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1
Lagarde, Antoine. "Birth, life and death of a granular raft." Thesis, Sorbonne université, 2020. http://www.theses.fr/2020SORUS054.
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Nous étudions le devenir d'une monocouche de particules à une interface huile-eau, appelée radeau granulaire, depuis sa formation jusqu'à son naufrage. Nous nous attaquons d'abord à l'interaction capillaire entre deux particules, que nous généralisons ensuite à deux radeaux granulaires. Cette force dépend fortement du nombre de particules, une conséquence directe de la déformation que chacun des radeaux impose à l'interface. Nous explorons ensuite l'interaction entre de nombreux radeaux granulaires répartis aléatoirement à l'interface. Leur agrégation est d'autant plus rapide que la distance initiale qui les sépare est faible. Le mouvement de chaque radeau ne peut être résolu analytiquement, mais l'agrégation dans son ensemble peut être décrite statistiquement. La distribution des tailles de radeaux évolue ainsi de manière auto-similaire. Nous nous tournons ensuite vers les changements structuraux qu'un radeau granulaire peut subir au cours de son mouvement, à savoir son érosion. Sa cohésion est bien supérieure à ce que prédit la théorie classique, un résultat que nous retrouvons également pour deux billes en contact. La description précise de la géométrie de la ligne de contact permet d'expliquer cette résistance étonnement grande à l'érosion. Pour finir, nous nous concentrons sur le naufrage d'un radeau granulaire, lorsque la déflexion verticale de l'interface devient trop grande. Le filament d'huile formé s'amincit en suivant un régime transitoire inhabituel, ce qui retarde l'apparition du régime final attendu. Ce résultat met l'accent sur le rôle décisif que les conditions aux limites peuvent jouer dans la transition entre deux régimes auto-similaires<br>We study the life of an axisymmetric monolayer of particles called a granular raft floating at an oil-water interface, from its formation to its sinking. We first look at the capillary interaction between a pair of beads, and generalize the result to a pair of granular rafts. The force strongly depends on the number of particles in each raft, a result that we understand by looking at the interfacial deformation each individual raft creates. Then, we explore the interaction between numerous granular rafts of different sizes randomly distributed. The aggregation is faster when the particles are initially more concentrated at the interface. The individual motion of each bead cannot be solved, but the overall clustering can be described statistically. The cluster-size distribution appears to answer to a self-similar evolution that we characterize. After that, we focus on the structural changes a granular raft can experience during its motion, and more precisely to its erosion. The cohesion of an entire raft is far higher than expected by the usual capillary theory. The same high cohesion is found between two beads in contact. A precise description of the position of the contact line accounts for the unexpectedly high resistance to erosion. Finally, we explore the dynamics of sinking of a granular raft, which happens when the vertical deflection of the interface exceeds a critical deformation. The oil thread formed during the sinking thins following an unusual path between the two classical self-similar regimes, delaying the onset of the final regime. This result emphasizes the decisive role boundary conditions can play in the transition between self-similarities
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Bozon, Aurelie. "Le RAFT-RGD radiomarqué avec un émetteur °- comme nouvel agent de radiothérapie interne vectorisée." Phd thesis, Université de Grenoble, 2013. http://tel.archives-ouvertes.fr/tel-00820235.
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Le RAFT-RGD radiomarqué avec un émetteur β- comme nouvel agent de radiothérapie interne vectorisée. L'intégrine αvβ3 est fortement impliquée en oncogenèse à travers son rôle dans la néoangiogenèse tumorale, dans la prolifération et la survie des cellules cancéreuses et dans le processus métastatique. L'intégrine αvβ3 est exprimée faiblement dans la plupart des tissus. Par contre, elle est fortement exprimée par les cellules endothéliales activées lors de l'angiogenèse et par les cellules de nombreux types de cancers invasifs. Ces caractéristiques font de l'intégrine αvβ3 une excellente cible pour l'imagerie et la thérapie de ces tumeurs. Le RAFT-RGD (Regioselectively Addressable Functionalized Template-(cyclo-[RGDfK])4) est un derivé polypeptidique constitué de quatre peptides cyclo-RGD (spécifiques de l'intégrine αvβ3) fixés sur un groupe porteur RAFT. Le RAFT-RGD cible spécifiquement l'intégrine αvβ3 in vitro et in vivo et permet la détection par imagerie nucléaire ou par fluorescence de tumeurs exprimant αvβ3 sur des modèles précliniques. Le RAFT-RGD un excellent vecteur potentiel pour cibler les tumeurs exprimant αvβ3 et pour y délivrer des traitements, que ce soit des molécules de chimiothérapie ou des radionucléides de thérapie. Cette étude est la première à évaluer le potentiel thérapeutique du RAFT-RGD radiomarqué avec un émetteur β- sur un modèle de souris Nude porteuses de tumeurs exprimant l'intégrine αvβ3. Une injection de 37 MBq de 90Y-RAFT-RGD ou de 177Lu-RAFT-RGD permet de ralentir significativement la croissance de tumeurs exprimant l'intégrine αvβ3 par rapport aux souris contrôles non traitées ou traitées avec la même activité de la molécule de contrôle non spécifique de la cible, le RAFT-RAD. En comparaison, une injection de 30 MBq de 90Y-RAFT-RGD ne permet pas de ralentir la croissance de tumeurs n'exprimant pas l'intégrine αvβ3. Le RAFT-RGD présente un bon potentiel pour le traitement de tumeurs exprimant l'intégrine αvβ3 lorsqu'il est radiomarqué avec des émetteurs β-. Mots clés : intégrine αvβ3, RAFT-RGD, ciblage tumoral, radiothérapie interne vectorisée.
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Ghadban, Ali. "Synthèse et caractérisation de glycopolymères à base d'oligoalginates en milieu aqueux." Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00923140.
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La synthèse de glycomonomères à base d'oligoalginate (AlgiMERs) et leur polymérisations conventionnelles et RAFT en solution aqueuse ont été étudiés. Premièrement, l'oligoalginates de départ ont été transformés soit dans le glycosylamines correspondant ou en amino alditols (via une amination réductrice). A cette étape, l'optimisation des protocoles d'amination ont été identifiées par la réalisation d'une étude systématique sur un simple acide uronique (acide D-glucuronique). Deuxièmement, les sucres aminés ont été obtenus a réagi avec une électrophile portant un groupe vinyle polymérisable à céder AlgiMERs. Le glycomonomères résultant n'a pas homopolymérisé même en haute force ionique et pour temps de réaction longs, mais leur copolymérisations radicalaire conventionnelles avec N-(2-hydroxyéthyl)méthacrylamide (HEMAm) donne de glycopolymères avec de haute mass molaires (Mw ≈ 1.500.000 Da) contenant jusqu'à 50% en masse de oligoalginate. Une étude cinétique a confirmé que la consommation des deux monomères suivi une cinétique de premier ordre et que les AlgiMERs ont été intégrées tôt dans le processus de polymérisation. Basé sur ces résultats, l'enquête a été étendue à la copolymérisation radicalaire vivante en milieu aqueuse et glycopolymères gradient bien définies ont été obtenues (Mn = 12 000 Da - 90 000 Da; PDI ≤ 1,20). Enfin, j'ai pu prouver qu'un polymère synthétique portant des résidus d'oligo (1→4)-α-L-guluronan conduit des gels en présence d'ions Ca2+ et offre un hydrogel transparent et stable.
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Delaunay, Jean-Louis. "Rôle des microdomaines membranaires dans le ciblage apical de la nucléotide pyrophosphatase NPP3 dans les cellules MDCK." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2007. http://tel.archives-ouvertes.fr/tel-00429983.
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La membrane plasmique des cellules épithéliales polarisées comporte deux domaines distincts, le domaine apical et le domaine basolatéral. Chaque domaine a une composition en lipides et en protéines déterminée, leur permettant d'assurer des fonctions spécifiques. Les mécanismes moléculaires responsables du tri et de l'adressage des protéines transmembranaires vers le pôle apical sont encore mal connus. La membrane apicale est enrichie en glycosphingolipides et en cholestérol qui forment des microdomaines appelés « rafts ». Expérimentalement, les rafts peuvent être isolés sous forme de DRM (detergent-resistant membranes) définis par leur résistance à un détergent non ionique, le Triton X-100. Il a été proposé que les rafts recrutent les protéines apicales au niveau du réseau trans-golgien et servent de plateforme pour leur adressage au pôle apical. Effectivement les protéines ancrées par le glycosylphosphatidyl-inositol sont résistantes au Triton et sont localisées en général à la membrane apicale. En revanche, la plupart des protéines transmembranaires apicales sont solubles dans le Triton, bien qu'elles soient résistantes à l'action de détergents plus doux comme le Lubrol WX. L'objectif des travaux de thèse a été d'étudier le rôle des rafts dans l'adressage apical de protéines transmembranaires et de comprendre l'effet différentiel du Triton et du Lubrol sur leur solubilisation. Les nucléotides pyrophosphatases NPP1 (basolatérale) et NPP3 (apicale) exprimées de façon stable dans les cellules MDCK ont servi de modèles. NPP3 est insoluble dans le Lubrol et partiellement insoluble dans le Triton, tandis que NPP1 est essentiellement solubilisée. L'étude de la localisation et de la sensibilité aux détergents de mutants et de chimères combinant des domaines cytoplasmiques, transmembranaires et extracellulaires de NPP3 et NPP1, a montré qu'il n'existait pas de corrélation stricte entre l'adressage apical et la résistance aux détergents. La résistance de NPP3 à la solubilisation par le Lubrol est acquise précocement au cours de sa biosynthèse, indépendamment de sa destination finale. Cette résistance dépend d'acides aminés chargés positivement situés dans la queue cytoplasmique, proches de la membrane. Afin de comprendre la sélectivité du Triton et du Lubrol dans l'extraction des protéines et des lipides membranaires, la composition lipidique des DRM obtenus après extraction par le Triton et le Lubrol a été comparée. Les DRM extraits par le Triton et le Lubrol sont enrichis en cholestérol ce qui correspond à la définition des rafts. Cependant, les DRM Triton sont appauvris en lipides du feuillet interne tandis que les DRM Lubrol sont enrichis en phosphatidyléthanolamine. Les DRM Lubrol sont également enrichis en protéines associées au feuillet interne de la membrane. En conclusion, ces travaux montrent que la résistance de la protéine apicale NPP3 à l'extraction par le Lubrol, et en partie par le Triton, est une propriété intrinsèque qui correspond probablement à une adaptation de la protéine à la composition lipidique du domaine apical, mais que cette propriété ne détermine pas son adressage polarisé. De plus, ces travaux montrent que les détergents sont des outils très intéressants pour étudier les interactions entre les protéines et les lipides membranaires, mais qu'il n'existe probablement pas de détergent capable d'isoler de façon stricte des microdomaines membranaires tels que sont définis les rafts. Nos résultats suggèrent que le feuillet interne des rafts est enrichi en phosphatidyléthanolamine et en cholestérol, qu'il est en partie solubilisé par le Triton, ce qui déstabiliserait les protéines transmembranaires et entraînerait leur extraction. Mots clés: détergent, raft, , ciblage apical, cholestérol, microdomaine membranaire, feuillet interne de la membrane, phosphatidyléthanolamine.
