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The widely-used passenger and car ferries, sailing regularly and carrying heavy loads, form a unique type of marine vessel, providing vital transportation links to the coastal regions. Modern ferry ships usually are equipped with multiple diesel engines as prime movers. These diesel engines consume a large amount of marine diesel fuel with high fuel costs, and high emissions of greenhouse gas (GHG) and other harmful air pollutants, including CO2, HC, NOx, SO2, CO, and PM. To reduce fuel costs and the harmful emissions, the marine industry and ferry service providers have been seeking clean ship propulsion solutions. In this work, the model-based design (MBD) and optimization methodology for developing advanced electrified vehicles (EV) are applied to the modelling, design and control optimizations of clean marine vessels with a hybrid electric propulsion system. The research focuses on the design and optimization of the hybrid electric ship propulsion system and uses an open deck passenger and car ferry, the MV Tachek, operated by the British Columbia Ferry Services Inc. Canada, as a test case. At present, the ferry runs on the Quadra Island – Cortes Island route in British Columbia, Canada, with dynamically changing ocean conditions in different seasons over a year. The research first introduces the ship operation profile, using statistical ferry operation data collected from the ferry’s voyage data recorder and a data acquisition system that is specially designed and installed in this research. The ship operation profile model with ship power demand, travelling velocity and sailing route then serves as the design and control requirements of the hybrid electric marine propulsion system. The development of optimal power control and energy management strategies and the optimization of the powertrain architecture and key powertrain component sizes of the ship propulsion system are then carried out. Both of the series and parallel hybrid electric propulsion architectures have been studied. The sizes of crucial powertrain components, including the diesel engine and battery energy storage system (ESS), are optimized to achieve the best system energy efficiency. The optimal power control and energy management strategies are optimized using dynamic programming (DP) over a complete ferry sailing trip. The predicted energy efficiency and emission reduction improvements of the proposed new ship with the optimized hybrid propulsion system are compared with those of two benchmark vessels to demonstrate the benefits of the new design methodology and the optimized hybrid electric ship propulsion system design. These two benchmarks include a conventional ferry with the old diesel-mechanical propulsion system, and the Power Take In (PTI) hybrid electric propulsion systems installed on the MV Tachek at present. The simulation results using the integrated ship propulsion system model showed that the newly proposed hybrid electric ship could have 17.41% fuel saving over the conventional diesel-mechanical ship, and 22.98% fuel saving over the present MV Tachek. The proposed optimized hybrid electric propulsion system, combining the advantages of diesel-electric, pure electric, and mechanical propulsions, presented considerably improved energy efficiency and emissions reduction. The research forms the foundation for future hybrid electric ferry design and development. / Graduate

<p dir="ltr">Plant immunity to pathogens involves a network of genetic, molecular, and cellular processes that culminate in activation of responses that restrict pathogen ingress and reduce diseases symptoms. Mechanisms of pathogen recognition, signaling, and activation of immune responses are well understood especially for (hemi) biotrophic pathogens. By contrast, there is paucity of knowledge on immune signaling for responses to broad host necrotrophic fungi such as <i>Botrytis cinerea (Botrytis</i><i>)</i>. Plant resistance to such pathogens is genetically complex with no complete resistance observed in any host species. However, genetic variation for quantitative resistance has been documented although the molecular mechanisms are poorly understood. In the current study, we focused on functional dissection of components of tomato immune signaling underlying quantitative resistance to <i>Botrytis</i>. Tomato BIK1-family receptor-like cytoplasmic kinases (RLCKs) were studied using gene edited mutants, and subsequent