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  • 1990-1994  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 75 (1994), S. 7983-7988 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The angular dependence of magnetic Barkhausen noise (MBN) on eight surfaces through the thickness of a 2% Mn steel pipeline sample was investigated. The MBN signal was analyzed by integrating the square of the MBN voltage signal with respect to the time axis. The resulting value, referred to as the MBN energy signal, was modeled by considering the irreversible motion of 180° domain walls, under the influence of an oriented magnetic field. An expression for the angular dependence of the MBN energy signal was derived and was given by energy=α cos2 θ+β, where α and β are the fitting parameters and θ is the angle between the maximum MBN signal and the applied sweep field. The α parameter was associated with the irreversible motion of 180° walls that contributed to the net macroscopic easy axis near the surface of the sample, while the β parameter was associated with the isotropic background MBN signal. The energy equation could be used to fit the data for all sweep field amplitudes in which the MBN spectrum was observed. A dependence of the α and β parameters on the applied sweep field amplitude was observed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Homology with the mouse bare patches mutant suggests that the gene for the X-linked dominant chondrodysplasia punctata / ichthyosis / cataract / short stature syndrome (Happle syndrome) is located in the human Xq28 region. To test this hypothesis, we performed a linkage study in three families comprising a total of 12 informative meioses. Multiple recombinations appear to exclude the Xq28 region as the site of the gene. Surprisingly, multiple crossovers were also found with 26 other markers spread along the rest of the X chromosome. Two-point linkage analysis and analysis of recombination chromosomes seem to exclude the gene from the entire X chromosome. Three different mechanisms are discussed that could explain the apparent exclusion of an X-linked gene from the X chromosome by linkage analysis: (a) different mutations on the X chromosome disturbing X inactivation, (b) metabolic interference, i.e. allele incompatibility of an X-linked gene, and (c) an unstable pre-mutation that can become silent in males. We favour the last explanation, as it would account for the unexpected sex ratio (M∶F) of 1.2∶1 among surviving siblings, and for the striking clinical variability of the phenotype, including stepwise increases in disease expression in successive generations.
    Type of Medium: Electronic Resource
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