Fragment Grammars: Exploring Computation and Reuse in Language

Language relies on a division of labor between stored units and structure building operations which combine the stored units into larger structures. This division of labor leads to a tradeoff: more structure-building means less need to store while more storage means less need to compute structure. We develop a hierarchical Bayesian model called fragment grammar to explore the optimum balance between structure-building and reuse. The model is developed in the context of stochastic functional programming (SFP) and in particular using a probabilistic variant of Lisp known as the Church programming language (Goodman, Mansinghka, Roy, Bonawitz, & Tenenbaum, 2008). We show how to formalize several probabilistic models of language structure using Church, and how fragment grammar generalizes one of them---adaptor grammars (Johnson, Griffiths, & Goldwater, 2007). We conclude with experimental data with adults and preliminary evaluations of the model on natural language corpus data

How Gibbs distributions may naturally arise from synaptic adaptation mechanisms. A model-based argumentation

This paper addresses two questions in the context of neuronal networks dynamics, using methods from dynamical systems theory and statistical physics: (i) How to characterize the statistical properties of sequences of action potentials ("spike trains") produced by neuronal networks ? and; (ii) what are the effects of synaptic plasticity on these statistics ? We introduce a framework in which spike trains are associated to a coding of membrane potential trajectories, and actually, constitute a symbolic coding in important explicit examples (the so-called gIF models). On this basis, we use the thermodynamic formalism from ergodic theory to show how Gibbs distributions are natural probability measures to describe the statistics of spike trains, given the empirical averages of prescribed quantities. As a second result, we show that Gibbs distributions naturally arise when considering "slow" synaptic plasticity rules where the characteristic time for synapse adaptation is quite longer than the characteristic time for neurons dynamics.Comment: 39 pages, 3 figure

Gene Expression and its Discontents: Developmental disorders as dysfunctions of epigenetic cognition

Systems biology presently suffers the same mereological and sufficiency fallacies that haunt neural network models of high order cognition. Shifting perspective from the massively parallel space of gene matrix interactions to the grammar/syntax of the time series of expressed phenotypes using a cognitive paradigm permits import of techniques from statistical physics via the homology between information source uncertainty and free energy density. This produces a broad spectrum of possible statistical models of development and its pathologies in which epigenetic regulation and the effects of embedding environment are analogous to a tunable enzyme catalyst. A cognitive paradigm naturally incorporates memory, leading directly to models of epigenetic inheritance, as affected by environmental exposures, in the largest sense. Understanding gene expression, development, and their dysfunctions will require data analysis tools considerably more sophisticated than the present crop of simplistic models abducted from neural network studies or stochastic chemical reaction theory

The cultural epigenetics of psychopathology: The missing heritability of complex diseases found?

We extend a cognitive paradigm for gene expression based on the asymptotic limit theorems of information theory to the epigenetic epidemiology of mental disorders. In particular, we recognize the fundamental role culture plays in human biology, another heritage mechanism parallel to, and interacting with, the more familiar genetic and epigenetic systems. We do this via a model through which culture acts as another tunable epigenetic catalyst that both directs developmental trajectories, and becomes convoluted with individual ontology, via a mutually-interacting crosstalk mediated by a social interaction that is itself culturally driven. We call for the incorporation of embedding culture as an essential component of the epigenetic regulation of human mental development and its dysfunctions, bringing what is perhaps the central reality of human biology into the center of biological psychiatry. Current US work on gene-environment interactions in psychiatry must be extended to a model of gene-environment-culture interaction to avoid becoming victim of an extreme American individualism that threatens to create paradigms particular to that culture and that are, indeed, peculiar in the context of the world's cultures. The cultural and epigenetic systems of heritage may well provide the 'missing' heritability of complex diseases now under so much intense discussion