207 research outputs found
Causality, Information and Biological Computation: An algorithmic software approach to life, disease and the immune system
Biology has taken strong steps towards becoming a computer science aiming at
reprogramming nature after the realisation that nature herself has reprogrammed
organisms by harnessing the power of natural selection and the digital
prescriptive nature of replicating DNA. Here we further unpack ideas related to
computability, algorithmic information theory and software engineering, in the
context of the extent to which biology can be (re)programmed, and with how we
may go about doing so in a more systematic way with all the tools and concepts
offered by theoretical computer science in a translation exercise from
computing to molecular biology and back. These concepts provide a means to a
hierarchical organization thereby blurring previously clear-cut lines between
concepts like matter and life, or between tumour types that are otherwise taken
as different and may not have however a different cause. This does not diminish
the properties of life or make its components and functions less interesting.
On the contrary, this approach makes for a more encompassing and integrated
view of nature, one that subsumes observer and observed within the same system,
and can generate new perspectives and tools with which to view complex diseases
like cancer, approaching them afresh from a software-engineering viewpoint that
casts evolution in the role of programmer, cells as computing machines, DNA and
genes as instructions and computer programs, viruses as hacking devices, the
immune system as a software debugging tool, and diseases as an
information-theoretic battlefield where all these forces deploy. We show how
information theory and algorithmic programming may explain fundamental
mechanisms of life and death.Comment: 30 pages, 8 figures. Invited chapter contribution to Information and
Causality: From Matter to Life. Sara I. Walker, Paul C.W. Davies and George
Ellis (eds.), Cambridge University Pres
The Thermodynamics of Network Coding, and an Algorithmic Refinement of the Principle of Maximum Entropy
The principle of maximum entropy (Maxent) is often used to obtain prior
probability distributions as a method to obtain a Gibbs measure under some
restriction giving the probability that a system will be in a certain state
compared to the rest of the elements in the distribution. Because classical
entropy-based Maxent collapses cases confounding all distinct degrees of
randomness and pseudo-randomness, here we take into consideration the
generative mechanism of the systems considered in the ensemble to separate
objects that may comply with the principle under some restriction and whose
entropy is maximal but may be generated recursively from those that are
actually algorithmically random offering a refinement to classical Maxent. We
take advantage of a causal algorithmic calculus to derive a thermodynamic-like
result based on how difficult it is to reprogram a computer code. Using the
distinction between computable and algorithmic randomness we quantify the cost
in information loss associated with reprogramming. To illustrate this we apply
the algorithmic refinement to Maxent on graphs and introduce a Maximal
Algorithmic Randomness Preferential Attachment (MARPA) Algorithm, a
generalisation over previous approaches. We discuss practical implications of
evaluation of network randomness. Our analysis provides insight in that the
reprogrammability asymmetry appears to originate from a non-monotonic
relationship to algorithmic probability. Our analysis motivates further
analysis of the origin and consequences of the aforementioned asymmetries,
reprogrammability, and computation.Comment: 30 page
Approximations of Algorithmic and Structural Complexity Validate Cognitive-behavioural Experimental Results
We apply methods for estimating the algorithmic complexity of sequences to
behavioural sequences of three landmark studies of animal behavior each of
increasing sophistication, including foraging communication by ants, flight
patterns of fruit flies, and tactical deception and competition strategies in
rodents. In each case, we demonstrate that approximations of Logical Depth and
Kolmogorv-Chaitin complexity capture and validate previously reported results,
in contrast to other measures such as Shannon Entropy, compression or ad hoc.
Our method is practically useful when dealing with short sequences, such as
those often encountered in cognitive-behavioural research. Our analysis
supports and reveals non-random behavior (LD and K complexity) in flies even in
the absence of external stimuli, and confirms the "stochastic" behaviour of
transgenic rats when faced that they cannot defeat by counter prediction. The
method constitutes a formal approach for testing hypotheses about the
mechanisms underlying animal behaviour.Comment: 28 pages, 7 figures and 2 table
Evidence of Highly Regulated Genes (in-Hubs) in Gene Networks of Saccharomyces Cerevisiae
Uncovering interactions between genes, gene networks, is important to increase our understanding of intrinsic cellular processes and responses to external stimuli such as drugs. Gene networks can be computationally inferred from repeated measurements of gene expression, using algorithms, which assume that each gene is controlled by only a small number of other proteins. Here, by extending the transcription network with cofactors (defined from protein-protein binding data) as active regulators, we identified the effective gene network, providing evidence of in-hubs in the gene regulatory networks of yeast. Then, using the notion that in-hub genes will be differentially expressed over several experimental conditions, we designed an algorithm, the HubDetector, enabling identification of in-hubs directly from gene expression data. Applying the HubDetector to 488 genome-wide expression profiles from two independent datasets, we identified putative in-hubs overlapping significantly with in-hubs in the effective gene network
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