molecular, biochemical, and genomic characterizations of the mutants and the corresponding proteins. In addition, <i>Botrytis</i> induced transcriptome of Arabidopsis and tomato were compared to explain observed differences in their resistance to the fungus. The results from these studies are described in four chapters. Chapter 1 provides a review of RLCKs and their function in plant responses to biotic and abiotic stresses. Chapter 2 presents the genetic, molecular, and biochemical characterization of tomato RLCK, TPK1B RELATED PROTEIN KINASE (TPK09) in fungal resistance and responses to light stress. Chapter 3 highlights observations on the functions of TPK1B RELATED PROTEIN KINASE7 (TPK07) in fungal and bacterial resistance. Lastly, Chapter 4 covers comparative transcriptome analysis of Arabidopsis and tomato responses to <i>Botrytis</i>.</p><p dir="ltr">Specialized cell-surface receptors mediate the perception of environmental changes. A subset of plant cell surface receptors recognizes pathogen-associated molecular patterns (PAMPs), which are immunogenic pathogen or host-derived molecules, peptides (phytocytokines), lipids, and carbohydrates. PAMPs are perceived by surface receptors designated as pattern recognition receptors (PRRs) that are categorized as receptor like kinases (RLKs) or receptor like proteins (RLPs). Recognition of PAMPs through PRR is an evolutionarily conserved pathway that aids plants in specific recognition of pathogens. The signaling events initiated by PRRs are connected to PRR-associated RLCKs, which amplify the signal and activate other regulatory proteins. PRR-RLCK activation is linked to immune messengers ROS, Ca⁺, and MAPKs based on extensive research in Arabidopsis which also established the paradigm for RLCKs functions in integrating signals from various PRRs. However, insufficient attention was given to RLCK functions in crop plant responses to biotic and abiotic stressors and, thus, limited data exists on RLCKs from crops of agronomic and horticultural significance. To address this gap, we conducted genetic, genomic, and molecular studies on the biological functions of tomato TPK1B RELATED KINASES TPK09 and TPK07.</p><p dir="ltr">To determine the function of TPK09 and TPK07, mutant alleles of these two RLCKs were generated through CRISPR-Cas9 gene editing. Loss of function mutants of <i>tpk09</i> exhibited increased susceptibility to <i>Botrytis</i> but showed no altered responses to the bacterial pathogen <i>P. syringae</i>. Plants carrying mutant alleles displayed reduced immune gene expression and impaired accumulation of reactive oxygen species in response to chitin and flg22. In addition to <i>Botrytis</i> and several plant hormones, the expression of <i>TPK09</i> gene is induced by light but suppressed by darkness. The exposure of wildtype tomato plants to light-emitting diodes (LEDs) reduced hypocotyl length but <i>tpk09</i> mutants were insensitive. Furthermore, <i>tpk09</i> mutants also exhibited increased accumulation of H₂O₂ and extensive necrosis, suggesting a disturbance in cellular homeostasis in response to changes in light spectra, ultimately leading to enhanced susceptibility to <i>Botrytis</i>. Although the global impact of TPK09 on <i>Botrytis</i> induced transcriptome was limited, the expression of the tomato negative regulator of cell death SlBI-like1 gene was significantly reduced in the mutant, particularly in response to the combined effect of <i>Botrytis</i> and LED light. The data suggest TPK09 regulates SlBI-like1 gene expression, but the mechanism is unclear. Further, the impairment of the light stress response in <i>tpk09</i> mutants was substantiated by a reduction in chlorophyll content and damage to the photosynthetic machinery, along with a clear reduction in the expression of genes related to light harvesting and photosynthesis. Regulatory network analysis using RNA-seq data identified TPK09 regulated genes related to stress and oxidative damage. This was further supported from proteomic studies of tomato TPK09-HA transgenic plants. Immunoprecipitation coupled with mass spectrometry revealed that proteins associated with photosynthesis and photosystem subunits were enriched in TPK09 overexpressing plant. Our data establishes that TPK09 is required for fungal resistance and light stress by maintaining functional photosynthetic machinery and ROS homeostasis.