription Factor PU.1 Via Its Evolutionarily Conserved Upstream Regulatory Element Is Critical in Adult Mouse Hematopoiesis." Blood 114, n.º 22 (20 de noviembre de 2009): 1468. http://dx.doi.org/10.1182/blood.v114.22.1468.1468.
Texto completoResumen
Abstract Abstract 1468 Poster Board I-491 Background: Levels of the Ets transcription factor PU.1 control normal hematopoietic differentiation and even modest alterations can lead to leukemia and lymphoma. Regulation of PU.1 levels at different stages of hematopoiesis requires multiple interactions between several regulatory elements and transcription factors. Our previous studies identified a potential autoregulatory mechanism of the PU.1 gene through the combined activity of the proximal promoter and an evolutionarily conserved upstream regulatory element (URE), located at –14 kb relative to the transcription start site in mice. PU.1 binds to a conserved PU.1 site in the PU.1 URE both in vitro and in vivo. Approach: To ask at which stages of hematopoietic differentiation autoregulation of PU.1 via binding to its URE might play a role, we developed a mouse model with targeted disruption of the PU.1 binding site in the PU.1 URE. Results: Targeted mutation of the PU.1 autoregulatory site in PU.1 URE abolished PU.1 binding as verified by Chromatin Immuno-precipitation (ChIP). PU.1 URE activity was manifestly reduced resulting in a variety of lineage-specific abnormalities. As shown here in adult mice, the absence of the autoregulatory PU.1 site affected PU.1 expression in a lineage dependent manner. PU.1 expression was markedly decreased in phenotypic long term hematopoietic stem cells (LT-HSC: CD150+/CD48−/ c-kit+/sca-1+/lin−) and short term HSCs (ST-HSCs: CD150−/CD48+/ c-kit+/sca-1+/lin−) and, to a lesser extent, in Common Myeloid Progenitors (CMPs: lin−/c-kit+/Sca-1−/CD34+/FcrRlow), and Megakaryocyte/Erythrocyte Progenitors (MEPs: lin−/c-kit+/Sca-1−/CD34−/FcrRhigh). Within the lymphoid linage, PU.1 levels were unchanged in Common Lymphoid Progenitors (CLPs: lin−/c-kitlow/Sca-1low /IL-7Ra+/Thy1.1−) and pre-B-cells (B220+/ CD43−), up in pro-B-cells (B220+/CD43+), and down in mature B cells. Myeloid cells appeared to be unaffected. Interestingly, while PU.1 levels were decreased in LT- and ST-HSC populations, only phenotypic LT-HSCs were reduced in number. To further analyze HSC function of PU.1 site mutated mice we performed limiting dilution transplantation assays and measured the frequency of competitive repopulation units (CRU) using the congenic Ly5.1/Ly5.2 system. Our preliminary data indicated a decrease of LT-HSC function in PU.1 site mutated mice, although their homing and engraftment functions were not affected. This was also observed in mice with targeted disruption of all three AML-1 sites that are in close proximity of the PU.1 site at the PU.1 URE. While AML-1 itself appeared not to influence LT-HSC function (M. Ichikawa, T. Asai et al. Nature Medicine, 2004), we found that the conformational changes of the URE present in mice with disrupted AML-1 binding sites, as measured by Quantitative Chromosome Conformation Capture, impede PU.1 binding to its autoregulatory site. Conclusion: PU.1 indeed autoregulates its expression via binding to the -14kb URE in a lineage specific manner in vivo. Our data point to a critical role of PU.1 autoregulation especially for long-term hematopoietic stem cell function. Disclosures: No relevant conflicts of interest to declare.
8
Bonfield, Tracey L., Baisakhi Raychaudhuri, Anagha Malur, Susamma Abraham, Bruce C. Trapnell, Mani S. Kavuru y Mary Jane Thomassen. "PU.1 regulation of human alveolar macrophage differentiation requires granulocyte-macrophage colony-stimulating factor". American Journal of Physiology-Lung Cellular and Molecular Physiology 285, n.º 5 (noviembre de 2003): L1132—L1136. http://dx.doi.org/10.1152/ajplung.00216.2003.
