"Affordance" is an ecological psychology which can explain the interaction between the natural environment and its physical property of material with a combination of biology. This concept is first applied on interface design by Norman. Gaver also uses this theory to provides a evaluate framework for separating affordances from the perceptual information available about them. To those traditional book readers, the interface design of e-book is one of the reasons they refuse to use it. The user experiences of traditional reading are also have a serious effect on the e-book design. Designers of e-book cannot determine they should provide more traditional way to read or they can just make a whole new user experience on electronic reading. The goal of this study is to use ¡§Affordances¡¨ to discuss the difference between electronic and traditional reading, by using common tasks of traditional and electronic reading to observe user¡¦s action and performance. The main results are the following: the performance of e-book which this study used is lower than traditional book, because 1) Information on the interface is not clear that users may confuse, or make a wrong action. 2) Some functions didn¡¦t provide any instructions or information that can help users to know how to action. 3) The hardware of e-book is too slow that cannot reflect user¡¦s action. The main discussions of e-book as affordance approach are the following. 1) When there are multiple affordances available to choose, users will pick the most efficient one they perceived. 2) If users experienced some difficulty during action, they may choose another affordance to complete task. 3) If the perceived information of icon has multiple meanings to the users, it will cause a false or hidden affordance.

This paper outlines the development of a second screen marketing campaign to raise awareness of the importance of hydration among male students at The University of Texas at Austin. Existing literature, communication theories, and current second screen campaigns are used to inform campaign development. The development process and key recommendations for this, and future second screen marketing campaigns, is then discussed. / text

This paper seeks to understand the landscape of social TV, which takes place when an audience member engages with social media while watching television programming, and second screen experiences, and more specifically how these technologies can be employed by advertisers. By reviewing existing literature, examining field studies and data, and analyzing case studies, the report identifies how marketers can best tie their television advertising to social media to increase engagement and keep brands top of mind, even during breaks from traditional programming. The paper will conclude by discussing the current limitations of the emerging technologies surrounding the phenomenon of social TV, as well as providing recommendations that can be applied to brands and marketers alike. / text

Influenza virus is a globally significant infectious agent with the potential to cause catastrophic pandemic outbreaks. Present treatment of influenza infections is restricted to only four anti-viral drugs, but there are increasing global reports of anti-viral resistance in several seasonal strains and also the 2009 pandemic swine-origin influenza virus H1N1. Possible future pandemic outbreaks, emerging new strains and drug resistance underscore the need to understand this complex virus and its pathogenicity with the goal that novel targets can be uncovered for future therapeutic development. Extensive lung tissue damage during influenza virus infection is proposed to contribute to the development of aberrant host immune responses. Strong evidence now demonstrates the significance of the cellular death pathway in promoting efficient influenza virus replication and disease progression. Viruses rely heavily on the machinery of their host for productive replication, which is also an Achilles’ heel that could be targeted for treatment. In pursuit of unraveling the complex nature of influenza virus replication, I carried out a global shRNA screen to identify specific host factors and signaling pathways that are involved in influenza-induced cell death and replication. In this study I identified 138 genes required for influenza viruses to induce infected host cell death. These genes were found to be involved in Protein Kinase A, NF-kB and PI3K signaling cascades. These signaling pathways are well known regulators of cell death and survival, which suggests influenza viruses may carefully regulate these pathways to reach a balance that suit their requirements for efficient proliferation, eventually at the cost of the host cell. I chose five candidate genes—BAD, MxB, TNFSF12-13,TNFSF13, and USP47—that were associated with apoptosis and the major signaling pathways determined in my network analysis to further verify the genome-wide screen as well as elucidate the role of these potentially novel host factors in influenza virus replication. I show in my study that influenza virus-induced cytopathology and cell death are considerably inhibited in BAD knockdown cells and both virus replication and viral protein production also are dramatically reduced. I also report here that MxB depletion protected cells from virus-mediated cytopathology and resulted in significant inhibition of influenza virus replication for H1N1 and H3N2 subtypes. Additionally, I report that TNFSF12-13, TFNSF13, and USP47, similarly, are required for efficient influenza virus replication and induction of cell death. Depletion of these proteins resulted in significant inhibition of viral propagation and conferred protection of host cells to virus killing. Overall, my study has provided a list of novel host factors that play significant roles during influenza virus infection. Further studies on these potential genes and their encoded protein products may uncover possible new targets for drug development for future therapeutic treatment. In addition to providing greater understanding of influenza virus infection, these studies will also highlight important fundamentals of cellular processes that may be broadly applicable to other fields of research.

