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Kipkeew, Friederike [Verfasser], Elke [Akademischer Betreuer] Winterhager, and Andrea [Akademischer Betreuer] Vortkamp. "Die CCN Proteine CCN1 (CYR61) und CCN3 (NOV) : Regulatoren der Trophoblastproliferation und -migration / Friederike Kipkeew. Gutachter: Andrea Vortkamp. Betreuer: Elke Winterhager." Duisburg, 2014. http://d-nb.info/1049647432/34.
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Bohr, Wilhelm [Verfasser]. "Expression, Aufreinigung und Charakterisierung von rekombinantem hCTGF (CCN2) und rNOV (CCN3) in einem eukaryontischen Zellsystem / Wilhelm Bohr." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2010. http://d-nb.info/1015149219/34.
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Guo, Yanping. "The mechanism of Nov (CCN3) function in haematopoiesis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:5785f3b9-3206-4bb4-b486-d90cded680f8.
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Haematopoietic stem cells (HSC) are strictly regulated by intrinsic regulators and extrinsic signals from the microenvironment. Nov (CCN3), a matricellular protein of the CCN family, has been reported as a suppressor gene in solid tumours and chronic myeloid leukaemia (CML). Recent study identified Nov as a positive regulator in human cord blood CD34+ stem cells. However, the functions of Nov in haematopoiesis and adult HSC remain largely unknown.
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Le, Dréau Gwenvaël. "NOV/CCN3 et système nerveux central : étude du rôle de NOV/CCN3 dans les précurseurs de neurones granulaires et des astrocytes." Paris 6, 2008. http://www.theses.fr/2008PA066063.
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NOV/CCN3 est une protéine sécrétée et multifonctionnelle impliquée dans le développement de différents tissus. Le système nerveux central représentant l’un de ses sites majeurs d’expression au cours du développement, nous avons ainsi émis l’hypothèse que NOV participe au développement de ce tissu. Les résultats obtenus en étudiant le rôle potentiel de NOV durant la phase postnatale de développement du cervelet chez le rat suggèrent que NOV participe à la mise en place des neurones granulaires en inhibant la prolifération et stimulant la migration de leurs précurseurs. Par ailleurs, nous avons observé in vitro que l’expression de NOV est induite au cours de la différenciation de lignées de précurseurs astrocytaires mais que NOV ne semble pas réguler ce processus. Ces résultats soutiennent l’hypothèse que NOV soit impliquée dans le développement du système nerveux central, en particulier dans le devenir de populations neuronales.
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Lu, W. "Characterisation of CCN3 signalling pathway in Chronic Myeloid Leukaemia (CML)." Thesis, Queen's University Belfast, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517404.
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Li, Chang Long. "Etude de la protéine CCN3/NOVH dans la signalisation cellulaire." Paris 7, 2003. http://www.theses.fr/2003PA077223.
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Ricard, Anne-Sophie. "Les molécules d’adhésion CCN3 et DDR1 au cours du vitiligo." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21854/document.
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Le vitiligo généralisé est une leucodermie acquise qui touche 0,5 à 1% de la population mondiale et qui résulte d’une perte progressive des mélanocytes.Le mécanisme à l’origine de la perte des mélanocytes au cours du vitiligo reste obscur et la destruction des mélanocytes n’a jamais été observée.De nombreuses hypothèses ont été avancées pour expliquer la disparition des mélanocytes : une susceptibilité génétique, l’auto-immunité, la théorie neurale et la théorie oxydative.Notre équipe a développé une théorie intégrée qui reprend ces différents mécanismes. Cette théorie considère que le vitiligo est lié au détachement des mélanocytes et à leur élimination à travers l’épiderme ou mélanocytorrhagie. Dans cette théorie, un défaut d’adhésion des mélanocytes est le facteur prédisposant au vitiligo.L’interaction des mélanocytes avec les kératinocytes environnants et avec la membrane basale est médiée par les intégrines et les cadhérines. L’expression de l’intégrine et de la E-cadhérine n’est pas modifiée dans le vitiligo généralisé.En 2006, Fukunaga-Kalabis et al. montrent que l’attachement des mélanocytes à la membrane basale est en partie dû à DDR1 qui est sous le contrôle de la protéine CCN3. Ils ont observé que l’inhibition de CCN3 induit le détachement des mélanocytes.Récemment, des variants génétiques de DDR1 ont été observés chez des patients d’origine ethnique différente atteints de vitiligo. Nous avons décidé d’étudier d’une part l’expression de CCN3 au niveau de la peau lésionnelle et non lésionnelle de patients atteints de vitiligo et d’autre part l’impact de l’inhibition de CCN3 et de DDR1 au niveau de mélanocytes utilisés pour des reconstructions épidermiques. Nos résultats in vitro et in vivo suggèrent que CCN3 est impliqué dans la physiopathologie du vitiligoCommon generalized vitiligo is an acquired hypopigmentation which is found in 0, 5-1% of individuals world-wide and which results in progressive loss of melanocytes.The mechanism underlying the elimination of melanocytes in vitiligo remains unclear and melanocyte destruction has never been clearly demonstrated in non segmental vitiligo. Various hypotheses have been put forward to explain the disappearance of melanocytes in vitiligo: genetic susceptibility, autoimmunity, neural and impared redox status. We previously proposed a new theory that integrates those pathomechanisms. This theory considers vitiligo as a disease caused by the chronic detachment and transepidermal loss of melanocytes named melanocytorrhagy. In this theory, the defective adhesion of melanocytes is the predisposing factor.Interactions between melanocytes and the basement membrane are mediated by integrins and interactions between melanocytes and keratinocytes are mediated by cadherins in association with β-catenin. But integrin expression is not affected in NSV and a normal expression of E-cadherin in lesional and non lesional vitiligo skin is observed.In 2006, Fukunaga-Kalabis et al. reported that attachment of melanocytes to basal lamina is in part due to DDR1, which is under control of CCN3. They have observed that inhibition of CCN3 induces the detachment of melanocytes.Recently, DDR1 genetics variants have been associated with vitiligo in patients of different ethnic origin. We have decided to study in parallel the expression of CCN3 and DDR1 in lesional and non lesional skin of vitiligo patients and the impact of inhibition of CCN3 and DDR1 in melanocytes on their behaviour in reconstructed epidermis.In conclusion, our in vivo and in vitro data suggest that CCN3 is implicated in vitiligo etiology
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Wang, Wen. "Investigating the role of CCN1, CCN2, and CCN6 in osteoclast and osteoblast physiology." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=204059.
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CCN protein family members (CYR61, CTGF, Nov, Wisp-1, Wisp-2 and Wisp-3) have important roles in many different processes including angiogenesis, inflammation, remodelling of extracellular matrix and tumorigenesis. In bone, CCN1 increases osteoblastogenesis via Wnt3A signalling and activation of -catenin which, in turn, upregulates CCN1 expression. The exact role of CCN1, CCN2, and CCN6 in osteoclast physiology are not known but we have recently shown that recombinant human (rh)CCN1 inhibits osteoclastogenesis in vitro. The aim of this study was to determine: 1) the expressions of all six members of the CCN protein family in osteoblasts and osteoclasts; 2) the functions of recombinant human CCN2, CCN6 in osteoclastogenesis; 3) whether osteoblast-derived CCN1 may mediate the effect of CCN1 on osteoclast formation and the roles of osteoblast-derived CCN1 and/or osteoclast-derived CCN1 in osteoblast and/or osteoclast differentiation; 4) which signalling pathways are involved in the function of CCN1 in osteoclasts and osteoblasts. We found CCN1-5 but not CCN6 expressed in murine osteoclasts and osteoblasts. All six members were expressed in human OA osteoblasts but only CCN1-3 were detected in human osteoclasts using quantitative RT-PCR. rhCCN1 (in agreement with our previous observations), and also 2 and 6 inhibited human and mouse osteoclast formation in a concentration-dependent manner. We generated and validated an expression construct to specifically overexpress CCN1 in osteoblasts. Incorporation of CCN1-specific siRNA reduced CCN1 expression to between 12.5% and 50% of control osteoblast cultures. In both co-cultures with direct contact between osteoblasts and osteoclast co-cultures as well as Transwell cultures, overexpression of CCN1 in osteoblasts decreased the formation of TRAP positive multinucleated osteoclast-like cells, while siRNA mediated knockdown of CCN1 in the osteoblasts resulted in increased osteoclast-like cell formation. These data suggest that osteoblast-derived CCN1 is a secreted negative regulator of osteoclastogenesis. Moreover, overexpression or knockdown of CCN1 in osteoclast precursors inhibited or increased osteoclast differentiation whilst overexpression or knockdown CCN1 in osteoblasts increased or inhibited osteoblast mineralization respectively. Further investigation found that CCN1 increased Wnt and MAPK signalling in osteoblasts cultured in mineralization medium and inhibited Wnt and IGF-1 signalling during osteoclast differentiation. In conclusion, paracrine and autocrine effects of CCN1 have been demonstrated in osteoclasts and osteoblasts in this study and Wnt, MAPK, amd IGF-1 signalling pathways, may be involved in these effects.
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O''''Hagan, Thomas P. "The role of regulatory T cells and CCN3 in CNS myelination and remyelination." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.728386.
