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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
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Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
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Showing 41 to 47 of 47 (0.02 seconds)| 41 |
Natriuretic peptides as a humoral link between the heart and the gastrointestinal system /Addisu, Anteneh. January 2008 (has links)
Dissertation (Ph.D.)--University of South Florida, 2008. / Includes vita. Includes bibliographical references (leaves 102-128).
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Le récepteur nucléaire de l'acide rétinoïque alpha (RARa) : nouveaux effets non-génomiques et nouveaux partenairesPiskunov, Aleksandr 25 June 2012 (has links) (PDF)
Les récepteurs nucléaires de l'acide rétinoïque (AR) appelés RAR, se comportent comme des facteurs de transcription inductibles par le ligand. La transcription des gènes cibles induite par l'AR, nécessite la fixation des RAR au niveau de séquences spécifiques des promoteurs et met en jeu des changements conformationnels des récepteurs qui contrôlent l'association/dissociation de toute une panoplie de corégulateurs. Cependant, en plus de ce modèle génomique et nucléaire bien établi, l'équipe du Dr Cécile Rochette-Egly a montré récemment que l'AR a aussi des effets non-génomiques et induit rapidement la voie de signalisation p38MAPK/MSK1 qui ensuite cible les RAR pour des cascades de phosphorylations et module la transcription des gènes cibles. Pendant mon travail de thèse, j'ai mis en exergue trois nouveaux concepts originaux du mécanisme d'action du sous-type RARα. J'ai montré qu'une sous-population de RARα est présente dans des microdomaines membranaires, les radeaux lipiques ou "lipid rafts"où elle interagit avec les protéines Gαq. Cette interaction est le signal des effets non génomiques de l'AR, l'activation de la voie de la p38MAPK. Ces effets ont été corrélés à l'activité des gènes cibles de l'AR, prouvant ainsi leur nécessité. J'ai identifié un nouveau partenaire de RARα, la profiline IIA. J'ai analysé le mécanisme moléculaire de l'interaction et démontré qu'elle a lieu dans le noyau. La profiline IIA s'est révélée être un régulateur des effects génomiques de RARα et est recrutée avec RARα au niveau des promoteurs des gènes cibles. Finalement j'ai mis en évidence une nouvelle fonction de RARα dans le contrôle de l'adhésion et de l'étalement des cellules. D'où l'hypothèse de nouveaux effets génomiques de RARα avec la profiline IIA dans le contrôle de l'expression des protéines d'adhésion. Cependant, de manière inattendue, j 'ai identifié une nouvelle population de RARα dans le cytoplasme de ces cellules. D'où l'hypothèse de nouveaux effets non génomiques dans le cytoplasme, via l'interaction de RARα avec des protéines d'adhésion.
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Tumour-selective apoptosis : identification of NMHCIIa as novel death receptor interactor regulating the response to TRAILSchulz, Cathrin 26 September 2012 (has links) (PDF)
The cytokine TRAIL is a promising cancer therapeutic candidate as it induces apoptosis selectively in transformed cells. TRAIL-induced clustering of its receptors (DR) is essential for the DISC complex formation, which induces cell death. The mechanism for TRAIL's tumour selective effect is largely unknown. We identified the cytoskeleton proteins non-muscle myosin heavy chain IIa, IIb (NMHCIIa, NMHCIIb), myosin regulatory light chain (MLC2) and ß-actin as novel DR-interactors. An initially weak and TRAIL-induced abrogation of NMHCII/DR interaction correlated with efficient DISC formation in tumour cells. In contrast, a robust NMHCII/DR interaction that was sustained upon TRAIL stimulus was accompanied by incomplete DISC arrangement. Weakening the NMHCII/DR interaction in normal cells using chemical inhibitors enhanced TRAIL-induced apoptosis. Intriguingly, siRNA-mediated NMHCIIa- but not NMHCIIb depletion potently released TRAIL resistance in normal cells and influenced DISC composition. Reduced NMHCII/DR interaction in transformed cells was characterised by diminished MLC2 phosphorylation and altered protein expression of upstream regulatory kinases. Our results suggest that normal cell resistance to TRAIL-apoptosis is based on the interaction of cytoskeleton components with DR that is impaired upon transformation. Since NMHCII function in cell adhesion and migration, it will be interesting to study possible roles of the interaction in cell detachment and altered TRAIL sensitivity; moreover this link may provide clues as to the cause of TRAIL resistance in some cancers.
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Natriuretic peptides as a humoral link between the heart and the gastrointestinal systemAddisu, Anteneh. January 2008 (has links)
Dissertation (Ph.D.)--University of South Florida, 2008. / Title from PDF of title page. Document formatted into pages; contains 132 pages. Includes vita. Includes bibliographical references.
