900 resultados para 2016 model


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The organisational decision making environment is complex, and decision makers must deal with uncertainty and ambiguity on a continuous basis. Managing and handling decision problems and implementing a solution, requires an understanding of the complexity of the decision domain to the point where the problem and its complexity, as well as the requirements for supporting decision makers, can be described. Research in the Decision Support Systems domain has been extensive over the last thirty years with an emphasis on the development of further technology and better applications on the one hand, and on the other hand, a social approach focusing on understanding what decision making is about and how developers and users should interact. This research project considers a combined approach that endeavours to understand the thinking behind managers’ decision making, as well as their informational and decisional guidance and decision support requirements. This research utilises a cognitive framework, developed in 1985 by Humphreys and Berkeley that juxtaposes the mental processes and ideas of decision problem definition and problem solution that are developed in tandem through cognitive refinement of the problem, based on the analysis and judgement of the decision maker. The framework facilitates the separation of what is essentially a continuous process, into five distinct levels of abstraction of manager’s thinking, and suggests a structure for the underlying cognitive activities. Alter (2004) argues that decision support provides a richer basis than decision support systems, in both practice and research. The constituent literature on decision support, especially in regard to modern high profile systems, including Business Intelligence and Business analytics, can give the impression that all ‘smart’ organisations utilise decision support and data analytics capabilities for all of their key decision making activities. However this empirical investigation indicates a very different reality.

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This chapter describes the adaptation of a parent report instrument on early language development to a bilingual context. Beginning with general issues of adapting tests to any language, particular attention is placed on the issue of using parents as evaluators of child language acquisition of a minority language in a bilingual context. In Ireland, Irish is the first official language and is spoken by about 65,000 people on a daily basis. However all Irish speakers are bilingual, and children are exposed to the dominant English language at an early age. Using an adaptation of a parent report instrument, 21 typically developing children between 16 and 40 months were assessed repeatedly over two years to monitor their language development. The form allowed parents to document their children’s vocabulary development in both languages. Results showed that when knowledge of both languages was accounted for, the children acquired vocabulary at rates similar to those of monolingual speakers and used translational equivalents relatively early in language development. The study also showed that parents of bilingual children could accurately identify and differentiate language development in both of the child’s languages. Recommendations for adapting and using parent report instruments in bilingual language acquisition contexts are outlined.

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Due to their informality, the favelas of Rio de Janeiro are in a precarious position. Though the informal neighborhoods have long served as sites of affordable housing for Rio’s poorest residents, changes within in the city related to public security, mega-events, real estate speculation, and urban revitalization jeopardize their permanence. As one possible solution, this study, conducted for the client Catalytic Communities, investigated collective titling in favelas modeled after quilombos, territories recognized and titled by Brazilian federal law as patrimonies of black cultural traditions.

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Perceived discrimination is associated with increased engagement in unhealthy behaviors. We propose an identity-based pathway to explain this link. Drawing on an identity-based motivation model of health behaviors (Oyserman, Fryberg, & Yoder, 2007), we propose that erceptions of discrimination lead individuals to engage in ingroup-prototypical behaviors in the service of validating their identity and creating a sense of ingroup belonging. To the extent that people perceive unhealthy behaviors as ingroup-prototypical, perceived discrimination may thus increase motivation to engage in unhealthy behaviors. We describe our theoretical model and two studies that demonstrate initial support for some paths in this model. In Study 1, African American participants who reflected on racial discrimination were more likely to endorse unhealthy ingroup-prototypical behavior as self-characteristic than those who reflected on a neutral event. In Study 2, among African American participants who perceived unhealthy behaviors to be ingroup-prototypical, discrimination predicted greater endorsement of unhealthy behaviors as self-characteristic as compared to a control condition. These effects held both with and without controlling for body mass index (BMI) and income. Broader implications of this model for how discrimination adversely affects health-related decisions are discussed.

