74 research outputs found

    Auswirkungen von Bodenperforation und Kalkung auf Bodeneigenschaften von Rückegassen in einem Buchenbestand des Sollings

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    Einhergehend mit der Befahrung des Waldes durch tonnenschwere Forstmaschinen, kann es auf Rückegassen zu erheblichen Schäden am Waldboden in Form von Strukturveränderungen kommen. Die resultierende Bodenverformung und -verdichtung bewirkt Veränderungen von Bodeneigenschaften, u.a. des Porensystems, welche sich in einer Uniformierung der Poren bei gleichzeitigem Rückgang des Porenvolumens sowie der Porenkontinuität äußern (1). Infolge der Strukturveränderungen ist es insbesondere der modifizierte Gashaushalt, der sich auf vielfältige Prozesse auswirkt und die Lebensraumfunktion des Waldbodens verringert (2). Von erheblicher Bedeutung ist die Frage nach der natürlichen Regenerationsfähigkeit verdichteter Waldböden unter Rückegassen. Seitens des RÜWOLA-Projektes wird in einem Feldversuch auf einem Lösslehmstandort im Solling (Braunerde) geprüft, ob mit dem Verfahren der Bodenperforation und der Kombination weiterer Maßnahmen wie Kalkung, eine Technik zur Verfügung steht, die es ermöglicht, regenerative Prozesse im Boden zu initiieren bzw. zu beschleunigen. Drei Jahre nach Anlage von Lochstanzungen wurden Schürfgruben quer zu den Fahrspuren gegraben, die Stanzlöcher freigelegt und mittels verschiedener Methoden die Auswirkungen auf Bodeneigenschaften geprüft. Unter Verwendung der KA 5 (3) erfolgte ein direkter Vergleich zwischen Fahrspur und Mittelstreifen sowie eine detaillierte Untersuchung der Stanzlöcher mit Hilfe eines Zählrahmens (u.a. Durchwurzelung). Des Weiteren fanden Infiltrationsversuche, Bestimmung mikrobieller Biomasse (CFE-Methode), saurer Phosphataseaktivität und physikalischer Kenngrößen (z.B. TRD, GPV) statt. Die Ergebnisse verdeutlichen, dass Unterschiede zwischen Fahrspur und Mittelstreifen insbesondere bzgl. Eigenschaften der Bodenstruktur und der Durchwurzelung gegeben sind. Kontraste bestehen ebenfalls im Vergleich der Stanzlöcher und dem umgebenden, ungestanzten Bodenareal. Die Summe der betrachteten Parameter weist auf eine mögliche Wirkung der Maßnahmenkombination „Lochstanzung + Kalkung“ hin. Bodenperforation scheint auch zu erhöhter Verdunstung und Drainage beizutragen, wohingegen die Ergebnisse der Stechzylinderproben eher als indifferent zu beurteilen sind

    MAP3K8 (TPL2/COT) Affects Obesity-Induced Adipose Tissue Inflammation without Systemic Effects in Humans and in Mice

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    Chronic low-grade inflammation in adipose tissue often accompanies obesity, leading to insulin resistance and increasing the risk for metabolic diseases. MAP3K8 (TPL2/COT) is an important signal transductor and activator of pro-inflammatory pathways that has been linked to obesity-induced adipose tissue inflammation. We used human adipose tissue biopsies to study the relationship of MAP3K8 expression with markers of obesity and expression of pro-inflammatory cytokines (IL-1ß, IL-6 and IL-8). Moreover, we evaluated obesity-induced adipose tissue inflammation and insulin resistance in mice lacking MAP3K8 and WT mice on a high-fat diet (HFD) for 16 weeks. Individuals with a BMI >30 displayed a higher mRNA expression of MAP3K8 in adipose tissue compared to individuals with a normal BMI. Additionally, high mRNA expression levels of IL-1ß, IL-6 and IL-8, but not TNF -a, in human adipose tissue were associated with higher expression of MAP3K8. Moreover, high plasma SAA and CRP did not associate with increased MAP3K8 expression in adipose tissue. Similarly, no association was found for MAP3K8 expression with plasma insulin or glucose levels. Mice lacking MAP3K8 had similar bodyweight gain as WT mice, yet displayed lower mRNA expression levels of IL-1ß, IL-6 and CXCL1 in adipose tissue in response to the HFD as compared to WT animals. However, MAP3K8 deficient mice were not protected against HFD-induced adipose tissue macrophage infiltration or the development of insulin resistance. Together, the data in both human and mouse show that MAP3K8 is involved in local adipose tissue inflammation, specifically for IL-1ß and its responsive cytokines IL-6 and IL-8, but does not seem to have systemic effects on insulin resistance

    IFI16 and cGAS cooperate in the activation of STING during DNA sensing in human keratinocytes

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    Many human cells can sense the presence of exogenous DNA during infection though the cytosolic DNA receptor cyclic GMP-AMP synthase (cGAS), which produces the second messenger cyclic GMP-AMP (cGAMP). Other putative DNA receptors have been described, but whether their functions are redundant, tissue-specific or integrated in the cGAS-cGAMP pathway is unclear. Here we show that interferon-γ inducible protein 16 (IFI16) cooperates with cGAS during DNA sensing in human keratinocytes, as both cGAS and IFI16 are required for the full activation of an innate immune response to exogenous DNA and DNA viruses. IFI16 is also required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phosphorylation and translocation. We propose that the two DNA sensors IFI16 and cGAS cooperate to prevent the spurious activation of the type I interferon response

    Function of SSA Subfamily of Hsp70 Within and Across Species Varies Widely in Complementing Saccharomyces cerevisiae Cell Growth and Prion Propagation

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    BACKGROUND:The cytosol of most eukaryotic cells contains multiple highly conserved Hsp70 orthologs that differ mainly by their spatio-temporal expression patterns. Hsp70s play essential roles in protein folding, transport or degradation, and are major players of cellular quality control processes. However, while several reports suggest that specialized functions of Hsp70 orthologs were selected through evolution, few studies addressed systematically this issue. METHODOLOGY/PRINCIPAL FINDINGS:We compared the ability of Ssa1p-Ssa4p from Saccharomyces cerevisiae and Ssa5p-Ssa8p from the evolutionary distant yeast Yarrowia lipolytica to perform Hsp70-dependent tasks when expressed as the sole Hsp70 for S. cerevisiae in vivo. We show that Hsp70 isoforms (i) supported yeast viability yet with markedly different growth rates, (ii) influenced the propagation and stability of the [PSI(+)] and [URE3] prions, but iii) did not significantly affect the proteasomal degradation rate of CFTR. Additionally, we show that individual Hsp70 orthologs did not induce the formation of different prion strains, but rather influenced the aggregation properties of Sup35 in vivo. Finally, we show that [URE3] curing by the overexpression of Ydj1p is Hsp70-isoform dependent. CONCLUSION/SIGNIFICANCE:Despite very high homology and overlapping functions, the different Hsp70 orthologs have evolved to possess distinct activities that are required to cope with different types of substrates or stress situations. Yeast prions provide a very sensitive model to uncover this functional specialization and to explore the intricate network of chaperone/co-chaperone/substrates interactions
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