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Dissertations / Theses on the topic 'JNK'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Rogge, Dorothea Elisabeth [Verfasser]. "JNK und Schlaganfall / Dorothea Elisabeth Rogge." Kiel : Universitätsbibliothek Kiel, 2012. http://d-nb.info/1023870363/34.

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2

Pietkiewicz, Sabine [Verfasser], Reiner [Akademischer Betreuer] Jänicke, and Matthias U. [Akademischer Betreuer] Kassack. "Die Bedeutung der JNK-Isoformen JNK1 und JNK2 für die Apoptose nach proteasomaler Inhibition / Sabine Pietkiewicz. Gutachter: Reiner Jänicke ; Matthias U. Kassack." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/102435475X/34.

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3

Rogers, Jeffrey Scott. "Characterization of JNK Binding Proteins: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/222.

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The JNK signal transduction pathway mediates a broad, complex biological process in response to inflammatory cytokines and environmental stress. These responses include cell survival and apoptosis, proliferation, tumorigenesis and the immune response. The divergent cellular responses caused by the JNK signal transduction pathway are often regulated by spatial and cell type contexts, as well as the interaction with other cellular processes. The discovery of additional components of the JNK signal transduction pathway are critical to elucidate the stress response mechanisms in cells. This thesis

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4

Cosolo, Andrea [Verfasser], and Anne-Kathrin [Akademischer Betreuer] Classen. "Patterning of tissue stress responses by JNK and JAK/STAT / Andrea Cosolo ; Betreuer: Anne-Kathrin Classen." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1202011772/34.

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5

Collura, Kaitlin Marie. "Palmitoylation-Dependent Regulation of the DLK/JNK/cJun and the GP130/JAK/STAT Retrograde Signaling Pathways." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/426710.

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Biomedical Sciences<br>Ph.D.<br>Palmitoylation is the post-translational addition of the 16-carbon fatty acid palmitate to protein cysteine residues. This process is best known for its roles in targeting proteins to lipid membranes, including both the plasma membrane and vesicles. Palmitoylation occurs in all eukaryotic cells, but appears to be particularly important in neurons, because genetic mutation or loss of several palmitoyl acyltransferases (PATs, the enzymes that catalyze palmitoylation), leads to predominantly neuropathological defects. In addition, a growing number of recent studies

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6

Willoughby, Emma Alexandra. "Interaction between dual specificity phosphatases and JNK scaffolds." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446531/.

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The c-Jun N-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) are activated by signals including environmental stresses, growth factors and hormones. In some pathways, scaffold proteins bind JNK and upstream kinases in order to activate subsets of JNK and localise them to specific subcellular sites. For example, the JNK-interacting protein (JIP) scaffold binds JNK, MKK7 and MLKs. The G protein coupled receptor (GPCR) adaptor protein ?-arrestin 2 has also recently been identified as a JNK scaffold, binding JNK3, ASK1 and indirectly MKK4. The work presented here shows that

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7

Girardin, Stephen. "Régulation de la voie de signalisation intracellulaire JNK/SAPK." Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13179.

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8

Shirakawa, Takashi. "Deactivation of STAT6 through serine 707 phosphorylation by JNK." Kyoto University, 2011. http://hdl.handle.net/2433/142114.

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9

Fujikawa, Risako. "EP4 Receptor-Associated Protein in Microglia Promotes Inflammation in the Brain." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225462.

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10

Le-Niculescu, Helen. "Characterization of the biological roles of the JNK MAPK pathways in mammalian cells : specific and stringent activation of the JNKK2-JNK signaling module /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9984810.

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11

Morbach, Anne. "The Role of Cdep in the Embryonic Morphogenesis of Drosophila melanogaster." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-203534.

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Many organs and structures formed during the embryonic morphogenesis of animals derive from epithelia. Epithelia are made up of apicobasally polarized cells which adhere to and communicate with each other, allowing for epithelial integrity and plasticity. During embryonic morphogenesis, epithelia change their shape and migrate in a coordinated manner. How these epithelial processes are regulated is still not fully understood. In a forward genetic screen using the embryo of the fruit fly Drosophila melanogaster, candidate genes influencing the morphogenesis of epithelial structures were identif

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12

Çavusoglu, Kader 1982. "The Crosstalk between LXR and JNK pathways : mechanisms and mediators." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/116934.