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Zgheib, Nancy. "Élaboration de particules de latex composites à base d'oxyde de cérium par polymérisation radicalaire en milieu aqueux dispersé." Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00862401.
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Nous décrivons dans ce travail l'élaboration de latex nanocomposites à base d'oxyde de cérium en vue d'applications dans le domaine des revêtements. Deux procédés originaux ont été développés afin de contrôler la morphologie des particules. Dans un premier temps, nous avons tiré parti de la forte densité de charges des nanoparticules d'oxyde de cérium pour stabiliser des particules de latex obtenues par polymérisation en émulsion ou en miniémulsion " de Pickering ". Dans les deux cas, la réaction est conduite en présence des particules inorganiques et d'un agent complexant à caractère acide, l'acide méthacrylique, en l'absence de tout tensioactif. Des particules de latex, décorées en surface par les nanoparticules d'oxyde de cérium ont été ainsi synthétisées. Par la suite, une stratégie qui consiste à utiliser des chaînes de polymères hydrophiles, réactivables (macro-agent RAFT) et préalablement adsorbées à la surface des nanoparticules d'oxyde de cérium a été envisagée. Ces chaînes polymères comportant à la fois des fonctions carboxyliques et un groupe trithiocarbonate terminal sont capables de stabiliser la suspension colloïdale des nanoparticules et de réamorcer la polymérisation en mode semi-continu permettant ainsi l'encapsulation de l'oxyde de cérium. Une optimisation visant à utiliser un procédé batch a également été évaluée. Quelle que soit la stratégie employée, une attention toute particulière a été portée à la stabilité colloïdale du milieu ainsi qu'à la cinétique de la réaction. La morphologie des particules composites a été caractérisée par MET et cryo-MET et reliée aux conditions de modification de surface et de polymérisation
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Granlund, Andreas, and Jonas Torvaldsson. "Övergivande av fartyg i isfarvatten : En kvalitativ studie över svenska rederiers beredskap inför nödsituationer i isfarvatten." Thesis, Linnéuniversitetet, Sjöfartshögskolan, SJÖ, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-11916.
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Trots att isen lagt sig på Bottenhavet avstannar inte handeln med de norrländska hamnarna. Många av de fartyg som anlöper dessa hamnar har som primär överlevnadsfarkost en frifallslivbåt, en typ av livbåt som av experter har blivit utdömda som värdelösa i samband med is. Även fartygens sekundära överlevnadssystem, som består av uppblåsbara flottar, har blivit kritiserat. Syftet med detta arbete var att undersöka vad svenska rederier med fartyg som bär denna typ av livbåt har för beredskap inför en eventuell nödsituation i isen. Undersökningen har grundats på en kvalitativ intervjustudie med representanter från tre svenska rederier som bedriver vintersjöfart. Studien har visat på stora skillnader mellan de olika rederierna gällande rutiner för att operera i is. Inget av rederierna som intervjuats har haft en speciell plan för övergivandet av fartyg i isförhållanden, trots att de har en säkerhetsorganisation som blivit godkänd av den svenska Transportstyrelsen.<br>Even though the ice has formed on the Gulf of Bothnia the trade with the northern ports of Sweden and Finland does not cease. Many of the ships calling these ports have their primary survival craft in form the of a freefall lifeboat, a survival craft that experts have condemned as useless in ice. Even the ship's secondary survival system consisting of inflatable rafts has been criticized. The purpose of this study was to examine what kind of plan Swedish shipping companies, who operate vessels that carry this type of lifeboat, have to deal with a possible emergency situation in the ice. The study was based on qualitative interviews with representatives from three Swedish shipping companies operating in winter conditions. The study revealed great differences between the various companies in routine procedures when operating in ice. None of the interviewed companies had a special plan for the abandonment of ships in ice conditions, although they have a safety organization approved by the Swedish Transport Agency.
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Yu, Lingli. "Nerve Growth Factor Signaling from Membrane Microdomain to Nucleus : Differential Regulation by Caveolins." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2012. http://tel.archives-ouvertes.fr/tel-00796393.
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At the plasma membrane, both NGF receptors have been shown to localized to lipid rafts, specific subdomains that are enriched in cholesterol, sphingolipids and the presence of caveolin proteins (Cav1 and/or Cav2). The focus of this work is on this membrane microenvironment mediated modulation of NGF signaling which via two receptors: p75NTR and TrkA. In the present work we found that overexpression of Cav-1 in mouse dorsal root ganglia neurons significantly impacted neurite extension. Similarly, overexpression of Cav-1 in PC12 cells strongly inhibits their ability to grow neurites in response to NGF. It inhibits NGF signaling without, impairing transient MAPK pathway activation. Rather, it does so by sequestering NGF receptors in lipid rafts, which correlates with the cell surface localization of downstream effectors, and phosphorylated-Rsk2, resulting in the prevention of the phosphorylation of CREB. By contrast, overexpression of Cav-2 potentiates NGF induced differentiation, which is accompanied by sustained activation of downstream effectors, and standard internalization of the receptors. This differential effect could be due to the different localization of Caveolins, that modifies the microenvironment, thereby affecting NGF signaling. Furthermore, PC12 cells expressing the non-phosphorylatable Cav-1 mutant (S80V), neither TrkA trafficking or CREB phosphorylation are inhibited and the response resembles that observed in Cav-2 expressing PC12 cells. These studies underline the interplay between caveolins and NGF signalling, offering insight into the potential impact of Caveolin-1 and mutations thereof in certain cancers where NGF signaling is involved.
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Wenk, Christiane. "Chirurgie guidée par fluorescence des fibrosarcome félin et développement et caractérisation d'un vecteur bi-fonctionnel pour le ciblage du cancer." Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00843015.
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Actuellement, la chirurgie représente la première indication pour la thérapie du cancer. Néanmoins, la résection complète du tissu tumoral, la détection des micrométastases et la préservation des tissus sains pendant l'intervention représentent un enjeu majeur et influencent fortement le pronostic du patient. Les récents développements technologiques en imagerie pour la chirurgie guidée des cancers ont conduit à des résultats précliniques prometteurs et les premiers essais cliniques utilisant des traceurs non-spécifiques confirment déjà le potentiel de ces systèmes pour l'amélioration de la chirurgie. De plus, le diagnostic précoce des tumeurs, ainsi que le développement de thérapies ciblées sont également des axes majeurs de recherche en cancérologie. Dans ce contexte notre équipe a précédemment développé un vecteur synthétique ciblant un récepteur cellulaire l'intégrine αVβ3. Ce vecteur est constitué d'un châssis décapeptidique cyclique RAFT (Regioselectively Addressable Functionalized Template) et présentant deux domaines indépendants permettant de séparer les deux fonctions du vecteur. Sur un domaine, la fonction de ciblage est assurée par la présentation multivalente de ligands -RGD- spécifiques du récepteur. L'autre domaine du vecteur porte les molécules d'intérêt à vectoriser, agents thérapeutiques ou de détection pour l'imagerie médicale. Dans la première partie de ces travaux, nous avons évalué la combinaison de ce vecteur couplé à un fluorophore avec une sonde portative pour imager et guider le chirurgien pendant la chirurgie des fibrosarcomes spontanés chez le chat. Cette étude représente une preuve de concept pour la translation clinique chez l'homme. Les résultats ont montré que l'injection du traceur ne provoquait pas d'effets toxiques chez le chat et permettait un marquage spécifique de la tumeur avec un bon ratio tumeur/tissu sain, qui devrait améliorer la qualité de la résection tumorale en aidant le chirurgien à mieux délimiter les marges du tissu tumoral. Dans la seconde partie de ces travaux nous avons développé un nouveau vecteur bi-fonctionnel dérivé du RAFT-RGD. Au composé d'origine a été ajoutée une séquence peptidique clivable par la matrixmetalloprotease-9, une enzyme surexprimée dans la tumorigénèse. Cette molécule à fluorescence activable a montré une amélioration du ciblage tumoral in vitro et in vivo comparée au RAFT-RGD suggérant un effet additionnel lié au double ciblage. Ces résultats préliminaires encouragent la poursuite de sa caractérisation pour son potentiel de " pro-drug " mais également pour l'étude des interactions entre l'intégrine et l'environment tumoraux.
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Grauby-Heywang, Christine. "Etude à l'interface air-eau de mélanges lipidiques susceptibles de former des RAFTS membranaires." Habilitation à diriger des recherches, Université Sciences et Technologies - Bordeaux I, 2008. http://tel.archives-ouvertes.fr/tel-00685610.
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La première partie de ce manuscrit concerne l'étude en monocouches à l'interface air-eau de mélanges lipidiques susceptibles de former des "rafts" dans les membranes cellulaires, c'est-à-dire des domaines enrichis spécifiquement en certains lipides (glycolipides, sphingolipides, cholestérol) et certaines protéines. Du fait de leur composition spécifique, ces domaines sont caractérisés par une phase particulière ("liquid ordered phase") présentant des caractéristiques intermédiaires entre celles des phases fluides et condensées. Les principales méthodes mises en oeuvre dans cette étude sont des mesures de pression de surface (isothermes de compression, analyse des aires moléculaires moyennes, études de désorption en présence de beta-cyclodextrine), la microscopie de fluorescence (après marquage de la monocouche à l'aide d'une sonde fluorescente), ou la microscopie à l'angle de Brewster. Une des parties les plus importantes de ce travail concerne le comportement de monocouches constituées d'un glycolipide, le GM3, en présence de phospholipides (phase fluide), de sphingomyéline ou de cholestérol (phase "raft"). Les mesures montrent que le GM3 n'a pas d'affinité particulière pour la sphingomyéline. De même, son interaction avec le cholestérol induit une condensation de la monocouche similaire à celle observée avec les phospholipides en phase fluide, et ne permet pas le maintien du cholestérol dans la monocouche lors d'une désorption induite par la beta-cyclodextrine. Ce manque d'interaction spécifique du GM3 avec des lipides présents dans les "rafts" permet donc d'expliquer sa répartition assez large dans les membranes d'adipocytes, tant dans la phase fluide que dans les "rafts". La seconde partie concerne l'étude de molécules organiques de type hémicyanine organisées en monocouches de Langmuir et films de Langmuir-Blodgett, étudiés par des méthodes complémentaires (absorption, spectroscopie de fluorescence stationnaire et résolue en temps), mesures de pression de surface et microscopie de fluorescence. Ces hémicyanines comportent une chaîne hydrophobe nécessaire à la réalisation de films organisés stables. Ces derniers peuvent avoir de multiples applications dans la collecte et le transfert de l'énergie lumineuse ou les analyses chimiques ou biochimiques (reconnaissance sélective de cations lors de pollutions par exemple).
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Minshall, Brianna Lynn. "Sex differences in stress-enhanced fear learning and anxiety-like behavior following acute early life stress: Role for circulating gonadal steroid hormones." Miami University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=miami1618562926270776.
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Pflughaupt, Robin L. "In pursuit of RAFT-functional polyethylene : exploration of a novel class of Sn-RAFT agents and the preparation and application of RAFT-functional polyethylene-like poly(ω-pentadecalactone)". Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/64038/.
