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  • 1
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    1,4-Dibromo-2,5-di-p-toluoylbenzene (2013)
    International Union of Crystallography (IUC)
    Details
    Publication Date: 2013-08-18
    Description: In the title compound, C22H16Br2O2, which has approximate non-crystallographic inversion symmetry, the dihedral angles between the central ring and the pendant rings are 89.1 (4) and 82.4 (3)°; the dihedral angle between the pendant rings is 12.1 (4)°. In the crystal, the packing is influenced by van der Waals forces and no aromatic π–π stacking is observed.
    Electronic ISSN: 1600-5368
    Topics: Chemistry and Pharmacology , Geosciences
    Published by International Union of Crystallography (IUC)
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  • 2
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    Homogenization of anisotropic elastoplastic behaviors of a porous polycrystal with interface effects (2013)
    Wiley-Blackwell
    Details
    Publication Date: 2013-05-03
    Description: SUMMARY This paper is devoted to develop a theoretical framework to predict the macroscopic transversely isotropic elastoplastic behavior of clay-like material, which is viewed as a porous polycrystal. We consider evolutions of two local plastic mechanisms of grains and interface simultaneously, for which a Schmid criterion is used for the strength of sheet-like grains and a Tresca criterion for the strength of interfaces between particles. By adapting the standard incremental method, we propose firstly a classic self-consistent model, which does not consider the effect of interface, then a generalized self-consistent model in which the solid phase is represented by laminated (or isotropic) spherical grains surrounded by interfaces. Comparisons of numerical predictions between these two methods are performed and have demonstrated the validity of the generalized self-consistent model taking account of interface effects. Numerical simulations of uniaxial compression tests have shown that the macroscopic elastoplastic behavior of polycrystalline (clay-like) material can be successfully predicted by the way of considering the two local plastic mechanisms at microscopic scale. Copyright © 2013 John Wiley & Sons, Ltd.
    Print ISSN: 0363-9061
    Electronic ISSN: 1096-9853
    Topics: Architecture, Civil Engineering, Surveying , Geosciences
    Published by Wiley-Blackwell
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  • 3
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    Nonlinear effects of group size [Sustainability Science] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-07-03
    Description: For decades, scholars have been trying to determine whether small or large groups are more likely to cooperate for collective action and successfully manage common-pool resources. Using data gathered from the Wolong Nature Reserve since 1995, we examined the effects of group size (i.e., number of households monitoring a single...
    Keywords: Sustainability Science
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Neuroprotective Effect of CYGB in a Neonatal Rat HI Model [Gene Regulation] (2013)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publication Date: 2013-06-01
    Description: This study was designed to investigate the expression profile of CYGB, its potential neuroprotective function, and underlying molecular mechanisms using a model of neonatal hypoxia-ischemia (HI) brain injury. Cygb mRNA and protein expression were evaluated within the first 36 h after the HI model was induced using RT-PCR and Western blotting. Cygb mRNA expression was increased at 18 h in a time-dependent manner, and its level of protein expression increased progressively in 24 h. To verify the neuroprotective effect of CYGB, a gene transfection technique was employed. Cygb cDNA and shRNA delivery adenovirus systems were established (Cygb-cDNA-ADV and Cygb-shRNA-ADV, respectively) and injected into the brains of 3-day-old rats 4 days before they were induced with HI treatment. Rats from different groups were euthanized 24 h post-HI, and brain samples were harvested. 2,3,5-Triphenyltetrazolium chloride, TUNEL, and Nissl staining indicated that an up-regulation of CYGB resulted in reduced acute brain injury. The superoxide dismutase level was found to be dependent on expression of CYGB. The Morris water maze test in 28-day-old rats demonstrated that CYGB expression was associated with improvement of long term cognitive impairment. Studies also demonstrated that CYGB can up-regulate mRNA and protein levels of VEGF and increase both the density and diameter of the microvessels but inhibits activation of caspase-2 and -3. Thus, this is the first in vivo study focusing on the neuroprotective role of CYGB. The reduction of neonatal HI injury by CYGB may be due in part to antioxidant and antiapoptotic mechanisms and by promoting angiogenesis.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