Texto completoResumen
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is critically implicated in lung homeostasis in the GM-CSF knockout mouse model. These animals develop an isolated lung lesion reminiscent of pulmonary alveolar proteinosis (PAP) seen in humans. The development of the adult form of human alveolar proteinosis is not due to the absence of a GM-CSF gene or receptor defect but to the development of an anti-GM-CSF autoimmunity. The role of GM-CSF in the development of PAP is unknown. Studies in the GM-CSF knockout mouse have shown that lack of PU.1 protein expression in alveolar macrophages is correlated with decreased maturation, differentiation, and surfactant catabolism. This study investigates PU.1 expression in vitro and in vivo in human PAP alveolar macrophages as well as the regulation of PU.1 by GM-CSF. We show for the first time that PU.1 mRNA expression in PAP bronchoalveolar lavage cells is deficient compared with healthy controls. PU.1-dependent terminal differentiation markers CD32 (FCγII), mannose receptor, and macrophage colony-stimulating factor receptor (M-CSFR) are decreased in PAP alveolar macrophages. In vitro studies demonstrate that exogenous GMCSF treatment upregulated PU.1 and M-CSFR gene expression in PAP alveolar macrophages. Finally, in vivo studies showed that PAP patients treated with GM-CSF therapy have higher levels of PU.1 and M-CSFR expression in alveolar macrophages compared with healthy control and PAP patients before GM-CSF therapy. These observations suggest that PU.1 is critical in the terminal differentiation of human alveolar macrophages.
9
Mak, Ka Sin, Alister P. W. Funnell, Richard C. M. Pearson y Merlin Crossley. "PU.1 and Haematopoietic Cell Fate: Dosage Matters". International Journal of Cell Biology 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/808524.
Texto completoResumen
The ETS family transcription factor PU.1 is a key regulator of haematopoietic differentiation. Its expression is dynamically controlled throughout haematopoiesis in order to direct appropriate lineage specification. Elucidating the biological role of PU.1 has proved challenging. This paper will discuss how a range of experiments in cell lines and mutant and transgenic mouse models have enhanced our knowledge of the mechanisms by which PU.1 drives lineage-specific differentiation during haematopoiesis.
10
Ghisi, Margherita, Mark D. McKenzie, Ethan P. Oxley, Emilia Simankowicz, Cynthia Liu, Aleksandar Dakic, Stephen L. Nutt, Matthew E. Ritchie, Johannes Zuber y Ross A. Dickins. "Uncovering Key Downstream Effectors of PU.1 Tumor Suppression in Acute Myeloid Leukemia". Blood 128, n.º 22 (2 de diciembre de 2016): 2698. http://dx.doi.org/10.1182/blood.v128.22.2698.2698.
Texto completoResumen
Abstract Mutation or altered expression of key transcription factors resulting in aberrant myeloid differentiation is a critical step in the pathogenesis of acute myeloid leukemia (AML). The ETS-domain hematopoietic transcription factor PU.1 (SPI1) is an essential regulator of myeloid differentiation. While genetic mutation of PU.1 is rare, PU.1 is down-regulated or functionally repressed in about 50% of AML patients as a consequence of recurrent translocations (such as AML1-ETO and PML-RARα) or mutations (such as FLT3-ITD). While it is well-established that the inhibition of PU.1 function promotes AML development, our understanding of the downstream targets mediating its tumor-suppressor role is still incomplete. In order to study PU.1-driven differentiation in AML, our laboratory has recently developed a mouse model of AML driven by doxycycline (Dox)-regulated knockdown of the PU.1 gene (shPU.1) on a p53-deficient background. This is an aggressive AML model that mimics high risk disease in the clinic, as loss of function mutations of p53 characterize a subset of AML patients with particularly poor prognosis. In this system, Dox treatment shuts off a GFP-linked shRNA specifically targeting PU.1. Restoration of PU.1 expression in the context of established leukemias in vivo, and in culture-adapted cell lines derived from them, triggered myeloid differentiation and induction of cell death. In order to study the dynamic transcriptional changes underpinning these effects, we performed genome-wide transcriptome analysis on shPU.1/p53-/- AML cells isolated from the bone marrow of multiple leukemic mice transplanted with 2 different primary AML (246 and 410) that were either untreated or Dox-treated for 2, 4, or 6 days. Dox-induced restoration of PU.1 expression led to dramatic transcriptional changes closely resembling those associated with the maturation of normal mouse granulocyte/macrophage progenitors (GMPs) into neutrophils. Among the differentially expressed genes at day 2 of Dox-treatment we identified 12 "early response" genes commonly induced in both 246 and 410 AML. This group of genes included the macrophage colony-stimulating factor receptor (Csf1r), a well-known target of PU.1, as well as other genes previously implicated in myeloid differentiation, cytokine signalling, survival and cancer. In order to explore the contribution of these "early-response" genes to the range of anti-leukemic effects exerted by PU.1 restoration, we have generated retroviral shRNA vectors to test whether specifically silencing each of these genes alters PU.1-induced differentiation, inhibition of proliferation and/or death of p53-/- AML cells in vitro. In conclusion, in this work we have used a novel AML mouse model driven by reversible PU.1 inhibition to identify the PU.1-regulated transcriptome in AML, and to screen for key PU.1-response genes mediating its pro-differentiation and anti-leukemic effects in the context of this disease. Disclosures No relevant conflicts of interest to declare.