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This work explores the preparation of Reversible Addition-Fragmentation chain-Transfer (RAFT)-functional polyethylene (PE). Challenges in developing methods to control the polymerization of primary radicals and prepare functional polyethylene are significant. Modest control over ethylene polymerization demonstrated via F-RAFT polymerization inspired our interest in RAFT agent design and we envisaged that metallo-RAFT agents could present different reactivities towards primary radicals. Considering the challenge of attempting to develop chemistry for the controlled radical polymerization of primary radicals, preparation of RAFT-functional polyethylene-like poly(ω-pentadecalactone) (PPDL) was also investigated. We envisaged the preparation of RAFT-functional PPDL to be more convenient than reported strategies to prepare functional polyethylene all whilst being a “green” alternative to PE that may be suitable for some applications. Chapter 1 discusses challenges in preparing functional polyethylene via controlled radical polymerization techniques. Furthermore, metallo-RAFT chemistry and the ring-opening polymerization of macrocyclic esters are reviewed. Chapter 2 describes the synthesis of PPDL via enzymatic ring-opening polymerization (eROP). Using a bifunctional initiator appropriate for the RAFT polymerization of acrylic and styrenic monomers, RAFT-functional poly(ω-pentadecalactone) was prepared. Furthermore, chain extension of the macro-chain-transfer agent was utilized to prepare acrylic and styrenic block copolymers of PPDL. To our knowledge, this is the first preparation of block copolymers of poly(ω-pentadecalactone) via a combination of eROP and RAFT polymerization techniques. Chapter 3 describes the large scale synthesis and characterization of a selection of acrylic block copolymers of PPDL suitable for fuels applications. Furthermore, the fuels testing of these copolymers for cold flow applications is described. In general, all block copolymers of PPDL, in particular poly(ω-pentadecalactone)-b-poly(isodecyl acrylate) improved the cold flow performance of various diesel fuels. Chapter 4 reports the synthesis of Sn-RAFT agents and their subsequent use in the controlled radical polymerization of several vinylic monomers. Chapter 5 summarizes the findings in chapters 2 – 4 and Chapter 6 communicates the associated experimental data.
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Muschol, Waldemar, Gerhard Püschel, Martina Hülsmann, and Kurt Jungermann. "Eicosanoid-mediated increase in glucose and lactate output as well as decrease and redistribution of flow by complement-activated rat serum in perfused rat liver." Universität Potsdam, 1991. http://opus.kobv.de/ubp/volltexte/2010/4589/.
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Rat serum, in which the complement sytem had been activated by incubation with zymosan, increased the glucose and lactate output, and reduced and redistributed the flow in isolated perfused rat liver clearly more than the control serum. Heat inactivation of the rat serum prior to zymosan incubation abolished this difference. Metabolic and hemodynamic alterations caused by the activated serum were dose dependent. They were almost completely inhibited by the cyclooxygenase inhibitor indomethacin and by the thromboxane antagonist 4-[2-(4-chlorobenzenesulfonamide)-ethyl]-benzene-acetica cid (BM 13505), but clearly less efficiently by the 5’-lipoxygenase inhibitor nordihydroguaiaretic acid and the leukotriene antagonist N-{3-[3-(4-acetyl-3-hydroxy-2-propyl-phenoxy)-propoxy]-4-chlorine-6-methyl-phenyl}-1H-tetrazole-5-carboxamide sodium salt (CGP 35949 B). Control serum and to a much larger extent complement-activated serum, caused an overflow of thromboxane B₂ and prostaglandin F₂α into the hepatic vein. It is concluded that the activated complement system of rat serum can influence liver metabolism and hemodynamics via release from nonparenchymal liver cells of thromboxane and prostaglandins, the latter of which can in turn act on the parenchymal cells.
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Chainani, Rick. "THE EFFECTS OF NEUROTENSIN ON THE RAT DISTAL COLON." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3205.
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The enteric nervous system controls the gut through the release of specific neurotransmitter and neuromodulators at specific sites such as mucosal secretory cell or smooth muscle cell. In the present study, we have examined the response to one of these neurohumoral agents, Neurotensin, in the rat distal colon. Neurotensin is a paracrine and endocrine modulator of the digestive tract. Even though these effects have been seen in colonic preparations, there are very few functional studies of the effects of Neurotensin in the rat colon, especially the distal colon. In the current study we propose the following hypothesis that Neurotensin will lead to contractile effect on basal tone and phasic contraction in the distal rat colon and will mediate this process primarily through the NT1 receptor. This hypothesis is based on evidence from the mixed action of Neurotensin in other regions of the gut and the more widespread distribution of the NT1 receptor. We have identified two specific aims to investigate this hypothesis. Aim 1 is to investigate the role of Neurotensin in tonic contraction and phasic contraction of the distal rat colon. In this aim, we will expose distal rat colon strips to varying doses of Neurotensin and record changes in basal tone and phasic activity. For our second aim, we will investigate the receptors mediating these responses to Neurotensin. In this aim, we will introduce NT1, NT2, and nonspecific inhibitors to distal rat colon and observe modulation in Neurotensin effects. We will also determine the existence of the receptors via Western Blot. The rat distal colon did respond in a dose-response fashion to varying doses of Neurotensin, but elicited different effects dependent on the strip preparation. When the mucosa was intact, circular muscle responded with an inhibitory effect to phasic activity, but there was little to no change in tonic activity. When the mucosa was removed, the circular muscle responded to Neurotensin by eliciting an increase in tonic activity, but had no effect on phasic activity. The use of SR48692, a specific NT1 receptor inhibitor, showed that the effects that were observed due to Neurotensin were not mediated through the NT1 receptor. With the use of SR142948, a non-selective NT1/NT2 inhibitor, the effects of Neurotensin was completely abolished. This led us to believe that the observed effects were mediated through a Neurotensin receptor and that receptor is likely the NT2 receptor. This was confirmed by the use of the specific NT2 receptor antagonist, levocabastine. The existence of the receptor in rat colon had to be confirmed in order to ensure that the effects observed were mediated through the NT2 receptor and not from an outside mediator. Western Blot analysis confirmed the existence of the NT2 receptor within the mucosa, within the muscle, and within the intact preparation of the distal rat colon. Although these results conflict with our hypothesis, it provides for an interesting template and avenue of exploration.
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Neuschäfer-Rube, Frank, Gerhard Püschel та Kurt Jungermann. "Characterization of prostaglandin-F₂α-binding sites on rat hepatocyte plasma membranes". Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2010/4586/.
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Prostaglandin (PG)F₂α has previously been shown to increase glucose output from perfused livers and isolated hepatocytes, where it stimulated glycogen phosphorylase via an inositol-trisphosphatedependent signal pathway. In this study, PGF₂α binding sites on hepatocyte plasma membranes, that might represent the putative receptor, were characterized.
Binding studies could not be performed with intact hepatocytes, because PGF₂α accumulated within the cells even at 4°C. The intracellular accumulation was an order of magnitude higher than binding to plasma membranes.
Purified hepatocyte plasma membranes had a high-affinity/low-capacity and a low-affinity/highcapacity binding'site for PGF₂α. The respective binding constants for the high-affinity site were Kd = 3 nM and Bmax = 6 fmol/mg membrane protein, and for the low-affinity site Kd = 426 nM and Bmax = 245 fmol/mg membrane protein.
Specific PGF₂α binding to the low-affinity site, but not to the high-affinity site, could be enhanced most potently by GTP[γS] followed by GDP[ϐS] and GTP, but not by ATP[γS] or GMP.
PGF₂α competed most potently with [³H]PGF₂α for specific binding to hepatocyte plasma membranes, followed by PGD₂ and PGE₂.
Since the low-affinity PGF₂α-binding site had a Kd in the concentration range in which PG had previously been shown to be half-maximally active, and since this binding site showed a sensitivity to GTP, it is concluded that it might represent the receptor involved in the PGF₂α signal chain in hepatocytes. A biological function of the high-affinity site is currently not known.
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Hespeling, Ursula, Gerhard Püschel, Kurt Jungermann, Otto Götze, and Jörg Zwirner. "Stimulation of glycogen phosphorylase in rat hepatocytes via prostanoid release from Kupffer cells by recombinant rat anaphylatoxin C5a but not by native human C5a in hepatocyte/Kupffer cell co-cultures." Universität Potsdam, 1995. http://opus.kobv.de/ubp/volltexte/2010/4590/.
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Human anaphylatoxin C3a had previously been shown to increase glycogenolysis in perfused rat liver and prostanoid formation in rat liver macrophages. Surprisingly, human C5a, which in other systems elicited stronger responses than C3a, did not increase glycogenolysis in perfused rat liver. Species incompatibilities within the experimental system had been supposed to be the reason. The current study supports this hypothesis: (1) In rat liver macrophages that had been maintained in primary culture for 72 h recombinant rat anaphylatoxin C5a in concentrations between 0.1 and 10 pg/ml increased the formation of thromboxane A₂, prostaglandin D₂, E₂ and F₂α6- to 12-fold over basal within 10 min. In contrast, human anaphylatoxin C5a did not increase prostanoid formation in rat Kupffer cells. (2) The increase in prostanoid formation by recombinant rat C5a was specific. It was inhibited by a neutralizing monoclonal antibody. (3) In co-cultures of rat hepatocytes and rat Kupffer cells but not in hepatocyte mono-cultures recombinant rat C5a increased glycogen phosphorylase activity 3-fold over basal. This effect was inhibited by incubation of the co-cultures with 500 μM acetylsalicyclic acid. Thus, C5a generated either locally in the liver or systemically e.g. in the course of sepsis, may increase hepatic glycogenolysis by a prostanoid-mediated intercellular communication between Kupffer cells and hepatocytes.
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Bruce, Kamilla. "Jag hade aldrig rast... : En lärare berättar." Thesis, Karlstad University, Faculty of Arts and Education, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-4759.
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<p>Syftet med mitt arbete är att få en fördjupad insikt i en lärares arbete, och få kunskap om hur stress och utbrändhet kan påverka arbetet som lärare. För att få denna förståelse har jag intervjuat en manlig lärare, Ove. Han har arbetat som lärare i fyrtio år. Genom att använda mig utav livsberättelsemetoden har jag fått tagit del av hans erfarenheter. I hans berättelse framkommer det att stress var inledningsvis något som var positivt för hans arbete. Han berättar att det är lätt att brinna för sitt arbete och lägga ner all sin tid och energi för det man tycker är roligt och intressant. Genom berättelsen får man ta del av hur den positiva stressen vänder, och Ove blir sjukskriven. Genom berättelsen framkommer Oves frustration över hur lärarrollen har förändrats genom åren. Det framkommer att det finns många faktorer som är avgörande hur en lärare ska fördela sin tid. Exempel på sådana faktorer är hur samhället och hur lärarrollen har förändrats genom åren.</p><br><p>The purpose with my work is to get a deeper insight into a teacher's job, and gain insight into how stress and burnout can affect the work as a teacher. To obtain this understanding, I interviewed a male teacher, Ove. He has worked as a teacher for forty years. The method I have used is a personal life story around this person. In his story it becomes clear that stress was initially something that was positive for his work. He says that it is easy to burn for their work and spend all their time and energy for what we think is fun and interesting. Through the story may take some of the positive stress turns, and Ove become sick. Through the story emerges Oves frustration with how the teacher's role has changed over the years. It is found that there are many factors that determine how a teacher should allocate their time. Examples of these factors is how society and how the teacher's role has changed over the years.</p>
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Püschel, Gerhard, C. Kirchner, A. Schröder, and Kurt Jungermann. "Glycogenolytic and antiglycogenolytic prostaglandin E₂ actions in rat hepatocytes are mediated via different signalling pathways." Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2010/4585/.