    Published by The American Society for Biochemistry and Molecular Biology (ASBMB)
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  • 5
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    Human osteosarcoma CD49f−CD133+ cells: impaired in osteogenic fate while gain of tumorigenicity (2013)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2013-09-06
    Description: Human osteosarcoma CD49f−CD133+ cells: impaired in osteogenic fate while gain of tumorigenicity Oncogene 32, 4252 (5 September 2013). doi:10.1038/onc.2012.438 Authors: M Ying, G Liu, H Shimada, W Ding, W A May, Q He, G B Adams & L Wu
    Keywords: osteosarcoma-initiating cellsself-renewaltumorigenicitylineage differentiationosteosarcoma-forming cellsosteogenic differentiation
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 6
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    The G-protein-coupled estrogen receptor agonist G-1 suppresses proliferation of ovarian cancer cells by blocking tubulin polymerization (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-10-18
    Description: The G-protein-coupled estrogen receptor agonist G-1 suppresses proliferation of ovarian cancer cells by blocking tubulin polymerization Cell Death and Disease 4, e869 (October 2013). doi:10.1038/cddis.2013.397 Authors: C Wang, X Lv, C He, G Hua, M-Y Tsai & J S Davis
    Keywords: GPERG-1ovarian cancercell proliferationapoptosis
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Nature Publishing Group (NPG)
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  • 7
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    Endothelial microparticles increase in mitral valve disease and impair mitral valve endothelial function (2013)
    The American Physiological Society (APS)
    Details
    Publication Date: 2013-04-02
    Description: Mitral valve endothelial cells are important for maintaining lifelong mitral valve integrity and function. Plasma endothelial microparticles (EMPs) increased in various pathological conditions related to activation of endothelial cells. However, whether EMPs will increase in mitral valve disease and their relationship remains unclear. Here, 81 patients with mitral valve disease and 45 healthy subjects were analyzed for the generation of EMPs by flow cytometry. Human mitral valve endothelial cells (HMVECs) were treated with EMPs. The phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), the association of eNOS and heat shock protein 90 (HSP90), and the generation of nitric oxide (NO) and superoxide anion (O 2 – ) were measured. EMPs were increased significantly in patients with mitral valve disease compared with those in healthy subjects. EMPs were negatively correlated with mitral valve area in patients with isolated mitral stenosis. EMPs were significantly higher in the group with severe mitral regurgitation than those in the group with mild and moderate mitral regurgitation. Furthermore, EMPs were decreased dramatically in both Akt and eNOS phosphorylation and the association of HSP90 with eNOS in HMVECs. EMPs decreased NO production but increased O 2 – generation in HMVECs. Our data demonstrated that EMPs were significantly increased in patients with mitral valve disease. The increase of EMPs can in turn impair HMVEC function by inhibiting the Akt/eNOS-HSP90 signaling pathway. These findings suggest that EMPs may be a therapeutic target for mitral valve disease.
    Print ISSN: 0193-1849
    Electronic ISSN: 1522-1555
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 8
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    AMP-Activated Protein Kinase Induces p53 by Phosphorylating MDMX and Inhibiting Its Activity [Articles] (2013)
    The American Society for Microbiology (ASM)
    Details
    Publication Date: 2013-12-20
    Description: AMP-activated protein kinase (AMPK) has been shown to activate p53 in response to metabolic stress. However, the underlying mechanisms remain unclear. Here we show that metabolic stresses induce AMPK-mediated phosphorylation of human MDMX on Ser342 in vitro and in cells, leading to enhanced association between MDMX and 14-3-3. This markedly inhibits p53 ubiquitylation and significantly stabilizes and activates p53. By striking contrast, no phosphorylation of MDM2 by AMPK was noted. AMPK-mediated MDMX phosphorylation, MDMX–14-3-3 binding, and p53 activation were drastically reduced in mouse embryo fibroblasts harboring endogenous MDMX with S341A (mouse homologue of human serine 342), S367A, and S402A (mouse homologue of human serine 403) mutations. Moreover, deficiency of AMPK prevented MDMX–14-3-3 interaction and p53 activation. The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin). Together, the results unveil a mechanism by which metabolic stresses activate AMPK, which, in turn, phosphorylates and inactivates MDMX, resulting in p53 stabilization and activation.
