731 research outputs found

    Prekarität als kollektive Herausforderung im Haushaltskontext

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    Zu Formen und Folgen prekärer Beschäftigung liegen umfangreiche sozialwissenschaftliche Kenntnisse vor. Sehr viel weniger wissen wir hingegen über die sozialen Kontexte, die das Gefährdungs- und Ausgrenzungspotential unsicherer Erwerbsbeteiligung entscheidend bestimmen. Insbesondere der Haushalt als Lebenszusammenhang und Wirtschaftsgemeinschaft bedarf diesbezüglich deutlich stärkerer soziologischer Aufmerksamkeit. Deshalb stehen Bewältigungsstrategien von Haushalten, die mit prekären Beschäftigungswirklichkeiten konfrontiert sind, und die Frage, inwieweit unsichere Beschäftigungsformen prekäre Muster der Haushalts- und Lebensführung hervorbringen, im Mittelpunkt eines DFG-Forschungsprojekts am Soziologischen Forschungsinstitut (SOFI) Göttingen. Zentrale Fragen des Projekts lauten: Bildet der Haushalt eine Kraftquelle, um prekäre Arbeits- und Lebenssituationen bewältigen zu können oder wirkt er eher als Prekaritätsbeschleuniger? Welche Rolle spielen zudem Unterstützungsformen von außen (z.B. soziale Nahbeziehungen, öffentliche Infrastrukturangebote, staatliche Transferleistungen)? Kommt es aufgrund der Veränderung der Lebensformen und Haushaltsstrukturen zu einem Bedeutungsgewinn familiärer Bindungen oder sozialer Netzwerke bei der Bewältigung prekärer sozialer Lagen? Um diese Fragen beantworten zu können, werden im Projekt unterschiedliche Haushaltskonstellationen, die von unsicheren Beschäftigungsformen getragen werden, mittels biografisch-narrativer Haushaltsinterviews untersucht. Der Schwerpunkt wird damit von Individualbiografien auf Haushalte, auf deren gemeinsame Geschichte sowie auf deren Lebensführungsmuster und Bewältigungsstrategien verschoben. Das Projekt erweitert damit den Blick auf die sozialen Folgen prekärer Beschäftigung: Prekarität wird nicht mehr als individuelles Problem betrachtet, sondern als eine kollektive Herausforderung im Haushaltskontext

    Transmission of a Protease-Secreting Bacterial Symbiont Among Pea Aphids via Host Plants

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    Aphids are economically important pest insects that damage plants by phloem feeding and the transmission of plant viruses. Their ability to feed exclusively on nutritionally poor phloem sap is dependent on the obligatory symbiotic bacterium Buchnera aphidicola, but additional facultative symbionts may also be present, a common example of which is Serratia symbiotica. Many Serratia species secrete extracellular enzymes, so we hypothesised that S. symbiotica may produce proteases that help aphids to feed on plants. Molecular analysis, including fluorescence in situ hybridization (FISH), revealed that S. symbiotica colonises the gut, salivary glands and mouthparts (including the stylet) of the pea aphid Acyrthosiphon pisum, providing a mechanism to transfer the symbiont into host plants. S. symbiotica was also detected in plant tissues wounded by the penetrating stylet and was transferred to naïve aphids feeding on plants containing this symbiont. The maintenance of S. symbiotica by repeated transmission via plants may explain the high frequency of this symbiont in aphid populations. Proteomic analysis of the supernatant from a related but cultivable S. symbiotica strain cultured in liquid medium revealed the presence of known and novel proteases including metalloproteases. The corresponding transcripts encoding these S. symbiotica enzymes were detected in A. pisum and in plants carrying the symbiont, although the mRNA was much more abundant in the aphids. Our data suggest that enzymes from S. symbiotica may facilitate the digestion of plant proteins, thereby helping to suppress plant defense, and that the symbionts are important mediators of aphid–plant interactions

    Development of Mast Cell and Eosinophil Hyperplasia and HLH/MAS-Like Disease in NSG-SGM3 Mice Receiving Human CD34+ Hematopoietic Stem Cells or Patient-Derived Leukemia Xenografts.