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Prostaglandin E₂ has been reported both to stimulate glycogen-phosphorylase activity (glycogenolytic effect) and to inhibit the glucagon-stimulated glycogen-phosphorylase activity (antiglycogenolytic effect) in rat hepatocytes. It was the purpose of this study to resolve this apparent contradiction and to characterize the signalling pathways and receptor subtypes involved in the opposing prostaglandin E₂ actions.
Prostaglandin E₂ (10 μM) increased glucose output, glycogen-phosphorylase activity and inositol trisphosphate formation in hepatocyte cell culture andor suspension. In the same systems, prostaglandin E₂ decreased the glucagon-stimulated (1 nM) glycogen-phosphorylase activity and cAMP formation.
The signalling pathway leading to the glycogenolytic effect of PGE₂ was interrupted by incubation of the hepatocytes with 4P-phorbol 12-myristate 13-acetate (100 nM) for 10 min, while the antiglycogenolytic effect of prostaglandin E₂ was not attenuated.
The signalling pathway leading to the antiglycogenolytic effect of prostaglandin E₂ was interrupted by an incubation of cultured hepatocytes with pertussis toxin (100 ng/ml) for 18 h, whereas the glycogenolytic effect of prostaglandin E₂ was enhanced.
The EP₁/EP₃ prostaglandin-E₂-receptor-specific prostaglandin E₂ analogue Sulproston had a stronger glycogenolytic potency than the EP₃ prostaglandin-E₂-receptor-specific prostaglandin E₂ analogue Misoprostol. The antiglycogenolytic potency of both agonists was equal.
It is concluded that the glycogenolytic and the antiglycogenolytic effects of prostaglandin E₂ are mediated via different signalling pathways in hepatocytes possibly involving EP₁ and EP₃ prostaglandin E₂ receptors, respectively.
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Ismail, Zul Izhar Mohd. "The effects of cocaine exposure during early life on rat brain development /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18177.pdf.
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Kakio, Atsuko. "Formation Mechanisms and Properties of Ganglioside-Bound Altzheimer's Amyloid β-Protein in Raft-Like Membranes". 京都大学 (Kyoto University), 2003. http://hdl.handle.net/2433/148530.
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Nasa, Zeyad, and nasa zeyad@med monash edu au. "Characterization of the Rat Relaxin-like Factor Gene." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080514.100729.
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Relaxin-like factor (RLF), also known as Leydig insulin-like peptide (Ley-I-L) or Insulin 3 (INSL3), is a newly characterized member of the insulin peptide family. Amino acid sequence homology revealed that RLF is more closely related to relaxin than any other insulin-like hormones. The main aim of this thesis was to sequence the rat RLF (Relaxin-like factor) gene and determine the structure and organisation of the gene. Secondly to compare the structural organisation of the rat RLF/JAK3 genomic region with that of the mouse and human, using bioinformatic databases. Thirdly to further investigate the signalling pathways for the RLF receptor, in particular the NFÛB pathway. The homology between rat and mouse in the JAK3/RLF region revealed 84.4 % similarity over 1262 bp of DNA sequence, observing that unlike the mouse, the rat RLF promoter is separated from the JAK3 gene by around 700-1000 bp. Similarly in humans, the RLF gene is located around 4 kb downstre am from JAK3. Also Protein kinase A (PKA) was the only signalling pathway which dispalyed major induction and no inhibitory effects were observed through the NFÛB signalling pathway.
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Kim, Michael. "Effect of Hemoglobin-Based Oxygen Carriers on Arterial Pressure and Vasoactivity in the Rat Mesentery." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1675.
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Hemoglobin-based oxygen carriers provide a promising future as an alternative to human blood transfusions. Hemoglobin-based oxygen carriers, HBOCs, provide a lowcost, easy to maintain, and safe solution. They require no refrigeration and are universally compatible, and the required transfusion volume is less than that of a normal transfusion. HBOCs have been known to have adverse side effects such as renal toxicity, gastrointestinal dismotility, and hypertension. Many of these problems stem from the lack of a membrane, which protects the hemoglobin from dissociating and extravasating into the blood vessel wall. Extracellular hemoglobin, like that found in HBOCs, has a greater affinity for nitric oxide, NO, than oxygen due to the lack of a protective membrane like that of a red blood cell. This NO scavenging effect has been used to explain the increase in mean arterial pressure, MAP, as well as any other smooth muscle dysfunction. NO has been accepted as the endothelial derived relaxing factor which serves to dilate or maintain the vascular tone of the arterioles. It is theorized that the drop in NO due to scavenging by hemoglobin causes an increase in MAP. In this study, using the mesentery of rats as a model to observe the microcirculation, various doses of HBOC 201, HBOC 205 (MW 400), and HBOC 205 (MW 600) were infused into the rats. Measurements of MAP and arteriolar diameter were taken in response to increasing doses of each HBOC to establish a dose-response relationship. Chemicals such as sodium nitrite, NaNO2, and Nw- Nitro-L-arginine methyl ester hydrochloride, L-NAME, a NOS inhibitor, were used to chemically alter the levels of NO. The purpose was to see if modifying the levels of NO could alter the changes in MAP due to the HBOCs. MAP rose in response to the increasing doses of HBOCs, but the arterioles failed to show any vasomotor responses. NaNO2 showed an ability to reduce the increase in MAP as a result of the HBOC, but again had no affect on arteriolar diameter. L-NAME was able to reproduce changes in MAP similar to that of the HBOCs, but again had no effect on diameter. The results support the theory of NO scavenging by the HBOC leading to an increase in MAP. The lack of activity in arterioles indicates that NO may not be a major factor in controlling vascular tone in this tissue. The results support that HBOC’s side effects are a result of NO scavenging, but further work is needed to better understand vasoactivity in the mesentery.
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Meliagros, Pete. "Effects of Hemoglobin-Based Oxygen Carriers on the Vasoactivity of the Spinotrapezius Muscle of the Rat." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1674.
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Hemoglobin-based oxygen carriers (HBOCs) offer a safe, more plentiful and long term alternate to blood banks. However, they have been found to increase blood pressure which can be attributed to an increase in total peripheral resistance (TPR). Lumenal nitric oxide (NO) scavenging by these HBOCs seems to be responsible for this hypertensive effect. In addition, it is believed that hemoglobin (Hb) tetramers and dimers may extravasate and consume additional nitric oxide in the perivascular and interstitial space. The purpose of the present study was to elucidate the role of NO scavenging and to confirm extravasation as a contributor to HBOC vasopressor effects in the spinotrapezius muscle. The present study investigated the vessel reactivity and mean arterial pressure response to three HBOCs: HBOC 201, HBOC 205 MW 400, and HBOC 205 MW 600. These varied in molecular weight (MW) and percentage of tetramers and dimers. It was found that larger polymers of HBOC showed no significant decrease in vasoactivity. Although larger polymers are less likely to extravasate, the remaining tetramers and dimers seem sufficient to contribute to the observed vasoactivity. Using NaNO2, a NO donor, in conjunction with the HBOCs almost completely abolished this hypertensive effect at higher concentrations. Further examination utilizing a nitric oxide synthase (NOS) inhibitor to mimic the HBOC vasopressor effects demonstrated that lower concentrations of NaNO2 were able to abolish the hypertensive effect. In vitro studies only further supported these results by demonstrating that NO consumption increases with HBOC dose. HBOC labeled with TRITC showed conclusive evidence that extravasation also plays a role in NO scavenging, even when minimal amounts of tetramers and dimers are present. In conclusion, the present study offers strong evidence that NO scavenging is responsible for the observed vasopressor effects. It also offers evidence supporting the theory that HBOC extravasation may be contributing to these vasopressor effects as well.
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Aitchison, Lara Karyn. "Exposure to benzylpiperazine (BZP) in adolescent rats: Adulthood changes in anxiety-like behaviour." Thesis, University of Canterbury. Psychology, 2006. http://hdl.handle.net/10092/1291.
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Increasingly, individuals in New Zealand are taking "herbal highs" with little knowledge of their possible long-term effects. Benzylpiperazine (BZP) is the predominant base drug in most herbal highs. The limited research into BZP has suggested that it produces similar effects to amphetamine, but could be 10 times less potent. There are to date, however, no long-term behavioural studies of BZP exposure. This study therefore, investigated effects of BZP exposure in adolescent male and female rats on subsequent measures of anxiety-like behaviours in adulthood. One group of experimental animals was treated daily with BZP, whereas another group received the same total amount of drug via a four day "binge" regime. The results suggested that, when observed in a Y-maze, social interaction test and a light/dark emergence test, BZP-treated rats were more anxious than control animals. In the Y-maze, male controls were more active than female controls, but BZP-treated females were more active than treated males. Results of this interaction indicate that the male rats may have been more affected by the administration of BZP during adolescence than females. Additionally, rats given the binge dose regime showed significantly increased anxiety in the Y-maze relative to the daily-exposed or control rats'. This suggests that larger quantities of BZP over a shorter time frame produce more detrimental effects than smaller quantities of BZP over a longer time frame. Overall, it would appear that the administration of BZP to adolescent animals produces behavioural changes in emotionality that are detectable in adulthood.
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Taylor, Simon John. "'On-Line' detection of release of acetylcholinesterase from the brain in vivo." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238155.
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Stanislas, Thomas. "Rôle de la Dynamique Membranaire dans la Mise en Place des Mécanismes de Défense chez le Tabac." Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00800206.