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Ein simultanes Erzeugungs-, Verteilungs-, Aufteilungs- und RoutenwahlmodellDugge, Birgit 13 April 2006 (has links)
In dieser Arbeit wird ein simultanes Quell-, Ziel-, Verkehrsmittel- und Routenwahlmodell (Modell EVA-U) entwickelt, welches ein stochastisches Nutzergleichgewicht erreicht. Die Routenwahlmodelle der Verkehrsarten sind nicht mehr Teil der Umlegungsalgorithmen, sondern in das Nachfragemodell integriert. Dadurch ist eine konsistente Bewertung aller Alternativen (der Verkehrsarten) möglich. Das Simultanmodell EVA-U stellt eine Weiterentwicklung des Simultanmodells EVA von LOHSE dar. Das EVA-U-Modell ist den universalen Logit-Modellen zuzuordnen. Die Randsummenbedingungen der Verkehrsverteilung werden beachtet. Die Bewertung der Alternativen erfolgt mittels Generalisierter Kosten. Die Abhängigkeit von Routen wird berücksichtigt, ebenso die Tagesganglinie der Verkehrsnachfrage und die Fahrpläne des ÖV-Systems. Das Modell EVA-U erlaubt auch die Berücksichtigung von Routen intermodaler Verkehrsarten (z.B. P+R). Darüber hinaus ist die Integration eines Modells des ruhenden Verkehrs möglich. / In this thesis a simultaneous Trip Generation-, Distribution-, Modal-Split and Route Choice Model (modell EVA-U) is elaborated. The model tends to reach a stochastic user equilibrium. The route choice algorithms are not longer part of an assignment procedure but part of the demand model. A consistent assessment of properties of all transport systems is possible. The simultaneous model EVA-U is an advancement of the EVA-Model by Lohse. The model EVA-U is to be assigned to the generalised logit-models. All matrix constrains are taken into account. The assessment is effected by generalised costs. The dependence of routes is taken into account. Moreover, the integration of day time and the schedules of private transport lines is possible. Furthermore, it is possible to integrate a model of parked cars and circuits of inter-modal traffic forms (park and ride) in the Model EVA-U.
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人力資本及勞工流動之研究：理論與台灣實證李鈞元, Lee Chun-Yuan Unknown Date (has links)
雖然人力資本在理論上的重要地位早已確立，但是，因為人力資本的衡量不易周延精確，使得其實證研究難有突破性的發展；所以，本論文嘗試透過具備個體基礎的理論架構，使用「人力運用調查」的原始資料進行實證分析，希望能進一步瞭解人力資本的性質、勞工流動的成因及這兩者如何影響個人的薪資與整體的成長。而在編排上，本論文則是由三篇可分割獨立的論文所組成。
第2章的重點是從同質人力資本的角度討論人力資本的衡量問題：基於薪資可以反映勞動生產力的概念，本章嘗試使用各個勞工與基礎勞工間推估預期薪資的比率做為代表人力品質之權數，以建構較完整的台灣人力資本指標；從成長會計分析及總合生產函數迴歸估計的實證結果來看，考量人力品質提升的勞動投入約可解釋18% 至35% 的經濟成長，遠高於實際工時的15%；惟近年來台灣人力品質的提升似乎逐漸減緩，不利於後續的經濟成長。
第3章的重點是使用多項式logit模型討論勞工的流動現象，而且其估計結果亦成為第4章必需的實證基礎：鑑於台灣的產業結構一再歷經巨幅的改變，本章將勞工是否異動視為共包括「不換工作」、「換工作但不換產業」及「換工作又換產業」三個選項的決策問題，並援引非巢式logit模型及巢式logit模型對其進行分析。從總括值迴歸係數的檢測來看，巢式模型與隨機效用理論是互不相容的，只有非巢式模型具有較完整堅固的個體基礎。
第4章的重點是從異質人力資本的角度討論產業特定型人力資本是否存在的問題：因為台灣現有的資料庫缺少產業年資等相關資料，所以，本章擬將重點置於轉換工作者，研究轉換產業是否會影響其現職前一般經驗與現職工資之間的關係，以間接分析產業特定型人力資本在台灣的存在性及重要性。從實證結果來看，一般而言，產業特定型人力資本也許並不是非常重要，但應該仍是存在的，亦即仍會對勞工在不同產業間的重新配置產生一定的影響。
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Appeal mechanisms and Investment Court Systems in Investor-State Dispute Settlement : An analysis of AM and ICS suggestions, in light of contemporary reformDrakopoulos, David January 2021 (has links)
We begin with a short analysis of the history of Investor-State Dispute Settlement (ISDS). We then discuss the merits and demerits of the regime, such as the arguments between finality, speediness, and correctness. Following from this, historical reforms are discussed, and whether those issues have gotten worse or better since these discussions. The modern problems are discussed, leading to the explanation of the “legitimacy crisis”. As Appellate Mechanisms (AM) and Investment Court Systems (ICS) both propose multi layered systems, we argue whether ISDS must be a “one bite at the apple” system. We expand on the issues of regulatory chill, before showing the contradictions in the granting of awards. From this, a discussion is raised on the advantages of a tenured system of adjudicators, particularly in reference to their apparent bias. We delve deeper into the direct consequences of the perceived issues of ISDS, in the context of human rights, the environment, and other issues of sovereignty.As more reforms are suggested, the question of “what makes arbitration, arbitration?” is raised. From here, we may begin to suggest reforms based on which key factors are to be preserved. Firstly, we discuss current reform options, such as the Mauritius Convention. We take inspiration from existing AM, and prior discussions on the implementation of such a system across the International Centre for Settlement of Investment Disputes (ICSID) and United Nations Commission on International Trade Law (UNCITRAL) frameworks. We analyse whether these discussions have led to change by comparing trends in drafting.Thereon, we offer suggestions of reform. ICS and how this would be implemented, what it would look like structurally, and its positive and negative effects. Using the Comprehensive Economic and Trade Agreement (CETA) and other contemporary ICS reform suggestions, we gain some knowledge of what an ICS regime could and should look like, the implementation of AM previously discussed in this regime, and other. Finally, we offer a different solution to the problems, yet less pragmatic, the termination of arbitration.
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