    Print ISSN: 0270-7306
    Electronic ISSN: 1098-5549
    Topics: Biology , Medicine
    Published by The American Society for Microbiology (ASM)
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  • 9
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    Regulation of acute graft-versus-host disease by microRNA-155 (2012)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2012-05-18
    Description: Acute graft-versus-host disease (aGVHD) remains a major complication of allogeneic hematopoietic stem cell transplant (alloHSCT), underscoring the need to further elucidate its mechanisms and develop novel treatments. Based on recent observations that microRNA-155 (miR-155) is up-regulated during T-cell activation, we hypothesized that miR-155 is involved in the modulation of aGVHD. Here we show that miR-155 expression was up-regulated in T cells from mice developing aGVHD after alloHSCT. Mice receiving miR-155–deficient donor lymphocytes had markedly reduced lethal aGVHD, whereas lethal aGVHD developed rapidly in mice recipients of miR-155 overexpressing T cells. Blocking miR-155 expression using a synthetic anti–miR-155 after alloHSCT decreased aGVHD severity and prolonged survival in mice. Finally, miR-155 up-regulation was shown in specimens from patients with pathologic evidence of intestinal aGVHD. Altogether, our data indicate a role for miR-155 in the regulation of GVHD and point to miR-155 as a novel target for therapeutic intervention in this disease.
    Keywords: Transplantation
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 10
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    c-Src-Initiated Erlotinib Resistance Involves c-Met (2013)
    The American Association for Cancer Research (AACR)
    Details
    Publication Date: 2013-01-18
    Description: Purpose: Strategies to inhibit the EGF receptor (EGFR) using the tyrosine kinase inhibitor erlotinib have been associated with limited clinical efficacy in head and neck squamous cell carcinoma (HNSCC). Co-activation of alternative kinases may contribute to erlotinib resistance. Experimental Design: We generated HNSCC cells expressing dominant-active c-Src (DA-Src) to determine the contribution of c-Src activation to erlotinib response. Results: Expression of DA-Src conferred resistance to erlotinib in vitro and in vivo compared with vector-transfected control cells. Phospho-Met was strongly upregulated by DA-Src, and DA-Src cells did not produce hepatocyte growth factor (HGF). Knockdown of c-Met enhanced sensitivity to erlotinib in DA-Src cells in vitro , as did combining a c-Met or c-Src inhibitor with erlotinib. Inhibiting EGFR resulted in minimal reduction of phospho-Met in DA-Src cells, whereas complete phospho-Met inhibition was achieved by inhibiting c-Src. A c-Met inhibitor significantly sensitized DA-Src tumors to erlotinib in vivo , resulting in reduced Ki67 labeling and increased apoptosis. In parental cells, knockdown of endogenous c-Src enhanced sensitivity to erlotinib, whereas treatment with HGF to directly induce phospho-Met resulted in erlotinib resistance. The level of endogenous phospho-c-Src in HNSCC cell lines was also significantly correlated with erlotinib resistance. Conclusions: Ligand-independent activation of c-Met contributes specifically to erlotinib resistance, not cetuximab resistance, in HNSCC with activated c-Src, where c-Met activation is more dependent on c-Src than on EGFR, providing an alternate survival pathway. Addition of a c-Met or c-Src inhibitor to erlotinib may increase efficacy of EGFR inhibition in patients with activated c-Src. Clin Cancer Res; 19(2); 380–92. ©2012 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
    Published by The American Association for Cancer Research (AACR)
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