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La cryptogéine, une protéine sécrétée par l'oomycète Phytophthora cryptogea, provoque la mise en place de mécanismes de défense chez le tabac, mobilisant au cours des étapes précoces de la signalisation associée, des protéines localisées dans la membrane plasmique (MP). Une fraction membranaire résistante à la solubilisation par les détergents (DIM pour Detergent Insoluble Membrane), enrichie en stérols et en sphingolipides avait été purifiée à partir de la MP de tabac : cette fraction contenait plusieurs protéines impliquées dans la cascade de signalisation induite par la cryptogéine. Chez l'animal, l'association dynamique de protéines à des microdomaines riches en stérols et sphingolipides en réponse à un stress biotique joue un rôle essentiel dans la régulation de la signalisation cellulaire. L'objectif de ce travail était de tester l'hypothèse qu'un tel phénomène puisse se produire dans notre modèle d'étude. La comparaison du protéome de fractions DIMs, purifiées à partir de cellules traitées ou non pendant 5 minutes à la cryptogéine a été réalisée à l'aide d'un marquage isotopique (15N ou 14N) et d'une approche de protéomique quantitative. Le premier résultat est que l'abondance de la majorité des protéines n'est pas modifiée dans les DIMs en réponse à la cryptogéine. Une seule protéine est enrichie dans les DIMs, une isoforme de 14-3-3, tandis que quatre dynamines (DRPs pour Dynamin Related Proteins), impliquées dans le trafic vésiculaire, sont exclues des DIMs en réponse à la cryptogéine. L'étude d'une des dynamines identifiées, DRP1A, a été menée. Nous avons caractérisé les différents gènes codant DRP1A dans le génome du tabac, puis utilisé une approche ARN antisens pour altérer l'expression de cette protéine et nous avons étudié sa localisation subcellulaire à l'aide d'anticorps spécifiques et en observant en microscopie confocale cette protéine fusionnée à la GFP. Cette approche a permis de confirmer la présence de DRP1A dans la fraction DIMs et la diminution transitoire de son association à cette fraction en réponse à la cryptogéine, suite à une dissociation de la fraction membranaire. Ces travaux constituent la première mise en évidence d'une association/dissociation dynamique de protéines aux DIMs de plantes en réponse à un stimulus biologique
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MORENS, Céline. "Assimilation et distribution de l'azote alimentaire en situation de régime hyperprotéique chez le rat et chez l'homme." Phd thesis, INAPG (AgroParisTech), 2002. http://tel.archives-ouvertes.fr/tel-00005628.
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Püschel, Gerhard P., Martin Oppermann, Frank Neuschäfer-Rube, Otto Götze, and Kurt Jungermann. "Differential effects of human anaphylatoxin C3a on glucose output and flow in rat liver during orthograde and retrograde perfusion : the periportal scavenger cell hypothesis." Universität Potsdam, 1991. http://opus.kobv.de/ubp/volltexte/2008/1674/.
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1) During orthograde perfusion of rat liver human anaphylatoxin C3a caused an increase in glucose and lactate output and reduction of flow. These effects could be enhanced nearly twofold by co-infusion of the carboxypeptidase inhibitor MERGETPA, which reduced inactivation of C3a to C3adesArg. 2) During retrograde perfusion C3a caused a two- to threefold larger increase in glucose and lactate output and reduction of flow than in orthograde perfusions. These actions tended to be slightly enhanced by MERGETPA. 3) The elimination of C3a plus C3adesArg immunoreactivity during a single liver passage was around 67%, irrespective of the perfusion direction and the presence of the carboxypeptidase inhibitor MERGETPA; however, less C3adesArg and more intact C3a appeared in the perfusate in the presence of MERGETPA in orthograde and retrogade perfusions
It is concluded that rat liver inactivated human anaphylatoxin C3a by conversion to C3adesArg and moreover eliminated it by an additional process. The inactivation to C3adesArg seemed to be located predominantly in the proximal periportal region of the liver sinusoid, since C3a was less effective in orthograde perfusions, when C3a first passed the proximal periportal region before reaching the predominant mass of parenchyma as its site of action, than in retrograde perfusions, when it first passed the perivenous area. These data may be evidence for a periportal scavenger mechanism, by which the liver protects itself from systemically released mediators of inflammation that interfere with the local regulation of liver metabolism and hemodynamics.
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Püschel, Gerhard, and Kurt Jungermann. "Activation of inositol phosphate formation by circulating noradrenaline but not by sympathetic nerve stimulation with a similar increase of glucose release in perfused rat liver." Universität Potsdam, 1988. http://opus.kobv.de/ubp/volltexte/2010/4584/.
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In the isolated rat liver perfused in situ, stimulation of the nerve bundles around the hepatic artery and portal vein caused an increase of glucose and lactate output and a reduction of perfusion flow. These changes could be inhibited completely by α-receptor blockers. The possible involvement of inositol phosphates in the intracellular signal transmission was studied.
1. In cell-suspension experiments, which were performed as a positive control, noradrenaline caused an increase in glucose output and, in the presence of 10 mM LiCl, a dose-dependent and time-dependent increase of inositol mono, bis and trisphosphate.
2. In the perfused rat liver 1 μM noradrenaline caused an increase of glucose and lactate output and in the presence of 10 mM LiCl a time-dependent increase of inositol mono, bis and trisphosphate that was comparable to that observed in cell suspensions.
3. In the perfused rat liver stimulation of the nerve bundles around the portal vein and hepatic artery caused a similar increase in glucose and lactate output to that produced by noradrenaline, but in the presence of 10 mM LiCl there was a smaller increase of inositol monophosphate and no increase of inositol bis and trisphosphate.
These findings are in line with the proposal that circulating noradrenaline reaches every hepatocyte, causing a clear overall increase of inositol phosphate formation and thus calcium release from the endoplasmic reticulum, while the hepatic nerves reach only a few cells causing there a small local change of inositol phosphate metabolism and thence a propagation of the signal via gap junctions.
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Uys, Joachim De Klerk. "The effects of early life trauma on the neurochemistry and behaviour of the adult rat." Thesis, Link to the online version, 2006. http://hdl.handle.net/10019/1249.
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Warnock, Amy Louise. "Influence of early life and positive affect on feeding behaviour and food choice in the rat." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31559.
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In recent years, worldwide obesity rates have risen dramatically, putting major strain on public health systems and the economy. Obesity is a multifaceted disease and its development can be influenced by a variety of factors including genetic, psychological and environmental influences. One area of current focus in obesity research is that of early life programming. It has been well-established that certain early life factors can impact the physiology and behaviour of the offspring. Because of this, early life programming has become increasingly well studied in order to develop a deeper understanding of how early life can influence obesity development. Another area of interest lies in positive mood. While there has been much research into the effects of negative states such as stress and anxiety on feeding behaviour, there is still very little known about how positive states can influence food choice. Using rat models of prenatal stress, neonatal overnutrition and positive affect, this thesis aimed to investigate the effects of early life and mood factors on feeding behaviour and food choice. Prenatal stress has been extensively studied and is characterised by an enhanced stress response in the offspring. Using two rat models of prenatal stress- social and restraint stress, the effects of prenatal stress on feeding behaviour and food choice in the offspring were examined. In both models, no effects of prenatal stress on either food intake or food choice were observed. However, in both cases the expected alterations to the offspring's stress responses when exposed to an acute stressor were not replicated. This may suggest that models of prenatal stress are not as robust as often cited in the literature. As well as the prenatal environment, the early postnatal environment is also able to influence physiology and behaviour. In terms of obesity, a well-studied model is that of small litter size. Rats from small litters are over-nourished as neonates and because of this illustrate an increased body weight that persists throughout life. While this increase in weight gain has been well-established, there is no evidence examining the impact of neonatal overnutrition on long-term food choice. Therefore, food intake and food choice were measured in small and control litter rats over a 10-week period. When placed on an ad lib diet of bland chow, sucrose and lard, small litter rats consumed significantly more chow than control litter rats, whilst maintaining similar consumption of lard and sucrose. However, when offered a high-fat high-sugar (HFHS) pellet for two hours a day alongside ad lib chow, small litter rats illustrated increased consumption of the HFHS pellet compared to controls. This suggests that small litter rats may be programmed to adjust their food choices to enable them to maintain their increased body weight in comparison to controls. To examine the effects of positive affect on feeding behaviour, ultrasonic vocalisations (USVs, specifically those at 50 kHz) were used as a measure of positive affect in rats. In order to examine whether access to a food reward could induce a positive affect (as measured by an increase in 50 kHz USVs), rats were schedule-fed sweetened condensed milk and USVs measured before, during and after consumption. No differences in 50 kHz USVs were observed suggesting that a palatable food, whilst rewarding, does not alter affective state in the rat. Using heterospecific social contact (a tickling interaction simulating rough and tumble play) to induce positive affect, rats were presented with an hour-long sucrose preference test following social contact in order to examine the impact of positive affect on food choice. While no differences in sucrose consumption were found, a reduced sucrose preference was observed in rats receiving social contact compared to controls, suggesting that positive affect may play a role in mediating food choice. Finally, the effects of fasting (a negative stimulus thought to reduce 50 kHz USVs) and a food reward on motivation for social contact were examined. Both fasting and access to a food reward resulted in no differences in conditioned place preference to receive social interaction. Overall, the results obtained in this thesis implicate both neonatal overnutrition and, for the first time, positive affect as possible mediators of food choice, although further studies are required to fully establish these effects. Importantly, these results also raise questions regarding the reproducibility of some early life models, such as prenatal stress, and highlights the importance of sharing precise experimental protocols across laboratories. Through further investigation of the effects of early life and affective states on food consumption and choice, and the mechanisms behind these, this may enable the development of therapeutic interventions and preventative measures that can help slow, or even reverse, the global obesity epidemic.
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Neuschäfer-Rube, Frank, DeVries Christa, Kristina Hänecke, Kurt Jungermann та Gerhard Püschel. "Molecular cloning and expression of a prostaglandin E₂ receptor of the EP₃ϐ subtype from rat hepatocytes". Universität Potsdam, 1994. http://opus.kobv.de/ubp/volltexte/2010/4583/.
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Rat hepatocytes have previously been reported to possess prostaglandin E₂ receptors of the EP₃-type (EP₃-receptors) that inhibit glucagonstimulated glycogenolysis by decreasing cAMP. Here, the isolation of a functional EP₃ϐ receptor cDNA clone from a rat hepatocyte cDNA library is reported. This clone can be translated into a 362-amino-acid protein, that displays over 95% homology to the EP₃ϐ receptor from mouse mastocytoma. The amino- and carboxy-terminal region of the protein are least conserved. Transiently transfected HEK 293 cells expressed a single binding site for PGE₂ with an apparent Kd of 15 nM. PGE₂ > PGF₂α > PGD₂ competed for [³H]PGE₂ binding sites as did the EP₃ receptor agonists M&B 28767 = sulprostone > misoprostol but not the EP₁ receptor antagonist SC 19220. In stably transfected CHO cells M&B 28767 > sulprostone = PGE₂ > misoprostol > PGF₂α inhibited the forskolin-elicited cAMP formation. Thus, the characteristics of the EP₃ϐ receptor of rat hepatocytes closely resemble those of the EP₃ϐ receptor of mouse mastocytoma.
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AL-Thabhani, Hanaa A. "Steriods Protect Against Doxorubicin-Induced Cytotoxicity in Rat Cardiac Myoblastic H9C2 Cells." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd_retro/18.
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Doxorubicin is one of the most potent anticancer drugs used in the treatment of wide spectrum of neoplastic diseases including breast, thyroid, colon and liver cancer. However, doxorubicin use is associated with undesirable side effects including cardiomyopathy and congestive heart failure. In the present study we have established that treatment of rat cardiac myoblasts (H9c2 cells) with doxorubicin resulted in H9c2 cell injury in a dose and time dependent manner with almost 50% cell death obtained at 5 μM of doxorubicin treatment for 24 hours. We have selected about 50% cell injury as optimum doxorubicin-induced cell injury because once this threshold is reached, cells became irreversibly injured and could not respond to protective treatment. Another potent antineoplastic drug cyclophosphamide had no cardiotoxic effects on H9c2 cells even at 35 μM concentration and up to 72 hours of treatment. Pretreatment of H9c2 cells for 24 hours with dexamethasone, cortisol, corticosterone or progesterone, significantly protect H9c2 myoblasts against subsequent 5 μM doxorubicin treatment for 24 hours in a concentration dependent manner with maximum protection obtained at 100 nM dexamethasone, 100 nM progesterone, 500 nM cortisol and 500 nM corticosterone. However, testosterone or dehydroepiandrosterone had no protective effects even at 10 μM concentration. It is concluded that both glucocorticoids and progesterone protect H9c2 cells against doxorubicin-induced cell injury.