Tesis sobre el tema "Mousse PU"
1
Njeugna, Yotchou Nicole Suzie. "Contribution au développement et à l'industrialisation d'un système non-tissé 3D". Phd thesis, Université de Haute Alsace - Mulhouse, 2009. http://tel.archives-ouvertes.fr/tel-00487989.
Texto completoResumen
Réalisé dans le cadrr du pôle de compétitivité Véhicule du Futur » de la région ,11k.c Franche Comté_ cc uas_ul de thèse porta sur la hmblcmatsque du remplacement des étoffes complexes textiles utilisées dans les applications d'habillage intérieur automobile. La législation sur les véhicules hors d'usage impose des produits automobiles a 1$" ), rccyclablcs et t 95' réutilisables dl ici janvier 2015. Alin de rebondie u la problématique posée ainsi qua la législation Europécnnc, des industriels et des acteurs de la recherche de la regain mulhousienne ont lias aillé ensemble dans le cadre du poilez VERTILAP" sur le développement d'un nouveau textile non-tissé 3D. Ce travail de thèse a eu pour objectif de développer le proucde de ! abris ation de ces nouveaux matériaux ainsi que les produits non-tisses 3D obtenus. La démarche de développements procédé produits a consisté Ii faire évoluer le prototype expérimental VERTILAP' au travers de la caractérisation physique et mécanique en compression des produits obtenus. Des méthodes ci dcsj outils de caractérisations adaptés a ces nouveaux produits ont etc mis au point. L'analyse de résultats obtenus s'est appuyée sur les outils statistiques i abn de valider ces résultats. Une étude comparative avec les produits contenant de la mousse polyuréthane (PU) a permis de montrer que ces nouveaux non-tissés 3D pouvaient être utilisés en remplacement des mousses PU. La réalisation de prototypes pour des applications d'habitacle autinnobilu a été faite et a prouvé la faisabilité industrielle d'un tel remplacement. Les résultats de ce travail ont été utilisés pour [élaboration du cahier des charges d'ur prototype semi industriel VERTILAP".
2
Jaussaud, Quentin. "Génération in situ d’isocyanates par décarboxylation d’acides oxamiques pour l’élaboration de matériaux polyuréthanes". Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0139.
