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  • Animal models of human disease, Cell signalling/signal transduction, Other arteriosclerosis, Mechanism of atherosclerosis/growth factors, Other Vascular biology  (1)
  • Grain size  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Bulletin of volcanology 57 (1996), S. 512-529 
    ISSN: 1432-0819
    Keywords: Facies ; Grain size ; Components ; Pyroclastic flows ; Subaerial ; Emplacement process
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences
    Notes: Abstract The majority of tephra generated during the paroxysmal 1883 eruption of Krakatau volcano, Indonesia, was deposited in the sea within a 15-km radius of the caldera. Two syneruptive pyroclastic facies have been recovered in SCUBA cores which sampled the 1883 subaqueous pyroclastic deposit. The most commonly recovered facies is a massive textured, poorly sorted mixture of pumice and lithic lapilli-to-block-sized fragments set in a silty to sandy ash matrix. This facies is indistinguishable from the 1883 subaerial pyroclastic flow deposits preserved on the Krakatau islands on the basis of grain size and component abundances. A less common facies consists of well-sorted, planarlaminated to low-angle cross-bedded, vitric-enriched silty ash. Entrance of subaerial pyroclastic flows into the sea resulted in subaqueous deposition of the massive facies primarily by deceleration and sinking of highly concentrated, deflated components of pyroclastic flows as they traveled over water. The basal component of the deposit suggests no mixing with seawater as inferred from retention of the fine ash fraction, high temperature of emplacement, and lack of traction structures, and no significant hydraulic sorting of components. The laminated facies was most likely deposited from low-concentration pyroclastic density currents generated by shear along the boundary between the submarine pyroclastic flows and seawater. The Krakatau deposits are the first well-documented example of true submarine pyroclastic flow deposition from a modern eruption, and thus constitute an important analog for the interpretation of ancient sequences where subaqueous deposition has been inferred based on the facies characteristics of encapsulating sedimentary sequences.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2012-08-16
    Description: Objective— Bone morphogenetic proteins (Bmps) are important mediators of inflammation and atherosclerosis, though their mechanism of action is not fully understood. To better understand the contribution of the Bmp signaling pathway in vascular inflammation, we investigated the role of Bmper (Bmp endothelial cell precursor–derived regulator), an extracellular Bmp modulator, in an induced in vivo model of inflammation and atherosclerosis. Methods and Results— We crossed apolipoprotein E–deficient (ApoE –/– ) mice with mice missing 1 allele of Bmper (Bmper +/– mice used in the place of Bmper –/– mice that die at birth) and measured the development of atherosclerosis in mice fed a high-fat diet. Bmper haploinsufficiency in ApoE –/– mice (Bmper +/– ;ApoE –/– mice) led to a more severe phenotype compared with Bmper +/+ ;ApoE –/– mice. Bmper +/– ;ApoE –/– mice also exhibited increased Bmp activity in the endothelial cells in both the greater and lesser curvatures of the aortic arch, suggesting a role for Bmper in regulating Bmp-mediated inflammation associated with laminar and oscillatory shear stress. Small interfering RNA knockdown of Bmper in human umbilical vein endothelial cells caused a dramatic increase in the inflammatory markers intracellular adhesion molecule 1 and vascular cell adhesion molecule 1 at rest and after exposure to oscillatory and laminar shear stress. Conclusion— We conclude that Bmper is a critical regulator of Bmp-mediated vascular inflammation and that the fine-tuning of Bmp and Bmper levels is essential in the maintenance of normal vascular homeostasis.
    Keywords: Animal models of human disease, Cell signalling/signal transduction, Other arteriosclerosis, Mechanism of atherosclerosis/growth factors, Other Vascular biology
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
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