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This project was carried out in the Cell Signaling Research Group headed by Dr. Carme Caelles at IRB Barcelona. As a part of the research-line that deals with physiological and pharmacological (anti-inflammatory and/or anti-diabetic) actions conducted by some nuclear receptor (NR) ligands through negative interference with the c-Jun N-terminal kinase (JNK) signaling pathway, this project was focused on studying the mechanism of cross-talk between those pathways. The results of the study show the ligand-dependent LXR inhibition of the LPS-activated SAPK (JNK and p38MAPK) pathways. Moreov

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13

Klingler, Barbara [Verfasser], and Harald [Gutachter] Wajant. "Mechanismen der Todesrezeptorinduzierten JNK-Aktivierung / Barbara Klingler. Gutachter: Harald Wajant." Würzburg : Universität Würzburg, 2015. http://d-nb.info/1110984898/34.

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14

Gazin, Vincent. "Etude cellulaire et moléculaire de la toxicité chimique de l'uranium au niveau pulmonaire." Paris 7, 2004. http://www.theses.fr/2004PA077079.

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15

Mateos, Stéphanie. "Interférence de la voie de signalisation Notch avec les mécanismes de transformation des cellules de neurorétine aviaires par v-Src." Paris 7, 2004. http://www.theses.fr/2004PA077126.

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16

Barutcu, Seda. "Role of JIP1-JNK Signaling in Beta-Cell Function and Autophagy." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/954.

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Proper functioning of endocrine cells is crucial for organismal homeostasis. The underlying mechanisms that fine-tune the amount, and the timing of hormone secretion are not clear. JIP1 / MAPK8IP1 (JNK interacting protein 1) is a scaffold protein that mediates cellular stress response, and is highly expressed in endocrine cells, including insulin secreting b-cells in pancreas islets. However, the role of JIP1 in b-cells is unclear. This study demonstrates that b-cell specific Jip1 ablation results in decreased glucose-induced insulin secretion, without a change in Insulin1 and Insulin2 gene ex

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17

Wylie, Paul. "Muscarinic acetylcholine receptor regulation of ERK and JNK in CHO cells." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29924.

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Extracellular signal-regulated kinases (ERKs) and the c-Jun N-terminal kinases/stress- activated protein kinases (JNKs/SAPKs) are activated by an array of extracellular signals to mediate a variety of cellular responses e.g. mitogenesis, differentiation, hypertrophy and apoptosis. The study investigated the regulation of ERK and JNK by agonist-mediated stimulation of the human m2-AChR or m3-AChR stably expressed in CHO cells. Stimulation of both receptors dramatically activated ERK, although stimulation by the m3-AChR was more sustained. The m3-AChR is efficiently coupled to JNK activation, wh

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18

Murai, Norihiko. "Activation of JNK in the Inner Ear Following Impulse Noise Exposure." Kyoto University, 2008. http://hdl.handle.net/2433/124329.

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19

Jacinto, Estela. "Signal integration in T lymphocytes : the role of JNK and ERK /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9814546.

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20

Eminel, Sevgi [Verfasser]. "Functions of JNK stresskinases in neuronal apoptosis and differentiation / Sevgi Eminel." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019542004/34.

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21

Diouani, Sara. "Implication de PiT1 dans l’apoptose induite par le TNF-α dans des modèles in vivo et in vitro". Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T036.

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PiT1/SLC20A1 a été identifiée pour la première fois comme récepteur rétroviral, puis de nombreuses autres études réalisées in vitro ont permis de révéler ces différentes fonctions. PiT1 est notamment un transporteur de phosphate-sodium dépendant. Par le biais de cette activité de transporteur de phosphate inorganique (Pi), PiT1 est impliqué dans plusieurs processus cellulaires comme la minéralisation osseuse, la calcification vasculaire (dans certaines pathologies), et la réabsorption rénale et intestinale de Pi. Dans notre laboratoire, afin de mieux caractériser les fonctions physiologiques d

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22

Vonkavaara, Malin. "Host-pathogen interactions between Francisella tularensis and Drosophila melanogaster." Doctoral thesis, Umeå universitet, Institutionen för klinisk mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-54604.