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Multiple Sclerosis (MS) is an immune-mediated disease, characterised by demyelination in the central nervous system (CNS)- In MS, the regeneration of myelin sheaths (remyelination) can occur. However, when this regenerative process fails, patients can develop permanent disability. The promotion of remyelination is currently an unmet clinical need that holds significant potential to improve the lives of MS patients. Despite the pathological role of CD4+ T cells in MS, T cells have been shown to support remyelination in experimental models. However, previous studies have investigated total CD4+ T cells without addressing distinct CD4+ T cell subsets. CD4+ Regulatory T cells (Treg) have been identified in multiple organ systems as having a role in repair and regeneration; therefore, we aimed to characterise the role of the anti-inflammatory, CD4+ T cell subset, Treg, in CNS remyelination. To determine if Treg have a direct effect on neural cells we utilised an organotypic brain stem slice model that myelinates ex vivo. In both inflammatory and stabilised brain slice cultures, Treg and/or conditioned media from Treg cultures promoted the maturation of oligodendrocytes, developmental myelination and remyelination as measured by the co-localisation of fluorescent staining of myelin and axons. Treg-deficient mice exhibited impaired oligodendrocyte differentiation during remyelination that was rescued by the adoptive transfer of Treg in vivo. Proteome profiling of conditioned media identified CCN3 as a novel Treg-derived factor that promoted myelination and was required for Treg-enhanced myelination in brain slices. This is the first evidence of CCN3 in CNS regeneration and of CCN3 production by T cells. These findings uncover a new role of Treg in promoting oligodendrocyte differentiation and remyelination in the CNS, distinct from, but complementary to, the classical anti-inflammatory roles of Treg.
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Marchal, Pierre-Olivier. "Rôle de NOV/CCN3 dans différents modèles in vivo de néphropathies et pathologies cardiovasculaires." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066321.
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La maladie rénale chronique (MRC) est un véritable problème de santé publique. Bien qu'elle puisse avoir plusieurs origines, celle-ci est caractérisée par le développement d'une inflammation chronique ainsi qu'une fibrose conduisant à une diminution progressive de la fonction rénale. Il est nécessaire de trouver de nouvelles cibles thérapeutiques pour arrêter la progression de cette pathologie. La protéine NOV/CCN3 a été identifiée comme étant une cible potentiellement intéressante. Dans cette étude, nous avons montré que dans un modèle in vivo de néphropathie obstructive, NOV avait un rôle proinflammatoire et profibrotique. Dans un autre modèle in vivo de néphropathie hypertensive, nous avons montré que NOV était régulée par l'Angiotensine II (AngII) et pouvait inhiber l'expression du récepteur AT1R de l'AngII et ainsi limiter les effets délétères de cette hormone. Bien que contradictoires, ces résultats montrent un rôle important de NOV au cours du développement des néphropathies indiquant que cette protéine peut avoir des effets opposés en fonction du contexte pathologique. Enfin, du fait de l'étroite relation entre NOV et l'AngII, nous avons montré que NOV était aussi régulée par cette hormone au niveau aortique et avait un effet proinflammatoire au niveau vasculaire dans des conditions d'hypertension. L'ensemble de nos résultats montrent un rôle important de NOV dans ces différents types de pathologies et que cette protéine pourrait être une cible intéressante pour traiter les néphropathies ou encore les pathologies cardiovasculairesChronic kidney disease (CKD) is a major public health problem. Regardless of the primary cause, CKD is characterized by the development of chronic inflammation and fibrosis leading to progressive decline of renal function and eventually end-stage renal disease (ESRD). Actually, regular hemodialysis and renal transplantation are the only available therapies for ESRD patients. Therefore, there is an urgent need for new therapeutically targets against this incurable disease. Recently, the NOV/CNN3 protein was shown to be an interesting candidate. In this study we have shown that, in obstructive nephropathy in mice, NOV has profinflammatory and profibrotic effects. In addition, we have shown in a mouse model of hypertensive nephropathy, that NOV was regulated by Angiotensin II (AngII) and could inhibit AT1R receptor expression to limit the deleterious effects of this hormone. These results show an important role of NOV during the development of two different types of nephropathies and may indicate that this protein can have model specific effects. Finally, we have shown that NOV itself was also regulated by AngII in the aorta and has proinflammatory effects in hypertensive conditions. Taken together our results show an important role of NOV in these different types of pathologies and that this protein could be a key player in the development of CKD as well as vascular diseases. Nevertheless, further investigations are still required to better characterize the precise role of NOV in these pathological contexts
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Henrot, Pauline. "Implication de CCN3 (NOV) dans la vasculopathie et la pigmentation cutanées de la Sclérodermie Systémique." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0198.
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Près de la moitié des patients atteints de sclérodermie systémique (ScS) présentent des troubles de la pigmentation cutanée. La mélanogenèse est sous la dépendance, outre les facteurs épidermiques, de facteurs dermiques produits par les fibroblastes et les cellules endothéliales. Parmi ces facteurs se trouve NOV (CCN3) (protéine appartenant à la même famille que CTGF (CCN2), protéine pro-fibrotique augmentée dans la ScS) qui aurait un rôle anti-fibrotique. Nous souhaitons ainsi disséquer le lien entre la composante fibrotique dermique et la pigmentation épidermique. Pour cela, des biopsies cutanées ont été réalisées chez 21 patients ScS, en zone lésionnelle (scléreuse avec ou sans trouble de pigmentation) et non lésionnelle pour 12 d’entre eux. Ces biopsies ont été séparées en 3 fragments qui ont été soit fixés pour analyses histologiques et immunohistochimiques, soit congelés à -80°C pour analyse protéomique ou transcriptomique, soit dissociés pour isoler les cellules cutanées afin de les analyser en protéomique ou transcriptomique. Des témoins de peau et des cellules saines sont utilisées en contrôle. Nous avons dégagé deux types de troubles pigmentaires : une hyperpigmentation s’apparentant à un photo-vieillissement, et une dépigmentation péri-folliculaire apparaissant de manière précoce. Les niveaux d’expression de CCN2 et CCN3 varient chez les patients en fonction des données cliniques, aussi bien au niveau protéique qu’au niveau immunohistochimique. S’il existe des différences en fonction de l’atteinte pigmentaire, il semble que dans les fibroblastes sclérodermiques, la balance CCN2/CCN3 soit déséquilibrée tant au niveau de la zone lésionnelle que cliniquement non lésionnelle, suggérant que CCN2 et 3 pourraient être dérégulés intrinsèquement ou à des stades précoces. Ce travail pourrait aboutir à l’identification d’un phénotype précoce basé sur l’atteinte pigmentaire, et au développement d’une thérapie basée sur la rééquilibration du ratio CCN2/CCN3Systemic Sclerosis (SSc) is a rare but potentially deadly connective tissue disease. Its pathophysiology remains partly unknown but combines auto-immunity, small and large vessels involvement and fibrosis of the connective tissue, affecting all organs. Skin features are considered as diagnostic and prognosis markers and include for some patients the presence of pigmentary disorders. In this work, we looked into pigmentary disorders in SSc and their relationship with the pathophysiology of the disease. First, we analyzed the presence of pigmentary disorders among a local cohort of 239 patients as well as their association with systemic involvement in the disease. We have found that diffuse hyperpigmentation was associated with an increased risk of vascular involvement in SSc, particularly digital ulcers. Then, we investigated the molecular basis behind this association. Proteins of the CCN (CYR61 / CTGF / NOV) family are multimodular proteins secreted in the extra-cellular matrix, where they take part in numerous biological processes, such as cell proliferation, adhesion, collagen secretion. Within this family, CCN3 (also called NOV) is a promising candidate, being implicated both in angiogenesis and epidermal homeostasis. We studied CCN3 expression in the skin of SSc patients presenting or not pigmentary disorders, as compared to healthy controls. We found that CCN3 expression was particularly decreased in the dermal vessels in situ, as well as in endothelial cells in vitro. CCN3 inhibition in endothelial cells resulted in altered angiogenesis in vitro, through a decrease in cell migration. We also studied CCN3 expression in SSc epidermis. SSc patients presenting hyperpigmentation exhibited decreased CCN3 in their melanocytes as well as increased CCN3 in their keratinocytes, compared to patients without pigmentary disorders. Overall, CCN3 represents a promising therapeutic lead for SSc patients with vascular involvement, which could bespotted early thanks to the presence of hyperpigmentation
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Schenk, Rita. "Impact of the CCN-proteins CYR61/CCN1 and WISP3/CCN6 on mesenchymal stem cells and endothelial progenitor cells." Doctoral thesis, kostenfrei, 2007. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2776/.
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Pakradouni, Jihane. "NOV/CCN3, une protéine d'intérêt dans les pathologies tumorales et dans les facteurs de risque des maladies cardiovasculaires?" Paris 6, 2011. http://www.theses.fr/2011PA066544.
