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  • Blackwell Publishing Ltd  (3)
  • American Physical Society (APS)  (1)
  • The American Association of Immunologists (AAI)  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Genotypic variation for resistance to Septoria nodorum in triticale (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Plant breeding 119 (2000), S. 0 
    Details
    ISSN: 1439-0523
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: Septoria nodorum leaf and glume blotch is an important disease of triticale (×_Triticosecale Wittm.) and can cause severe losses of grain yield in some regions. Quantitative genetic parameters for resistance were estimated for 2 years in two locations in triticale genotypes artificially inoculated with S. nodorum. The effect of infection was assessed by a visual symptom rating of flag leaves and spikes and by grain yield traits relative to an uninoculated control. The mean ratings of flag leaves and spikes, calculated from two to four ratings, were 2.6 and 3.9, respectively, with a range of six ratings for spikes and over five for flag leaves. Infection caused an 11.5% mean reduction in kernel weight per spike, which was the result of 13.2% lower 1000-kernel weight. The number of kernels per spike and 50-ml weight were little affected. For all relative grain yield traits, genotypic variation was small with high genotype-environment interaction effects and thus moderate to low heritabilities. In contrast, for visual ratings genotypic variation was high, with low interaction effects leading to high heritabilities. Phenotypic correlation between flag leaf and spike ratings was low, indicating independent disease resistance mechanisms. The best association, although still moderate, was obtained between flag leaf rating and relative 1000-kernel weight. Therefore, visual disease ratings do not satisfactorily assess the effect of Septoria infection on grain yield traits. The reduction in 1000-kernel and possibly 50-ml weight are good indicators, provided that multi-environment tests are conducted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1439-0523.2000.00519.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Doxycycline Inhibition of Cartilage Matrix Degradation (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 732 (1994), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1994.tb24770.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of CD44 isoforms in basal cell carcinomas (1996)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The expression of CD44 isoforms (CD44std, CD44v6, CD44v10) was investigated by an immuno-histochemical technique in 42 basal cell carcinomas (BCC) of the superficial and nodular variety. All BCCs studied displayed very low amounts of CD44std, a receptor for hyaluronic acid. Except for single CD44std-positive cells located preferentially in the central parts of the BCC nests, the bulk of the tumour formations were CD44std-negative. CD44v6 showed a heterogeneous distribution pattern accentuated in the peripheral palisading tumour cells. In superficial BCCs, the labelling intensity for CD44v6) increased with the size of the tumour nests. CD44v10 was not detectable in BCCsOur findings support the notion that CD44v6 is not linked to the metastatic proclivity of tumours originating from keratinocytes. We suggest that the very low expression of the receptor for hyaluronic acid (CD44std) may be one of the factors which block the formation of metastases from BCCs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.1996.32793.x
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  • 4
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    Electron Rearrangement Dynamics in Dissociating I2n+ Molecules Accessed by Extreme Ultraviolet Pump-Probe Experiments (2014)
    American Physical Society (APS)
    Details
    Publication Date: 2014-08-12
    Description: Author(s): K. Schnorr, A. Senftleben, M. Kurka, A. Rudenko, G. Schmid, T. Pfeifer, K. Meyer, M. Kübel, M. F. Kling, Y. H. Jiang, R. Treusch, S. Düsterer, B. Siemer, M. Wöstmann, H. Zacharias, R. Mitzner, T. J. M. Zouros, J. Ullrich, C. D. Schröter, and R. Moshammer The charge rearrangement in dissociating I2n+ molecules is measured as a function of the internuclear distance R using extreme ultraviolet pulses delivered by the free-electron laser in Hamburg. Within an extreme ultraviolet pump-probe scheme, the first pulse initiates dissociation by multiply ioniz... [Phys. Rev. Lett. 113, 073001] Published Mon Aug 11, 2014
    Keywords: Atomic, Molecular, and Optical Physics
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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  • 5
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    A New Immunomodulatory Role for Peroxisomes in Macrophages Activated by the TLR4 Ligand Lipopolysaccharide [INNATE IMMUNITY AND INFLAMMATION] (2017)
    The American Association of Immunologists (AAI)
    Details
    Publication Date: 2017-03-07
    Description: Peroxisomes are proposed to play an important role in the regulation of systemic inflammation; however, the functional role of these organelles in inflammatory responses of myeloid immune cells is largely unknown. In this article, we demonstrate that the nonclassical peroxisome proliferator 4-phenyl butyric acid is an efficient inducer of peroxisomes in various models of murine macrophages, such as primary alveolar and peritoneal macrophages and the macrophage cell line RAW264.7, but not in primary bone marrow–derived macrophages. Further, proliferation of peroxisomes blocked the TLR4 ligand LPS-induced proinflammatory response, as detected by the reduced induction of the proinflammatory protein cyclooxygenase (COX)-2 and the proinflammatory cytokines TNF-α, IL-6, and IL-12. In contrast, disturbing peroxisome function by knockdown of peroxisomal gene Pex14 or Mfp2 markedly increased the LPS-dependent upregulation of the proinflammatory proteins COX-2 and TNF-α. Specifically, induction of peroxisomes did not affect the upregulation of COX-2 at the mRNA level, but it reduced the half-life of COX-2 protein, which was restored by COX-2 enzyme inhibitors but not by proteasomal and lysosomal inhibitors. Liquid chromatography–tandem mass spectrometry analysis revealed that various anti-inflammatory lipid mediators (e.g., docosahexaenoic acid) were increased in the conditioned medium from peroxisome-induced macrophages, which blocked LPS-induced COX-2 upregulation in naive RAW264.7 cells and human primary peripheral blood–derived macrophages. Importantly, LPS itself induced peroxisomes that correlated with the regulation of COX-2 during the late phase of LPS activation in macrophages. In conclusion, our findings identify a previously unidentified role for peroxisomes in macrophage inflammatory responses and suggest that peroxisomes are involved in the physiological cessation of macrophage activation.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
    Published by The American Association of Immunologists (AAI)
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