Texto completoResumen
Ces travaux de thèse portent sur la synthèse de polyuréthanes par génération in situ d’isocyanates, à travers différentes voies de moindre toxicité que la voie classique faisant appel à l’utilisation directe d’isocyanates. Dans un premier temps, la décarboxylation oxydante des acides oxamiques conduisant à la formation d’isocyanates a été réalisée par activation thermique grâce à l’utilisation d’un iodure hypervalent, jouant le rôle d’oxydant. Une étude cinétique sur des réactions modèles en présence d’alcool, associé à une modélisation numérique, ont notamment mis en évidence un effet catalytique de l’acide acétique, sous-produit de la réaction, sur la formation de liaisons uréthane. La formation de CO2 généré par cette réaction menant à la formation d’isocyanates, a ensuite été exploitée, pour la synthèse de mousses polyuréthanes réticulées. Les effets de différents paramètres, tels la nature des monomères ou la température de réaction, sur la morphologie et les propriétés des mousses obtenues ont ensuite été étudiés. Cette réaction d’activation des acides oxamiques a ensuite été réalisée par irradiation lumineuse en présence d’un photocatalyseur, permettant d’élaborer des films polyuréthanes. La modification des composés du mélange réactionnel a permis de développer des formulations homogènes, notamment en changeant la nature de l’iodure hypervalent utilisé. Enfin, la synthèse d’uréthanes et de polyuréthanes à partir de 1,4,2-dioxazol-5-ones a été explorée. Après une optimisation des conditions catalytiques permettant la génération d’isocyanates par ouverture de ces hétérocycles, le CO2 aussi formé a été exploité pour la production de mousses polyuréthanesThis PhD work focus on the synthesis of polyurethanes through the in situ generation of isocyanates, using pathways with lower toxicity compared to the classical approach involving the direct use of isocyanates. The oxidative decarboxylation of oxamic acids leading to the formation of isocyanates was, first, carried out by thermal activation using a hypervalent iodine as an oxidant. A kinetic study on model reactions in the presence of alcohol, combined with computational modeling, notably revealed a catalytic effect of acetic acid, a by-product of the reaction, on the formation of urethane bonds. The CO2 generated by this reaction, leading to the formation of isocyanates, was then exploited for the synthesis of cross-linked polyurethane foams. The effects of various parameters, such as the nature of the monomers or the reaction temperature, on the morphology and properties of the obtained foams were thereafter studied. This activation reaction of oxamic acids was then carried out by light irradiation in the presence of a photocatalyst, allowing the production of polyurethane films. Modifying the components of the reaction mixture enabled the development of homogeneous formulations, particularly by changing the nature of the hypervalent iodine used. Finally, the synthesis of urethanes and polyurethanes from 1,4,2-dioxazol-5-ones was explored. After optimizing the catalytic conditions for generating isocyanates through the opening of these heterocycles, the generated CO2 was exploited for the production of polyurethane foams
3
Vafiadès, Virginie. "Caractérisations microstructurale et mécanique de mousses de nickel à cellules ouvertes pour batteries de véhicules hybrides". Paris, ENMP, 2004. http://www.theses.fr/2004ENMP1199.
Texto completoResumen
"Le procédé de fabrication des mousses de nickel consiste à déposer environ 10 microns de nickel sur une mousse de polyuréthanne. Le principal objectif de cette étude est la réduction des coûts de production. La dégradation du polymère est étudiée par analyse thermogravimétrique et conduit à la superposition de trois phénomènes. Après déconvolution des courbes ATG, un modèle de dégradation thermique est proposé. L'influence de la taille de grains sur les propriétés mécaniques de la mousse est étudiée. Les parois des brins de nickel étant fines, les résultats sont comparés avec ceux de feuillards de nickel. Lorsque la microstructure devient " bambou ", la limite d'élasticité reste constante. Un modèle mécanique est présenté en incorporant l'effet de la taille des grains. Les piles à combustible, fonctionnant à de plus hautes températures, constituent un autre marché. Des essais de fluage en traction ont été réalisés et les paramètres de fluage ont été incorporés dans deux modèles mécaniques. "The nickel foam production at NiTECH starts with a 10 microns thick coating of nickel onto an open-cell polyurethane foam. The major aim of this study is to reduce the costs of production. For that purpose, the thermal degradation of the polyurethane foam is studied by thermogravimetric analysis and involves three superimposed phenomena. Afterwards, the three phenomena are separated and the thermal degradation is modeled. The dependence of the mechanical behavior of nickel foams upon grain size is studied. The foam walls being very thin, the result is compared with that of nickel foils. Once the microstructure becomes "bamboo", the yield strength remains constant. A mechanical model is finally presented incorporating the grain size effect. Besides, an other application of nickel foam could be found in the fuel cells operating at high temperatures. Tensile creep tests were carried out and the creep parameters were estimated experimentally and incorporated in two mechanical models
4
Olme, Carl-Henrik Axel. "Role and functional consequences of PU.1 transcriptional factor loss and mutations in a mouse model of radiation-induced acute myeloid leukaemia". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9122.
