80,634 research outputs found
Artificial Hydrocarbon Networks Fuzzy Inference System
This paper presents a novel fuzzy inference model based on artificial hydrocarbon networks, a computational algorithm for modeling problems based on chemical hydrocarbon compounds. In particular, the proposed fuzzy-molecular inference model (FIM-model) uses molecular units of information to partition the output space in the defuzzification step. Moreover, these molecules are linguistic units that can be partially understandable due to the organized structure of the topology and metadata parameters involved in artificial hydrocarbon networks. In addition, a position controller for a direct current (DC) motor was implemented using the proposed FIM-model in type-1 and type-2 fuzzy inference systems. Experimental results demonstrate that the fuzzy-molecular inference model can be applied as an alternative of type-2 Mamdani’s fuzzy control systems because the set of molecular units can deal with dynamic uncertainties mostly present in real-world control applications
Bringing Molecules Back into Molecular Evolution
Much molecular-evolution research is concerned with sequence analysis. Yet these sequences represent real, three-dimensional molecules with complex structure and function. Here I highlight a growing trend in the field to incorporate molecular structure and function into computational molecular-evolution work. I consider three focus areas: reconstruction and analysis of past evolutionary events, such as phylogenetic inference or methods to infer selection pressures; development of toy models and simulations to identify fundamental principles of molecular evolution; and atom-level, highly realistic computational modeling of molecular structure and function aimed at making predictions about possible future evolutionary events
Birth/birth-death processes and their computable transition probabilities with biological applications
Birth-death processes track the size of a univariate population, but many
biological systems involve interaction between populations, necessitating
models for two or more populations simultaneously. A lack of efficient methods
for evaluating finite-time transition probabilities of bivariate processes,
however, has restricted statistical inference in these models. Researchers rely
on computationally expensive methods such as matrix exponentiation or Monte
Carlo approximation, restricting likelihood-based inference to small systems,
or indirect methods such as approximate Bayesian computation. In this paper, we
introduce the birth(death)/birth-death process, a tractable bivariate extension
of the birth-death process. We develop an efficient and robust algorithm to
calculate the transition probabilities of birth(death)/birth-death processes
using a continued fraction representation of their Laplace transforms. Next, we
identify several exemplary models arising in molecular epidemiology,
macro-parasite evolution, and infectious disease modeling that fall within this
class, and demonstrate advantages of our proposed method over existing
approaches to inference in these models. Notably, the ubiquitous stochastic
susceptible-infectious-removed (SIR) model falls within this class, and we
emphasize that computable transition probabilities newly enable direct
inference of parameters in the SIR model. We also propose a very fast method
for approximating the transition probabilities under the SIR model via a novel
branching process simplification, and compare it to the continued fraction
representation method with application to the 17th century plague in Eyam.
Although the two methods produce similar maximum a posteriori estimates, the
branching process approximation fails to capture the correlation structure in
the joint posterior distribution
Genealogical lineage sorting leads to significant, but incorrect Bayesian multilocus inference of population structure
Over the past decades, the use of molecular markers has revolutionized biology and led to the foundation of a new research discipline—phylogeography. Of particular interest has been the inference of population structure and biogeography. While initial studies focused on mtDNA as a molecular marker, it has become apparent that selection and genealogical lineage sorting could lead to erroneous inferences. As it is not clear to what extent these forces affect a given marker, it has become common practice to use the combined evidence from a set of molecular markers as an attempt to recover the signals that approximate the true underlying demography. Typically, the number of markers used is determined by either budget constraints or by statistical power required to recognize significant population differentiation. Using microsatellite markers from Drosophila and humans, we show that even large numbers of loci (>50) can frequently result in statistically well-supported, but incorrect inference of population structure using the software baps. Most importantly, genomic features, such as chromosomal location, variability of the markers, or recombination rate, cannot explain this observation. Instead, it can be attributed to sampling variation among loci with different realizations of the stochastic lineage sorting. This phenomenon is particularly pronounced for low levels of population differentiation. Our results have important implications for ongoing studies of population differentiation, as we unambiguously demonstrate that statistical significance of population structure inferred from a random set of genetic markers cannot necessarily be taken as evidence for a reliable demographic inference
Defining a robust biological prior from Pathway Analysis to drive Network Inference
Inferring genetic networks from gene expression data is one of the most
challenging work in the post-genomic era, partly due to the vast space of
possible networks and the relatively small amount of data available. In this
field, Gaussian Graphical Model (GGM) provides a convenient framework for the
discovery of biological networks. In this paper, we propose an original
approach for inferring gene regulation networks using a robust biological prior
on their structure in order to limit the set of candidate networks.
Pathways, that represent biological knowledge on the regulatory networks,
will be used as an informative prior knowledge to drive Network Inference. This
approach is based on the selection of a relevant set of genes, called the
"molecular signature", associated with a condition of interest (for instance,
the genes involved in disease development). In this context, differential
expression analysis is a well established strategy. However outcome signatures
are often not consistent and show little overlap between studies. Thus, we will
dedicate the first part of our work to the improvement of the standard process
of biomarker identification to guarantee the robustness and reproducibility of
the molecular signature.
Our approach enables to compare the networks inferred between two conditions
of interest (for instance case and control networks) and help along the
biological interpretation of results. Thus it allows to identify differential
regulations that occur in these conditions. We illustrate the proposed approach
by applying our method to a study of breast cancer's response to treatment
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