26 research outputs found

    Evolutionary suicide through a non-catastrophic bifurcation : adaptive dynamics of pathogens with frequency-dependent transmission

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    Evolutionary suicide is a riveting phenomenon in which adaptive evolution drives a viable population to extinction. Gyllenberg and Parvinen (Bull Math Biol 63(5):981-993, 2001) showed that, in a wide class of deterministic population models, a discontinuous transition to extinction is a necessary condition for evolutionary suicide. An implicit assumption of their proof is that the invasion fitness of a rare strategy is well-defined also in the extinction state of the population. Epidemic models with frequency-dependent incidence, which are often used to model the spread of sexually transmitted infections or the dynamics of infectious diseases within herds, violate this assumption. In these models, evolutionary suicide can occur through a non-catastrophic bifurcation whereby pathogen adaptation leads to a continuous decline of host (and consequently pathogen) population size to zero. Evolutionary suicide of pathogens with frequency-dependent transmission can occur in two ways, with pathogen strains evolving either higher or lower virulence.Peer reviewe

    Зубелевич Я. Аксиоцентризм в философии образования

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    Рецензія на монографію: Зубелевич Я. Аксиоцентризм в философии образования / пер. с польского О. Гирного ; Ян Зубелевич. – СПб. : Изд-во Политех. ун-та, 2008. – 220 с

    joint work with Eva Kisdi and Stefan A.H. Geritz

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    FAN, a Novel WD-Repeat Protein, Couples the p55 TNF-Receptor to Neutral Sphingomyelinase

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    AbstractThe initiation of intracellular signaling events through the 55 kDa tumor necrosis factor–receptor (TNF-R55) appears to depend on protein intermediates that interact with specific cytoplasmic domains of TNF-R55. By combined use of the yeast interaction trap system and a peptide scanning library, the novel WD-repeat protein FAN has been identified, which specifically binds to a cytoplasmic nine amino acid binding motif of TNF-R55. This region has been previously recognized as a distinct functional domain that is both required and sufficient for the activation of neutral sphingomyelinase (N-SMase). Overexpression of full-length FAN enhanced N-SMase activity in TNF–treated cells, while truncated mutants of FAN produced dominant negative effects. The data suggest that FAN regulates ceramide production by N-SMase, which is a crucial step in TNF signaling
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