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NOV/CCN3 (Nephroblastoma overexpressed), est un membre fondateur de la famille des CCN. Il code une protéine sécrétée intervenant dans des situations physiologiques (développement, angiogenèse et cicatrisation) et pathologiques (fibrose, tumorigenèse). Ce projet de thèse en CIFRE vise à mettre en évidence les propriétés anti-tumorales et anti-angiogéniques de NOV et de son fragment C-terminal (NOV C-ter) dans des modèles tumoraux. Nous avons évalué les effets thérapeutiques de NOV et NOV C-ter dans trois modèles de tumeurs angiogéniques et avons démontré l’efficacité de NOV C-ter dans le glioblastome. Ces résultats constituent les premières preuves d’une action thérapeutique de NOV C-ter dans le cancer. Nous avons parallèlement développé une thématique portant sur le rôle de NOV dans les facteurs de risque de maladies cardiovasculaires (MCV). Nous avons mis en évidence une augmentation de l’expression de NOV in vitro et in vivo dans un contexte de surexpression d’angiotensine II et de TNFα, deux acteurs essentiels de la composante inflammatoire de l’hypertension. NOV induit par ailleurs l’expression de deux chimiokines CCL2 et CCL5 impliquées dans la physiopathologie hypertensive. Une étude réalisée sur une cohorte de patients présentant des facteurs de risque de MCV nous a permis de déterminer les facteurs responsables de 40% de la variabilité de la concentration plasmatique de NOV et de mettre en évidence une corrélation entre l’expression locale et systémique de NOV et les paramètres de l’obésité. L’ensemble de ces résultats suggère que NOV est impliquée dans la physiopathologie de l’hypertension et de l’obésité et serait un nouvel acteur des facteurs de risque des MCV
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Calhabeu, Frédérico. "NOV / CCN3 et CKIP-1 régulent respectivement la détermination et la migration des myoblastes au cours de la différenciation musculaire." Paris 6, 2006. http://www.theses.fr/2006PA066453.
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CKIP-1 et NOV sont deux protéines qui ont été récemment impliquées dans la régulation de la différenciation myogéniques. CKIP-1 est une protéine à domaine pleckstrin (PH) qui a été initialement isolée à partir d’un criblage double hybride. Au laboratoire, une forme courte, CKIP-1p28, dépourvue du domaine PH a été mise en évidence dans les myoblastes C2. Les deux formes de CKIP-1 ont des effets antagonistes sur la différenciation PI3-K dépendante des myoblastes. Tandis que CKIP-1 potentialise la différenciation, l’expression de CKIP-1p28 l’inhibe en interférant avec la polymérisation de l’actine. Ces deux isoformes sont deux nouvelles protéines adaptatrices qui, en modulant le remodelage du cytosquelette, permettent la translocation et la phosphorylation d’Akt à la membrane régulant ainsi la migration cellulaire aussi bien in vitro qu’in vivo, lors du développement du Zebrafish. La protéine NOV appartient à une famille de protéines secrétées, liant la matrice, la famille CCN (Cyr61, CTGF, NOV). La surexpression de NOV dans les myoblastes C2 inhibe leur différenciation. Ces cellules C2-NOV sont incapables d’induire les marqueurs de différenciation tels que la Myogénine, la p21WAF1 et la troponine. De plus, nous avons observé que NOV inhibe fortement l’expression des gènes de détermination MyoD et Myf5 ainsi que celle d’IGF-II. La surexpression de MyoD dans les C2-NOV est suffisante pour rétablir la différenciation, alors que l’ajout d’insuline à 10-6 M n’a aucun effet. En conclusion, l’ensemble de nos résultats ont montré que NOV est un régulateur de l’engagement des cellules dans le lignage myogénique et interfère dans la boucle de régulation positive MyoD/IGF-II, alors que CKIP-1 joue le rôle d’une protéine adaptatrice nécessaire à la différenciation terminale via l’activation de la voie PI3K/Akt et le remodelage du cytosquelette d’actine.
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Wagener, Jessica [Verfasser], Elke [Akademischer Betreuer] Winterhager, and Andrea [Akademischer Betreuer] Vortkamp. "NOV(CCN3)-vermittelte Signalkaskaden zur Regulation der Migration und Proliferation der humanen Trophoblastzelllinie Jeg3 / Jessica Wagener. Gutachter: Elke Winterhager ; Andrea Vortkamp." Duisburg, 2011. http://d-nb.info/101861222X/34.
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Hlavatý, Martin. "Bezpečnostní problémy obsahově centrických sítí." Master's thesis, Vysoké učení technické v Brně. Fakulta informačních technologií, 2012. http://www.nusl.cz/ntk/nusl-235479.
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Today, computer networks are dominated by data distribution and content retrieval, but technology was created for communication between hosts. Content and service access requires mappnig between what users want and where in network it can be found. Content-centric networks separate content from its location. This thesis aims to security of Content-centric networks, looks for weak spots in its design and suggests steps for improvements of their security.
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Lambi, Alex G. "The Intricate Role of Connective Tissue Growth Factor (CTGF/CCN2) in Prenatal Osteogenesis: A Heretofore Oversimplified Dogma of the CCN Field." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/233693.
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Cell BiologyPh.D.
Connective tissue growth factor (CTGF/CCN2) is axiomatically necessary for proper skeletal development and function. We need not look further than the studies that have been done to date utilizing mice genetically engineered to lack CTGF production. These CTGF null or knockout (KO) mice fail to form a normal murine skeleton and instead yield one littered with bony dysmorphisms, including incompetent craniofacial development, kinked limb bones, and misshapen ribs that are not conducive to proper respiratory function. As a result, the global lack of CTGF is incompatible with postnatal life. A closer look at several sites demonstrated defects in physiologic processes necessary for bone formation - angiogenesis, chondrogenesis, and osteogenesis. Therefore, the dogma in the CCN protein field to date has been that systemic ablation of CTGF production in vivo results in global defects in bone development. We believe this dogma is an oversimplification of the role of CTGF on skeletal development. Our initial impetus leading us to this belief was the gross identification of the specific skeletal sites malformed in CTGF KO mice, in particular the bones of the limbs. While in the lower limb of CTGF KO mice the tibiae and fibulae are misshapen, the adjacent femora and digits are phenotypically normal. The same is true for the upper limb, in which the radii and ulnae are phenotypically abnormal while the humeri and digits are normal. Therefore, we believe that the role of CTGF in skeletogenesis is site-specific such that its loss affects local skeletal patterning and/or mechanobiological cues resulting in the unique phenotype seen in CTGF KO mice. The research of this dissertation constitutes a comprehensive skeletal analysis of CTGF KO mice and in so doing we determined the extent and location of skeletal abnormalities. We found skeletal site-specific changes in growth plate organization, bone microarchitecture and shape and gene expression levels in CTGF KO compared to wild-type (WT) mice. Growth plate malformations included reduced proliferation zone and increased hypertrophic zone lengths. Appendicular skeletal sites demonstrated decreased metaphyseal trabecular bone, while having increased mid-diaphyseal bone and osteogenic expression markers. Axial skeletal analysis showed decreased bone in caudal vertebral bodies, mandibles, and parietal bones in CTGF KO mice, with decreased expression of osteogenic markers. Analysis of skull phenotypes demonstrated global and regional differences in CTGF KO skull shape resulting from allometric (size-based) and non-allometric shape changes. Localized differences in skull morphology included increased skull width and decreased skull length. We further continued the skeletal characterization of CTGF KO bones with an analysis of bone cell ultrastructure and matrix composition. These studies demonstrated that, while CTGF is not necessary for complete morphologic maturation of bone cells, global ablation results in ultrastructural features not commonly seen in WT bones. Our findings include drastically dilated rough endoplasmic reticulum (RER) in osteoblasts of the tibial diaphyseal region, comprising the phenotypic kink in CTGF KO mice and ultrastructural dysmorphologies of CTGF KO osteoclasts including multi-layered, membranous inclusions, decreased vacuolization and ruffled border extents, and disproportionately large clear zones. Lastly, FT-IR analysis demonstrated heterogeneity in CTGF KO bone composition. The results of this dissertation have revealed a more complex role for CTGF in osteogenesis and have identified potential mechanisms and future research directions to fully understand this intricate story.
Temple University--Theses
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Trembath, James. "Airborne CCN measurements." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/airborne-ccn-measurements(3e4249a8-c992-4408-b193-a48921b1caaf).html.
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This work tests the validity of using a commercial cloud condensation nuclei (CCN) counter (CCNc) on the Facility for Airborne Atmospheric Measurements (FAAM) research aircraft. The CCNc was suitable for aircraft work with sta- ble and repeatable supersaturation, temperature and pressure relationships. The sample architecture of the aircraft fitted CCNc was found to transmit particles with acceptable losses in the diameter range of interest as was a pressure control device designed for airborne work. Rosemount inlets, used to sample aerosol, were found to be sensitive to particle density resulting in disparate aerosol being sam- pled with different efficiencies. In dust dominated aerosol inlet efficiency peaks at 10.24 at an optical diameter of 2.91 μm, with a minimum inlet efficiency between 1.78 and 1.51 at 0.28μm. In less dense aerosol inlets sample representatively below 0.6 μm and comparably below 1.0 μm. The thorough testing of the CCNc, associated sampling architecture and mea- surement strategies, enabled vertical and horizontal CCN to be investigated along with other aerosol and cloud microphysical properties in the Southern Equato- rial Pacific (SEP). The primary source of particulates was the South American continent, with sulphate dominating composition. There were strong gradients in aerosol and gas phase chemistry concentration with distance from the coast and in the cloud microphysics measurements where highest droplet numbers and smallest diameters were close to the coast. These data represent an important validatory and parameterisation data set for models of all scales. CCN data were used to calculate the aerosol hygroscopicity parameter, the mean project value, κ, was 0.21 ± 0.18 . There was no evident variation in hygroscopicity with distance from the Chilean coastline suggesting a single dominant source and a well mixed boundary layer up to 907km to the west. CCN measurements were also com- pared to predictions from multiple models of different composition and mixing state assumptions. The best CCN closure used an external mixture of inorganic and organic aerosol components, with a modelled to observed ratio of 1.37 ± 0.32. It was hypothesised that this large ratio and the relatively low bulk hy- groscopicity was influenced by an external mixture. Incorporating this external mixture is imperative if CCN are to be accurately modelled and any subsequent cloud processes accurately captured.
