136 research outputs found

    A user profiling component with the aid of user ontologies

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    Abstract: What follows is a contribution to the field of user modeling for adaptive teaching and learning programs especially in the medical field. The paper outlines existing approaches to the problem of extracting user information in a form that can be exploited by adaptive software. We focus initially on the so-called stereotyping method, which allocates users into classes adaptively, reflecting characteristics such as physical data, social background, and computer experience. The user classifications of the stereotyping method are however ad hoc and unprincipled, and they can be exploited by the adaptive system only after a large number of trials by various kinds of users. We argue that the remedy is to create a database of user ontologies from which readymade taxonomies can be derived in such a way as to enable associated software to support a variety of different types of users

    Proinflammatory adipocytokines induce TIMP-1 expression in 3T3-L1 adipocytes

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    AbstractTissue inhibitor of metalloproteinase (TIMP)-1 is an adipocyte-secreted protein upregulated in obesity which promotes adipose tissue development. Furthermore, the proinflammatory adipocytokines tumor necrosis factor α (TNFα) and interleukin (IL)-6 induce insulin resistance, and plasma concentrations are increased during weight gain. In the current study, the impact of TNFα and IL-6 on TIMP-1 mRNA and protein expression was determined in 3T3-L1 adipocytes. Interestingly, TNFα and IL-6 induced TIMP-1 protein secretion more than 3- and 2-fold, respectively. Furthermore, TIMP-1 mRNA was upregulated in a time- and dose-dependent fashion. Inhibitor experiments suggested that nuclear factor κB and p44/42 mitogen-activated protein kinase are involved in both, basal and adipocytokine-induced TIMP-1 expression. Moreover, the thiazolidinedione troglitazone partly reversed TNFα- but not IL-6-induced TIMP-1 synthesis. Taken together, we demonstrate that TIMP-1 expression is selectively upregulated in fat cells by proinflammatory adipocytokines and might play a role in maintaining adipose tissue mass in obesity

    concept paper

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    In this concept paper, we outline our working plan for the next phase of the Corporate Semantic Web project. The plan covers the period from March 2009 to March 2010. Corporate ontology engineering will improve the facilitation of agile ontology engineering to lessen the costs of ontology development and, especially, maintenance. Corporate semantic collaboration focuses the human- centered aspects of knowledge management in corporate contexts. Corporate semantic search is settled on the highest application level of the three research areas and at that point it is a representative for applications working on and with the appropriately represented and delivered background knowledge. Each of these pillars will yield innovative methods and tools during the project runtime until 2013. We propose a concept draft and a working plan covering the next twelve months for an integrative architecture of a Corporate Semantic Web provided by these three core pillars

    prototypical implementations ; working packages in project phase II

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    In this technical report, we present the concepts and first prototypical imple- mentations of innovative tools and methods for personalized and contextualized (multimedia) search, collaborative ontology evolution, ontology evaluation and cost models, and dynamic access and trends in distributed (semantic) knowledge. The concepts and prototypes are based on the state of art analysis and identified requirements in the CSW report IV

    state of the art analysis ; working packages in project phase II

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    In this report, we introduce our goals and present our requirement analysis for the second phase of the Corporate Semantic Web project. Corporate ontology engineering will improve the facilitation of agile ontology engineering to lessen the costs of ontology development and, especially, maintenance. Corporate semantic collaboration focuses the human-centered aspects of knowledge management in corporate contexts. Corporate semantic search is settled on the highest application level of the three research areas and at that point it is a representative for applications working on and with the appropriately represented and delivered background knowledge

    prototypical implementations

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    In this technical report, we present prototypical implementations of innovative tools and methods developed according to the working plan outlined in Technical Report TR-B-09-05 [23]. We present an ontology modularization and integration framework and the SVoNt server, the server-side end of an SVN- based versioning system for ontologies in the Corporate Ontology Engineering pillar. For the Corporate Semantic Collaboration pillar, we present the prototypical implementation of a light-weight ontology editor for non-experts and an ontology based expert finder system. For the Corporate Semantic Search pillar, we present a prototype for algorithmic extraction of relations in folksonomies, a tool for trend detection using a semantic analyzer, a tool for automatic classification of web documents using Hidden Markov models, a personalized semantic recommender for multimedia content, and a semantic search assistant developed in co-operation with the Museumsportal Berlin. The prototypes complete the next milestone on the path to an integral Cor- porate Semantic Web architecture based on the three pillars Corporate Ontol- ogy Engineering, Corporate Semantic Collaboration, and Corporate Semantic Search, as envisioned in [23]

    Recurrent EZH1 mutations are a second hit in autonomous thyroid adenomas

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    Autonomous thyroid adenomas (ATAs) are a frequent cause of hyperthyroidism. Mutations in the genes encoding the TSH receptor (TSHR) or the Gs protein alpha subunit (GNAS) are found in approximately 70% of ATAs. The involvement of other genes and the pathogenesis of the remaining cases are presently unknown. Here, we performed whole-exome sequencing in 19 ATAs that were paired with normal DNA samples and identified a recurrent hot-spot mutation (c.1712A>G; p.Gln571Arg) in the enhancer of zeste homolog 1 (EZH1) gene, which codes for a catalytic subunit of the polycomb complex. Targeted screening in an independent cohort confirmed that this mutation occurs with high frequency (27%) in ATAs. EZH1 mutations were strongly associated with known (TSHR, GNAS) or presumed (adenylate cyclase 9 [ADCY9]) alterations in cAMP pathway genes. Furthermore, functional studies revealed that the p.Gln571Arg EZH1 mutation caused increased histone H3 trimethylation and increased proliferation of thyroid cells. In summary, this study revealed that a hot-spot mutation in EZH1 is the second most frequent genetic alteration in ATAs. The association between EZH1 and TSHR mutations suggests a 2-hit model for the pathogenesis of these tumors, whereby constitutive activation of the cAMP pathway and EZH1 mutations cooperate to induce the hyperproliferation of thyroid cells.IZKF Wurzburg [B-281]; ERA-NET E-Rare [01GM1407B]; Deutsche KrebshilfeDeutsche Krebshilfe [109994]; Wilhelm Sander Stiftung [2013.010.1]We wish to thank Eileen Bosenberg, Bianca Klupfel, and Ines Elsner for technical support and Ulrike Zabel for DNA cloning. This study was partially supported by grants from the IZKF Wurzburg (B-281, to DC and MF); the ERA-NET E-Rare (01GM1407B, to MF and DC); the Deutsche Krebshilfe (109994, to ME); and the Wilhelm Sander Stiftung (project 2013.010.1, to RP)

    Principles and Determinants of G-Protein Coupling by the Rhodopsin-Like Thyrotropin Receptor

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    In this study we wanted to gain insights into selectivity mechanisms between G-protein-coupled receptors (GPCR) and different subtypes of G-proteins. The thyrotropin receptor (TSHR) binds G-proteins promiscuously and activates both Gs (cAMP) and Gq (IP). Our goal was to dissect selectivity patterns for both pathways in the intracellular region of this receptor. We were particularly interested in the participation of poorly investigated receptor parts
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