Texto completoResumen
In a mouse model of radiation-induced acute myeloid leukaemia (rAML), the CBA/H strain, copy loss of Sfpi1 is found in up to 90 % of cases. The gene codes for the transcription factor PU.1, an important regulator of haematopoiesis, which acts as a tumour suppressor. Point mutations specifically in the DNA sequence encoding the binding domain of the protein are found at a high frequency, suggesting that the transcription factor has a reduced function in leukaemic blasts. Transgenic CBA/H mice expressing green fluorescent protein (GFP) under the control of the Sfpi1 promoter allowed the use of flow cytometry to, for the first time, study copy loss of Sfpi1 in cases of rAML by analysing the expression levels of GFP. Analysis of mRNA levels of Sfpi1 showed there probably is a different mechanism for leukaemogenesis in cases with point mutations in the sequence encoding the DNA binding domain compared to cases with a wild type Sfpi1, the former potentially through lack of function in the transcription factor PU.1 and the latter through suppression of Sfpi1 gene expression. Fluorescent activated cell sorting was used to isolate immature bone marrow cells (BMC) containing Sfpi1 deletions from previously irradiated mice. The isolated cells were transplanted into myeloablated hosts with some success, although this new approach to study radiation-induced leukaemogenesis needs refinement. A population of immature BMCs was found to be less radiosensitive in the CBA/H strain compared to the C57BL/6 strain, which is not susceptible to rAML. This gave an indication of where the target cell population for the initial leukaemic events may occur. The work in this thesis presents novel ways of studying early events in rAML induction in the CBA/H mouse and gives new insights into the mechanisms of leukaemogenesis in the model.
5
李淑貞. "The effect of Pu-Chung-I-Chi-Tang and its associated crude drugs on Glutathione homeostasis in mouse livers". Thesis, 2000. http://ndltd.ncl.edu.tw/handle/67939120662716052427.
Texto completoResumen
碩士國立臺灣大學
藥學研究所
88
Pu-Chung-I-Chi-Tang (abbreviated as PCICT) was an herbal formula developed by the renowned medical expert Lee, Tung-Yuan back in 1180-1251, which composed of Hedysarum polybotrys, Panax ginseng, Bupleurum chinense, Cimicifuga foetida, Atractylodes macrocephala, Angelica sinensis, Glycyrrhiza uralensis and Citrus reticulata. The formula has the functions of liver protection, overall fortification and enhancement of immunity defense mechanism, inhibition of tumor growth, and enhancement of chemotherapeutic effects. Clinically, it is applied in treatments of hepatitis, intestinal tuberculosis, gastroptosis, cold, flu, tuberculosis, anemia, various malignant tumors and neurasthenia. Glutathione is constituted by three types of amino acids; its bio-synthesis and metabolism inside the human body is generally regulated by enzyme system in -glutamyl cycle. The vital enzymes that participate in the cycle are as follows: -glutamylcysteine synthetase and glutathione synthetase, which controls the bio-synthesis of glutathione; glutathione reductase and glutathione peroxidase, which regulates redox cycle and is endowed with the function of biochemical protection, while glutathione S-transferase controls physical metabolism and detoxification. Glutathione has wide ranging biological rejuvenating properties; the most critical biological functions involve: anti-oxidation defense mechanism, detoxification, regulation in oxidation-reduction related message conveyance system, regulations in immunity reactions, cancer resistance, and chemotherapeutic agents. With respect to anti-oxidation, detoxification, liver protection, cell regulation, immunity build-up, and cancer prevention, PCICT shares the same biochemical function as glutathione. This study primarily investigates the relation between PCICT and glutathione in biochemical system; the concentration of glutathione and the activities of related enzymes have been analyzed, and through their relations in -glutamyl cycle and the biochemical potencies manifested, the effects of PCICT on -glutamyl cycle is elucidated. The result of this study reveals that PCICT drives up the concentration of glutathione; both Panax ginseng and Bupleurum chinense possess anti-oxidation effect; Bupleurum chinense, Angelica sinensis, Cimicifuga foetida and Atractylodes macrocephala can regulates redox cycle, while Hedysarum polybotrys, Bupleurum chinense, Angelica sinensis, Cimicifuga foetida and Atractylodes macrocephala induces synthesis of glutathione. Summarizing these results, it was established that PCICT and the related herbs are indeed endowed with specific bio-activities and anti-oxidation effects.
Libros sobre el tema "Mousse PU"
1
1820-1898, Taschereau E. A. y Église catholique. Archidiocèse de Québec. Archevêque (1870-1898 : Taschereau), eds. Circulaire au clergé: Comme j'ai pu le constater, le fléau de "la mouche à patate" continue a faire des ravages dans nos campagnes .. [S.l: s.n., 1986.
