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  • Proceedings of the National Academy of Sciences  (5)
  • 2005-2009  (5)
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  • Proceedings of the National Academy of Sciences  (5)
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  • 2005-2009  (5)
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Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Toll-like receptor 3 ligand attenuates LPS-induced liver injury by down-regulation of toll-like receptor 4 expression on macrophages
    Proceedings of the National Academy of Sciences ; 2005
    In:  Proceedings of the National Academy of Sciences Vol. 102, No. 47 ( 2005-11-22), p. 17077-17082
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 102, No. 47 ( 2005-11-22), p. 17077-17082
    Abstract: This study demonstrates that pretreatment with polyinosinic-polycytidylic acid (poly I:C) significantly decreased the mortality and liver injury caused by injection of lipopolysaccharide (LPS) in the presence of d -galactosamine ( d -GalN) in C57BL/6 mice. Depletion of natural killer, natural killer T, and T cells did not change the protective effect of poly I:C on LPS/ d -GalN-induced liver injury in vivo . However, depletion of macrophages abolished LPS/ d -GalN-induced fulminant hepatitis, which could be restored by adoptive transfer of macrophages but not by transfer of poly I:C-treated macrophages. Treatment with poly I:C down-regulated the expression of the toll-like receptor 4 (TLR4) on macrophages and reduced the sensitivity of macrophages (Kupffer cells and peritoneal macrophages from C57BL/6 mice, or RAW264.7 cells) to LPS stimulation. Poly I:C pretreatment also impaired the signaling of mitogen-activated protein kinases and NF-κB induced by LPS in RAW264.7 cells. Blockade of TLR3 with a TLR3 antibody abolished poly I:C down-regulation of TLR4 expression and LPS stimulation of TNF-α production in RAW264.7 cells. Taken together, our findings suggest that activation of TLR3 by its ligand, poly I:C, induced LPS tolerance by down-regulation of TLR4 expression on macrophages.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0504570102
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2005
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    HF( v′ = 3) forward scattering in the F + H 2 reaction: Shape resonance and slow-down mechanism
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 17 ( 2008-04-29), p. 6227-6231
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 17 ( 2008-04-29), p. 6227-6231
    Abstract: Crossed molecular beam experiments and accurate quantum dynamics calculations have been carried out to address the long standing and intriguing issue of the forward scattering observed in the F + H 2 → HF( v′ = 3) + H reaction. Our study reveals that forward scattering in the reaction channel is not caused by Feshbach or dynamical resonances as in the F + H 2 → HF( v′ = 2) + H reaction. It is caused predominantly by the slow-down mechanism over the centrifugal barrier in the exit channel, with some small contribution from the shape resonance mechanism in a very small collision energy regime slightly above the HF( v′ = 3) threshold. Our analysis also shows that forward scattering caused by dynamical resonances can very likely be accompanied by forward scattering in a different product vibrational state caused by a slow-down mechanism.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0710840105
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Probing the resonance potential in the F atom reaction with hydrogen deuteride with spectroscopic accuracy
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 35 ( 2008-09-02), p. 12662-12666
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 35 ( 2008-09-02), p. 12662-12666
    Abstract: Reaction resonances are transiently trapped quantum states along the reaction coordinate in the transition state region of a chemical reaction that could have profound effects on the dynamics of the reaction. Obtaining an accurate reaction potential that holds these reaction resonance states and eventually modeling quantitatively the reaction resonance dynamics is still a great challenge. Up to now, the only viable way to obtain a resonance potential is through high-level ab initio calculations. Through highly accurate crossed-beam reactive scattering studies on isotope-substituted reactions, the accuracy of the resonance potential could be rigorously tested. Here we report a combined experimental and theoretical study on the resonance-mediated F + HD → HF + D reaction at the full quantum state resolved level, to probe the resonance potential in this benchmark system. The experimental result shows that isotope substitution has a dramatic effect on the resonance picture of this important system. Theoretical analyses suggest that the full-dimensional FH 2 ground potential surface, which was believed to be accurate in describing the resonance picture of the F + H 2 reaction, is found to be insufficiently accurate in predicting quantitatively the resonance picture for the F + HD → HF + D reaction. We constructed a global potential energy surface by using the CCSD(T) method that could predict the correct resonance peak positions as well as the dynamics for both F + H 2 → HF + H and F + HD → HF + D, providing an accurate resonance potential for this benchmark system with spectroscopic accuracy.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0709974105
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Control of petal shape and floral zygomorphy in Lotus japonicus
    Proceedings of the National Academy of Sciences ; 2006
    In:  Proceedings of the National Academy of Sciences Vol. 103, No. 13 ( 2006-03-28), p. 4970-4975
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 103, No. 13 ( 2006-03-28), p. 4970-4975
    Abstract: Zygomorphic flowers, with bilateral (dorsoventral) symmetry, are considered to have evolved several times independently in flowering plants. In Antirrhinum majus , floral dorsoventral symmetry depends on the activity of two TCP-box genes, CYCLOIDEA ( CYC ) and DICHOTOMA ( DICH ). To examine whether the same molecular mechanism of floral asymmetry operates in the distantly related Rosid clade of eudicots, in which asymmetric flowers are thought to have evolved independently, we investigated the function of a CYC homologue LjCYC2 in a papilionoid legume, Lotus japonicus . We showed a role for LjCYC2 in establishing dorsal identity by altering its expression in transgenic plants and analyzing its mutant allele squared standard 1 ( squ1 ). Furthermore, we identified a lateralizing factor, Keeled wings in Lotus 1 ( Kew1 ), which plays a key role in the control of lateral petal identity, and found LjCYC2 interacted with Kew1 , resulting in a double mutant that bore all petals with ventralized identity to some extents. Thus, we demonstrate that CYC homologues have been independently recruited as determinants of petal identities along the dorsoventral axis in two distant lineages of flowering plants, suggesting a common molecular origin for the mechanisms controlling floral zygomorphy.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0600681103
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2006
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
  • 5
    Online Resource
    Online Resource
    NKG2D recognition mediates Toll-like receptor 3 signaling-induced breakdown of epithelial homeostasis in the small intestines of mice
    Proceedings of the National Academy of Sciences ; 2007
    In:  Proceedings of the National Academy of Sciences Vol. 104, No. 18 ( 2007-05), p. 7512-7515
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 104, No. 18 ( 2007-05), p. 7512-7515
    Abstract: Toll-like receptors (TLRs) and NK receptors are the two most important receptor families in innate immunity. Although it has been observed that TLR signaling can induce or up-regulate the expression of the ligands for stimulatory NK receptors on monocytes or muscle cells, there is not yet a report indicating whether TLR signaling can break down self-tolerance through NK receptors. The present work reports that TLR3 signaling by polyinosinic–polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8αα intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. The blockade of interaction between NKG2D and Rae1 inhibits the cytotoxicity of intraepithelial lymphocytes against IECs in a cell–cell contact-dependent manner and therefore alleviates polyinosinic–polycytidylic acid-induced epithelial destruction and acute mucosal injury of small intestine. These results demonstrate that TLR signaling induces tissue injury through the NKG2D pathway, suggesting that TLR signaling may break down self-tolerance through induction of abnormal expression of ligands for stimulatory NK receptors.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0700822104
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2007
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
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