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Träfflista för sökning "WFRF:(Bogdan S) srt2:(2005-2009)"

Sökning: WFRF:(Bogdan S) > (2005-2009)

  • Resultat 1-7 av 7
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1.
  • Wu, Xifeng, et al. (författare)
  • Genetic variation in the prostate stem cell antigen gene PSCA confers susceptibility to urinary bladder cancer.
  • 2009
  • Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:9, s. 991-5
  • Tidskriftsartikel (refereegranskat)abstract
    • We conducted a genome-wide association study on 969 bladder cancer cases and 957 controls from Texas. For fast-track validation, we evaluated 60 SNPs in three additional US populations and validated the top SNP in nine European populations. A missense variant (rs2294008) in the PSCA gene showed consistent association with bladder cancer in US and European populations. Combining all subjects (6,667 cases, 39,590 controls), the overall P-value was 2.14 x 10(-10) and the allelic odds ratio was 1.15 (95% confidence interval 1.10-1.20). rs2294008 alters the start codon and is predicted to cause truncation of nine amino acids from the N-terminal signal sequence of the primary PSCA translation product. In vitro reporter gene assay showed that the variant allele significantly reduced promoter activity. Resequencing of the PSCA genomic region showed that rs2294008 is the only common missense SNP in PSCA. Our data identify rs2294008 as a new bladder cancer susceptibility locus.
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2.
  • Bogdan, Cristian, et al. (författare)
  • Generating an Abstract User Interface from a Discourse Model Inspired by Human Communication
  • 2008
  • Ingår i: Proceedings of the 41st Annual Hawaii International Conference on System Sciences. ; , s. 36-46
  • Konferensbidrag (refereegranskat)abstract
    • Inspired by Human Communication Cristian Bogdan, Jürgen Falb, Hermann Kaindl, Sevan Kavaldjian, Roman Popp, Helmut Horacek, Edin Arnautovic and Alexander Szep Vienna University of Technology, Institute of Computer Technology A 1040 Vienna, Austria {bogdan, falb, kaindl, kavaldjian, popp, horacek, arnautovic, szep}@ict.tuwien.ac.at Abstract Programming user interfaces is hard, error-prone and expensive, but recent advances allow generating them from interaction design models. We present an approach for modeling interaction design that is inspired by human com- munication. Our interaction design models are discourse models, more precisely models of dialogues. They are based on theories of human communication and should, therefore, be more understandable to humans than programs imple- menting user interfaces. The main ingredients of our mod- els are communicative acts (Speech Act Theory), which are connected as adjacency pairs (Conversation Analysis) and via RST relations (Rhetorical Structure Theory). While RST provides useful means for modeling discourse in the sense of monologue, a dialogue results from connecting monologues via adjacency pairs. This paper presents a new metamodel that integrates these approaches. Based on it, we show how abstract user interfaces can be generated from such dis- course models. In a nutshell, we generate finite-state ma- chinery and employ rules devised by us to map parts of a discourse model to abstract widgets.
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4.
  • Kavaldjian, S., et al. (författare)
  • Transforming Discourse Models to Structural User Interface Models
  • 2008
  • Ingår i: Models in Software Engineering Workshops and Symposia at MoDELS 2007, Nashville, TN, USA, September 30 - October 5, 2007, Reports and Revised Selected Papers. - Berlin, Heidelberg : Springer Berlin/Heidelberg. - 9783540690696 ; , s. 77-88
  • Konferensbidrag (refereegranskat)abstract
    • User-interface design is still a time consuming and expensive task to do, but recent advances allow generating them from interaction design models. We present a model-driven approach for generating user interfaces out of interaction design models. Our interaction design models are discourse models, more precisely models of classes of dialogues. They are based on theories of human communication and should, therefore, be more understandable to humans than programs implementing user interfaces. Our discourse models also contain enough semantics to transform them automatically into user interfaces for multiple devices and modalities. This paper presents a two-step transformation approach with an intermediate user interface model. By showing specific transformation rules, we concentrate on a major part of the first step, transforming discourse models to structural user interface models.
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5.
  • Kroon, Lars, et al. (författare)
  • Bifurcation picture and stability of the gap and out-gap discrete solitons
  • 2007
  • Ingår i: Low temperature physics (Woodbury, N.Y., Print). - : AIP Publishing. - 1063-777X .- 1090-6517. ; 33:5, s. 481-483
  • Tidskriftsartikel (refereegranskat)abstract
    • The dynamics of a quaternary fragment of a discrete system of coupled nonlinear oscillators with modulated frequency parameters is investigated, and the stability of its gap and out-gap soliton-like excitations is studied.
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6.
  • Maynard, Christa J., et al. (författare)
  • Accumulation of ubiquitin conjugates in a polyglutamine disease model occurs without global ubiquitin/proteasome system impairment
  • 2009
  • Ingår i: Proceedings of the National Academy of Sciences. - : Proceedings of the National Academy of Sciences. - 1091-6490 .- 0027-8424. ; 106:33, s. 13986-13991
  • Tidskriftsartikel (refereegranskat)abstract
    • Aggregation-prone proteins have been suggested to overwhelm and impair the ubiquitin/proteasome system (UPS) in polyglutamine (polyQ) disorders, such as Huntington's disease (HD). Overexpression of an N-terminal fragment of mutant huntingtin (N-mutHtt), an aggregation-prone polyQ protein responsible for HD, obstructs the UPS in cellular models. Furthermore, based on the accumulation of polyubiquitin conjugates in brains of R6/2 mice, which express human N-mutHtt and are one of the most severe polyQ disorder models, it has been proposed that UPS dysfunction is a consistent feature of this pathology, occurring in both in vitro and in vivo models. Here, we have exploited transgenic mice that ubiquitously express a ubiquitin fusion degradation proteasome substrate to directly assess the functionality of the UPS in R6/2 mice or the slower onset R6/1 mice. Although expression of N-mutHtt caused a general inhibition of the UPS in PC12 cells, we did not observe an increase in the levels of proteasome reporter substrate in the brains of R6/2 and R6/1 mice. We show that the increase in ubiquitin conjugates in R6/2 mice can be primarily attributed to an accumulation of large ubiquitin conjugates that are different from the conjugates observed upon UPS inhibition. Together our data show that polyubiquitylated proteins accumulate in R6/2 brain despite a largely operative UPS, and suggest that neurons are able to avoid or compensate for the inhibitory effects of N-mutHtt.
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