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    Immunocompromised mouse strains expressing human transgenes are being increasingly used in biomedical research. The genetic modifications in these mice cause various cellular responses, resulting in histologic features unique to each strain. The NSG-SGM3 mouse strain is similar to the commonly used NSG (NOD scid gamma) strain but expresses human transgenes encoding stem cell factor (also known as KIT ligand), granulocyte-macrophage colony-stimulating factor, and interleukin 3. This report describes 3 histopathologic features seen in these mice when they are unmanipulated or after transplantation with human CD34+ hematopoietic stem cells (HSCs), virally transduced hCD34+ HSCs, or a leukemia patient-derived xenograft. The first feature is mast cell hyperplasia: unmanipulated, naĂŻve mice develop periductular pancreatic aggregates of murine mast cells, whereas mice given the aforementioned human cells develop a proliferative infiltrative interstitial pancreatic mast cell hyperplasia but with human mast cells. The second feature is the predisposition of NSG-SGM3 mice given these human cells to develop eosinophil hyperplasia. The third feature, secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome (HLH/MAS)-like disease, is the most pronounced in both its clinical and histopathologic presentations. As part of this disease, a small number of mice also have histiocytic infiltration of the brain and spinal cord with subsequent neurologic or vestibular signs. The presence of any of these features can confound accurate histopathologic interpretation; therefore, it is important to recognize them as strain characteristics and to differentiate them from what may be experimentally induced in the model being studied

    Hexapod Assassins’ Potion: Venom Composition and Bioactivity from the Eurasian Assassin Bug Rhynocoris iracundus

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    Assassin bug venoms are potent and exert diverse biological functions, making them potential biomedical goldmines. Besides feeding functions on arthropods, assassin bugs also use their venom for defense purposes causing localized and systemic reactions in vertebrates. However, assassin bug venoms remain poorly characterized. We collected the venom from the assassin bug Rhynocoris iracundus and investigated its composition and bioactivity in vitro and in vivo. It caused lysis of murine neuroblastoma, hepatoma cells, and healthy murine myoblasts. We demonstrated, for the first time, that assassin bug venom induces neurolysis and suggest that it counteracts paralysis locally via the destruction of neural networks, contributing to tissue digestion. Furthermore, the venom caused paralysis and melanization of Galleria mellonella larvae and pupae, whilst also possessing specific antibacterial activity against Escherichia coli, but not Listeria grayi and Pseudomonas aeruginosa. A combinatorial proteo-transcriptomic approach was performed to identify potential toxins responsible for the observed effects. We identified neurotoxic Ptu1, an inhibitory cystin knot (ICK) toxin homologous to ω-conotoxins from cone snails, cytolytic redulysins homologous to trialysins from hematophagous kissing bugs, and pore-forming hemolysins. Additionally, chitinases and kininogens were found and may be responsible for insecticidal and cytolytic activities. We demonstrate the multifunctionality and complexity of assassin bug venom, which renders its molecular components interesting for potential biomedical applications

    Exuberant fibroblast activity compromises lung function via ADAMTS4

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    © 2020, The Author(s), under exclusive licence to Springer Nature Limited. Severe respiratory infections can result in acute respiratory distress syndrome (ARDS)1. There are no effective pharmacological therapies that have been shown to improve outcomes for patients with ARDS. Although the host inflammatory response limits spread of and eventually clears the pathogen, immunopathology is a major contributor to tissue damage and ARDS1,2. Here we demonstrate that respiratory viral infection induces distinct fibroblast activation states, which we term extracellular matrix (ECM)-synthesizing, damage-responsive and interferon-responsive states. We provide evidence that excess activity of damage-responsive lung fibroblasts drives lethal immunopathology during severe influenza virus infection. By producing ECM-remodelling enzymes—in particular the ECM protease ADAMTS4—and inflammatory cytokines, damage-responsive fibroblasts modify the lung microenvironment to promote robust immune cell infiltration at the expense of lung function. In three cohorts of human participants, the levels of ADAMTS4 in the lower respiratory tract were associated with the severity of infection with seasonal or avian influenza virus. A therapeutic agent that targets the ECM protease activity of damage-responsive lung fibroblasts could provide a promising approach to preserving lung function and improving clinical outcomes following severe respiratory infections

    HMDB: the Human Metabolome Database

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    The Human Metabolome Database (HMDB) is currently the most complete and comprehensive curated collection of human metabolite and human metabolism data in the world. It contains records for more than 2180 endogenous metabolites with information gathered from thousands of books, journal articles and electronic databases. In addition to its comprehensive literature-derived data, the HMDB also contains an extensive collection of experimental metabolite concentration data compiled from hundreds of mass spectra (MS) and Nuclear Magnetic resonance (NMR) metabolomic analyses performed on urine, blood and cerebrospinal fluid samples. This is further supplemented with thousands of NMR and MS spectra collected on purified, reference metabolites. Each metabolite entry in the HMDB contains an average of 90 separate data fields including a comprehensive compound description, names and synonyms, structural information, physico-chemical data, reference NMR and MS spectra, biofluid concentrations, disease associations, pathway information, enzyme data, gene sequence data, SNP and mutation data as well as extensive links to images, references and other public databases. Extensive searching, relational querying and data browsing tools are also provided. The HMDB is designed to address the broad needs of biochemists, clinical chemists, physicians, medical geneticists, nutritionists and members of the metabolomics community. The HMDB is available at
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