29,234 research outputs found
Application of new probabilistic graphical models in the genetic regulatory networks studies
This paper introduces two new probabilistic graphical models for
reconstruction of genetic regulatory networks using DNA microarray data. One is
an Independence Graph (IG) model with either a forward or a backward search
algorithm and the other one is a Gaussian Network (GN) model with a novel
greedy search method. The performances of both models were evaluated on four
MAPK pathways in yeast and three simulated data sets. Generally, an IG model
provides a sparse graph but a GN model produces a dense graph where more
information about gene-gene interactions is preserved. Additionally, we found
two key limitations in the prediction of genetic regulatory networks using DNA
microarray data, the first is the sufficiency of sample size and the second is
the complexity of network structures may not be captured without additional
data at the protein level. Those limitations are present in all prediction
methods which used only DNA microarray data.Comment: 38 pages, 3 figure
Detection of regulator genes and eQTLs in gene networks
Genetic differences between individuals associated to quantitative phenotypic
traits, including disease states, are usually found in non-coding genomic
regions. These genetic variants are often also associated to differences in
expression levels of nearby genes (they are "expression quantitative trait
loci" or eQTLs for short) and presumably play a gene regulatory role, affecting
the status of molecular networks of interacting genes, proteins and
metabolites. Computational systems biology approaches to reconstruct causal
gene networks from large-scale omics data have therefore become essential to
understand the structure of networks controlled by eQTLs together with other
regulatory genes, and to generate detailed hypotheses about the molecular
mechanisms that lead from genotype to phenotype. Here we review the main
analytical methods and softwares to identify eQTLs and their associated genes,
to reconstruct co-expression networks and modules, to reconstruct causal
Bayesian gene and module networks, and to validate predicted networks in
silico.Comment: minor revision with typos corrected; review article; 24 pages, 2
figure
Parallel Implementation of Efficient Search Schemes for the Inference of Cancer Progression Models
The emergence and development of cancer is a consequence of the accumulation
over time of genomic mutations involving a specific set of genes, which
provides the cancer clones with a functional selective advantage. In this work,
we model the order of accumulation of such mutations during the progression,
which eventually leads to the disease, by means of probabilistic graphic
models, i.e., Bayesian Networks (BNs). We investigate how to perform the task
of learning the structure of such BNs, according to experimental evidence,
adopting a global optimization meta-heuristics. In particular, in this work we
rely on Genetic Algorithms, and to strongly reduce the execution time of the
inference -- which can also involve multiple repetitions to collect
statistically significant assessments of the data -- we distribute the
calculations using both multi-threading and a multi-node architecture. The
results show that our approach is characterized by good accuracy and
specificity; we also demonstrate its feasibility, thanks to a 84x reduction of
the overall execution time with respect to a traditional sequential
implementation
Intrusion Detection System using Bayesian Network Modeling
Computer Network Security has become a critical and important issue due to ever increasing cyber-crimes. Cybercrimes are spanning from simple piracy crimes to information theft in international terrorism. Defence security agencies and other militarily related organizations are highly concerned about the confidentiality and access control of the stored data. Therefore, it is really important to investigate on Intrusion Detection System (IDS) to detect and prevent cybercrimes to protect these systems. This research proposes a novel distributed IDS to detect and prevent attacks such as denial service, probes, user to root and remote to user attacks. In this work, we propose an IDS based on Bayesian network classification modelling technique. Bayesian networks are popular for adaptive learning, modelling diversity network traffic data for meaningful classification details. The proposed model has an anomaly based IDS with an adaptive learning process. Therefore, Bayesian networks have been applied to build a robust and accurate IDS. The proposed IDS has been evaluated against the KDD DAPRA dataset which was designed for network IDS evaluation. The research methodology consists of four different Bayesian networks as classification models, where each of these classifier models are interconnected and communicated to predict on incoming network traffic data. Each designed Bayesian network model is capable of detecting a major category of attack such as denial of service (DoS). However, all four Bayesian networks work together to pass the information of the classification model to calibrate the IDS system. The proposed IDS shows the ability of detecting novel attacks by continuing learning with different datasets. The testing dataset constructed by sampling the original KDD dataset to contain balance number of attacks and normal connections. The experiments show that the proposed system is effective in detecting attacks in the test dataset and is highly accurate in detecting all major attacks recorded in DARPA dataset. The proposed IDS consists with a promising approach for anomaly based intrusion detection in distributed systems. Furthermore, the practical implementation of the proposed IDS system can be utilized to train and detect attacks in live network traffi
Learning the structure of Bayesian Networks: A quantitative assessment of the effect of different algorithmic schemes
One of the most challenging tasks when adopting Bayesian Networks (BNs) is
the one of learning their structure from data. This task is complicated by the
huge search space of possible solutions, and by the fact that the problem is
NP-hard. Hence, full enumeration of all the possible solutions is not always
feasible and approximations are often required. However, to the best of our
knowledge, a quantitative analysis of the performance and characteristics of
the different heuristics to solve this problem has never been done before.
For this reason, in this work, we provide a detailed comparison of many
different state-of-the-arts methods for structural learning on simulated data
considering both BNs with discrete and continuous variables, and with different
rates of noise in the data. In particular, we investigate the performance of
different widespread scores and algorithmic approaches proposed for the
inference and the statistical pitfalls within them
Causal graphical models in systems genetics: A unified framework for joint inference of causal network and genetic architecture for correlated phenotypes
Causal inference approaches in systems genetics exploit quantitative trait
loci (QTL) genotypes to infer causal relationships among phenotypes. The
genetic architecture of each phenotype may be complex, and poorly estimated
genetic architectures may compromise the inference of causal relationships
among phenotypes. Existing methods assume QTLs are known or inferred without
regard to the phenotype network structure. In this paper we develop a
QTL-driven phenotype network method (QTLnet) to jointly infer a causal
phenotype network and associated genetic architecture for sets of correlated
phenotypes. Randomization of alleles during meiosis and the unidirectional
influence of genotype on phenotype allow the inference of QTLs causal to
phenotypes. Causal relationships among phenotypes can be inferred using these
QTL nodes, enabling us to distinguish among phenotype networks that would
otherwise be distribution equivalent. We jointly model phenotypes and QTLs
using homogeneous conditional Gaussian regression models, and we derive a
graphical criterion for distribution equivalence. We validate the QTLnet
approach in a simulation study. Finally, we illustrate with simulated data and
a real example how QTLnet can be used to infer both direct and indirect effects
of QTLs and phenotypes that co-map to a genomic region.Comment: Published in at http://dx.doi.org/10.1214/09-AOAS288 the Annals of
Applied Statistics (http://www.imstat.org/aoas/) by the Institute of
Mathematical Statistics (http://www.imstat.org
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