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Duchesnes, Cecile Emmanuelle. "Molecular characterisation of the chemokine receptor CCR3." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407171.
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Tarr, Joseph Thomas. "CTGF/CCN2: The Marionettist of Mammalian Palatogenesis." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/540676.
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Biomedical SciencesPh.D.
The mammalian palate develops early in embryogenesis by way of a carefully orchestrated series of temporally and spatially regulated signaling events. Molecular signaling pathways that have been proven to be vital to the process of palatogenesis include TGF-βs, BMPs, FGFs, EGF, and Wnts. The absence of connective tissue growth factor (CTGF/CCN2) has been shown previously to cause failure of proper palatogenesis, i.e. cleft palate. However, the details about the phenotype of this model of cleft palate were scarce. Additionally, CCN2 is known to interact with TGF-βs, BMPs, FGFs, EGF, and Wnts, though information on how these pathways were impacted in the developing palate lacking CCN2 were also not available. In Chapters 2 and 3, through our use of gross specimen and histological examination combined with cell and organ culture, we produced the most detailed characterization of the CCN2 knockout (KO) model of cleft palate with identification of negatively affected signaling pathways that lead to the clefting phenotype. Collection and examination of gross and histological sections revealed at 100% penetrance of cleft palate in which development is impaired around the phase of palatal shelf elevation. Organ culture also revealed that when artificially apposed, the CCN2 KO model system also suffers from a fusion deficit. Finally, utilizing cells isolated from the developing palates, we found a reduction in proliferation, adhesion, and spreading with an enhanced migratory ability. Addition of recombinant CCN2 was able to rescue cell spreading but not proliferation. CCN2 as an immobilized substrate did not rescue adhesive ability. Decreased adhesion and spreading in the KO cells are attributed to the inability of the KO cells to activate Rac1 and RhoA. Examination of gene expression differences by mRNA-sequencing and qRT-PCR revealed numerous gene expression alterations between the wild type (WT) and the KO palates, most notably FGF4 and EGFR. Addition of FGF4 or EGF to cell culture was unable to promote increased proliferation in the KO cells while producing a response in the WT cells. Examination of downstream signaling revealed highly amplified and prolonged ERK1/2 signaling in the FGF4 treated palate cells indicating that FGF signaling is significantly altered in the absence of CCN2. Treatment of the cells with EGF produced a response proportional to EGFR expression differences indicating that EGFR signaling is not impacted beyond the receptor protein levels. The link between EGFR protein levels and FGF mediated ERK1/2 activation is a protein called Spry2. We found greatly reduced Spry2 mRNA levels in the KO palates and upon FGF4 stimulation at 24 hours of exposure indicating that in the absence of CCN2, proper inhibition of FGF signaling and EGFR degradation is negatively altered. Collectively, the data demonstrate that CCN2 is vital to palatogenesis by impacting proliferation, shelf elevation, and shelf fusion through increased FGF signaling and reduced EGFR signaling resulting partially from reduced Spry2 activity.
Temple University--Theses
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Kiwanuka, Elizabeth. "CCN2 – Keratinocyte Interactions In Vitro and In Vivo." Doctoral thesis, Uppsala universitet, Plastikkirurgi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-213566.
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Cutaneous wound healing is a complex process involving the migration of inflammatory cells to the wound site, deposition of extracellular matrix, and the reestablishment of an intact epithelial barrier. Re-epithelialization depends on the proliferation and directional migration of keratinocytes from the wound edges. Initially, keratinocytes migrate over a provisional wound matrix that is rich in fibronectin, and as the wound heals the provisional matrix becomes replaced by one consisting of collagen and proteoglycans. Re-epithelialization is tightly regulated by a variety of peptides such as growth factors, cytokines and proteases, and abnormalities may result in chronic non-healing wounds or hypertrophic scars. CCN2 (Connective Tissue Growth Factor) is a multifunctional protein with effects on cells and their interactions with the connective tissue. CCN2 is expressed in a variety of cell types and regulates numerous cell functions including proliferation, differentiation, adhesion, migration and stimulation of collagen production. While the importance of CCN2 for the fibrotic response has been well studied, its involvement in keratinocyte function has not yet been fully explored. Using an in vivo wound model, the expression of CCN2 was captured at the leading keratinocyte edge during re-epithelialization. In vitro, exogenous addition of CCN2 to human keratinocyte cultures promoted keratinocyte migration. Subsequently, integrin a5b1 was identified as an important mediator of CCN2 enhancement of keratinocyte adhesion to fibronectin. CCN2 activated the FAK-MAPK signaling pathway, and pretreatment with MEK1 specific inhibitor PD98059 markedly reduced CCN2-promoted keratinocyte migration. In vitro, CCN2 expression was induced by TGF-β1. Compared with inhibiting the SMAD pathway, blocking MAPK was more effective in reducing TGF-β1-induced CCN2 mRNA and protein expression. In addition, CCN2-induced keratinocyte spreading required FAK. Treatment with CCN2 led to actin disassembly and altered the activity of the Rho proteins and p190RhoGAP in keratinocytes. Furthermore, Cdc42 mediated CCN2-induced cell polarity. In conclusion, using in vivo and in vitro models, CCN2 was shown to regulate keratinocyte function by promoting keratinocyte adhesion, spreading and migration. A complete understanding of CCN2 expression in keratinocytes is crucial in order to develop novel therapies for wound healing.
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Brasseit, Jennifer. "Mutagenese und funktionelle Charakterisierung des humanen CCR3-Rezeptors." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-61848.
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McLean, Celia. "Investigating the expression and function of CCN2 in articular cartilage." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5289.
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The pericellular matrix (PCM) is a distinct zone of matrix that surrounds individual chondrocytes throughout articular cartilage. Although not much is known about its function, our group has shown that it has a role in mechanotransduction by controlling the bioavailability of perlecan-bound FGF-2. The aim of this project was to determine the other structural components of the PCM, and to search for other heparin binding growth factors which might be sequestered in the matrix. By confocal microscopy I confirmed that the PCM was rich in type VI collagen and perlecan, although devoid of type II collagen and aggrecan. Isolation of individual chondrons (the chondrocyte together with its PCM) was performed by partial digestion of the matrix using dispase and collagenase, and proteomic analysis using mass spectrometry was performed to identify new proteins. As this method was only partially successful I looked for the presence of a known heparin binding growth factor, connective tissue growth factor (CCN2), in chondron preparations. CCN2, which is an abundant secreted protein of articular cartilage, was present in both the chondron preparation by western blot, and was visualised in the PCM of porcine and human articular cartilage by confocal microscopy. CCN2 is not commercially available so His-tagged recombinant protein was stably expressed and purified using nickel affinity chromatography. Biological activity of the purified protein was investigated in a number of established assays. No biological activity was demonstrated when purified CCN2 was used alone on murine mesenchymal stem cells, but was evident when assayed in combination with low dose TGF-β. The effect of exogenous CCN2 on fibroblasts was limited by the significant release of endogenous CCN2. High constitutive expression of CCN2 in articular cartilage may limit the effects seen by exogenous CCN2. However, the results presented in this thesis support the role of CCN2 as a modulator of TGF beta signalling, and suggest that, through potentiating TGF beta it may regulate matrix turnover in articular cartilage.
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Hebert, Ryan Matthew. "Functional analysis of CCM3 a gene contributing to cerebral cavernous malformations /." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12022008-120301/.
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Haouchine, Omar. "Ccna, une poésie féminine de Kabylie : complaintes, conflits et régulation sociale." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCF009.
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Ccna [ʃ:na], est une poésie féminine traditionnelle kabyle chantée publiquement lors des fêtes de mariages dans la région d’Ighil n Zekri de Tizi-Ouzou en Algérie. Elle traite essentiellement de la condition socio-affective de la composante féminine des communautés villageoises. Bien qu’elle s’apparente à d’autres types poétiques relevant de la tradition orale kabyle, cette poésie possède des spécificités propres et une originalité expressive, tant du point de vue de son contexte de performance que du point de vue des fonctions qu’elle assure au sein des sociétés productrices. En effet, les cérémonies de ccna donnent lieu à la production d’un espace virtuel de communication et de gestion des conflits qui mérite indéniablement une étude approfondie. Ce projet de recherche est construit autour d’un corpus traduit et annoté, son étude implique nécessairement une approche, à la fois proprement littéraire des textes et anthropologique (acteurs, conditions de création, diffusion et réception)Ccna [ʃ:na], is a female traditional Kabylian poem sung publicly at weddings in the area of Ighil n Zekri in Tizi-Ouzou, Algeria. It mainly deals with women’s socio-emotional conditions in rural communities. Although it is similar to other poetic types in the kabylian oral tradition, this poetry has specificities and a meaningful originality, from the point of view of its performance context as well as from the functions it ensures within the producing societies. Indeed, ccna ceremonies lead to the creation of a virtual space of communication and conflict management that deserves an in-depth study. This research project is built around a corpus translated and annotated, its study necessarily implies an approach, both literary of the texts and anthropological (actors, conditions of the creation, dissemination and reception)
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Yoshida, Yoshinori. "CCN1 protects cardiomyocytes from oxidative stress via β1 integrin-Akt pathway." Kyoto University, 2007. http://hdl.handle.net/2433/135780.