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Francisella tularensis is a highly virulent Gram-negative bacterium causing the zoonotic disease tularemia. Arthropod-borne transmission plays an important role in transferring the disease to humans. F. tularensis induces very low amounts of pro-inflammatory cytokines during infection, due to inhibition of immune signaling pathways and an unusual structure of its lipopolysaccharide (LPS). To date, there is no vaccine available that is approved for public use, although an attenuated live vaccine strain (LVS) is commonly used as a model of the more infectious Francisella strains. To produce an e

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23

Guo, Qianyu. "Skeletal muscle JNK activity after acute resistive exercise in elder adults with T2D: Metabolic and clinical correlates." Thesis, The University of Sydney, 2011. http://hdl.handle.net/2123/7207.

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Objective This study describes the results of the baseline sub-study of a randomized double-blind, sham-exercise controlled trial designed to assess the efficacy of power training in older adults with type 2 diabetes. The primary purpose of this sub-study was to define the state of total and activated JNK in skeletal muscle which had been exposed to an acute resistive bout of exercise. In addition, metabolic and clinical characteristics were investigated in an attempt to explain the variance and the metabolic relevance of the JNK expression (total JNK, tJNK) and activation (ratio of phosphor

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24

Vaisnav, Mahesh. "The role of JIP-1 in JNK signalling during stress and apoptosis." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29675.

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Recently, the JIP group of proteins was shown to organise the JNK pathway components into scaffolds. Transient transfection studies have shown that JIP-1 binds to JNK, MKK7, MLK3 and HPK1 and organises the JNK pathway in the form of a scaffold to selectively mediate JNK activation in response to stressful stimuli. An examination of the interaction of endogenous JIP-1 with JNK, MLK3 and HPK1 in vivo demonstrated that JIP-1 interacted with MLK3 and HPK1 in resting N1E-115 cells. In stressed N1E-115 cells, the activation of JNK coincided with the JIP-1-JNK1 interaction while the JIP-1-MLK3 intera

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25

Lamb, Jennifer A. "Role of the JNK Signal Transduction Pathway in Cell Survival: a Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/232.

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The c-Jun NH2-terminal kinases (JNK) are evolutionarily conserved serine/threonine protein kinases that are activated by proinflammatory cytokines, environmental stress, and genotoxic agents. These kinases play key regulatory roles within a cell by coordinating signals from the cell surface to nuclear transcription factors. JNK phosphorylates the amino terminal domain of all three Jun transcription factors (JunB, c-Jun and JunD) all members of the AP-1 family. The activated transcription factors modulate gene expression to generate appropriate biological responses, including cell migration, pr

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26

Römer, Lutz [Verfasser]. "Pro- and antidegenerative effects of JNK stresskinases in neuronal cells / Lutz Römer." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019541253/34.

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27

Cellurale, Cristina Arrigo. "Role of the cJun NH2-Terminal Kinase (JNK) in Cancer: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/478.

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cJun NH2-terminal kinase (JNK) is a member of the MAPK (mitogen- activated protein kinase) signaling family that responds to various extracellular stimuli, such as stress, growth factors, cytokines, or UV radiation. JNK activation can lead to cellular responses including gene expression, growth, survival, and apoptosis. JNK has been implicated in normal developmental processes, including tissue morphogenesis, as well as pathological processes, such as cellular transformation and cancer. JNK exists in three isoforms, and knockout mice have been generated for each isoform; the ubiquitously expre

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28

Loudhaief, Rihab. "Effets des bioinsecticides à base de Bacillus thuringiensis sur la physiologie intestinale de la Drosophile." Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4054/document.

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Le tube digestif est la première barrière contre les agresseurs présents dans la nourriture (virus, bactéries, produits chimiques, pesticides etc...). Il doit donc maintenir au mieux son intégrité structurale et fonctionnelle tout au long de la vie de l'individu. Bien que l'impact délétère d'une intoxication aiguë puisse être surmonté par la capacité de défense et de régénération de la muqueuse digestive, une agression prolongée ou répétée peut compromettre l'équilibre physiologique (l'homéostasie) du tube digestif. Parmi les agresseurs pouvant être ingérés avec la nourriture, on trouve la bac

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29

Etter, Paul, Radhakrishnan Narayanan, Zaneta Navratilova, et al. "Synaptic and genomic responses to JNK and AP-1 signaling in Drosophila neurons." BioMed Central, 2005. http://hdl.handle.net/10150/610070.

