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  • 1
    Publikationsdatum: 2021-02-08
    Beschreibung: High-resolution acoustic and seismic data acquired 100 km offshore Cape São Vicente, image with unprecedented detail one of the largest active reverse faults of the SW Iberian Margin, the Horseshoe Fault (HF). The HF region is an area seismogenically active, source of the largest magnitude instrumental and historical earthquake (Mw〉6) occurred in the SW Iberian Margin. The HF corresponds to a N40 trending, 110 km long, and NW-verging active thrust that affects the whole sedimentary sequence and reaches up to the seafloor, generating a relief of more than 1 km. The along-strike structural variability as well as fault trend suggests that the HF is composed by three main sub-segments: North (N25), Central (N50) and South (N45). Swath-bathymetry, TOBI sidescan sonar backscatter and parametric echosounder TOPAS profiles reveal the surface morphology of the HF block, characterized by several, steep (20º) small scarps located on the hangingwall, and a succession of mass transport deposits (i.e. turbidites) on its footwall, located in the Horseshoe Abyssal Plain. A succession of pre-stack depth-migrated multichannel seismic reflection profiles across the HF and neighboring areas allowed us to constrain their seismo-stratigraphy, structural geometry, tectono-sedimentary evolution from Upper Jurassic to present-day, and to calculate their fault parameters. Finally, on the basis of segment length, surface fault area and seismogenic depth we evaluated the seismic potential of the HF, which in the worst-case scenario may generate an earthquake of magnitude Mw 7.8 ± 0.1. Thus, considering the tectonic behavior and near-shore location, the HF should be recognized in seismic and tsunami hazard assessment models of Western Europe and North Africa.
    Materialart: Article , PeerReviewed
    Format: text
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    facet.materialart.
    Unbekannt
    GSL (Geological Society London)
    In:  In: Atlas of submarine glacial landforms: modern, Quaternary and ancient. , ed. by Dowdeswell, J. A., Canals, M., Jakobsson, M., Todd, B. J., Dowdeswell, E. K. and Hogan, K. A. Memoirs of the Geological Society of London, 46 . GSL (Geological Society London), London, pp. 411-412. ISBN 978-1-78620-268-0
    Publikationsdatum: 2021-05-10
    Beschreibung: Spreading is a type of mass movement where a sediment unit is extended and broken up into coherent blocks that are displaced and tilted along a planar slip. High-resolution seafloor data demonstrate that spreading is a common style of submarine mass movement. Submarine spreading is clearly exemplified in the Storegga Slide, Norwegian margin (Fig. 1a, b). The slide occurred 8100 + 250 cal a BP as a retrogressive slope failure (Haflidason et al. 2005). It is one of the largest known submarine slides and the site of repeated sliding activity. Failures on the Norwegian margin are linked strongly to the growth and retreat of the Fennoscandian ice sheets, in particular to the alternating deposition of glacigenic debrites and basal and deformation tills during glacial maxima (e.g. O1–O2 30–15 ka and O4–O7 200–130 ka sub-units of the Naust Formation), and of fine-grained glacimarine, hemipelagic and contouritic sediments during interglacials (e.g. O3 130–30 ka sub-unit of the Naust Formation). The Naust sub-units are described in full in Berg et al. (2005). Differences in the geotechnical properties of these sediments, coupled with seismicity, rapid sediment deposition, associated high pore pressures and the regional topography and structural setting, are responsible for .20 slope failures across the region during the Quaternary (Solheim et al. 2005).
    Materialart: Book chapter , NonPeerReviewed
    Format: text
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Publikationsdatum: 2015-02-20
    Beschreibung: The protein tyrosine phosphatase PRL-2 interacts with the magnesium transporter CNNM3 to promote oncogenesis Oncogene 34, 986 (19 February 2015). doi:10.1038/onc.2014.33 Authors: S Hardy, N Uetani, N Wong, E Kostantin, D P Labbé, L R Bégin, A Mes-Masson, D Miranda-Saavedra & M L Tremblay
    Print ISSN: 0950-9232
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Publikationsdatum: 2015-05-21
    Beschreibung: Objective— Liver X receptors (LXRs) modulate cholesterol and fatty acid homeostasis as well as inflammation. This study aims to decipher the role of LXRs in the regulation of polyunsaturated fatty acid (PUFA) synthesis in macrophages in the context of atherosclerosis. Approach and Results— Transcriptomic analysis in human monocytes and macrophages was used to identify putative LXR target genes among enzymes involved in PUFA biosynthesis. In parallel, the consequences of LXR activation or LXR invalidation on PUFA synthesis and distribution were determined. Finally, we investigated the impact of LXR activation on PUFA metabolism in vivo in apolipoprotein E–deficient mice. mRNA levels of acyl-CoA synthase long-chain family member 3, fatty acid desaturases 1 and 2, and fatty acid elongase 5 were significantly increased in human macrophages after LXR agonist treatment, involving both direct and sterol responsive element binding protein-1–dependent mechanisms. Subsequently, pharmacological LXR agonist increased long chain PUFA synthesis and enhanced arachidonic acid content in the phospholipids of human macrophages. Increased fatty acid desaturases 1 and 2 and acyl-CoA synthase long-chain family member 3 mRNA levels as well as increased arachidonic acid to linoleic acid and docosahexaenoic acid to eicosapentaenoic acid ratios were also found in atheroma plaque and peritoneal foam cells from LXR agonist–treated mice. By contrast, murine LXR-deficient macrophages displayed reduced expression of fatty acid elongase 5, acyl-CoA synthase long-chain family member 3 and fatty acid desaturases 1, as well as decreased cellular levels of docosahexaenoic acid and arachidonic acid. Conclusions— Our results indicate that LXR activation triggers PUFA synthesis in macrophages, which results in significant alterations in the macrophage lipid composition. Moreover, we demonstrate here that LXR agonist treatment modulates PUFA metabolism in atherosclerotic arteries.