</p><p dir="ltr">We also studied the function of tomato TPK07 which is another member of the RLCK-VII family. Through analysis of <i>tpk07</i> mutants, we show that TPK07 it required for resistance to both <i>Botrytis</i> and <i>P. syringae</i> expressing the cysteine protease type III effector AvrPphB which cleaved TPK07 protein. However, further studies are needed to understand the biological function of this cleavage. The expression of TPK07 was induced by <i>Botrytis</i> and the bacterial PAMPs flg22, flg28, and csp22. TPK07 belongs to the RLCK VII-5 subfamily and clusters in the same clade with Arabidopsis PBL34 (AT5G15080), PBL35 (AT3G01300), and PBL36 (AT3G28690) that functions in immunity to <i>P. syringae</i>. In addition, <i>tpk07</i> mutants showed reduced accumulation of ROS in response to chitin and lipopolysaccharide. Moreover, TPK07 is a plasma membrane-localized kinase with a unique N-terminal sequence, offering a research avenue for future structural analysis to understand its contribution in pathogen responses.</p><p dir="ltr">In the last chapter, we conducted comparative analyses of <i>Botrytis</i> induced transcriptome of Arabidopsis and tomato to explain the observed differences between the two plant species in their resistance to <i>Botrytis</i>. Over the years, we observed tomato is more susceptible to <i>Botrytis</i> than Arabidopsis under the same disease assay conditions, but the mechanism is not known. We sought to gain insight into the immune responses of the two species and identify targets for future functional analyses that can explain the differential pathogen responses. Many separate studies<i> </i>have demonstrated<i> </i>that <i>Botrytis</i> causes extensive transcriptional reprogramming in Arabidopsis and tomato. Our results from the comparative studies of in-house generated data identified differentially expressed genes (DEGs), Gene Ontology terms, and metabolic pathways that are specific or shared between the two species. Interestingly, some genes show distinct expression pattern in tomato and Arabidopsis consistent with previous observation that some genes in the two species show contrasting disease resistance functions. Genes with distinct expression patterns warrant further studies to better understand differences in host immune responses between the two species. In addition, transcription factors (TFs) and regulatory hub genes that could be important for further studies were identified.</p><p dir="ltr">In sum, our data establishes the functions of two tomato RLCKs in fungal resistance, interactions between fungal resistance and plant responses to light, and the conserved and contrasting gene expression profiles of tomato and Arabidopsis genes, laying the foundation for future studies.</p>

Plants are fundamental to life on earth, crucially providing the basis of our food supply. As world population continues to grow, so too does the pressure on our agricultural systems, with one of the biggest challenges being the control of plant pathogens to ensure a healthy crop. The interaction between plant and pathogen is complex, with subtleties at the molecular level dictating the boundary between health and disease. This is exemplified by pathogen effectors; secreted proteins which enter the plant cell and interact with host targets to facilitate infection. AVR2 is one such effector, secreted by the oomycete pathogen Phytophthora infestans; the pathogen responsible for potato late blight. AVR2 interacts with a family of kelch-repeat containing phosphatases in potato, the BSLs, implicated in brassinosteroid pathway signalling – a major hormone signalling pathway in plants associated with growth and development. This work investigates the role of AVR2 and its host targets in pathogen virulence, with focus on the link between the brassinosteroid pathway and immunity in S. tuberosum. StBSL1 is shown to be a ‘susceptibility factor’ in P. infestans infection – a host protein with a positive effect on pathogen virulence. AVR2 stabilises BSL1 in planta, and both AVR2 and BSL1 are shown to suppress primary defence responses in the plant. Transcriptional analysis of brassinosteroid-treated S. tuberosum is used to identify a set of marker genes for active BR signalling. Strikingly, AVR2 is shown to upregulatethis pathway, and specifically upregulates the transcription factor StHBI1-like, identified as a suppressor of immunity. These findings reveal a novel mechanism in oomycete effector biology; the exploitation of crosstalk between the brassinosteroid pathway and immune signalling in plants.

