233 research outputs found

    Biotoperfassung in der Tagebaufolgelandschaft des Osendorfer Sees (Halle, Saale)

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    Von den früher zahlreichen Braunkohlen-Tagebaubetrieben im Stadtgebiet von Halle (vgl. KRUMBIEGEL 1974) ist der Osendorfer See mit dem umliegenden Gelände ein wertvolles Zeugnis der Industriegeschichte. Über mehrere Jahrzehnte erfolgten nachhaltige Eingriffe mit überaus dramatischen Folgen in der Landschaft und im Naturhaushalt, die auch jetzt noch in vielen Punkten nicht zu übersehen sind (Abb. 1 u. 3). Nach dem Ende des Bergbaus und nachfolgenden Rekultivierungen sind größere Abschnitte des Geländes im Zustand des ausgelaufenen Kohleabbaus erhalten geblieben. Auf den vorerst vegetationsfreien Flächen aus überwiegend geschütteten Bodensubstraten haben sich in den folgenden Jahrzehnten zahlreich verschiedene Pflanzenarten und unterschiedliche Pflanzengesellschaften spontan angesiedelt (Abb. 2 u. 3). Dabei zeichnet sich ab, dass der bisherige Stand der Besiedlung auch in absehbarer Zeit längst noch nicht abgeschlossen sein wird. Das Gelände bietet sich damit langzeitlich für landschaftsökologische Studien an, bei denen die weitere Entwicklung und die Sukzessionen innerhalb des Grünflächen-Gürtels von Halle an einem besonders günstig gelegenen Objekt verfolgt werden können. In dem vorliegenden Beitrag soll ein Überblick über das Gelände, die bisher angesiedelten Pflanzenarten und die Pflanzengesellschaften gegeben werden. Dazu werden in Grundzügen die bisher erkennbaren Biotopstrukturen abgegrenzt und in einer Karte dargestellt (Abb. 2). Mit dieser Ersterfassung wollen wir eine Grundlage für spätere Untersuchungen legen

    Revision of the Transuranus PUREDI Model

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    The Transuranus PUREDI model calculates the plutonium redistribution across the fuel pellet due to thermal diffusion. This phenomenon is particularly significant in oxide fuels for fast breeder reactors (FBR) where temperatures and temperature gradients are extremely high. The first version of PUREDI was developed and implemented as a stand-alone model. Since plutonium redistribution due to transport can lead to significant modifications of the radial power profile, a coupling of the PUREDI model with TUBRNP (recently extended for FBRs) is needed to correctly predict the fuel temperature. To this purpose, a revision of PUREDI has been proposed and the main features will be outlined in this report.JRC.E.3-Materials researc

    Creep Simulations of Nuclear Fuel Cladding under long term Storage Conditions with TRANSURANUS

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    Within a joint research project between the Institute for Energy (IE) and the Institute for Transuranium Elements (ITU) on the integrity of spent nuclear fuel cladding the ITU code TRANSURANUS was used to simulate creep of Zircaloy cladding tubes under long term storage conditions. Since TRANSURANUS is designed to model the mechanical, thermal and physical behaviour of fuel rods during reactor operation it was the objective of this study firstly to explore the limitations of the present creep models in TRANSURANUS for the simulation of long term creep processes under dry storage conditions. If the present creep models in TRANSURANUS were found to be inappropriate then the next objective was to formulate the properties of an "ideal" creep model for dry storage. The creep models were compared with creep tests on unirradiated Zircaloy cladding tubes. It turned out that the standard creep model for Zircaloy cladding in TRANSURANUS, the model of Lassmann and Moreno, underestimated the creep strains of the tests significantly. The creep model of Mayuzumi and Onchi, which was designed to model long term creep processes under dry storage conditions, lead to reasonable agreement with the creep tests for temperatures of 350 degrees Celcius and above. It turned out that for the accurate prediction under low-temperature conditions (under 350 degrees Celcius) more sophisticated creep models, which account for a shift in creep mechanisms, are necessary.JRC.F.5-Safety of present nuclear reactor