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BACKGROUND:The transcription factor AP-1 positively controls synaptic plasticity at the Drosophila neuromuscular junction. Although in motor neurons, JNK has been shown to activate AP-1, a positive regulator of growth and strength at the larval NMJ, the consequences of JNK activation are poorly studied. In addition, the downstream transcriptional targets of JNK and AP-1 signaling in the Drosophila nervous system have yet to be identified. Here, we further investigated the role of JNK signaling at this model synapse employing an activated form of JNK-kinase<br>and using Serial Analysis of Gene

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30

Caswell, Patrick Tomas. "Subcellular distribution and function of the neuronal JNK signalling pathway scaffold protein JIP3." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29689.

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The JNKs have been shown to regulate cellular processes ranging from apoptosis to differentiation and survival, depending on cell-tissue type and cell context. JIP3 was identified as a putative scaffold protein functioning in the JNK signalling pathway. JIP3 is predominantly expressed in neurons, and is thought to have a role in neuronal vesicular transport. The function of JIP3 in the context of JNK signalling has, however, not been established.;A polyclonal JIP3 antiserum was generated in the course of this study, which was suitable for western blotting, immunprecipitation and indirect immun

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31

Rui, Hongliang. "Regulation of MAPK/JNK signaling pathway and TGF-beta signaling pathway by axin /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20RUI.

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Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2004.<br>CD-ROM contains electronic versons of the thesis in pdf and word format. Includes bibliographical references (leaves 129-151). Also available in electronic version. Access restricted to campus users.

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32

Lessel, Wiebke [Verfasser]. "Die Rolle des JNK-Signalwegs in der Colitis ulcerosa-assoziierten Karzinogenese / Wiebke Lessel." Magdeburg : Universitätsbibliothek, 2017. http://d-nb.info/1141230631/34.

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33

Dumont, Adélie. "L'action ambivalente de l'agent anti-cancéreux 5-Fluorouracile sur les cellules myéloïdes immunosuppressives sous contrôle de l'acide docosahexaénoïque : Rôle de l'inflammasome NLRP3 et de la voie JNK dans la sécrétion de l'IL-1beta." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCI013/document.

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Selon une étude précédente, une limitation à l'efficacité anticancéreuse du 5-Fluorouracile (5-FU) repose sur la sécrétion d'IL-1β par des cellules myéloïdes immunosuppressives (MDSC). La libération d'IL-1β mature provient de l'activation de NLRP3 induite par le 5- FU et de l’augmentation de l’activité de la caspase-1 dans les MDSC, qui favorise la reprise de la croissance tumorale chez des souris traitées avec 5-FU. L'acide docosahexaénoïque (DHA) appartient à la famille des acides gras oméga-3 et possède des propriétés anticancéreuses et anti-inflammatoires qui pourraient améliorer la chimio

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34

Willaime-Morawek, Sandrine. "Apoptose neuronale et second messager céramide : étude des voies de signalisation intracellulaires." Paris 6, 2003. http://www.theses.fr/2003PA066339.

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35

Feoktistov, Alexander. "Setting the Limit on Axon Growth: Multiple Overlapping Mechanisms Repress the MAP3K Wnd/DLK So That Growth Cones Can Remodel into Stationary Synaptic Boutons." Thesis, University of Oregon, 2016. http://hdl.handle.net/1794/20403.

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The development of a stereotyped pattern of neural connectivity depends upon the behavior of growth cones, motile structures at the tips of axons that propel axon growth and steer the axon to its targets. When growth cones reach their appropriate target cells, they halt and ultimately remodel into stationary presynaptic boutons. The influence of extracellular cues in directing growth cones to their targets is well studied, but cell-intrinsic factors are also increasingly appreciated for their role in driving much of growth cone behavior. Dual leucine zipper kinases (DLKs) promote growth co

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36

Busquets, Figueras Oriol. "Estudi del paper de les proteïnes JNK en el desenvolupament de trastorns metabòlics i cognitius = Study on the role of the JNK proteins in the development of metabolic and cognitive disruptions." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668381.

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Molts estudis previs sobre el paper de les cinases c-JUN N-terminal (JNK) no tenien en compte les diferències existents en l’activitat de cadascuna de les isoformes. Això va provocar que les propostes terapèutiques que regulaven les JNK de manera inespecífica es trobessin amb problemes importants. L’objectiu de la present tesi doctoral era ampliar els coneixements que es tenen actualment sobre el paper individual de les isoformes de les JNK i, avaluar qualsevol interès terapèutic que pugui derivar de la seva modulació per a l’epilèpsia del lòbul temporal i afectacions cognitives derivades del

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37

Arnold, Richard Graham. "The role of c-Jun-N-Terminal Kinase (JNK) in hindlimb ischaemia-reperfusion injury." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579569.