Influenza virus is a globally significant infectious agent with the potential to cause catastrophic pandemic outbreaks. Present treatment of influenza infections is restricted to only four anti-viral drugs, but there are increasing global reports of anti-viral resistance in several seasonal strains and also the 2009 pandemic swine-origin influenza virus H1N1. Possible future pandemic outbreaks, emerging new strains and drug resistance underscore the need to understand this complex virus and its pathogenicity with the goal that novel targets can be uncovered for future therapeutic development. Extensive lung tissue damage during influenza virus infection is proposed to contribute to the development of aberrant host immune responses. Strong evidence now demonstrates the significance of the cellular death pathway in promoting efficient influenza virus replication and disease progression. Viruses rely heavily on the machinery of their host for productive replication, which is also an Achilles’ heel that could be targeted for treatment. In pursuit of unraveling the complex nature of influenza virus replication, I carried out a global shRNA screen to identify specific host factors and signaling pathways that are involved in influenza-induced cell death and replication. In this study I identified 138 genes required for influenza viruses to induce infected host cell death. These genes were found to be involved in Protein Kinase A, NF-kB and PI3K signaling cascades. These signaling pathways are well known regulators of cell death and survival, which suggests influenza viruses may carefully regulate these pathways to reach a balance that suit their requirements for efficient proliferation, eventually at the cost of the host cell. I chose five candidate genes—BAD, MxB, TNFSF12-13,TNFSF13, and USP47—that were associated with apoptosis and the major signaling pathways determined in my network analysis to further verify the genome-wide screen as well as elucidate the role of these potentially novel host factors in influenza virus replication. I show in my study that influenza virus-induced cytopathology and cell death are considerably inhibited in BAD knockdown cells and both virus replication and viral protein production also are dramatically reduced. I also report here that MxB depletion protected cells from virus-mediated cytopathology and resulted in significant inhibition of influenza virus replication for H1N1 and H3N2 subtypes. Additionally, I report that TNFSF12-13, TFNSF13, and USP47, similarly, are required for efficient influenza virus replication and induction of cell death. Depletion of these proteins resulted in significant inhibition of viral propagation and conferred protection of host cells to virus killing. Overall, my study has provided a list of novel host factors that play significant roles during influenza virus infection. Further studies on these potential genes and their encoded protein products may uncover possible new targets for drug development for future therapeutic treatment. In addition to providing greater understanding of influenza virus infection, these studies will also highlight important fundamentals of cellular processes that may be broadly applicable to other fields of research.

No description available.

No description available.

Parkinson’s disease (PD) is a progressive neurodegenerative movement disorder characterized by the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta. The mechanism by which these DA neurons die is still unclear and under investigation. Although mostly idiopathic, about 10% of PD cases have shown familial inheritance. Mutations in leucine-rich repeat kinase 2 (LRRK2), a large multi-domain protein with unknown physiological and pathological roles, have been linked to PD cases of autosomal dominant inheritance. A PD Drosophilamelanogaster model over expressing the human LRRK2(I2020T) kinase mutant using the GAL4/UAS system has shown a loss of DA neurons and locomotor deficiency. Additionally, ectopic overexpression of human LRRK2 in the eye caused a damaged eye phenotype characterized by roughness of the surface, loss of pigmentation and presence of black lesions (Venderova Ket. al., 2009). The presence of this identifiable eye phenotype has allowed us to perform a suppressor/enhancer screen to identify possible genetic interactors of LRRK2. The LRRK2(I2020T) transgenic flies were crossed with genomic deficiency lines and the eye phenotype screened for either suppression or enhancement. Twenty-two genes, which are implicated in a variety of biological processes, have been identified thus far. Fourteen of these 22 interacting genes were assessed in the DA neurons of the D.melanogaster model. This functional screen is a rapid method to provide us with potential genetic interactions between LRRK2 and other genes, which will in turn, aid in elucidating the functional role of LRRK2 in PD pathology.

Due to rising energy prices as well as supply and ecological concerns, there is a strong interest in reducing the energy used in buildings. As such, it is desirable to model the operation of a building and predict its future energy use. In predicting the energy use of a building, the heat gain/loss through windows is an important factor. In order to accurately model this heat gain/loss, the convective heat transfer coefficient of any insect screens mounted adjacent to the windows needs to be known. This thesis describes an investigation into the heat transfer from insect screens mounted towards the indoor side of a window. The convective heat transfer coefficient of an insect screen varies based on several parameters. For implementation in building energy modelling software, it is desirable to be able to predict the convective heat transfer coefficient for an arbitrary insect screen. Due to the number of variables and the large dynamic range of the details required for modelling, direct simulation of a range of whole insect screens was not completed. Instead, a range of numerical models representing small sections of an insect screen were created. By comparing results from these to available correlations for simpler geometries, such as cylinders and flat plates, estimates for the heat transfer coefficient of a screen can be obtained. The results were non-dimensionalized for analysis and different methodologies for the prediction of heat transfer from an indoor window insect screen are described.

No description available.