    Schlagwort(e): Gene regulation, Lipid and lipoprotein metabolism
    Print ISSN: 1079-5642
    Digitale ISSN: 1524-4636
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Publikationsdatum: 2016-01-16
    Beschreibung: Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxrα in mice with hepatocyte-specific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxrα produced equivalent, non-additive effects on the lipogenic genes. Thus, insulin was unable to induce the lipogenic genes in the absence of Lxrα, and LXRα was unable to induce the lipogenic genes in the absence of insulin. However, insulin was not required for LXRα to modulate the phospholipid profile, or to suppress genes in the ER stress or inflammation pathways. These data show that insulin is required specifically for the lipogenic effects of LXRα and that manipulation of the insulin signaling pathway could dissociate the beneficial effects of LXR on cholesterol efflux, inflammation, and ER stress from the negative effects on lipogenesis.
    Print ISSN: 0021-9258
    Digitale ISSN: 1083-351X
    Thema: Biologie , Chemie und Pharmazie
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Publikationsdatum: 2015-11-06
    Beschreibung: Cohen Syndrome (CS) is a rare autosomal recessive disorder, with defective glycosylation secondary to mutations in the VPS13B gene, which encodes a protein of the Golgi apparatus. Besides congenital neutropenia, retinopathy and intellectual deficiency, CS patients are faced with truncal obesity. Metabolism investigations showed abnormal glucose tolerance tests and low HDL values in some patients, and these could be risk factors for the development of diabetes mellitus and/or cardiovascular complications. To understand the mechanisms involved in CS fat storage, we used two models of adipogenesis differentiation: (i) SGBS pre-adipocytes with VPS13B invalidation thanks to siRNA delivery and (ii) CS primary fibroblasts. In both models, VPS13B invalidation led to accelerated differentiation into fat cells, which was confirmed by the earlier and increased expression of specific adipogenic genes, consequent to the increased response of cells to insulin stimulation. At the end of the differentiation protocol, these fat cells exhibited decreased AKT2 phosphorylation after insulin stimulation, which suggests insulin resistance. This study, in association with the in-depth analysis of the metabolic status of the patients, thus allowed us to recommend appropriate nutritional education to prevent the occurrence of diabetes mellitus and to put forward recommendations for the follow-up of CS patients, in particular with regard to the development of metabolic syndrome. We also suggest replacing the term obesity by abnormal fat distribution in CS, which should reduce the number of inappropriate diagnoses in patients who are referred only on the basis of intellectual deficiency associated with obesity.
    Print ISSN: 0964-6906
    Digitale ISSN: 1460-2083
    Thema: Biologie , Medizin
    Publiziert von Oxford University Press
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Publikationsdatum: 2016-12-09
    Beschreibung: Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN cells and BPDCN cell lines restored LXR target gene expression and increased cholesterol efflux via the upregulation of adenosine triphosphate–binding cassette (ABC) transporters, ABCA1 and ABCG1. LXR agonist treatment was responsible for limiting BPDCN cell proliferation and inducing intrinsic apoptotic cell death. LXR activation in BPDCN cells was shown to interfere with 3 signaling pathways associated with leukemic cell survival, namely: NF-B activation, as well as Akt and STAT5 phosphorylation in response to the BPDCN growth/survival factor interleukin-3. These effects were increased by the stimulation of cholesterol efflux through a lipid acceptor, the apolipoprotein A1. In vivo experiments using a mouse model of BPDCN cell xenograft revealed a decrease of leukemic cell infiltration and BPDCN-induced cytopenia associated with increased survival after LXR agonist treatment. This demonstrates that cholesterol homeostasis is modified in BPDCN and can be normalized by treatment with LXR agonists which can be proposed as a new therapeutic approach.
    Schlagwort(e): Myeloid Neoplasia
    Print ISSN: 0006-4971
    Digitale ISSN: 1528-0020
    Thema: Biologie , Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Publikationsdatum: 2017-04-20
    Beschreibung: Chronic graft-versus-host disease (cGVHD) is frequent and severe after allogeneic hematopoietic stem cell transplantation (AHSCT), with unmet therapeutic needs. 1 A recent retrospective study has shown the potential efficacy of ruxolitinib, a selective Janus Kinase (JAK) 1/2 inhibitor, for the treatment of acute (n=54) and chronic GVHD (n=41) with a 81.5% and 85.4% overall response rate for acute and chronic GVHD respectively. 3 There are no specific studies evaluating the efficacy of ruxolitinib in sclerodermatous skin cGVHD, a rare and difficult-to-treat form of cGVHD. This article is protected by copyright. All rights reserved.
    Print ISSN: 0007-0963
    Digitale ISSN: 1365-2133
    Thema: Medizin
    Publiziert von Wiley-Blackwell
    Standort Signatur Einschränkungen Verfügbarkeit
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