本研究同時探討房貸違約與提前清償終止行為，並對提前清償動機『出售』與『轉貸』予兼容並蓄。蒐集自H銀行房貸資料，運用多項式邏吉斯廻歸模型分析法，以總體經濟因子之有無分兩階段，對應變數-房貸終止行為(Y1)及提前清償動機(Y2)，採取雙層次深入實證。 實證結果：從機率模型配適度與解釋力之實證分析中，獲得一致結論，對於含有總體經濟因子-經濟成長率與CPI 年增率之模型，其所計算Cox & Snell及Nagelkerke之假 值分別為0.534及0.611，均大於0.5以上，其相對性與獨立性上，均具備較高的模型解釋力，為一較優之房貸違約與提前清償終止行為模型，其相關顯著影響因子如下： 一、對違約具有顯著影響之因子，包括：借款年限、初貸利率、LTV、保證人、次級房貸、部分提前清償、購屋投資、 PTI、DBR＞22、軍警公教人員、設二胎、區域台北市、區域新北市及CPI年增率等14項。 二、對提前清償具有顯著影響之因子，包括：初貸利率、次級房貸、部分提前清償、購屋投資、購屋自住、年資、設二胎、CPI年增率及經濟成長率等9項。 三、對提前清償動機-『出售』之顯著因子：次級房貸、部分提前清償、購屋投資、設二胎等4項。 四、對提前清償動機-『轉貸』之顯著因子：初貸利率、次級房貸、購屋自住、年資、設二胎、CPI年增率及經濟成長率等7項。。 本實證結果所建構含有總體經濟因子之房貸終止行為機率模型，以其顯著影響因子再深入探討提前清償-『出售』與『轉貸』之動機，使提前清償行為模式更精確性地呈現，有助於提供金融機構，在計算違約機率與提前清償機率之模型架構上及授信審核評估上，具貢獻價值之參考資訊。 / This research explores the default and prepayment on the termination behaviors of residential mortgages, as well as the motives of prepayment in house selling or refinancing. Mortgage data are collected from the H bank in Taiwan, using the multi-nominal logistic regression analytic method to explore the factors affecting the default and prepayment behaviors. Empirical results show that loan period, initial mortgage rate, loan-to-value ratio (LTV), the existence of the guarantor, subprime mortgages, curtailment, investment purpose, payment-to-income (PTI), debt burden ratio exceeded 22 (DBR＞22), government employees or teachers, second lien, location in Taipei city, the new Taipei city and CPI annual rate of increase are the significant factors of default behavior. As for the variables on prepayment, the initial mortgage rate, subprime mortgages, curtailment, investment purpose, residential use, DBR＞22, the age of professional career, second lien, CPI annual rate of increase and economical growth rate are significant. For more detailed curtailment behavior, the empirical results show that house sale subprime mortgages, curtailment, residential investment purpose, second lien are significant factors. As for the variables in inter-bank refinancing initial interest rate, subprime mortgages, residential investment purpose, the age of professional career, second lien, CPI annual rate of increase and economical growth rate are significant factors. Results of this research may provide financial institutions precious references on the mortgage default and prepayment behaviors. The mortgage industry can take into account of the significant results on the capital planning in the future.

The need for a reduced dependence on fossil fuels is motivated by a wide range of factors: from increasing fuel costs, to national security implications of supply, to rising concern for environmental impact. Although much focus is given to terrestrial systems, over 90% of the world's freight is transported by ship. Likewise, naval warfighting systems are critical in supporting U.S. national interests abroad. Yet the vast majority of these vessels rely on fossil fuels for operation. The results of this thesis illustrate a common theme that hybrid mechanical-electrical marine propulsion systems produce substantially better fuel efficiency than other technologies that are typically emphasized to reduce fuel consumption. Naval and commercial powertrains in the 60-70 MW range are shown to benefit substantially from the utilization of mechanical drive for high speed propulsion; complemented by an efficient electric drive system for low speed operations. This hybrid architecture proves to be able to best meet the wide range of performance requirements for each of these systems, while also being the most easily integrated technology option. Naval analyses evaluate powertrain options for the DDG-51 Flight III. Simulation results using actual operational profile data show a CODLAG system produces a net fuel savings of up to 12% more than a comparable all-electric system, corresponding to a savings of 37% relative the existing DDG-51 powertrain. These results prove that a mechanical linkage for the main propulsion engine greatly reduces fuel consumption and that for power generation systems