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Baker, Natasha. "Investigating the Role of WISP-3/CCN6 in Osteoarthritis and Chondrocyte Biology." Thesis, University of East Anglia, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502368.
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Wntl Inducible Secreted Protein 3 (WISP-3/CCN6) is a member of the CCN (Cysteine rich 61/Connective tissue Growth Factor/Nephroblastoma Overexpressed) family of matricellular proteins. WISP-3/CCN6 is mutated in Progressive Pseudorheumatoid Dysplasia (pPRD), a rare disease of articular cartilage degeneration. The expression of WISP-3/CCN6 in osteoarthritis at the mRNA and protein level was investigated. To determine the role of WISP-3/CCN6 in chondrocyte biology the WISP-3/CCN6 gene was stably transfected into immortalised chondrocytic (C-281I2) cells. The effect of stable WISP-3/CCN6 over-expression on metalloproteinase gene expression was investigated.. The expression of WISP-3/CCN6 mRNA was significantly up-regulated in osteoarthritic cartilage extracts compared to post.-mortem .controls. Immunohistochemistry of osteoarthritic cartilage sections revealed that WISP-3/CCN6 protein expression was upregulated in areas of cartilage damage and was often localised to the pericellular matrix surrounding chondrocytes. The steady state mRNA levels for the aggrecanases ADAMTSI, ADAMTS4 and in particular, ADAMTS5 were significantly lower in clonal C-28/I2 cell lines stably over-expressing WISP-3/CCN6 compared to controls, while MMPIO mRNA was significantly up-regulated. Treatment with lithium chloride, which can mimic activation of canonical \Vnt signalling, led to a de-repression of ADAMTS5 mRNA and enhanced up-regulation ofMMPIO in the WISP-3/CCN6 clones. Treatment with the cytokines Interleukin In and Oncostatin M up-regulated ADAMTS5 mRNA and .down-regulated MMPI0 mRNA in the WISP-3/CCN6 clones. These data demonstrate that WISP-3/CCN6 may repress ADAMTS5 mRNA expression in chondrocytic cells by inhibiting canonical Wnt signalling. In addition, inflammatory pathways may oppose WISP-3/CCN6 activity. WISP-3/CCN6 may therefore be protective against cartilage degradation and could be up-regulated in osteoarthritis as a protective or reparative response. The WISP-3/CCN6 mediated up-regulation ofMMPlO also apparently involves Wnt signalling suggesting alternative mechanisms of WISP3/ CCN6 interaction with this signalling pathway. These divergent responses suggest that the role ofWISP-3/CCN6 is context dependent.
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Cabral, Carlos Manuel Silvestre 1988. "Mini-CCNx : uma plataforma de prototipagem rápida para redes orientadas à conteúdo." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/258852.
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Orientadores: Christian Rodolfo Esteve Rothenberg, Maurício Ferreira MagalhãesDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Engenharia Elétrica e de Computação
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Resumo: A pesquisa experimental em Redes Orientadas a Conteúdo (ROCs) é crucial para a validação de novas propostas arquiteturais que trazem o conteúdo como o elemento central das redes. Essa dissertação apresenta uma nova ferramenta de prototipagem rápida para o modelo CCN (Content-Centric Networking), o Mini-CCNx, que visa preencher uma lacuna existente entre as plataformas experimentais atualmente disponíveis. Usando emulação baseada em contêineres e técnicas de isolamento de recursos, o Mini-CCNx aparece como uma ferramenta flexível, escalável, com baixo custo e alta fidelidade de desempenho possibilitando experimentos em redes emuladas com centenas de nós CCN em um simples laptop. Assim, esse trabalho de Mestrado traz como principal contribuição a disponibilização do Mini-CCNx, o primeiro emulador genérico especificamente focado para o desenvolvimento e testes de propostas para o modelo CCN. O Mini-CCNx é publicado com seu código aberto e documentação online e, portanto, pode ser melhorado e estendido por qualquer pesquisador da área. Essa dissertação apresenta 18 experimentos utilizando o Mini- CCNx, abrangendo desde análises de escalabilidade e coerência até a distribuição de vídeo e protocolos de roteamento. A reprodução de comportamentos observados em redes reais utilizando o emulador também é uma contribuição importante, pois mostra que se pode utilizar o Mini-CCNx para detectar eventuais falhas em aplicações e algoritmos antes dos testes em testbeds reais, que certamente são mais complexos e custosos quando comparados ao ambiente emulado. Porém, as características de baixo custo e flexibilidade indicam que o Mini-CCNx também pode ser utilizado em atividades de ensino como uma ferramenta prática de aprendizado e introdução ás ROCs e ao modelo CCN
Abstract: Experimental research in Information-Centric Networking (ICN) is crucial to the evaluation of new architectural proposals that bring named pieces of content as the main element of networks. This thesis presents a new fast prototyping tool for the CCN (Content-Centric Networking) model, Mini-CCNx that aims at filling an existing gap in generally available experimental platforms. Using container-based emulation and resource isolation techniques, Mini-CCNx appears as a flexible, scalable, high-fidelity, and low-cost tool that enables experiments on emulated networks with hundreds of CCN nodes in a commodity laptop. Therefore, this Master's project's main contribution is making Mini-CCNx, the first generic emulator focused on the development and evaluation of new proposals for the CCN model, available. Mini-CCNx is opensource and its documentation is publicly available online so it can be extended by any researcher in the area. This thesis presents 18 experiments using Mini-CCNx, ranging from scalability and coherence analysis to video distribution and routing protocols. The reproduction of real networks behavior using the emulator is also an important contribution because it shows one can use Mini-CCNx to detect flaws in applications or algorithms prior to real testbeds tests, which are certainly more complex and costly when compared to the emulated environment. Finally, Mini-CCNx's low-cost and flexibility indicate it can also be used in teaching activities as a practical ICN and CCN learning tool
Mestrado
Engenharia de Computação
Mestre em Engenharia Elétrica
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Matsumae, Hironobu. "CCN1 Knockdown Suppresses Neointimal Hyperplasia In A Rat Artery Balloon Injury Model." Kyoto University, 2008. http://hdl.handle.net/2433/124230.
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Chinot, Olivier. "Gliomes malins : etude retrospective des patients traites de 1980 a 1988 avec chimiotherapie selon le protocole vm26-belustine." Aix-Marseille 2, 1992. http://www.theses.fr/1992AIX20816.
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Mishra, Subhashree. "Characterizing CCN spectra to investigate the warm rain process." abstract and full text PDF (free order & download UNR users only), 2006. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1438932.
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Theveneau, Eric. "Rôle du proto-oncogène Ets1 au cours du développement des cellules des crêtes neurales aviaires." Paris 6, 2006. http://www.theses.fr/2006PA066321.
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Funk, Maja C. [Verfasser], and Wolfgang [Akademischer Betreuer] Driever. "Roles of Cyclin O (CCNO) for ciliation and centriole amplification in multiciliated cells." Freiburg : Universität, 2015. http://d-nb.info/1124003444/34.
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Matthes, Constanze. "Immunmodulation Dendritischer Zellen durch Sekretionsprodukte mesenchymaler Stammzellen mit besonderem Focus auf hCyr61/CCN1." Doctoral thesis, kostenfrei, 2008. http://nbn-resolving.de/urn/resolver.pl?urn=nbn:de:bvb:20-opus-28129.
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Taddei, Silvana Rodrigues de Albuquerque. "O papel das quimiocinas CCL3, CCL2 e seus receptores na movimentação dentária ortodôntica." Universidade Federal de Minas Gerais, 2011. http://hdl.handle.net/1843/BUOS-8RCNJ8.
