The strength and toughness of engineering alloys, under conditions where general yielding and sub-critical crack growth precede catastrophic fracture, are critically dependent on the nucleation, growth and coalescence of microvoids in fracture process zones that are usually subjected to mean - normal stress approaching #delta#_m/2k=2.0. It is shown that at these high mean-normal stress levels, microvid nucleation and spontaneous void coalescence can become the controlling process of ductile fracture, with negligible dilational-plastic void growth prior to microvoid coalescence and the formation of a fracture surface. This effect is the direct result of high mean-normal stresses promoting the microvoid coalescence process when the newly-nucleated voids are still of the same size and spacing as the void-nucleating particles. Under these conditions virtually all the dilational void-growth is confined to the final void-coalescence fracture surface and is the result of a highly - localised limit-load failure (or internal microscopic necking) of the intervoid matrix.
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