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  • 1
    Electronic Resource
    Electronic Resource
    Wet Erosive Wear of Alumina Densified with Magnesium Silicate Additions (2001)
    Westerville, Ohio : American Ceramics Society
    Journal of the American Ceramic Society 84 (2001), S. 0 
    Details
    ISSN: 1551-2916
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: A study was made of the wet erosive wear of polycrystalline alumina of mean grain size 〉1 μm, containing up to 10 wt% of magnesium silicate sintering aid. For pure polycrystalline alumina, the dominant wear mechanism was grain-boundary microfracture, leading to partial or complete grain removal. In the case of the liquid-phase-sintered materials, wear rates could be as low as 25% of those of pure alumina of the same mean grain size, and the main material removal mechanism was transgranular fracture combined with tribochemical wear. The use of Cr3+ photoluminescence line broadening showed much higher levels of local stress in the magnesium silicate-sintered materials (∼450 MPa) than in the pure-alumina materials (∼200 MPa). Grain-boundary compressive hoop stresses, caused by the thermal expansion mismatch between a continuous magnesium silicate film and the alumina grains, provided an explanation for the improved wear resistance of the alumina sintered with magnesium silicate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1151-2916.2001.tb00913.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Crack Healing in a Silicon Nitride Ceramic (1998)
    Westerville, Ohio : American Ceramics Society
    Journal of the American Ceramic Society 81 (1998), S. 0 
    Details
    ISSN: 1551-2916
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: A detailed study has been undertaken on crack healing at high temperatures in a silicon nitride containing 10 wt% additives in order to identify the dominant mechanism responsible for the phenomenon. Fracture toughness increased with annealing time and the crack growth rate decreased until arrest with increasing testing time. Differentiation between possible operating mechanisms was obtained using critical experiments involving detailed compliance measurements, crack wake removal, and crack reinitiation tests and a comprehensive TEM study of healed cracks. It was found that crack healing was not uniform in the crack wake. When the original crack path was either transgranular or intergranular, healing was associated with the appearance of a thin layer of silica glass due to the oxidation of Si3N4 grains. But when the crack went through multigrain junctions, the former crack path was completely obliterated and replaced by a new, crystalline phase formed by diffusion of the preexisting glass phase. It is concluded that the increased crack growth resistance and fracture toughness at high temperature is attributable to the partial recovery of the original strength from the crack segments at multigrain junctions due to vitreous phase flow and subsequent crystallization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1151-2916.1998.tb02558.x
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    Paper (German National Licenses)
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  • 3
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    Role of the Primary Cilia on the Macula Densa and Thick Ascending Limbs in Regulation of Sodium Excretion and HemodynamicsNovelty and Significance [Kidney] (2017)
    American Heart Association (AHA)
    Details
    Publication Date: 2017-07-13
    Description: We investigated the significance of the primary cilia on the macula densa and thick ascending limb (TAL) in regulation of renal hemodynamics, sodium excretion, and blood pressure in this study. A tissue-specific primary cilia knock-out (KO) mouse line was generated by crossing NKCC2-Cre mice with IFT88-Δ/flox mice (NKCC2CRE; IFT88Δ/flox), in which the primary cilia were deleted from the macula densa and TAL. NO generation was measured with a fluorescent dye (4,5-diaminofluorescein diacetate) in isolated perfused juxtaglomerular apparatus. Deletion of the cilia reduced NO production by 56% and 42% in the macula densa and TAL, respectively. NO generation by the macula densa was inhibited by both a nonselective and a selective nitric oxide synthesis inhibitors, whereas TAL-produced NO was inhibited by a nonselective and not by a selective NO synthesis 1 inhibitor. The tubuloglomerular feedback response was enhanced in the KO mice both in vitro measured with isolated perfused juxtaglomerular apparatuses and in vivo measured with micropuncture. In response to an acute volume expansion, the KO mice exhibited limited glomerular filtration rate elevation and impaired sodium excretion compared with the wild-type mice. The mean arterial pressure measured with telemetry was the same for wild-type and KO mice fed a normal salt diet. After a high salt diet, the mean arterial pressure increased by 17.4±1.6 mm Hg in the KO mice. On the basis of these findings, we concluded that the primary cilia on the macula densa and TAL play an essential role in the control of sodium excretion and blood pressure.
