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  1. What makes biological organisation teleological?Matteo Mossio & Leonardo Bich - 2017 - Synthese 194 (4):1089-1114.
    This paper argues that biological organisation can be legitimately conceived of as an intrinsically teleological causal regime. The core of the argument consists in establishing a connection between organisation and teleology through the concept of self-determination: biological organisation determines itself in the sense that the effects of its activity contribute to determine its own conditions of existence. We suggest that not any kind of circular regime realises self-determination, which should be specifically understood as self-constraint: in biological systems, in particular, self-constraint (...)
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  • Toward a More General Understanding of Bohr’s Complementarity: Insights from Modeling of Ion Channels.Srdjan Kesić - 2021 - Acta Biotheoretica 69 (4):723-744.
    Some contemporary theorists such as Mazzocchi, Theise and Kafatos are convinced that the reformed complementarity may redefine how we might exploit the complexity theory in 21st-century life sciences research. However, the motives behind the profound re-invention of “biological complementarity” need to be substantiated with concrete shreds of evidence about this principle’s applicability in real-life science experimentation, which we found missing in the literature. This paper discusses such pieces of evidence by confronting Bohr’s complementarity and ion channel modeling practice. We examine (...)
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  • The challenges of purely mechanistic models in biology and the minimum need for a 'mechanism-plus-X' framework.Sepehr Ehsani - 2018 - Dissertation, University College London
    Ever since the advent of molecular biology in the 1970s, mechanical models have become the dogma in the field, where a "true" understanding of any subject is equated to a mechanistic description. This has been to the detriment of the biomedical sciences, where, barring some exceptions, notable new feats of understanding have arguably not been achieved in normal and disease biology, including neurodegenerative disease and cancer pathobiology. I argue for a "mechanism-plus-X" paradigm, where mainstay elements of mechanistic models such as (...)
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