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Upon activation, T cells require energy for growth, proliferation, and function. Effector T (Teff) cells, such as Th1 and Th17 cells, utilize high levels of glycolytic metabolism to fuel proliferation and function. In contrast, Treg cells require oxidative metabolism to fuel suppressive function. It remains unknown how Teff/Treg-cell metabolism is altered when nutrients are limited and leptin levels are low. We therefore examined the role of malnutrition and associated hypoleptinemia on Teff versus Treg cells. We found that both malnutrition-associated hypoleptinemia and T cell-specific leptin receptor knockout suppressed Teff-cell number, function, and glucose metabolism, but did not alter Treg-cell metabolism or suppressive function. Using the autoimmune mouse model EAE, we confirmed that fasting-induced hypoleptinemia altered Teff-cell, but not Treg-cell, glucose metabolism, and function in vivo, leading to decreased disease severity. To explore potential mechanisms, we examined HIF-1α, a key regulator of Th17 differentiation and Teff-cell glucose metabolism, and found HIF-1α expression was decreased in T cell-specific leptin receptor knockout Th17 cells, and in Teff cells from fasted EAE mice, but was unchanged in Treg cells. Altogether, these data demonstrate a selective, cell-intrinsic requirement for leptin to upregulate glucose metabolism and maintain function in Teff, but not Treg cells.

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Diffuse intrinsic pontine glioma (DIPG) is a rare and incurable brain tumor that arises predominately in children and involves the pons, a structure that along with the midbrain and medulla makes up the brainstem. We have previously developed genetically engineered mouse models of brainstem glioma using the RCAS/Tv-a system by targeting PDGF-B overexpression, p53 loss, and H3.3K27M mutation to Nestin-expressing brainstem progenitor cells of the neonatal mouse. Here we describe a novel mouse model targeting these same genetic alterations to Pax3-expressing cells, which in the neonatal mouse pons consist of a Pax3+/Nestin+/Sox2+ population lining the fourth ventricle and a Pax3+/NeuN+ parenchymal population. Injection of RCAS-PDGF-B into the brainstem of Pax3-Tv-a mice at postnatal day 3 results in 40% of mice developing asymptomatic low-grade glioma. A mixture of low- and high-grade glioma results from injection of Pax3-Tv-a;p53(fl/fl) mice with RCAS-PDGF-B and RCAS-Cre, with or without RCAS-H3.3K27M. These tumors are Ki67+, Nestin+, Olig2+, and largely GFAP- and can arise anywhere within the brainstem, including the classic DIPG location of the ventral pons. Expression of the H3.3K27M mutation reduces overall H3K27me3 as compared with tumors without the mutation, similar to what has been previously shown in human and mouse tumors. Thus, we have generated a novel genetically engineered mouse model of DIPG, which faithfully recapitulates the human disease and represents a novel platform with which to study the biology and treatment of this deadly disease.

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We analyzed projections of current and future ambient temperatures along the eastern United States in relationship to the thermal tolerance of harbor seals in air. Using the earth systems model (HadGEM2-ES) and representative concentration pathways (RCPs) 4.5 and 8.5, which are indicative of two different atmospheric CO2 concentrations, we were able to examine possible shifts in distribution based on three metrics: current preferences, the thermal limit of juveniles, and the thermal limits of adults. Our analysis focused on average ambient temperatures because harbor seals are least effective at regulating their body temperature in air, making them most susceptible to rising air temperatures in the coming years. Our study focused on the months of May, June, and August from 2041-2060 (2050) and 2061-2080 (2070) as these are the historic months in which harbor seals are known to annually come ashore to pup, breed, and molt. May, June, and August are also some of the warmest months of the year. We found that breeding colonies along the eastern United States will be limited by the thermal tolerance of juvenile harbor seals in air, while their foraging range will extend as far south as the thermal tolerance of adult harbor seals in air. Our analysis revealed that in 2070, harbor seal pups should be absent from the United States coastline nearing the end of the summer due to exceptionally high air temperatures.