requiring redundancy, diesel generators represent a vastly superior option to gas turbines. For the commercial application it is shown that an augmented PTO/PTI hybrid system can better reduce cruise fuel consumption than modern sail systems, while also producing significant benefit with regard to CO2 emissions. In addition, using such a shaft mounted hybrid system for low speed electric drive in ports reduces NOx emissions by 29-43%, while CO is reduced 57-66% and PM may be reduced up to 25%, depending on the specific operating mode. As an added benefit, fuel consumption rates under these conditions are reduced 20-29%. / text

Les cellules lymphoïdes innées (ILCs) sont des populations cellulaires d’identification récente, mais leur rôle in vivo chez l’homme reste mal connu. Dans une 1ère étude, nous avons pu montrer qu’un déficit sévère en NK au cours de déficits immunitaires communs variables est associé à un risque accru de manifestations non infectieuses et infectieuses bactériennes sévères, suggérant un rôle protecteur non redondant des cellules NK lorsque le système immunitaire adaptatif n’est pas fonctionnel. Dans une 2ème étude, nous avons montré que des patients atteints de déficits immunitaires combinés sévères ɣc et JAK3 déficients n’ont pas d’ILCs. Après allogreffe de moelle osseuse, le nombre d’ILCs circulantes reste indétectable, sans manifestation clinique notable associée. Ces résultats sont en faveur d’une redondance des fonctions des ILCs chez l’homme, lorsque les fonctions T et B sont conservées. Nous avons ensuite étudié les modifications phénotypiques et fonctionnelles des cellules NK au cours du purpura thrombopénique immunologique, et observé un défaut de production d’interféron-ɣ par les cellules NK circulantes et une augmentation de la cytotoxicité dépendante des anticorps des cellules NK spléniques. Une inhibition des fonctions des cellules NK par les immunoglobulines polyvalentes est également mise en évidence. Enfin, une étude des ILCs circulantes au cours de la maladie associée aux IgG4 ainsi qu’une revue de la littérature sur l’étude des ILCs au cours des pathologies inflammatoires sont rapportées. En conclusion, l’apparente redondance des ILCs chez l’homme ainsi que leur implication en pathologies inflammatoires en font de potentielles cibles thérapeutiques. / Innate lymphoid cells (ILCs) are recently identified components of the immune system, but their functions in vivo in humans are still elusive. In a first study, we show in patients with common variable immunodeficiency that non-infectious inflammatory complications and severe bacterial infections were more frequent in patients with severe NK cell lymphopenia, indicating potential non-redundant immune functions of NK cells when the adaptive immune response is not optimal. In a second study, we observe that in patients with ɣc and JAK3 severe combined immunodeficiencies, all ILC subsets are absent. After hematopoietic stem cell transplantation, ILCs remain indetectable with no susceptibility to disease, suggesting that ILCs might be redundant and dispensable in humans, if T and B cells functions are preserved. In the second part of this thesis, we study phenotypic and functional modifications of NK cell compartment in primary immune thrombocytopenia. Interferon gamma production by the peripheral blood NK cells of ITP patients is decreased. In contrast, splenic NK cells of ITP patients tend to be more efficient in antibody-dependent cell cytotoxicity. Intravenous polyvalent immunoglobulins lead to the inhibition of blood NK cell activation. Finally, we present the preliminary results of a study investigating the modifications of circulating ILCs in IgG4-related disease, and present an extensive litterature review concerning the role of ILCs in inflammatory diseases. In conclusion, the apparent redundancy of ILCs for protective immunity and their pathogenic role in inflammatory diseases make their targeting in humans for therapeutic purposes particularly promising.