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Smith, Roger David. "Regulation of proliferation in a cultured rat intestinal epithelial cell line." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240063.
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Low, Brian. "A Cellular Mechanism for Dendritic Spine Loss Following Traumautic Brain Injury in Rat." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1892.
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Traumatic brain injury is a leading cause of death and disability in the United States. The injury is often composed of two processes: the primary injury, which can involve irreversible loss of tissue, and the secondary injury, which involves a cascade of reactive processes such as excitotoxicity that occur in the hours and days after the initial insult. Excitotoxic stimulation of neuronal circuits can lead to cellular dysfunction and modulation of neuronal sensitivity. One mechanism of dysfunction involves the calcium-regulated phosphatase, calcineurin. Calcineurin has been shown to be involved in the modulation of the neuronal post-synaptic structures known as dendritic spines. One means by which CaN regulates spine structure is through the dephosphorylation of the down-stream effector proteins such as, cofilin. This study tracks the changes in CaN activity levels as well as the phosphorylation state of cofilin in the cortex and hippocampus in each hemisphere of the laterally injured brain. We report that the lateral brain injury causes an increase in CaN activity in the hippocampus with a corresponding dephosphorylation of cofilin. Trauma-induced changes in CaN follow a slightly different time course in cortical tissue, as there is a biphasic modulation of cofilin that begins with an increased phosphorylation which is followed by an extended dephosphorylation. This dephosphorylation is partially prevented by a single post-injury injection of FK506, a calcineurin inhibitor. Since dephosphorylation of cofilin is a rate-limiting step in dendritic spine collapse, the results of this study demonstrate a potential cellular mechanism through which traumatic brain injury results in altered neuronal function.
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Püschel, Gerhard, Hisayuki Miura, Frank Neuschäfer-Rube та Kurt Jungermann. "Inhibition by the protein kinase C activator 4β-phorbol 12-myristate 13-acetate of the prostaglandin F₂α-mediated and noradrenaline-mediated but not glucagon-mediated activation of glycogenolysis in rat liver". Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2010/4588/.
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In perfused rat livers, infusion of prostaglandin F₂α (PGF₂α) or noradrenaline increased glucose and lactate output and reduced flow. Glucagon increased glucose output and decreased lactate output without influence on flow. Infusion of phorbol 13-myristate 14-acetate (PMA) for 20 min prior to these stimuli strongly inhibited the metabolic and hemodynamic effects of noradrenaline, reduced the metabolic actions of PGF₂α but did not alter the effects of glucagon.
In isolated rat hepatocytes PGF₂α, noradrenaline and glucagon activated glycogen phosphorylase but only PGF₂α and noradrenaline increased intracellular inositol 1,4,5-1risphosphalc (InsP₃). The noradrenaline- or PGF₂α-elicited activation of glycogen phosphorylase and increase in InsP₃ were largely reduced after preincubation of the cells for 10 min with PMA, whereas the glucagon-mediated enzyme activation was not affected. In contrat to PMA, the phorbol ester 4a-phorbol 13,14-didecanoate. which does not activate protein kinase C, did not attenuate the PGF₂α- and noradrenaline-elicited stimulation of glucose output, glycogen phosphorylase and InsP, formation. Stimulation of InsP₃ formation by AlF₄⁻, which activates phospholipase C independently of the receptor, was not attenuated by prior incubation with PMA.
Plasma membranes purified from isolated hepatocytes had both a high-capacity, low-affinity and a low-capacity, high-affinity binding site for PGF₂α. The Kd of the high-capacity, low-affinity binding site was close to the concentration of PGF₂α that increased glycogen phosphorylase activity halfmaximally. Binding to the high-capacity, low-affinity binding site was enhanced by guanosine 5'- 0-(3-thio)triphosphate (GTP[S]). This high-capacity, low-affinity site might thus represent the receptor. The Bmax and Kd of the high-capacity site, as well as the enhancement by GTP[S] of PGF₂α binding to this site, remained unaffected by PMA pretreatment.
It is concluded that, in hepatocytes, activation of protein kinase C by PMA interrupted the InsP₃-mediated signal pathway from PGF₂α via a PGF₂α receptor and phospholipase C to glycogen phosphorylase at a point distal of the receptor prior to phospholipase C.
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Addou, Benounan Samia. "Conséquences de l'adaptation à un régime hyperprotéique sur la structure de l'épithélium intestinal chez le rat Wistar." Phd thesis, AgroParisTech, 2008. http://pastel.archives-ouvertes.fr/pastel-00004489.
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Les protéines alimentaires se trouvent principalement dans des aliments traditionnels d'origine animale et végétale. L'évaluation de la qualité nutritionnelle de différents sources de protéines alimentaires consiste à mettre en relation les caractéristiques de l'apport alimentaire et les caractéristiques de la demande métabolique concept relatif à l'état de l'individu. La recommandation de base WHO/UNU est de 0,8g /kg /j de protéine de bonne qualité pour l'homme adulte. L'objet de ce travail est d'évaluer les conséquences d'une adaptation à un régime hyperprotéique sur des modifications fonctionnelles et morphologique chez le rat en croissance. Plus particulièrement, on a analysé les effets d'un régime à 50% en protéines sur l'évolution du poids corporel, le poids de certains organes ainsi que sur la structure intestinale du rat. Dans ce but, 96 rats mâles de souche wistar pesant entre 175 et 185g (180±2,27g), sont répartis en 5 groupes : le 1er groupe (n=30) reçoit un régime normoprotéique à base de protéine totale de lait (14%) et constitue le groupe témoin, le 2ème groupe (n=30) reçoit un régime hyperprotéique (50%) à base de protéine totale de lait, le 3ème groupe (n=12) reçoit un régime normoprotéique (14,5%) à base de protéine végétale onab , le 4ème groupe (n=12) reçoit un régime hyperprotéique (50%) à base de protéine de soja, le 5ème groupe (n=12) reçoit un régime hyperprotéique (50%) à base de gluten. Tous ces régimes sont administrés pendant 60 jours, durée de l'expérimentation. Les résultats montrent qu'une surconsommation de protéines s'accompagne d'une diminution significative du poids corporel et d'une modification de la structure histologique de l'épithélium intestinal qui se traduit par une atrophie villositaire et par une augmentation des lymphocytes intra-épithéliaux. Ces modifications seraient la manifestation de phénomènes induits par l'exposition chronique de l'épithélium intestinal à des teneurs élevés en protéines. Nous avons conclu qu'une surconsommation de protéines n'est pas sans conséquence sur la composition corporelle et la fonction intestinale. Il convient donc d'observer une certaine prudence dans l'utilisation à long terme de formules diététiques enrichies en protéines chez l'homme.
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Moore, Wayne Allen Jr. "Acute and Chronic Effects of Artificial Rearing on Rat Genioglossus Muscle." VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/885.
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In most mammals, nutritive suckling is critical during the early neonatal period. The genioglossus (GG) muscle in rat plays an important role in protruding the tongue for efficient suckling. The purpose of this study was to examine the contractile properties and myosin heavy chain (MHC) phenotype of the GG following an early period of artificial rearing, which reduced nutritive suckling. Beginning at three days of age Sprague-Dawley rats were fed via implanted gastric cannula until postnatal day 14 (P14). At P14, artificially reared (AR) rat pups were either placed with a lactating dam until the end of the weaning period and allowed to mature until postnatal day 42 (P42), or anesthetized and prepared for physiological experimentation. GG contractile properties at P14 and P42 in AR and dam reared (DR) rats were obtained with a force transducer and digital recording system through stimulation of the medial branch of the hypoglossal nerve. Following physiological experimentation, muscle samples were removed and stored for MHC analysis. Comparisons were made between AR and DR groups at P14 and P42. At P14 maximum tetanic tension and fatigue index were lower in the AR group than the DR group and no differences were found in MHC distribution. By day 42, AR rats had a higher fatigue index that DR rats and DR rats had a higher percentage of MHCIIa than AR rats. The artificial rearing technique employed in this study was adequate to produce chronic changes in fatigue resistance and MHC distribution in GG muscle. GG muscle of premature human infants requiring early artificial feedings may develop similar changes in their contractile characteristics and MHC phenotype.
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KOJIMA, KIYOHIDE, HIROMU NAKAMURA, and SHONEN YOSHIDA. "Occurrence of a Terminal Deoxynucleotidyl Transferase-Like Activity in N-2-Fluorenylacetamide-treated Rat Liver." Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17476.
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Basiouni, Shereen. "The modulating effects of polyunsaturated fatty acids on membrane composition and phospholipase D in a canine mast cell line as a model for atopic dermatitis." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142529.