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With the importance of renewable energy well-established worldwide, and targets of such energy quantified in many cases, there exists a considerable interest in the assessment of wind and wave devices. While the individual components of these devices are often relatively well understood and the aspects of energy generation well researched, there seems to be a gap in the understanding of these devices as a whole and especially in the field of their dynamic responses under operational conditions. The mathematical modelling and estimation of their dynamic responses are more evolved but research directed towards testing of these devices still requires significant attention. Model-free indicators of the dynamic responses of these devices are important since it reflects the as-deployed behaviour of the devices when the exposure conditions are scaled reasonably correctly, along with the structural dimensions. This paper demonstrates how the Hurst exponent of the dynamic responses of a monopile exposed to different exposure conditions in an ocean wave basin can be used as a model-free indicator of various responses. The scaled model is exposed to Froude scaled waves and tested under different exposure conditions. The analysis and interpretation is carried out in a model-free and output-only environment, with only some preliminary ideas regarding the input of the system. The analysis indicates how the Hurst exponent can be an interesting descriptor to compare and contrast various scenarios of dynamic response conditions.

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Tumor angiogenesis is critical to tumor growth and metastasis, yet much is unknown about the role vascular cells play in the tumor microenvironment. A major outstanding challenge associated with studying tumor angiogenesis is that existing preclinical models are limited in their recapitulation of in vivo cellular organization in 3D. This disparity highlights the need for better approaches to study the dynamic interplay of relevant cells and signaling molecules as they are organized in the tumor microenvironment. In this thesis, we combined 3D culture of lung adenocarcinoma cells with adjacent 3D microvascular cell culture in 2-layer cell-adhesive, proteolytically-degradable poly(ethylene glycol) (PEG)-based hydrogels to study tumor angiogenesis and the impacts of neovascularization on tumor cell behavior.

In initial studies, 344SQ cells, a highly metastatic, murine lung adenocarcinoma cell line, were characterized alone in 3D in PEG hydrogels. 344SQ cells formed spheroids in 3D culture and secreted proangiogenic growth factors into the conditioned media that significantly increased with exposure to transforming growth factor beta 1 (TGF-β1), a potent tumor progression-promoting factor. Vascular cells alone in hydrogels formed tubule networks with localized activated TGF-β1. To study cancer cell-vascular cell interactions, the engineered 2-layer tumor angiogenesis model with 344SQ and vascular cell layers was employed. Large, invasive 344SQ clusters developed at the interface between the layers, and were not evident further from the interface or in control hydrogels without vascular cells. A modified model with spatially restricted 344SQ and vascular cell layers confirmed that observed 344SQ cluster morphological changes required close proximity to vascular cells. Additionally, TGF-β1 inhibition blocked endothelial cell-driven 344SQ migration.

Two other lung adenocarcinoma cell lines were also explored in the tumor angiogenesis model: primary tumor-derived metastasis-incompetent, murine 393P cells and primary tumor-derived metastasis-capable human A549 cells. These lung cancer cells also formed spheroids in 3D culture and secreted proangiogenic growth factors into the conditioned media. Epithelial morphogenesis varied for the primary tumor-derived cell lines compared to 344SQ cells, with far less epithelial organization present in A549 spheroids. Additionally, 344SQ cells secreted the highest concentration of two of the three angiogenic growth factors assessed. This finding correlated to 344SQ exhibiting the most pronounced morphological response in the tumor angiogenesis model compared to the 393P and A549 cell lines.

Overall, this dissertation demonstrates the development of a novel 3D tumor angiogenesis model that was used to study vascular cell-cancer cell interactions in lung adenocarcinoma cell lines with varying metastatic capacities. Findings in this thesis have helped to elucidate the role of vascular cells in tumor progression and have identified differences in cancer cell behavior in vitro that correlate to metastatic capacity, thus highlighting the usefulness of this model platform for future discovery of novel tumor angiogenesis and tumor progression-promoting targets.