    Li/MgO with spin sensors as catalyst for the oxidative coupling of methane

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    Co-doping of Li/MgO, a well-known catalyst for the oxidative coupling of methane, was investigated. It is demonstrated that Gd3+ and Fe3+ can be used as spin sensors in these solids to investigate the structure via EPR spectroscopy. These aliovalent ions occupy Mg2+ sites in the lattice; the expected coupling with charge-compensating neighboring Li+ was detected. A strong increase of the activity was observed. However, all samples suffered from deactivation. The solubility of Gd3+ in MgO turned out to be inhibited. No such restriction was observed for Fe3+

    Patients with colorectal cancer and brain metastasis: The relevance of extracranial metastatic patterns predicting time intervals to first occurrence of intracranial metastasis and survival

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    To investigate the predictive impact of extracranial metastatic patterns on course of disease and survival in patients with colorectal cancer (CRC) and brain metastasis (BM). A total of 228 patients (134 male [59%], 94 female [41%]) with histologically proven CRC and BM were classified into different groups according to extracranial metastatic patterns. Time intervals to metastatic events and survival times from initial CRC diagnosis, extracranial and intracranial metastasis were analyzed. Extracranial organs mostly affected were liver (102 of 228 [44.7%]) and lung (96 of 228 [42.1%]). Liver and lung metastasis were detected in 31 patients (13.6%). Calculated over the entire course of disease, patients with lung metastasis showed longer OS than patients with liver metastasis or patients without lung metastasis (43.9 vs. 34.6 [p=0.002] vs. 35.0 months [p=0.002]). From the date of initial CRC diagnosis, lung metastasis occurred later in CRC history than liver metastasis (24.3 vs. 7.5 months). Once lung metastasis was diagnosed BM occurred faster than in patients with liver metastasis (15.8 vs. 26.0 months; Δ 10.2 months). Accordingly, OS from the diagnosis of liver metastasis was longer than from lung metastasis (27.1 vs. 19.6 months [p=0.08]). Once BM was present patients with lung metastasis lived longer than patients with liver metastasis (3.8 vs. 1.1 months [p=0.028]). Shortest survival times in all survival categories analyzed revealed patients with concurrent liver and lung metastasis. Patients with CRC and BM form a heterogenous cohort where EM to liver or lung predict survival

    Connexin30.2:<i>In vitro</i> interaction with connexin36 in hela cells and expression in AII amacrine cells and intrinsically photosensitive ganglion cells in the mouse retina

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    Electrical coupling via gap junctions is an abundant phenomenon in the mammalian retina and occurs in all major cell types. Gap junction channels are assembled from different connexin subunits, and the connexin composition of the channel confers specific properties to the electrical synapse. In the mouse retina, gap junctions were demonstrated between intrinsically photosensitive ganglion cells and displaced amacrine cells but the underlying connexin remained undetermined. In the primary rod pathway, gap junctions play a crucial role, coupling AII amacrine cells among each other and to ON cone bipolar cells. Although it has long been known that connexin36 and connexin45 are necessary for the proper functioning of this most sensitive rod pathway, differences between homocellular AII/AII gap junctions and AII/ON bipolar cell gap junctions suggested the presence of an additional connexin in AII amacrine cells. Here, we used a connexin30.2-lacZ mouse line to study the expression of connexin30.2 in the retina. We show that connexin30.2 is expressed in intrinsically photosensitive ganglion cells and AII amacrine cells. Moreover, we tested whether connexin30.2 and connexin36 – both expressed in AII amacrine cells – are able to interact with each other and are deposited in the same gap junctional plaques. Using newly generated anti-connexin30.2 antibodies, we show in HeLa cells that both connexins are indeed able to interact and may form heteromeric channels: both connexins were co-immunoprecipitated from transiently transfected HeLa cells and connexin30.2 gap junction plaques became significantly larger when co-expressed with connexin36. These data suggest that connexin36 is able to form heteromeric gap junctions with another connexin. We hypothesize that co-expression of connexin30.2 and connexin36 may endow AII amacrine cells with the means to differentially regulate its electrical coupling to different synaptic partners