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Polyunsaturated fatty acids (PUFA) have been used with some success in the treatment of canine atopic dermatitis (CAD). Correspondent in vitro studies revealed that PUFA play a crucial role in the exocytosis of mast cells. n3 PUFA such as α-linolenic acid (LNA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), as well as the n6 PUFA linoleic acid (LA) have been shown to arrest the secretion of inflammatory mediators. Contrary, the n-6 PUFA arachidonic acid (AA) has been proven to promote the production of mast cell inflammatory mediators. However, we are still lacking a complete picture of the mode of action. The goal of this work was to further characterize the modulatory effects of PUFA supplementation on the plasma membrane lipid composition of mast cells. Furthermore the consequences of a membrane modulation of mast cells by PUFA on the localization and activity on of the membrane bound enzyme phospholipases D (PLD) were investigated. Canine mastocytoma cells (C2) were supplemented with one of the following PUFA: LNA, EPA, DHA, LA or AA. To investigate the influence of PUFA on the lipid composition of membrane microdomains, lipid rafts were separated from non-raft plasma membranes of mast cells for the first time using a detergent-free isolation technique. Results show that PUFA are significantly increased in rafts as well as in non-rafts microdomains (Publication 1). The incorporation of PUFA into the membrane goes along with an increase of the unsaturation status and the fluidity of the membrane. This rise in membrane fluidity may result in a reorganization of membrane signaling molecules and enzymes such as the PLD. To define the impact of a PUFA supplementation on PLD trafficking, C2 were transfected with green fluorescent protein (GFP) fusion plasmids encoding PLD1 or PLD2. Since the transfection ability of the suspension cell line C2 is limited, a special transfection protocol was established, suitable for non-adherent cell lines. Transfection succeeded using chicken egg white as coating material for the cell culture plates. The transfection efficiency rose to 50% versus 5% in uncoated plates. In addition to the obvious increase in the transfection efficiency, the new technique is simple and economic and might be suitable for a wide range of suspension cell lines (Publication 2). Using this optimized protocol the influence of PUFA on the trafficking of PLD isoforms was studied. LNA, EPA, DHA and LA but not AA prevented the stimulation-induced translocation of PLD1 to the plasma membrane. Since the translocation of PLD1 is important for mast cell exocytosis, LNA, EPA, DHA and LA do have an inhibiting effect on the stimulation-induced release of pro-inflammatory mediators. All PUFA tested boosted the total PLD activity. In order to rule out, which PLD isoform was affected by the PUFA, the mast cells were supplemented with DHA or AA in the presence of specific PLD isoform inhibitors. DHA completely abolished the inhibitiory effect of the PLD1 inhibitor but had no effect on the inhibitory effect of PLD2 inhibitor. On the other hand, AA suppressed the inhibitory effect of both PLD1 and PLD2 inhibitor (Publication 3). Taking together, the studies provide a mechanistic base for the role of PUFA in the exocytosis processes of mast cells. PUFA of the n3 and the n6 families impact the lipid composition of membrane microdomains, which in turn lead to a modulation of the physiochemical properties of the membrane. LNA, EPA, DHA and LA suppress the release of inflammatory mediators through their inhibitory action on the stimulation-induced translocation of the PLD1. Contrariwise, AA permits the stimulation-induced migration of PLD1 to the plasma membrane and increases the activity of both PLD isoforms. Therefore, LNA, EPA, DHA and LA but not AA inhibit the release of mast cell inflammatory mediators upon stimulation<br>Mehrfach ungesättigte Fettsäuren (PUFA) können mit einigem Erfolg zur Behandlung der caninen atopischen Dermatitis (CAD) eingesetzt werden. In vitro-Studien zeigten, dass PUFA eine entscheidende Rolle in der Exozytose von Mastzellen spielen. N-3-PUFA wie α-Linolensäure (LNA), Eicosapentaensäure (EPA), Docosahexaensäure (DHA) sowie die n-6-PUFA Linolsäure (LA) können die Sekretion von Entzündungsmediatoren vermindern. Arachidonsäure (AA) als n-6 mehrfach ungesättigte Fettsäure hingegen fördert die Entzündungsmediatoren-Freisetzung aus den Mastzellen. Eine vollständige Aufklärung der Wirkungsweise fehlt aber weiterhin. Das Ziel dieser Arbeit war eine weitergehende Charakterisierung der modulierenden Effekte einer PUFA-Supplementierung auf die Lipidzusammensetzung der Plasmamembran von Mastzellen. Darüber hinaus wurden die Auswirkungen von PUFA auf die Lokalisation und Aktivität des Membran-gebundenen Enzyms Phospholipase D (PLD) untersucht. Canine Mastozytom-Zellen (C2) wurden mit einer der folgenden PUFA kultiviert: LNA, EPA, DHA, LA oder AA. Um den Einfluss von PUFA auf die Lipidzusammensetzung der Membran-Mikrodomänen zu untersuchen, konnten sowohl Lipid Raft als auch Nicht-Raft Plasmamembran-Anteile von Mastzellen zum ersten Mal mittels einer Detergenzien-freien Isolationsmethode getrennt werden. Hervorzuheben ist, dass PUFA signifikant vermehrt in Raft- sowie in Nicht-Raft Membranmikrodomänen eingelagert werden (Publikation 1). Die Integration von PUFA in die Membran geht mit einer Steigerung der Doppelbindungsanzahl und der Fluidität der Membran einher. Diese Erhöhung der Membranfluidität kann zu einer Reorganisation von membranären Signalmolekülen und Enzymen wie der PLD führen. Um die Auswirkungen einer PUFA-Supplementierung auf den intrazellulären Transport der PLD in C2 zu bestimmen, wurden die Zellen mit PLD1- oder PLD2-codierenden grün fluoreszierenden Protein-(GFP-)Fusionsplasmiden transfiziert. Da die Transfektionsfähigkeit der Suspensions-Zelllinie C2 begrenzt ist, wurde ein für nicht-adhärente Zelllinien geeignetes Transfektionsprotokoll etabliert. Mit Hühnereiweiß als Beschichtungsmaterial für die Zellkultur-Platten stieg die Transfektionseffizienz auf 50% im Vergleich zu 5% bei unbeschichteten Platten. Neben der deutlichen Erhöhung der Transfektionseffizienz ist die neu etablierte Technik einfach durchzuführen sowie wirtschaftlich und kann für eine Vielzahl von Suspension-Zelllinien geeignet sein (Publikation 2). Unter Verwendung dieses optimierten Protokolls wurde der Einfluss von PUFA auf die Translokation der PLD-Isoformen untersucht. LNA, EPA, DHA und LA, nicht aber AA verhindern die stimulationsinduzierte Translokation der PLD1 an die Plasmamembran. Die Translokation der PLD1 ist wichtig für die Mastzell-Exozytose. LNA, EPA, DHA und LA haben hier eine hemmende Wirkung auf die stimulationsinduzierte Freisetzung von proinflammatorischen Mediatoren. Alle getesteten PUFA verstärken die Gesamt-PLD-Aktivität. Um zu unterscheiden, welche PLD-Isoform durch PUFA beeinflusst ist, wurden die Mastzellen mit DHA oder AA in Gegenwart von PLD-Isoform-Inhibitoren supplementiert. DHA hebt die inhibitorische Wirkung des PLD1-Inhibitors vollständig auf, zeigte aber keinen Einfluss auf die hemmende Wirkung des PLD2-Inhibitors. Andererseits unterdrückt AA die hemmende Wirkung des PLD1- als auch des PLD2-Inhibitors (Publikation 3). Zusammenfassend bietet die Studie eine mechanistische Basis für die Rolle von PUFA bei Exozytose-Prozessen von Mastzellen. PUFA der n-3- und n-6-Familie beeinflussen die Lipidzusammensetzung von membranären Mikrodomänen, was wiederum zu einer Modulation der physikalisch-chemischen Eigenschaften der Membran führt. LNA, EPA, DHA und LA verhindern die Freisetzung von Entzündungsmediatoren durch ihre hemmende Wirkung auf die stimulationsinduzierte Translokation der PLD1. Umgekehrt erlaubt AA eine stimulationsinduzierte Migration der PLD1 zur Plasmamembran und steigert die Aktivität der beiden Isoformen der PLD. Somit hemmen LNA, EPA, DHA und LA, aber nicht AA die Freisetzung von Mastzell-Entzündungsmediatoren nach Stimulation
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Bastide, Kristell. "Caractérisation moléculaire de tumeurs pulmonaires radon-induites chez le rat." Phd thesis, Université Paris Sud - Paris XI, 2008. http://tel.archives-ouvertes.fr/tel-00349902.
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Le radon est un carcinogène pulmonaire avéré chez l'homme à fortes doses mais l'existence d'un risque de cancer à faibles doses n'est pas établie car les approches épidémiologiques se heurtent, à ce niveau de doses, à de nombreux facteurs confondants. Ces données soulignent la nécessité de disposer d'un modèle d'étude des tumeurs pulmonaires chez l'animal. <br />Le but de ce travail de thèse est de caractériser, sur le plan moléculaire, une série de tumeurs pulmonaires radon-induites chez le rat qui comprend des adénocarcinomes (AC), des carcinomes épidermoïdes (Sq) et des carcinomes adénosquameux (ASq) formés des composantes cellulaires AC et Sq. Une analyse cytogénétique globale de ces tumeurs par la technique de CGH a permis de définir des déséquilibres récurrents de régions chromosomiques, sur lesquelles ont été ciblés des gènes candidats potentiellement impliqués dans le développement des tumeurs, comme p16Ink4a, p19Arf, Rb1, K-Ras ou c-Myc. Une analyse plus précise des voies p16Ink4a/Cdk4/Rb1 et p19Arf/Mdm2/Tp53 a été menée et a permis de mettre en évidence une inactivation fréquente de la voie Rb1, par la perte d'expression de la protéine p16Ink4a, indiquant que cette voie joue un rôle majeur dans le développement de ces tumeurs pulmonaires. Enfin, une analyse transcriptomique comparative des trois types de tumeurs induites a révélé que les tumeurs complexes ASq ont un profil d'expression génique qui reflète leur nature composite mais qu'elles présentent également des spécificités. <br />L'ensemble de ce travail à mis à jour des caractéristiques moléculaires communes aux tumeurs pulmonaires murines et humaines qui encouragent à poursuivre l'étude des spécificités des tumeurs pulmonaires radio-induites chez le rat pour aider à une meilleure caractérisation de ces tumeurs chez l'homme.
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Elgrabli, Dan. "Toxicité et clairance pulmonaires des nanotubes de carbone." Phd thesis, Université Paris-Diderot - Paris VII, 2008. http://tel.archives-ouvertes.fr/tel-00347713.
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Les nanotubes de carbone (NTC) sont difficilement détectables dans les matrices biologiques. Ceci rend l'étude de leur toxicité et de leur biodistribution plus difficile. Lors de ce travail, nous avons étudié, dans un premier temps, l'effet de l'albumine sérique de veau (BSA) sur la dispersion des NTC puis dans un second temps, la toxicité, la biodistribution ainsi que la clairance d'un NTC multi-feuillet (MWCNT) chez le rat en utilisant le nickel, une impureté métallique présente dans le nanotube étudié. Après une unique instillation intratrachéale de 100 μg de MWCNT, nos résultats ne montrent ni inflammation, ni lésions pulmonaires, ni modifications des paramètres physiologiques pulmonaires. De plus, l'absence de passage de la barrière alvéolo-capillaire et la mise en place d'un long mécanisme de clairance ont été observées dans le poumon. Afin de mieux comprendre ce mécanisme et à l'aide de la microscopie electronique et de la spectroscopie infrarouge, nous avons montré que les MWCNT sont chimiquement modifiés et sont clivés dans le poumon. Ces résultats, ainsi que l'étude de la phagocytose des MWCNT et de l'apoptose des macrophages alvéolaires, ont permis d'émettre l'hypothèse d'un mécanisme de clairance selon laquelle l'élimination des MWCNT dans le poumon serait liée à la phagocytose, l'apoptose, la dégradation de MWCNT par les macrophages alvéolaires puis la phagocytose de cellules apoptotiques.
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Gut, Chester P. Jr. "Hyperbaric Oxygen in the Prevention of Carbon Monoxide Induced Delayed Neurological Sequelae in Male Sprague Dawley Rats (Rattus norvegicus)." Wright State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=wright1278639454.
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Campanac, Emilie. "Plasticité de l'excitabilité des neurones de la région CA1 de rat." Phd thesis, Université de la Méditerranée - Aix-Marseille II, 2008. http://tel.archives-ouvertes.fr/tel-00346412.
