57 research outputs found

    Eine gute Wahl: Wissenschaftliche Arbeiten mit LaTeX verfassen

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    In diesem Artikel wird das Textverarbeitungsprogramm LaTeX im Hinblick auf das Verfassen wissenschaftlicher Arbeiten besprochen. Dabei werden die Vorteile von LaTeX im Vergleich zu klassischen Textverarbeitungsprogrammen aufgezeigt sowie Software-Empfehlungen gegeben

    Low nadir CD4+ T-cell counts predict gut dysbiosis in HIV-1 infection

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    Human immunodeficiency virus (HIV)-1 infection causes severe gut and systemic immune damage, but its effects on the gut microbiome remain unclear. Previous shotgun metagenomic studies in HIV-negative subjects linked low-microbial gene counts (LGC) to gut dysbiosis in diseases featuring intestinal inflammation. Using a similar approach in 156 subjects with different HIV-1 phenotypes, we found a strong, independent, dose-effect association between nadir CD4+ T-cell counts and LGC. As in other diseases involving intestinal inflammation, the gut microbiomes of subjects with LGC were enriched in gram-negative Bacteroides, acetogenic bacteria and Proteobacteria, which are able to metabolize reactive oxygen and nitrogen species; and were depleted in oxygen-sensitive methanogenic archaea and sulfate-reducing bacteria. Interestingly, subjects with LGC also showed increased butyrate levels in direct fecal measurements, consistent with enrichment in Roseburia intestinalis despite reductions in other butyrate producers. The microbiomes of subjects with LGC were also enriched in bacterial virulence factors, as well as in genes associated with beta-lactam, lincosamide, tetracycline, and macrolide resistance. Thus, low nadir CD4+ T-cell counts, rather than HIV-1 serostatus per se, predict the presence of gut dysbiosis in HIV-1 infected subjects. Such dysbiosis does not display obvious HIV-specific features; instead, it shares many similarities with other diseases featuring gut inflammation.Fundació Glòria SolerFundació Catalunya-La PedreraGala SIDA 2015-2016Nit per la Recerca a la Catalunya Central 2015 editionPeople in Red-Barcelona 2016 editionRED de SIDA RD16/0025/0041ISCIIIEuropean Regional Develpment Fund (ERDF)Agencia de Gestio d´Ajuts Universitaris i de Recerca (AGAUR)Secretaria d´Universitats i Recerca del Departament d´Economia i Coneixement de la Generalitat de CatalunyaMinisterio de Economia y Competitividad. EspañaUniversidad de Whashingto

    Low nadir CD4+ T-cell counts predict gut dysbiosis in HIV-1 infection

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    Human immunodeficiency virus (HIV)-1 infection causes severe gut and systemic immune damage, but its effects on the gut microbiome remain unclear. Previous shotgun metagenomic studies in HIV-negative subjects linked low-microbial gene counts (LGC) to gut dysbiosis in diseases featuring intestinal inflammation. Using a similar approach in 156 subjects with different HIV-1 phenotypes, we found a strong, independent, dose-effect association between nadir CD4+ T-cell counts and LGC. As in other diseases involving intestinal inflammation, the gut microbiomes of subjects with LGC were enriched in gram-negative Bacteroides, acetogenic bacteria and Proteobacteria, which are able to metabolize reactive oxygen and nitrogen species; and were depleted in oxygen-sensitive methanogenic archaea and sulfate-reducing bacteria. Interestingly, subjects with LGC also showed increased butyrate levels in direct fecal measurements, consistent with enrichment in Roseburia intestinalis despite reductions in other butyrate producers. The microbiomes of subjects with LGC were also enriched in bacterial virulence factors, as well as in genes associated with beta-lactam, lincosamide, tetracycline, and macrolide resistance. Thus, low nadir CD4+ T-cell counts, rather than HIV-1 serostatus per se, predict the presence of gut dysbiosis in HIV-1 infected subjects. Such dysbiosis does not display obvious HIV-specific features; instead, it shares many similarities with other diseases featuring gut inflammation

    Speech Communication

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    Contains reports on five research projects.C.J. Lebel FellowshipNational Institutes of Health (Grant 5 T32 NS07040)National Institutes of Health (Grant 5 R01 NS04332)National Science Foundation (Grant 1ST 80-17599)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0254)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0341)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0290

    Speech Communication

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    Contains table of contents for Part IV, table of contents for Section 1 and reports on five research projects.Apple Computer, Inc.C.J. Lebel FellowshipNational Institutes of Health (Grant T32-NS07040)National Institutes of Health (Grant R01-NS04332)National Institutes of Health (Grant R01-NS21183)National Institutes of Health (Grant P01-NS23734)U.S. Navy / Naval Electronic Systems Command (Contract N00039-85-C-0254)U.S. Navy - Office of Naval Research (Contract N00014-82-K-0727

    Speech Communication

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    Contains reports on five research projects.C.J. Lebel FellowshipNational Institutes of Health (Grant 5 T32 NSO7040)National Institutes of Health (Grant 5 R01 NS04332)National Institutes of Health (Grant 5 R01 NS21183)National Institutes of Health (Grant 5 P01 NS13126)National Institutes of Health (Grant 1 PO1-NS23734)National Science Foundation (Grant BNS 8418733)U.S. Navy - Naval Electronic Systems Command (Contract N00039-85-C-0254)U.S. Navy - Naval Electronic Systems Command (Contract N00039-85-C-0341)U.S. Navy - Naval Electronic Systems Command (Contract N00039-85-C-0290)National Institutes of Health (Grant RO1-NS21183), subcontract with Boston UniversityNational Institutes of Health (Grant 1 PO1-NS23734), subcontract with the Massachusetts Eye and Ear Infirmar

    SCOPE

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    One of the objectives of the Open Access movement is to establish institutional repositories at universities and other research institutions in order to support selfarchiving. While a lot of software solutions have already been presented in recent years they lack a seamless integration of authoring tools, support for authors, and other technical publishing tools. This paper presents SCOPE (Servic e Core for open Publishing Environments) – an integrated publishing platform which facilita tes distributed electronic publishing on a central repository. This platform targets to extend the services provided by the edoc server of Humboldt University (http://edoc.hu-berlin.de/), and to support both, editors and authors during the creation phase of scholarly publications. Coinstantaneously, SCOPE focuses on XML based publishing technologies – especially on XML as the basic document format. To represent the basis of publishing processes, so called publication components (authoring tools, document models, conversion and transformation tools, styles, etc.) have been defined. Being developed for a variety of different publication series, these atomic modules, their versions, properties, and interdependencies are managed by a component management system. This syste m rests upon a formal application model and enables abstract specifica tions of the technological parts of publishing processes. Based upon this management system the second layer of SCOPE comes into function. It allows editors to access the repository and to manage their publication series. In order to model and control both, the organisational and the technical parts of complex publishing processes, a general sta te machine is applied with the help of which workflows can be defined and monitored conveniently. It enables the combination of automatically processed actions (e.g. conversion processes) and user driven activities (e.g. metadata management). The SCOPE architecture is currently used by research institutes both, inside and outside the university.Peer Reviewe
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