    The Hsc/Hsp70 Co-Chaperone Network Controls Antigen Aggregation and Presentation during Maturation of Professional Antigen Presenting Cells

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    The maturation of mouse macrophages and dendritic cells involves the transient deposition of ubiquitylated proteins in the form of dendritic cell aggresome-like induced structures (DALIS). Transient DALIS formation was used here as a paradigm to study how mammalian cells influence the formation and disassembly of protein aggregates through alterations of their proteostasis machinery. Co-chaperones that modulate the interplay of Hsc70 and Hsp70 with the ubiquitin-proteasome system (UPS) and the autophagosome-lysosome pathway emerged as key regulators of this process. The chaperone-associated ubiquitin ligase CHIP and the ubiquitin-domain protein BAG-1 are essential for DALIS formation in mouse macrophages and bone-marrow derived dendritic cells (BMDCs). CHIP also cooperates with BAG-3 and the autophagic ubiquitin adaptor p62 in the clearance of DALIS through chaperone-assisted selective autophagy (CASA). On the other hand, the co-chaperone HspBP1 inhibits the activity of CHIP and thereby attenuates antigen sequestration. Through a modulation of DALIS formation CHIP, BAG-1 and HspBP1 alter MHC class I mediated antigen presentation in mouse BMDCs. Our data show that the Hsc/Hsp70 co-chaperone network controls transient protein aggregation during maturation of professional antigen presenting cells and in this way regulates the immune response. Similar mechanisms may modulate the formation of aggresomes and aggresome-like induced structures (ALIS) in other mammalian cell types

    Suppression of Mcl-1 via RNA interference sensitizes human hepatocellular carcinoma cells towards apoptosis induction

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    BACKGROUND: Hepatocelluar carcinoma (HCC) is one of the most common cancers worldwide and a major cause of cancer-related mortality. HCC is highly resistant to currently available chemotherapeutic drugs. Defects in apoptosis signaling contribute to this resistance. Myeloid cell leukemia-1 (Mcl-1) is an anti-apoptotic member of the Bcl-2 protein family which interferes with mitochondrial activation. In a previous study we have shown that Mcl-1 is highly expressed in tissues of human HCC. In this study, we manipulated expression of the Mcl-1 protein in HCC cells by RNA interference and analyzed its impact on apoptosis sensitivity of HCC cells in vitro. METHODS: RNA interference was performed by transfecting siRNA to specifically knock down Mcl-1 expression in HCC cells. Mcl-1 expression was measured by quantitative real-time PCR and Western blot. Induction of apoptosis and caspase activity after treatment with chemotherapeutic drugs and different targeted therapies were measured by flow cytometry and fluorometric analysis, respectively. RESULTS: Here we demonstrate that Mcl-1 expressing HCC cell lines show low sensitivity towards treatment with a panel of chemotherapeutic drugs. However, treatment with the anthracycline derivative epirubicin resulted in comparatively high apoptosis rates in HCC cells. Inhibition of the kinase PI3K significantly increased apoptosis induction by chemotherapy. RNA interference efficiently downregulated Mcl-1 expression in HCC cells. Mcl-1 downregulation sensitized HCC cells to different chemotherapeutic agents. Sensitization was accompanied by profound activation of caspase-3 and -9. In addition, Mcl-1 downregulation also increased apoptosis rates after treatment with PI3K inhibitors and, to a lower extent, after treatment with mTOR, Raf I and VEGF/PDGF kinase inhibitors. TRAIL-induced apoptosis did not markedly respond to Mcl-1 knockdown. Additionally, knockdown of Mcl-1 efficiently enhanced apoptosis sensitivity towards combined treatment modalities: Mcl-1 knockdown significantly augmented apoptosis sensitivity of HCC cells towards chemotherapy combined with PI3K inhibition. CONCLUSION: Our data suggest that specific downregulation of Mcl-1 by RNA interference is a promising approach to sensitize HCC cells towards chemotherapy and molecularly targeted therapies
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