Buscar texto completoCapítulos de libros sobre el tema "Mousse PU"
1
Zou, Gang-Ming, Meredith A. Thompson y Mervin C. Yoder. "RNAi Knockdown of Transcription Factor Pu.1 in the Differentiation of Mouse Embryonic Stem Cells". En Methods in Molecular Biology, 127–36. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-536-7_10.
Texto completoActas de conferencias sobre el tema "Mousse PU"
1
Solomon, Lauren A., Stephen K. h. Li, Jan Piskorz, Li S. Xu y Rodney P. DeKoter. "Abstract 2098: Genome-wide comparison of PU.1 and Spi-B binding sites in a mouse B lymphoma cell line". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2098.
Texto completo
2
de Cidrac, L., L. Radoï, R. Pecorari y T. Nguyen. "Tumeur à cellules géantes : à propos d’un cas récidivant et agressif à localisation mandibulaire". En 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603021.
Texto completoResumen
Introduction : La tumeur à cellules géantes (TCG) est une lésion osseuse qui se développe préférentiellement au niveau de l’épiphyse des os longs chez des sujets de 20 à 40 ans, mais exceptionnellement au niveau des maxillaires. D’étiologie inconnue, elle fait partie du groupe des tumeurs osseuses bénignes. Ce groupe nosologique comprend le granulome central à cellules géantes (GCCG), le chérubisme, le kyste anévrismal ainsi que les TCG et les tumeurs brunes liées à l’hyperthyroïdie. L’histologie ne permet pas de poser un diagnostic de certitude entre la TCG et le GCCG. Cependant, les TCG présentent un tableau clinique plus agressif et récidivant. Il existe un risque de transformation maligne en sarcome dans 10 à 20% des cas (Barthélemy 2009) et un fort potentiel métastatique (Martin-Duverneuil 2004). Observation : Le cas rapporté est celui d’une patiente de 28 ans qui présentait une tuméfaction intrabuccale douloureuse de 35mm de grand axe, en distal de 47. Le Cone Beam (CBCT) montrait une lésion osseuse radioclaire sous-jacente de 22mm de grand axe, à proximité d’un apex résiduel de 48. Le diagnostic initial était celui d’un kyste résiduel compliqué d’une cellulite. Le traitement a consisté en une énucléation simple. L’examen anatomopathologique suspectait un granulome périphérique à cellules géantes (GPCG) avec atteinte osseuse. La patiente a été perdue de vue 4 mois jusqu’à la récidive de la lésion. Le nouveau CBCT montrait une lésion ostéolytique de 40mm de grand axe, au niveau de l’angle mandibulaire, envahissant la branche montante avec perforation des corticales et atteinte des tissus mous. Une chirurgie interruptrice mandibulaire en marges saines avec reconstruction par attelle en titane préformée a été réalisée. L’examen anatomopathologique de la pièce d’exérèse n’a pas pu conclure entre GCCG et TCG. La patiente a été suivie 2 ans sans récidive. Discussion : Contrairement au GPCG, le GCCG et la TCG se développent d’abord dans l’os spongieux puis de manière excentrique jusqu’aux corticales osseuses qui peuvent être détruites et aux tissus mous qui sont refoulés ou envahis. Le contenu est mou, de couleur brun-rouge, parfois vacuolaire ou hémorragique. L’examen histologique montre un stroma assez homogène, très vasculaire, contenant, à côté de cellules mononuclées, de grandes cellules multinucléées : les cellules géantes. Le nombre de noyaux serait corrélé avec l’agressivité de la tumeur (Ficarra 1987). Moins fréquente que le GCCG, la TCG est plus agressive. Elle récidive dans environ 50% des cas. La recommandation actuelle est de la traiter par exérèse chirurgicale réglée avec des limites histologiques saines. Le curetage est insuffisant pour prévenir le risque de récidive et de transformation maligne (Barthélémy 2009). Dans le cas rapporté, la forme particulièrement agressive de la tumeur chez cette jeune patiente (récidive en 4 mois avec perforation des corticales et envahissement des parties molles) nous a orienté vers le diagnostic de TCG et un traitement radical de sa récidive. Conclusion : La TCG nécessite un diagnostic précoce et une exérèse en marges saines dès la première intervention afin de diminuer le risque de récidive et d’éviter des traitements plus mutilants.