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Orthodontic tooth movement (OTM) is achieved by the remodeling of periodontal ligament (PDL) and alveolar bone in response to mechanical loading. This process is regulated by pro-inflammatory mediators, such as cytokines and chemokines. CCL2, CCL3 and CCL5 are chemokines involved in osteoclastogenesis and are upregulated in periodontium after mechanical loading. As their cellular effects are mediated by binding to receptors, this study aimed to investigate the role of the chemokines and receptors CCL3/CCR1/CCR5 and CCL2/CCR2 in osteoclast recruitment and activation during OTM. An orthodontic appliance was placed in wild-type mice (WT), CCR5-deficient mice (CCR5-/-), CCR1-deficient mice (CCR1-/-), CCL3-deficient mice (CCL3-/-), CCR2-deficient mice (CCR2-/-) and mice treated with Met-RANTES (antagonist of CCR1 and CCR5), P8A (analog of CCL2) and vehicle (PBS). The number of TRAP-positive osteoclasts and the amount of OTM were quantified histomorphometrically. Moreover, the expression of mediators involved in bone remodeling was evaluated by Real-time PCR. Our data showed that the number of TRAP-positive cells, the amount of OTM and RANKL, Cathepsin K and MMP13 levels were significantly higher in CCR5-/- compared to WT mice. On the other hand, the number of osteoclasts and the amount of OTM were significantly diminished in CCL3-/- mice, CCR1-/- mice and Met-RANTES treated mice when compared to WT and vehicle treated mice, respectively. In accordance with these results, the levels of RANK, RANKL and TNF- decreased in CCL3-/- mice. Moreover, the treatment with Met-RANTES also reduced the expression of Cathepsin K and MMP13. These results suggest that CCR1 is one of the main pro-resorbing chemokine receptors, while CCR5 is an anti-resorbing receptor involved in OTM. In addition, the CCR1 action is dependent, at least in part, on CCL3 binding. Furthermore, TRAP-positive cells and the amount of OTM were significantly decreased in CCR2-/- and P8A-treated mice, when compared to WT and vehicle treated mice, respectively. In agreement with these data, the expression of the RANKL/RANK axis was lower in CCR2-/- than in WT mice. In summary, our results suggest that the CCL2/CCR2 axis might be involved in osteoclast activity and recruitment during OTMO movimento dentário ortodôntico (MDO) é obtido pela remodelação do ligamento periodontal (LP) e osso alveolar em resposta à carga mecânica. Este processo é regulado por mediadores pró-inflamatórios, como citocinas e quimiocinas. Entre as quimiocinas, CCL2, CCL3 e CCL5 têm um papel importante na osteoclastogênese e seus níveis são aumentados nos tecidos periodontais após a aplicação de uma força ortodôntica. Como o efeito destas quimiocinas é mediado pela ligação aos seus receptores, nesta tese objetivou-se investigar o papel das quimiocinas e receptores CCL3/CCR1/CCR5 e CCL2/CCR2 no recrutamento e ativação dos osteoclastos durante a MDO. Para tal, um aparelho ortodôntico foi instalado em camundongos selvagens (WT) e animais deficientes para os receptores CCR5 (CCR5-/-), CCR1 (CCR1-/-), e CCR2 (CCR2-/-), para a quimiocina CCL3 (CCL3-/-) e animais tratados com Met-RANTES (antagonista dos receptores CCR1 e CCR5), com P8A (análogo de CCL2) e com veículo (PBS). O número de osteoclastos TRAP-positivos e a quantidade de movimentação ortodôntica foram quantificados histomorfometricamente. Além disso, real-time PCR foi utilizado para avaliar a expressão dos mediadores envolvidos na remodelação óssea. Nossos resultados demonstraram que o número de células TRAP-positivas, a quantidade de MDO e a expressão de RANKL, Catepsina K e MMP13 aumentaram significativamente nos camundongos CCR5-/-. Por outro lado, o número de osteoclastos e a MDO foram reduzidos nos animais CCL3-/- e CCR1-/- comparados aos WT, bem como nos tratados com Met-RANTES em relação aos tratados com veículo. Estes resultados foram consistentes com a menor expressão de RANK, RANKL e TNF- no grupo CCL3-/-. O tratamento com o Met-RANTES resultou ainda 11 na redução da expressão de Catepsina K e MMP13. Os resultados sugerem que o CCR5 tem um papel anti-reabsortivo, enquanto o receptor CCR1 apresenta função pró-reabsortiva. Além disso, a ação do CCR1 é dependente, ao menos em parte, de sua ligação à quimiocina CCL3. Os resultados também mostraram que o número de células TRAP-positivas e a quantidade de MDO diminuíram nos camundongos CCR2-/- e nos animais tratados com P8A. Paralelamente, a diminuição da expressão do eixo RANKL/RANK foi observada no grupo CCR2-/-. Estes dados sugerem que o eixo CCL2/CCR2 está relacionado ao recrutamento e ativação de osteoclastos, durante a MOD
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Fulkerson, Patricia C. "A Critical Role for Eosinophils and CCR3 Signal Transduction in Allergic Airway Disease." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120337075.
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Holmes, Alan Matthew. "Regulation of connective tissue growth factor/CCN2 gene expression in systemic sclerosis fibroblasts." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445639/.
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Systemic sclerosis (Scleroderma, SSc) is a chronic, connective tissue disease of unknown etiology, characterised by vascular dysfunction, iriflarnmation and organ fibrosis. Involving both genetic and environmental components, the specific mechanisms which result in fibrosis remain largely unknown. A cardinal feature of SSc is increased synthesis of extracellular matrix (ECM). Dermal fibroblasts cultured from SSc patients maintain many of the abnormal properties seen in vivo, including excess production of collagen type I, and growth factors such as connective tissue growth factor (CTGF/CCN2). CTGF, like many genes dysregulated in SSc, is induced by TGF- p in normal fibroblasts. The overall aim of my studies was to determine the mechanism(s) controlling CTGF over-expression in SSc dermal fibroblasts (SDF). Induction of CTGF by TGF-p was found to be dependent upon elements in the proximal portion of the CTGF promoter, distinct from those of the previously characterised TGF- P response element (TRE). The TRE acts, in NIH/3T3 and HFF cells, as a regulator of basal expression, and is not essential for TGF-P induction of CTGF. Instead TGF-p induces CTGF expression via a Smad3 complex, binding to a bona fide SMAD transcription factor binding site. Over-expression CTGF in SDF is independent of autocrine expression of TGF-P and the SMAD binding element and rather dependent on a functional Sp-binding site. Inhibition of Spl-like DNA binding reduces excessive CTGF expression in SDF. Consistent with this Spl-DNA binding activity is elevated in SDF nuclear extracts. Investigation of the mechanism of elevated Spl-like binding found that SDF exhibited constitunVely active ERK1/2 and JNK1. Inhibition of ERK1/2 repressed elevated Sp-binding and CTGF over-expression observed in SDF. In summary, the data presented in this thesis provide evidence that dysregulation of ERK1/2 in SDF is involved in CTGF over-expression via a Spl-like DNA binding. Thus repression of ERK may represent a candidate in targeting fibrosis in SSc.
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Mihalcea, Rada. "The language of humour." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:a1cc3d1e-cc83-44dd-a2dd-6910fde3d252.
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Humour is one of the most interesting and puzzling aspects of human behaviour. Despite the attention it has received from fields such as philosophy, linguistics, and psychology, there have been only few attempts to create computational models for humour recognition and analysis. In this thesis, I use corpus-based approaches to formulate and test hypotheses concerned with the processing of verbal humour. The thesis makes two important contributions. First, it brings empirical evidence that computational approaches can be successfully applied to the task of humour recognition. Through experiments performed on very large data sets, I show that automatic classification techniques can be effectively used to distinguish between humorous and non-humorous texts, using content-based features or models of incongruity. Moreover, using a method for measuring feature saliency, I identify and validate several dominant word classes that can be used to characterize humorous text. Second, the thesis provides corpus-based support toward the validity of previously formulated linguistic theories, indicating that humour is primarily due to incongruity and humour-specific language. Experiments performed on collections of verbal humour show that both incongruity and content-based features can be successfully used to model humour, and that these features are even more effective when used in tandem.
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Abraham, Adam. "Spurious Victorians : imitation and the nineteenth-century novel." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:cbf24b85-cc63-42be-ba84-2f065942c4d8.
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In 'A Critique of Modern Textual Criticism', Jerome J. McGann writes, '[A]n author's work possesses autonomy only when it remains an unheard melody'. For the published and successful writer in the nineteenth century, such autonomy was often unattainable. Publications such as The Pickwick Papers inspired an array of opportunistic successors, including stage plays, unauthorized sequels, jest books, song books, and shilling and penny imitations. Despite the proliferation, this strain of writing is rarely studied. This thesis recovers ephemeral, scurrilous texts, often anonymous or pseudonymous, and reads them in the context of their canonical sources. Retrieving bibliographical environments, it demonstrates how plagiaristic, parodic, and willfully unoriginal works impacted on the careers of three novelists: Charles Dickens, Edward Bulwer Lytton, and George Eliot. The thesis argues that formal distinctions among modes of Victorian writing - criticism, parody, and plagiarism - often blur. Further, it argues that our understanding of a particular novelist's work must be broadened to include sequels, spinoffs, and imitations: to know a particular author means to know the spurious and oftentimes bad (morally or aesthetically) works that the author inspired. The Spurious Victorians of the title form something of countercanon to the 'major' writers of the period. Thomas Peckett Prest, Rosina Bulwer Lytton, and Joseph Liggins, among many others, informed and influenced the literary history that has in turn denied them admission. William Makepeace Thackeray wrote, 'If only men of genius were to write, Lord help us! how many books would there be?' Of course, Victorian print culture found room for the genius and the subgenius, Boz as well as Bos. 'Spurious Victorians' recovers works that have been lost from view in order to better understand the process by which an individual authorial voice emerged amid an echo chamber of competing, imitative voices.
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Wilkins, Sam. "The dominant party system in Uganda : subnational competition and authoritarian survival in the 2016 elections." Thesis, University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:cba1f2e5-cc83-4c9d-a0f3-ca065da0b98f.
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This thesis studies the authoritarian dominant party system in Uganda during the 2016 general election. It focuses on how subnational competition within the ruling National Resistance Movement (NRM) prolongs the tenure of its leader, 30-year incumbent President Yoweri Kaguta Museveni. In three districts where the NRM has been historically strong - Kyenjojo, Kayunga, and Bugiri - the thesis traces three processes to this end: the decentralisation and localisation of accountability politics away from the regime and toward expendable local politicians (H1); the relationship between local elite rivalry and the NRM's collective mobilisation for Museveni's simultaneous re-election (H2); and how competitive electoral pressures on NRM MPs alter the national elite bargain in the president's favour (H3). It concludes that in strong NRM areas, the fractious divisions that characterise intra-party competition are not a by-product of its near monopolistic domination of politics, but the very basis of that dominance. This emphasis on subnational intra-party competition brings a new variable into a literature on non-democratic survival that tends to focus on more narrowly coercive and clientelist regime strategies. The thesis presents this argument in a qualitative single case study driven by an open and inductive fieldwork component throughout the 2016 election period. Its three hypotheses are built on data from interviews (with voters and elites), ethnographic observations, official data, and secondary sources. This data is used in a process-tracing design before its conclusions are fortified by a subnational comparative analysis of the election results in the three case districts.