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Mobile Cloud Computing promises to overcome the physical limitations of mobile devices by executing demanding mobile applications on cloud infrastructure. In practice, implementing this paradigm is difficult; network disconnection often occurs, bandwidth may be limited, and a large power draw is required from the battery, resulting in a poor user experience. This thesis presents a mobile cloud middleware solution, Context Aware Mobile Cloud Services (CAMCS), which provides cloudbased services to mobile devices, in a disconnected fashion. An integrated user experience is delivered by designing for anticipated network disconnection, and low data transfer requirements. CAMCS achieves this by means of the Cloud Personal Assistant (CPA); each user of CAMCS is assigned their own CPA, which can complete user-assigned tasks, received as descriptions from the mobile device, by using existing cloud services. Service execution is personalised to the user's situation with contextual data, and task execution results are stored with the CPA until the user can connect with his/her mobile device to obtain the results. Requirements for an integrated user experience are outlined, along with the design and implementation of CAMCS. The operation of CAMCS and CPAs with cloud-based services is presented, specifically in terms of service description, discovery, and task execution. The use of contextual awareness to personalise service discovery and service consumption to the user's situation is also presented. Resource management by CAMCS is also studied, and compared with existing solutions. Additional application models that can be provided by CAMCS are also presented. Evaluation is performed with CAMCS deployed on the Amazon EC2 cloud. The resource usage of the CAMCS Client, running on Android-based mobile devices, is also evaluated. A user study with volunteers using CAMCS on their own mobile devices is also presented. Results show that CAMCS meets the requirements outlined for an integrated user experience.

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterised by motor and non-motor symptoms, resulting from the degeneration of nigrostriatal dopaminergic neurons and peripheral autonomic neurons. Given the limited success of neurotrophic factors in clinical trials, there is a need to identify new small molecule drugs and drug targets to develop novel therapeutic strategies to protect all neurons that degenerate in PD. Epigenetic dysregulation has been implicated in neurodegenerative disorders, while targeting histone acetylation is a promising therapeutic avenue for PD. We and others have demonstrated that histone deacetylase inhibitors have neurotrophic effects in experimental models of PD. Activators of histone acetyltransferases (HAT) provide an alternative approach for the selective activation of gene expression, however little is known about the potential of HAT activators as drug therapies for PD. To explore this potential, the present study investigated the neurotrophic effects of CTPB (N-(4-chloro-3-trifluoromethyl-phenyl)-2-ethoxy-6-pentadecyl-benzamide), which is a potent small molecule activator of the histone acetyltransferase p300/CBP, in the SH-SY5Y neuronal cell line. We report that CTPB promoted the survival and neurite growth of the SH-SY5Y cells, and also protected these cells from cell death induced by the neurotoxin 6-hydroxydopamine. This study is the first to investigate the phenotypic effects of the HAT activator CTPB, and to demonstrate that p300/CBP HAT activation has neurotrophic effects in a cellular model of PD.

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Ce mémoire de maîtrise traite de la théorie de la ruine, et plus spécialement des modèles actuariels avec surplus dans lesquels sont versés des dividendes. Nous étudions en détail un modèle appelé modèle gamma-omega, qui permet de jouer sur les moments de paiement de dividendes ainsi que sur une ruine non-standard de la compagnie. Plusieurs extensions de la littérature sont faites, motivées par des considérations liées à la solvabilité. La première consiste à adapter des résultats d’un article de 2011 à un nouveau modèle modifié grâce à l’ajout d’une contrainte de solvabilité. La seconde, plus conséquente, consiste à démontrer l’optimalité d’une stratégie de barrière pour le paiement des dividendes dans le modèle gamma-omega. La troisième concerne l’adaptation d’un théorème de 2003 sur l’optimalité des barrières en cas de contrainte de solvabilité, qui n’était pas démontré dans le cas des dividendes périodiques. Nous donnons aussi les résultats analogues à l’article de 2011 en cas de barrière sous la contrainte de solvabilité. Enfin, la dernière concerne deux différentes approches à adopter en cas de passage sous le seuil de ruine. Une liquidation forcée du surplus est mise en place dans un premier cas, en parallèle d’une liquidation à la première opportunité en cas de mauvaises prévisions de dividendes. Un processus d’injection de capital est expérimenté dans le deuxième cas. Nous étudions l’impact de ces solutions sur le montant des dividendes espérés. Des illustrations numériques sont proposées pour chaque section, lorsque cela s’avère pertinent.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.