    Keywords: High Blood Pressure
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 4
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    T-Cell Mineralocorticoid Receptor Controls Blood Pressure by Regulating Interferon-GammaNovelty and Significance [Integrative Physiology] (2017)
    American Heart Association (AHA)
    Details
    Publication Date: 2017-05-12
    Description: Rationale:Hypertension remains to be a global public health burden and demands novel intervention strategies such as targeting T cells and T-cell–derived cytokines. Mineralocorticoid receptor (MR) antagonists have been clinically used to treat hypertension. However, the function of T-cell MR in blood pressure (BP) regulation has not been elucidated.Objective:We aim to determine the role of T-cell MR in BP regulation and to explore the mechanism.Methods and Results:Using T-cell MR knockout mouse in combination with angiotensin II–induced hypertensive mouse model, we demonstrated that MR deficiency in T cells strikingly decreased both systolic and diastolic BP and attenuated renal and vascular damage. Flow cytometric analysis showed that T-cell MR knockout mitigated angiotensin II–induced accumulation of interferon-gamma (IFN-γ)–producing T cells, particularly CD8+ population, in both kidneys and aortas. Similarly, eplerenone attenuated angiotensin II–induced elevation of BP and accumulation of IFN-γ–producing T cells in wild-type mice. In cultured CD8+ T cells, T-cell MR knockout suppressed IFN-γ expression whereas T-cell MR overexpression and aldosterone both enhanced IFN-γ expression. At the molecular level, MR interacted with NFAT1 (nuclear factor of activated T-cells 1) and activator protein-1 in T cells. Finally, T-cell MR overexpressing mice manifested more elevated BP compared with control mice after angiotensin II infusion and such difference was abolished by IFN-γ–neutralizing antibodies.Conclusions:MR may interact with NFAT1 and activator protein-1 to control IFN-γ in T cells and to regulate target organ damage and ultimately BP. Targeting MR in T cells specifically may be an effective novel approach for hypertension treatment.
    Keywords: Pathophysiology, Hypertension
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 5
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    Activation of Adiponectin Receptor Regulates Proprotein Convertase Subtilisin/Kexin Type 9 Expression and Inhibits Lesions in ApoE-Deficient MiceHighlights [Basic Sciences] (2017)
    American Heart Association (AHA)
    Details
    Publication Date: 2017-06-22
    Description: Objective—The reduced adiponectin levels are associated with atherosclerosis. Adiponectin exerts its functions by activating adiponectin receptor (AdipoR). Proprotein convertase subtilisin kexin type 9 (PCSK9) degrades LDLR protein (low-density lipoprotein receptor) to increase serum LDL-cholesterol levels. PCSK9 expression can be regulated by PPARγ (peroxisome proliferator–activated receptor γ) or SREBP2 (sterol regulatory element-binding protein 2). The effects of AdipoR agonists on PCSK9 and LDLR expression, serum lipid profiles, and atherosclerosis remain unknown.Approach and Results—At cellular levels, AdipoR agonists (ADP355 and AdipoRon) induced PCSK9 transcription/expression that solely depended on activation of PPAR-responsive element in the PCSK9 promoter. AdipoR agonists induced PPARγ expression; thus, the AdipoR agonist-activated PCSK9 expression/production was impaired in PPARγ deficient hepatocytes. Meanwhile, AdipoR agonists transcriptionally activated LDLR expression by activating SRE in the LDLR promoter. Moreover, AMP-activated protein kinase α (AMPKα) was involved in AdipoR agonist-activated PCSK9 expression. In wild-type mice, ADP355 increased PCSK9 and LDLR expression and serum PCSK9 levels, which was associated with activation of PPARγ, AMPKα and SREBP2 and reduction of LDL-cholesterol levels. In contrast, ADP355 reduced PCSK9 expression/secretion in apoE-deficient (apoE−/−) mice, but it still activated hepatic LDLR, PPARγ, AMPKα, and SREBP2. More importantly, ADP355 inhibited lesions in en face aortas and sinus lesions in aortic root in apoE−/− mice with amelioration of lipid profiles.Conclusions—Our study demonstrates that AdipoR activation by agonists regulated PCSK9 expression differently in wild-type and apoE−/− mice. However, ADP355 activated hepatic LDLR expression and ameliorated lipid metabolism in both types of mice and inhibited atherosclerosis in apoE−/− mice.
    Keywords: Basic Science Research, Cell Signaling/Signal Transduction, Lipids and Cholesterol, Metabolism, Vascular Biology
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
    Published by American Heart Association (AHA)
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