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Seviour, William J. M. "Variability of the polar stratosphere and its influence on surface weather and climate." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:ed566f6a-cc23-40c7-8237-465646058eb5.
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Research during the last two decades has established that variability of the winter polar stratospheric vortex can significantly influence the troposphere, affecting the likelihood of extreme weather events and the skill of long-range weather forecasts. This influence is particularly strong following the rapid breakdown of the vortex in events known as sudden stratospheric warmings (SSWs). This thesis addresses some outstanding issues in our understanding of the dynamics of this stratospheric variability and its influence on the troposphere. First, a geometrical method is developed to characterise two-dimensional polar vortex variability. This method is also able to identify types of SSW in which the vortex is displaced from the pole and those in which it is split in two; known as displaced and split vortex events. It shown to capture vortex variability at least as well as previous methods, but has the advantage of being easily applicable to climate model simulations. This method is subsequently applied to 13 stratosphere-resolving climate models. Almost all models show split vortex events as barotropic and displaced vortex events as baroclinic; a difference also seen in observational reanalysis data. This supports the idea that split vortex events are caused by a resonant excitation of the barotropic mode. Models show consistent differences in the surface response to split and displaced vortex events which do not project stongly onto the annular mode. However, these differences are approximately co-located with lower stratospheric anomalies, suggesting that a local adjustment to stratospheric potential vorticity anomalies is the mechanism behind the different surface responses. Finally, the predictability of the polar stratosphere and its influence on the troposphere is assessed in a stratosphere-resolving seasonal forecast system. Little skill is found in the prediction of the strength of the Northern Hemisphere vortex at lead times beyond one month. However, much greater skill is found for the Southern Hemisphere vortex during austral spring. This allows for forecasts of interannual changes in ozone depletion to be inferred at lead times much beyond previous forecasts. It is further demonstrated that this stratospheric skill descends with time and leads to an enhanced surface skill at lead times of more than three months.
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Martins, Jorge Alberto. "\"Efeito dos núcleos de condensação na formação de nuvens e o desenvolvimento da precipitação na região amazônica durante a estação seca\"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/14/14133/tde-02042007-123958/.
Full textAbstract:
O objetivo deste trabalho foi estudar o papel dos aerossóis em modificar o desenvolvimento das nuvens e da precipitação. Esta tem sido uma das mais intrigantes questões no estudo das mudanças climáticas. Medidas da concentração de núcleos de condensação de nuvens (CCN) e distribuições de gotículas de nuvem durante o Experimento de Grande Escala da Biosfera-Atmosfera na Amazônia (LBA) revelaram características distintas entre condições atmosféricas limpas e poluídas. As medidas foram conduzidas no Sudoeste da Região Amazônica durante os meses de setembro e outubro de 2002, focando a transição do final da estação seca para o início da estação chuvosa. Durante a transição, a análise da concentração de CCN dentro da camada limite revelou um decréscimo geral, de valores acima de 1200 cm-3 para menos de 300 cm-3. A comparação entre áreas limpas e poluídas mostrou concentrações de CCN cerca de 5 vezes maiores em áreas poluídas. As diferenças não foram tão grandes nos níveis acima da camada limite. As medidas também mostraram um ciclo diurno acompanhando a atividade de queima de biomassa. Distribuições de tamanho de gotículas medidas em duas regiões com concentrações de aerossóis extremamente diferentes foram analisadas. Em condições poluídas pela queima de biomassa foi encontrada alta concentração de gotículas, com diâmetro médio e conteúdo de água de nuvem aumentando muito pouco com a altura, em comparação com regiões limpas. A função gama foi usada para ajustar as distribuições de gotículas e o parâmetro de forma da função foi usado como critério para definir adequadamente a melhor representação das distribuições de gotículas. De acordo com os valores encontrados, distribuições gama estreitas (parâmetro de forma em torno de 5) são mais bem indicadas para representar condições poluídas enquanto que aquelas mais largas se ajustam melhor em condições limpas (parâmetro de forma em torno de 2). Com base nesses resultados, experimentos numéricos foram conduzidos com o Brazilian Regional Atmospheric Modeling System (BRAMS) para investigar os efeitos da concentração de CCN e do parâmetro de forma das distribuições de gotículas no desenvolvimento da precipitação em nuvens convectivas tropicais. Os resultados mostraram uma grande sensibilidade devido às mudanças nesses parâmetros. Altas concentrações de CCN e distribuições de gotículas estreitas (parâmetros de forma maiores), típicas de dias poluídos, produziram baixos valores médios para água líquida integrada na coluna e precipitação acumulada na superfície. Por outro lado, tendência oposta a este efeito foi encontrada em condições limpas (baixos valores para ambos, a concentração de CCN e o parâmetro de forma). O parâmetro de forma se mostrou ser mais importante que a concentração de CCN. Os efeitos da concentração de CCN e do parâmetro de forma também influenciaram a distribuição espacial dos campos de nuvem e precipitação. Embora o valor médio desses campos tenha diminuído em condições poluídas, o valor máximo aumentou. Como conseqüência da menor dispersão nas nuvens em condições poluídas, mais radiação solar esteve disponível na superfície. Isto é oposto aos resultados dos modelos globais que mostram redução na radiação solar como conseqüência do segundo efeito indireto dos aerossóis. Da mesma forma, este estudo encontrou que as diferenças são reduzidas quando é incluído o efeito direto dos aerossóis em absorver ou refletir a radiação solar. Sobretudo, os resultados sugerem que um maior número de modelos com tratamento explícito dos processos microfísicos de nuvem são necessários. Esses modelos permitem comparações, podendo mostrar o melhor tratamento numérico a ser usado na representação dos efeitos dos aerossóis no processo de precipitação como um todo. Estes resultados são importantes porque melhoram a compreensão de como o clima será afetado como conseqüência das mudanças futuras.The objective of this work was to study the role of aerosols in modifying clouds and precipitation. This is one of the most difficult aspects in the study of climate changes. Field measurements of cloud condensation nuclei (CCN) and cloud size distributions performed during the Large Scale Biosphere-Atmosphere Experiment in Amazonia (LBA) campaign revealed distinct characteristics between clean and polluted atmospheric conditions. Measurements were conducted over the southwestern Amazon region during September-October 2002 focusing the transition from dry to wet seasons. During this period, analysis of CCN concentrations in the boundary layer revealed a general decreasing trend from mean values higher than 1200 cm-3 to values lower than 300 cm-3. The comparison between clean and polluted areas showed CCN concentrations 5 times higher than in polluted areas. These differences were not so strong above the boundary layer. Measurements also showed a diurnal cycle following the biomass burning activity. Cloud droplet size distributions at two regions with extremely different aerosols loading were also analyzed. During biomass-burning conditions, at high concentrations of cloud droplets, the mean diameter and liquid water content increased very little with altitude when compared with unpolluted conditions. A gamma distribution was used to fit the measured droplet spectra and the shape parameter was used as a criterion to define the best choice of spectra representation. According to the found values, narrow gamma distributions optimally fit polluted conditions (shape parameter around 5), while broad distributions are best fits for unpolluted conditions (shape parameter around 2). Based on these results, numerical experiments were carried out using the Brazilian Regional Atmospheric Modeling System (BRAMS) to investigate the effects of CCN concentrations and shape parameters of droplet spectra on the development of precipitation in tropical convective clouds. The results showed large sensitivity due to changes in these parameters. It was observed that high CCN concentrations and narrower cloud droplet distributions (high values for shape parameter), typical of the polluted days, produced low mean values of liquid water path and accumulated surface precipitation. On the other hand, an opposite trend to this effect was found under clean conditions (low CCN concentration and shape parameter values). Shape parameter showed to be much more important than CCN concentration. The effects of CCN concentration and shape parameter also influenced the spatial distribution of cloud and precipitation fields. Although mean values of these fields decreased under polluted conditions, maximum values were increased. Consequently, the less dispersion in clouds under polluted conditions, the more surface solar radiation was found. This is opposite to the results of global climate models, which predict reduction in solar radiation as a consequence of the second aerosol indirect effect. Also, it was found that the differences were reduced when the aerosols direct effect to absorb or reflect solar radiation is included. Moreover, the results suggest that additional models with explicit microphysics process treatment are necessary in order to allow further comparisons, which could show the best numerical treatment to be used in representing the aerosol effects on precipitation process. The importance of these results is to improve the understanding of future climate changes.
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Zhou, Erping. "An automated in-process measuring system for CCN machine tools." Thesis, Staffordshire University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295291.
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Mahajan, Salil. "CCM3 as applied to an idealized all land zonally symmetric planet, Terra Blanda 3." Texas A&M University, 2004. http://hdl.handle.net/1969.1/1422.
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Community Climate Model 3 (CCM3) is run on an idealized all land zonally
symmetric planet (Terra Blanda) with no seasonality, no snow and fixed soil moisture
to obtain a stationary time series effectively much longer than conventional runs with
geography and seasons. The surface temperature field generated is studied to analyze
the spatial and temporal spectra, estimate the length scale and time scale of the
model, and test the linearity of response to periodic and steady heat source forcings.