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Il a été préalablement montré dans les neurones pyramidaux de CA1 qu'en plus d'une plasticité synaptique à long terme, les protocoles de tétanisation des afférences (HFS/LFS) induisent une plasticité synergique de l'intégration des messages synaptiques. Dans ce contexte, nous avons abordé les questions suivantes: 1) des changements d'intégration dendritiques sont-ils associés à la STDP ? 2) quels sont les mécanismes d'expression de la facilitation de l'intégration observée après la LTP ? et 3) dans quelle mesure l'activité synaptique induit des changements persistants de l'excitabilité des interneurones GABAergiques ?<br />Nos résultats montrent que la règle préétablie de STDP pour la plasticité synaptique est aussi valide pour la plasticité de l'intégration et décrit aussi parfaitement les changements de la relation amplitude/pente des PPSE observés en parallèle. Ces changements sont spécifiques de la voie synaptique activée et nécessitent l'activation des récepteurs NMDA. <br />La plasticité de l'intégration met en jeu une régulation des conductances voltage-dépendantes présentes à la surface neuronale. Une réduction locale dendritique, NMDAR-dépendante du courant Ih est observée lors de l'augmentation d'intégration associée à la LTP. En présence de bloqueurs pharmacologiques du courant Ih, la LTP est toujours présente mais la facilitation de l'intégration n'est plus observée. Finalement, une facilitation de l'intégration similaire à celle observée après induction de la LTP est induite quand la conductance h est réduite dans la dendrite par la technique de courant imposé dynamique en temps réel.<br />Des changements de l'excitabilité neuronale ne sont pas restreints aux neurones pyramidaux et nous montrons qu'une augmentation de l'excitabilité intrinsèque, dépendante des récepteurs mGluR de type I est également observée dans certains interneurones GABAergiques de CA1 après une HFS. Cette augmentation d'excitabilité pourrait permettre de maintenir l‘équilibre entre excitation et inhibition au sein du réseau hippocampique en facilitant le recrutement des interneurones à la suite d'épisodes d'hyperactivité.<br />Nos résultats montrent donc qu'en parallèle des modifications de l'efficacité synaptique, des modifications de l'excitabilité intrinsèque des neurones peuvent participer au processus de stockage de l'information et permettent également de maintenir l'activité neuronale à un niveau physiologique.
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Dunphy-Doherty, F. "Isolation-rearing from weaning to investigate depressive-like behaviour in the rat." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/52211/.
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Depression is a heterogeneous condition characterised by low mood and a lack of motivation and enjoyment of regular activities. The response rate to current treatments coupled with adverse side effect profiles requires new avenues of investigation into the development of novel therapeutics to treat the condition. Rearing rats in isolation from weaning causes behavioural, cognitive and neurochemical changes which persist into adulthood; some of the symptoms produced have relevance to depression. In the current thesis, rats raised in social isolation from weaning consistently developed a hyperactive phenotype compared to group-housed littermates when placed into a novel environment. They also developed deficits in associative learning assessed by the conditioned fear response task. They displayed some anxiety-like behaviours in the open field and novelty-suppressed feeding task and deficits in visual memory in the novel object discrimination task, although these were not reliable across cohorts. There was a reduction in levels of hippocampal neurogenesis in a number of cohorts and for the first time it was demonstrated that rats reared in isolation exhibited changes in gut bacteria, opening up a potential new avenue of investigation into potential treatments. The efficacy of novel versus established antidepressant treatments was evaluated in isolated rats. Chronic fluoxetine had some anxiolytic effects in the open field, attenuated isolation induced changes in associative memory and increased neurogenesis but also had inconsistent effects on activity. Treatment with acute ketamine increased freezing time in the conditioned freezing response task, indicating an improvement in associative memory. The final study examined, for the first time, the effect of treatment with the JNK-1 inhibitor DJNKI in isolation reared rats. DJNKI had some positive cognitive effects in both the novel object discrimination task and the conditioned freezing response task. In conclusion, the isolation rearing model induced varying levels of depression-like deficits, which were responsive to some treatments. The model is a useful tool for investigating the symptoms of depression and evaluating novel treatment options.
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Loudon, Mary. "Arterial wall renin-like activity and blood pressure regulation in the rat." Thesis, University of Leicester, 1985. http://hdl.handle.net/2381/34141.
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In this study the Importance of the generation of angiotensin II within the blood vessel wall in determining the pressor response to injected renin was investigated. An injection of renin, given to rats after bilateral nephrectomy, produced a pressor response. The level of circulating renin, although initially elevated, returned to the normal range within three hours. However, the level of renin present in the aortic wall remained significantly elevated for six hours after the injection, as did the pressor response. Infusions of the angiotensin II antagonist saralasin at three and six hours after the renin injection confirmed that the pressor response was maintained by the renin-angiotensin system. An injection of renin into normal rats produced the same initial pressor response as was observed in the nephrectomised rats. However, the blood pressure subsequently returned to the pre-injection level after one hour. In the normal rats the pressor response was not related to the level of renin present within the aortic wall. It was concluded that the activity of the renin present within the blood vessel wall was more relevant to the control of blood pressure than the circulating level. However, when the kidneys were present this local action of the renin-angiotensin system was overriden by renal anti-hypertensive systems. This was not dependent on the presence of the renal medulla since the pressor response after chemical renal medullectomy was the same as that observed in the normal rats. The increase in the level of renin within the aortic wall after the injection of exogenous renin confirmed that renin can enter the walls of blood vessels from the circulation. It was concluded that this occurred by a process of passive diffusion.
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Püschel, Gerhard P., Ursula Hespeling, Martin Oppermann, and Peter Dieter. "Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a." Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2008/1671/.
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Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Kupffer cells); (b) the C3a-mediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a-elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C-terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a-dependent activation of hepatic glycogenolysis is mediated by way of a C3a-induced prostanoid production in Kupffer cells.
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Estebanez, Luc. "Caractérisation des traitements sensoriels dans le cortex à tonneaux du rat anesthésié." Phd thesis, Ecole Normale Supérieure de Paris - ENS Paris, 2011. http://tel.archives-ouvertes.fr/tel-00696553.
Full textAbstract:
Chez les rongeurs, le traitement par le cortex à tonneaux de l'information sensorielle en provenance des vibrisses est mal compris. En effet, malgré l'aide fournie par l'organisation de ce cortex en une reproduction stricte de la topographie de l'appareil sensoriel, il a été difficile jusqu'à présent d'identifier de façon indiscutable le système de filtrage linéaire et non-linéaire qu'utilisent les neurones du cortex à tonneaux durant leur traitement des scènes tactiles auxquelles ils sont exposés. Pour mieux identifier ces traitements corticaux, nous avons développé un système de stimulation vibrissale permettant d'appliquer des déflections sur un grand nombre de vibrisses indépendamment, dans toutes les directions possibles et ce à travers une vaste gamme fréquentielle. En utilisant ce dispositif de stimulation multivibrissale durant des enregistrements extracellulaires de l'activité électrique des neurones du cortex à tonneaux de rats anesthésiés, nous avons pu identifier plus précisément le filtrage linéaire des stimulations vibrissales, qui s'avère similaire pour tous les neurones que nous avons pu enregistrer. Par ailleurs, en explorant les aspects non-linéaires du traitement effectué par ces neurones, nous avons noté qu'ils se séparent en deux familles distinctes : d'un côté des neurones "locaux" qui se sont avérés sensibles à des contrastes locaux dans les déflections multivibrissales. De l'autre, des neurones "globaux" capables au contraire de détecter des situations où les déflections sont similaires pour de nombreuses vibrisses. Enfin, en effectuant d'autres enregistrements dans la couche II/III du cortex à tonneaux, cette fois à l'aide d'un microscope deux-photons, nous avons pu noter que les neurones appartenant aux familles locales et globales étaient séparés en groupes spatialement distincts et que la position spatiale des neurones était plus généralement étroitement liée à l'ensemble de leurs propriétés de filtrage des déflections vibrissales.
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Shen, Hua. "Responses Of paraoxonase 1 to dioxin-like pcb 126 ( 3,3',4,4',5-pentachlorobiphenyl): mechanisms and consequences." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2770.
Full textAbstract:
Polychlorinated biphenyls (PCBs) are ubiquitous environmental pollutants that have been associated with various adverse health effects in humans and wildlife. Dioxin-like PCBs elicit a broad spectrum of biochemical and toxic changes including cardiovascular disorders. Paraoxonase 1 (PON1), an antioxidant enzyme, prevents oxidative stress and plays key roles in the pathogenesis of atherosclerosis. The overall goal of this dissertation is to investigate the mechanism and role of PON1 in the antioxidant defense to the exposure of 3, 3', 4, 4', 5-pentachlorobiphenyl (PCB 126), the most potent congener in PCB family. My overall hypothesis is that: The up-regulation of PON1 is an antioxidant response to PCB 126 exposure, which involves the Ah receptor (AhR) and results in changes in the PON1 protein level and activity which in turn has an influence on the oxidative stress status. First, the responses of PON1 gene expression and activities in serum and liver upon the PCB126 treatment were evaluated in the rat model. I found that PCB 126 up-regulated PON1, gene expression and activities, in a time and dose dependent manner. Next, I investigated the molecular mechanism of this response. My results show that the up-regulation of PON1 by PCB 126 involves the AhR and the XRE-like sequence in the gene promoter region. The up-regulation of PON1 was tissue specific, and this response probably protected liver and serum from lipid oxidation to some extent. The structure-activity relationship studies with PCB congeners indicate that the up-regulation of PON1 was specific to dioxin-like PCB 126. Other different AhR ligands displayed different PON1 induction capabilities. Also, reduction of PON1 activity was found in male rats dosed with non-dioxin-like PCBs. Finally I investigated the interaction, and possible protection, of other antioxidants (Se and NAC) on the response to PCB 126. I found that these antioxidants reduced the magnitude of the response of PON1 to the PCB 126 exposure in liver. Both the increase of PON1 activities and addition of antioxidants may be the reason for the lack in increase of lipid peroxidation. In total, these findings support my hypothesis and suggest that up-regulation of PON1 by PCB 126 may be an adaptive antioxidant mechanism that is involved in the body's antioxidant system.
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Aviles, Alena E. "Flea and louse infestations of cotton rats (Sigmodon hispidus) in the southeastern United States." Click here to access thesis, 2009. http://www.georgiasouthern.edu/etd/archive/spring2009/alena_e_aviles/aviles_alena_e_200901_ms.pdf.
Full textAbstract:
Thesis (M.S.)--Georgia Southern University, 2009.<br>"A thesis submitted to the Graduate Faculty of Georgia Southern University in partial fulfillment of the requirements for the degree Master of Science." Directed by Lance A. Durden. ETD. Includes bibliographical references (p. 17-32) and appendices.
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Püschel, Gerhard P., Annegret Nath, and Kurt Jungermann. "Increase of urate formation by stimulation of sympathetic hepatic nerves, circulating noradrenaline and glucagon inthe perfused rat liver." Universität Potsdam, 1987. http://opus.kobv.de/ubp/volltexte/2008/1672/.
Full textAbstract:
In the isolated rat liver perfused in situ stimulation of the nerve bundles around the portal vein and the hepatic artery caused an increase of urate formation that was inhibited by the α1-blocker prazosine and the xanthine oxidase inhibitor allopurinol. Moreover, nerve stimulation increased glucose and lactate output and decreased perfusion flow. Infusion of noradrenaline had similar effects. Compared to nerve stimulation infusion of glucagon led to a less pronounced increase of urate formation and a twice as large increase in glucose output but a decrease in lactate release without affecting the flow rate. Insulin had no effect on any of the parameters studied.