The current study describes the impact of trauma on the perceptual thinking processes of participants who have sustained repeated criminal victimisation in South Africa. Fifteen adult males, (mean age 40.73 years) participated voluntarily in this descriptive study. The Rorschach Inkblot Method (RIM) is the psychometric instrument used to describe the participants and Exner’s Comprehensive System (CS) is the method of interpretation employed. The Perceptual Thinking Index (PTI) is the cluster of variables selected to describe each participant’s level of reality testing and perceptual functioning. Together with this, the D and Adjusted D Score variables are discussed to describe the participants’ overall and current coping capacities. From the research findings yielded in this study, it appears that the majority of these participants (73%) can be described as experiencing problems in terms of their perceptual thinking processes. They are also unable to appropriately engage in accurate reality testing. The results of the research study may serve as an incentive for further studies of this nature as according to the RIM, participants with this level of impaired reality testing generally present with psychotic features. However, these research results were found in participants who present with an absence of a psychotic or any schizophrenic type disorder diagnoses. Other researchers who used the RIM to assess trauma victims have found results similar to this. Furthermore, participants who present with this level of impaired reality testing, generally experience severe problems in coping with basic psychological aspects of daily functioning. This however, does not appear to be the case with this sample group, which was one of the motivating factors for conducting this research. A concluding suggestion is made for possible research into investigating how, and at what expense, other psychological features of functioning are employed, in order to manage in a seemingly well-adaptive manner. / Dissertation (MA (Clinical Psychology))--University of Pretoria, 2006. / Psychology / unrestricted

L’association entre déficits immunitaires primitifs (DIPs) et manifestations auto-immunes peut sembler paradoxale lorsque l’on aborde les DIPs comme des défauts d’immunité opposés à l’autoimmunité vue comme excès d’immunité adaptative à l’encontre du soi. Néanmoins, loin de se résumer à un simple défaut d’une ou plusieurs composantes du système immunitaire qui prédispose aux infections par divers agents pathogènes, les DIPs sont fréquemment associés à une autoimmunité; parfois révélatrice. Ainsi, les données épidémiologiques issues de registres ou de larges séries de patients atteints de DIPs s’accordent sur une prévalence globale de 25 à 30% de complications auto-immunes (au premier rang desquelles figurent les cytopénies auto-immunes). Différentes hypothèses sont avancées pour rendre compte de l’auto-immunité dans les DIPs. On peut citer : 1°) une perturbation profonde de l’homéostasie lymphocytaire, en particulier dans les déficits immunitaires combinés sévères (CID) avec lymphopénies T et B ; 2°) des défauts intrinsèques des lymphocytes B permettant une rupture de tolérance précoce des LB auto réactifs ; 3°) un comportement aberrant des LT (défaut de maturation, excès d’activation) ; 4°) une absence de lymphocytes T ou de B régulateurs ; 5°) une production inappropriée de certaines cytokines proinflammatoires comme dans les interféronopathies. Ces hypothèses concernent surtout les DIPs pédiatriques sévères. Mon travail de thèse explore la rupture de tolérance immunitaire adaptative au cours des DIPs de l’adulte par différentes approches. Nous nous sommes en particulier attachés au plus fréquent, le DICV (Déficit Immunitaire Commun Variable), déficit immunitaire humoral pas toujours bien défini sur le plan génétique et physiopathologique qui constitue un défi thérapeutique lorsqu’il est compliqué d’une auto-immunité nécessitant un traitement immunosuppresseur. / The association between primary immune deficiency (PID) and autoimmunity may seem paradoxical when PID is considered only as an immune response defect against pathogens and autoimmunity only as an excess of immunity. Nevertheless, far from being simple immune defects increasing the risk of infections, DIPs are frequently associated with autoimmunity. Even more, autoimmunes manifestations can sometimes reveal a PID. Thus, epidemiological data from registers or large series of patients with PIDs agree on an overall prevalence of 25 to 30% of autoimmune complications (with auto-immune cytopenias as first causes). Several hypotheses have been proposed with different underlying mechanisms to explain the tolerance breakdown in PIDs. We can cite : 1°) a severe disturbance of lymphocyte homeostasis, for example in severe combined immunodeficiencies ; 2°) an impaired B-cell developpement with earlystage defects of tolerance ; 3°) a dysregulation of T cells (developpement or activation impairments) ; 4°) a dysfunction of T-reg (or B-reg) ; 5°) an excess of production of proinflammatory cytokines. These hypotheses are especially true for early-onset PIDs (in infancy). In this work (PhD), we explore the mechanisms of tolerance breakdown involved in adults PIDs. We use several approaches to describe the pathways leading to autoimmunity, focusing on the most common PID in adult : CVID (common variable immunodeficiency). This syndrome is not well defined on the genetic and physiopathological level. It is still a therapeutic challenge when complicated by autoimmunity (requiring immunosuppressive therapy).