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In spite of improvements in the care of the critically ill patient, both elective and emergency vascular surgical interventions are associated with significant morbidity and mortality. Successful reperfusion of the ischaemic limb often initiates a systemic inflammatory response syndrome (SIRS), which may be complicated by multiple organ failure, including Acute Lung Injury (All) and the Acute Respiratory Distress Syndrome (ARDS). An exaggerated inflammatory response has been shown to play an integral role in the development of ARDS following lower torso or limb ischaemia-reperfusion injury. JN

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38

Zecchini, Vincent. "A novel function of Notch regulates JNK activity and apoptosis in the Drosophila embryo." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621033.

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39

Kyula, Joan Nduku. "HSV-1 induced activation of C-JUN-N-Terminal Kinase (JNK) and P38 MAPK." Thesis, Glasgow Caledonian University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413914.

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40

Kawauchi, Takeshi. "The in vivo roles of STEF/Tiam1, Rac1 and JNK in cortical neuronal migration." Kyoto University, 2004. http://hdl.handle.net/2433/147523.

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41

Pocivavsek, Ana. "Microglial LRP1 modulates JNK activation a signaling cascade that also regulates apolipoprotein E levels /." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/457179623/viewonline.

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42

Marchand, Benoît. "L'activité des glycogènes synthase kinases 3 est essentielle à la survie et à la prolifération des cellules pancréatiques tumorales humaines." Mémoire, Université de Sherbrooke, 2009. http://savoirs.usherbrooke.ca/handle/11143/4047.

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Depuis leur découverte, les glycogènes synthase kinases 3 (GSK3) ont été associées à de multiples fonctions cellulaires, incluant notamment la prolifération et la survie cellulaire. La délétion homozygote de GSK3? chez les souris est létale au stade embryonnaire E13,5 et il a été démontré que l'apoptose massive des hépatocytes due à une hypersensibilité au TNF? serait la principale cause de la létalité suggérant que l'activité de GSK3? est nécessaire pour la survie cellulaire. Plusieurs études suggèrent une activité des GSK3 plus élevée dans certains types de cancers, particulièrement au nivea

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43

Zhao, Jing. "Protein Kinases can differentially regulate transactivation activities of hLRH-1 through the modulation of cofactors interactions." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1271686070.

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44

Huang, Jie. "Depolarization-dependent pro-survival signaling in spiral ganglion neurons." Diss., University of Iowa, 2007. https://ir.uiowa.edu/etd/214.

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Membrane depolarization is an effective neurotrophic stimulus, with its trophic effect on spiral ganglion neurons (SGNs) even surpassing that of neurotrophins. Thus, SGN cultures are a favorable system to investigate pro-survival signal transduction downstream of depolarization. Depolarization promotes SGN survival by recruiting three distinct kinase pathways: cyclic AMP-dependent protein kinase (PKA), Ca2+/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV. CaMKIV mediates the pro-survival effect of depolarization by activating CREB in nucleus. However, the mechanisms by which PKA and

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45

Herdman, Michelle L. "Thimerosal-induced neurotoxicity apoptosis occurs through a mitochondrial-mediated pathway via the JNK signaling pathway /." Huntington, WV : [Marshall University Libraries], 2006. http://www.marshall.edu/etd/descript.asp?ref=685.

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46

Rui, Yanning. "Elucidation of molecular mechanisms and biological functions of axin-mediated JNK pathway and p53 signaling /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20RUI.

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47

Heywood, Darren J. "Investigating the involvement of the JNK and PKC signalling pathways in mediating neuronal cell death." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288333.

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48

Yeun, Pei. "The role of purinergic receptors in the modulation of JNK signalling endothelial and cancer cells." Thesis, University of Strathclyde, 2012. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=18196.

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49

Wong, Chung Kai. "The DIX domain protein Ccd1 inhibits JNK activation by axin and dishevelled through distinct mechanisms /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20WONG.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2004.<br>Includes bibliographical references (leaves 60-68). Also available in electronic version. Access restricted to campus users.

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Wan, Jun. "Elucidation of the JNK pathway mediated by Epstein-Barr virus encoded latent membrane protein 1 /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20WAN.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2004.<br>Includes bibliographical references (leaves 105-128). Also available in electronic version. Access restricted to campus users.

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