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  • 1985-1989  (2)
  • 1965-1969
  • 1989  (2)
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  • 1985-1989  (2)
  • 1965-1969
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Fatigue & fracture of engineering materials & structures 12 (1989), S. 0 
    ISSN: 1460-2695
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract— Two damage models were implemented into the finite element program ADINA to study the correlation between microscopical damage and macroscopical material failure. In the first model, based on the Gurson yield function the nucleation, growth and the coalescence of voids were incorporated into the constitutive relations. In the second model the void growth was determined according to the Rice and Tracey model using the von Mises yield function, and material failure was simulated by eliminating the elements where the critical void growth ratio was exceeded. The numerical results for the local and global behaviour of the specimens were compared with experiments. The generality of the damage parameters was checked by investigating several specimen geometries. Both damage models deliver qualitatively consistent results with regard to the influence of the stress triaxiality on the void growth and on the beginning of the material failure. However, the Gurson model gives a more accurate numerical simulation because the damage development and the stress drop continue after the onset of void coalescence while the critical void growth model causes less convergence problems in the simulation of large crack extension. The Jn-curve was estimated on the basis of both models.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Human genetics 〈Berlin〉 83 (1989), S. 93-96 
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary α2-Macrpglobulin (A2M) is a major human plasma protease inhibitor capable of inhibiting most endopeptidases tested so far. In the case of the other major plasma protease inhibitor, α1-antitrypsin, genetically determined deficiency states are known to increase the risk of chronic obstructive pulmonary disease (COPD) 20- to 30-fold in affected individuals. No defects of the A2M gene have been described as yet, but A2M may play a role in the regulation of protease activity in the lung, especially with respect to those proteases not inhibited by α1-antitrypsin. We report here the molecular genetic detection of an alteration of the A2M gene in a patient with serum A2M deficiency and chronic lung disease since childhood. The alteration involves restriction sites detected with 10 different enzymes and is most probably caused by a major deletion or rearrangement of the gene. Nine of the restriction enzymes used detected no polymorphisms in 40 healthy control subjects and 39 COPD patients. The polymorphism detected in this patient with the enzyme PvuII was different from another described previously, and was found in this patient only. The patient is heterozygous for an alteration in the A2M gene; this may be responsible for his serum A2M deficiency and may be relevant to the early onset of pulmonary disease in his case.
    Type of Medium: Electronic Resource
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