The length scale of the model is found to be in the range of 1000-2000 km and the time
scale is estimated to be 24 days for the global average surface temperature field. The
response of the global average temperature is found to be fairly linear to periodic and
the steady heat source forcings. The results obtained are compared with the results
of a similar study that used CCM0. Fluctuation Dissipation theorem is also tested
for applicability on CCM3. The response of the surface temperature field to a step
function forcing is demonstrated to be very similar to the decay of naturally occurring
anomalies, and the auto-correlation function. Return period of surface temperature
anomalies is also studied. It is observed that the length of the data obtained from
CCM3, though sufficient for analysis of first and second moments, is significantly
deficient for return period analysis. An AR1 process is simulated to model the global
averaged surface temperature of Terra Blanda 3 to assess the sampling error associated
with short runs.
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Kirchem, Antje. "Investigation of the signalling pathways coupled to the eotaxin receptor CCR3 in human eosinophils." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406094.
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Allen, Frederick Jr. "CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1513124234665339.
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Hablot, Julie. "Liens entre inflammations articulaire et digestive : étude expérimentale chez la souris et contribution de l’immunité mucosale." Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0095/document.
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Des cellules immunitaires appartenant à l’immunité de type 3 sont localisées dans muqueuse digestive. Les micro-organismes du microbiote stimulent le système immunitaire pour le maintenir en veille face à de potentiels agents infectieux, tout en ayant une tolérance pour les micro-organismes commensaux. Des études montrent des anomalies du microbiote intestinal chez les patients arthritiques. Ceci suggère une dérégulation de l’immunité mucosale digestive dans la survenue de l’inflammation articulaire. Des cellules de l’immunité mucosale pourraient migrer vers les sites articulaires, notamment grâce à des récepteurs aux chimiokines. Le facteur RORγt, indispensable à la différenciation des cellules de l’immunité de type 3, est régulé négativement par le récepteur PPARγ. A l’aide de modèle murins, nous avons étudié l’impact de l’invalidation de PPARγ et de l’inhibition du récepteur aux chimiokines CCR3 sur les relations entre sphères digestive et articulaire. Nous avons montré que l’induction d’une colite au cours d’une arthrite au collagène modifie le microbiote intestinal, retarde l’apparition et diminue la sévérité des lésions articulaires. Nous avons démontré que les souris PPARγ-/- développent spontanément une inflammation articulaire associées à des anomalies dans la répartition des cellules immunitaires de type 3 de la muqueuse digestive. Ces souris sont dysbiotiques avec une flore enrichie notamment en entérobactéries, mais non-arthritogène. Enfin, l’inhibition de CCR3 au cours du développement d’une arthrite au collagène retarde et diminue la sévérité de la pathologie et altère la répartition des leucocytes dans les articulations et de la muqueuse digestiveNumerous type 3 immune cells (Th17 and ILC3) are physiologically located in lamina propria of the intestine. Microbial agents within the gut shape the immune system to make it efficient against threats but peaceful with commensals. Recent studies demonstrated changes in gut microbiota composition (dysbiosis) in chronic inflammatory rheumatism. These results suggest a role for mucosal immunity alteration in articular inflammation occurrence. Indeed, some type 3 immune cells once activated by microbiota, are thought to migrate to joints, involving notably chemokines receptors. Transcription factor RORγt, the master regulator of type 3 immune cells, could be negatively regulated by nuclear receptor PPARγ. Using experimental murine models, we studied the consequence of PPARγ deficiency and consequence of the chemokine receptor CCR3 inhibition on the joint-gut axis. Firstly, we demonstrated that experimental colitis induces microbiota changes, delays and reduces collagen-induced arthritis severity. Secondly, we showed that PPARγ deficient mice display spontaneous joint inflammation associated with abnormal type 3 distribution within the gut. Dysbiosis with enrichment in facultative anaerobic Enterobacteriaceae was found in these mice. Fecal microbiota transfer demonstrated this microbiota is non-arthritogenic. Finally, we demonstrated that CCR3 inhibition has profound anti-arthritic potencies associated with changes in leukocytes distribution within the joint-gut axis
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Gasparini, Roberto. "Developing models of aerosol representation to investigate composition, evolution, optical properties, and CCN spectra using measurements of size-resolved hygroscopicity." Diss., Texas A&M University, 2003. http://hdl.handle.net/1969.1/3878.
Full textAbstract:
A Differential Mobility Analyzer/Tandem Differential Mobility Analyzer (DMA/TDMA) was used to measure size distributions, hygroscopicity, and volatility during the May 2003 Aerosol Intensive Operational Period at the Central Facility of the Atmospheric Radiation Measurement Southern Great Plains site. Hygroscopic growth factor distributions for particles at eight dry diameters ranging from 0.012 µm to 0.600 µm were measured. These measurements, along with backtrajectory clustering, were used to infer aerosol composition and evolution. The hygroscopic growth of the smallest and largest particles analyzed was typically less than that of particles with dry diameters of about 0.100 µm. Condensation of secondary organic aerosol on nucleation mode particles may be responsible for the minimal growth observed at the smallest sizes. Growth factor distributions of the largest particles typically contained a non-hygroscopic mode believed to be composed of dust. A model was developed to characterize the hygroscopic properties of particles within a size distribution mode through analysis of the fixed-size hygroscopic growth measurements. This model was used to examine three cases in which the sampled aerosol evolved over a period of hours or days. Additionally, size and hygroscopicity information were combined to model the aerosol as a population of multi-component particles. With this model, the aerosol hygroscopic growth factor f(RH), relating the submicron scattering at high RH to that at low RH, is predicted. The f(RH) values predicted when the hygroscopic fraction of the aerosol is assumed to be metastable agree better with measurements than do those predicted under the assumption of crystalline aerosol. Agreement decreases at RH greater than 65%. This multi-component aerosol model is used to derive cloud condensation nuclei (CCN) spectra for comparison with spectra measured directly with two Desert Research Institute (DRI) CCN spectrometers. Among the 1490 pairs of DMA/TDMA-predicted and DRI-measured CCN concentrations at various critical supersaturations from 0.02-1.05%, the sample number-weighted mean R2 value is 0.74. CCN concentrations are slightly overpredicted at both the lowest (0.02-0.04%) and highest (0.80-1.05%) supersaturations measured. Overall, this multi-component aerosol model based on size distributions and size-resolved hygroscopicity yields reasonable predictions of the humidity-dependent optical properties and CCN spectra of the aerosol.
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Irwin, Martin. "The characterisation of the interaction between atmospheric aerosol and water vapour." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/the-characterisation-of-the-interaction-between-atmospheric-aerosol-and-water-vapour(cdd6bbbb-8b8c-4ca4-82bb-0a3fc6ea8711).html.
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Understanding the interaction between atmospheric aerosol and water vapour is key in assessing the impacts of anthropogenic influences on the earth's radiative budget, both directly through scattering and absorbing incident solar radiation, and indirectly through changing cloud properties, with considerable uncertainty in the magnitude of the estimated forcings of the latter. Although aerosol particle water uptake is well defined for inorganic compounds, the effects of the aerosol organic fraction on cloud droplet formation and cloud condensation nuclei (CCN) properties are relatively poorly characterised, due to the large number of organic compounds present in atmosphere and their highly complex influences on properties such as water solubility and surface tension.This thesis presents extensive field measurements of CCN/aerosol hygroscopicity from three different environments, together with a novel error model, which has been developed to propagate instrumental uncertainties from measurements in the sub- and supersaturated regimes through to commonly used data products used in large-scale models. This study illustrates that a single hygroscopicity framework is not able to reconcile the measurements within errors, for different measurement environments. The sensitivity of this type of reconciliation study was assessed using several different scenarios, making different assumptions in each case; sensitivity tests using a 'typical' regional aerosol particle water uptake or number-size distribution, demonstrate that it is not possible to apply a constant correction to data to guarantee reconciliation, that the best reconciliation was achieved for size-resolved high-temporal water uptake and aerosol number-size distribution data, and that the application of single-parameter hygroscopicity models requires further examination. It is concluded that high-temporal size-resolved measurements of sub- and supersaturated particle water uptake are fundamental to providing a thorough characterisation of the interaction between atmospheric aerosol and water vapour, and are essential in order to achieve the best possible predictive capability from large-scale models.
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Elshaarani, Tarek. "An Investigation into the Application of Content-Centric Networking within Challenged Network Environments using CCNx." Thesis, Uppsala universitet, Institutionen för informationsteknologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-227044.
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Information Centric Network (ICN) architectures offer a viable design to cope with the disruptive nature of Challenged Network environments. They aim to address the challenges of unreliable connectivity and location transparency to offer a delay- and disruption-tolerant solution. Named Data Networking (NDN), a prominent ICN architecture, uses a publish/subscribe-driven model and relies on two main message units for communication, called Interests and Data. Instead of a host-based model for data retrieval, an addressing scheme based on named data is utilized. The naming of data allows for retrieval of data from the network without the knowledge of individual hosts. This thesis studies NDN behavior in a disruptive network environment. More specifically, we use CCNx as an implementation of a Content-Centric Networking protocol that inherits key characteristics from NDN. We study the behavior of CCNx using the Haggle testbed to simulate a simple disruptive network environment. We develop a delay/disruption-tolerant framework based on CCNx and implement the game Tic-Tac-Toe using that framework. The framework design is presented with an analysis into various alternatives that were considered. A more complex five-node experiment with link disruption is performed using the framework to evaluate CCNx in a real world scenario. We conclude that CCNx is good at handling disruptions associated with Challenged Networks.