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We have studied by electron microscopy and x-ray diffraction techniques the amorphous-to-crystalline phase transition which occurs during annealing of a highly Ge-rich and N-doped amorphous GeSbTe material. The crystallization onset occurs at 380 °C with the diffusion and segregation of Ge followed by the formation of Ge nanocrystals. The GeSbTe face-centered cubic (FCC) crystalline phase only appears at 400 °C. Phase separation occurs because the Ge concentration is well above what can be accommodated by the Ge2Sb2Te5 lattice. The possible formation of a two-phase material should be considered in order to simulate device characteristics and optimize material composition for electronic memory applications.
Inspired by the works of Landriault et al. (2011), (2014), we study the Gerber–Shiu distribution at Parisian ruin with exponential implementation delays for a spectrally negative Lévy insurance risk process. To be more specific, we study the so-called Gerber–Shiu distribution for a ruin model where at each time the surplus process goes negative, an independent exponential clock is started. If the clock rings before the surplus becomes positive again then the insurance company is ruined. Our methodology uses excursion theory for spectrally negative Lévy processes and relies on the theory of so-called scale functions. In particular, we extend the recent results of Landriault et al. (2011), (2014).
We study the distribution Ex[exp(-q∫0t1(a,b)(Xs)ds); Xt ∈ dy], where -∞ ≤ a < b < ∞, and where q, t > 0 and x ∈ R for a spectrally negative Lévy process X. More precisely, we identify the Laplace transform with respect to t of this measure in terms of the scale functions of the underlying process. Our results are then used to price step options and the particular case of an exponential spectrally negative Lévy jump-diffusion model is discussed.
Despite important differences between infectious diseases and cancers, tumour development (neoplasia) can nonetheless be closely compared to infectious disease because of the similarity of their effects on the body. On this basis, we predict that many of the life-history (LH) responses observed in the context of host–parasite interactions should also be relevant in the context of cancer. Parasites are thought to affect LH traits of their hosts because of strong selective pressures like direct and indirect mortality effects favouring, for example, early maturation and reproduction. Cancer can similarly also affect LH traits by imposing direct costs and/or indirectly by triggering plastic adjustments and evolutionary responses. Here, we discuss how and why a LH focus is a potentially productive but under-exploited research direction for cancer research, by focusing our attention on similarities between infectious disease and cancer with respect to their effects on LH traits and their evolution. We raise the possibility that LH adjustments can occur in response to cancer via maternal/paternal effects and that these changes can be heritable to (adaptively) modify the LH traits of their offspring. We conclude that LH adjustments can potentially influence the transgenerational persistence of inherited oncogenic mutations in populations.