Answer Sets for Consistent Query Answering in Inconsistent Databases

A relational database is inconsistent if it does not satisfy a given set of integrity constraints. Nevertheless, it is likely that most of the data in it is consistent with the constraints. In this paper we apply logic programming based on answer sets to the problem of retrieving consistent information from a possibly inconsistent database. Since consistent information persists from the original database to every of its minimal repairs, the approach is based on a specification of database repairs using disjunctive logic programs with exceptions, whose answer set semantics can be represented and computed by systems that implement stable model semantics. These programs allow us to declare persistence by defaults and repairing changes by exceptions. We concentrate mainly on logic programs for binary integrity constraints, among which we find most of the integrity constraints found in practice.Comment: 34 page

Turning an action formalism into a planner

The paper describes a case study that explores the idea of building a planner with a neat semantics of the plans it produces, by choosing some action formalism that is "ideal" for the planning application and building the planner accordingly. In general-and particularly so for the action formalism used in this study, which is quite expressive-this strategy is unlikely to yield fast and efficient planners if the formalism is used naively. Therefore, we adopt the idea that the planner approximates the theoretically ideal plans, where the approximation gets closer, the more run time the planner is allowed. As the particular formalism underlying our study allows a significant degree of uncertainty to be modeled and copes with the ramification problem, we end up in a planner that is functionally comparable to modern anytime uncertainty planners, yet is based on a neat formal semantics. To appear in the Journal of Logic and Computation, 1994. The paper is written in English

Characterizing and computing causes for query answers in databases from database repairs and repair programs

A correspondence between database tuples as causes for query answers in databases and tuple-based repairs of inconsistent databases with respect to denial constraints has already been established. In this work, answer-set programs that specify repairs of databases are used as a basis for solving computational and reasoning problems about causes. Here, causes are also introduced at the attribute level by appealing to a both null-based and attribute-based repair semantics. The corresponding repair programs are presented, and they are used as a basis for computation and reasoning about attribute-level causes

From cancer gene expression to protein interaction: Interaction prediction, network reasoning and applications in pancreatic cancer

Microarray technologies enable scientists to identify co-expressed genes at large scale. However, the gene expression analysis does not show functional relationships between co-expressed genes. There is a demand for effective approaches to analyse gene expression data to enable biological discoveries that can lead to identification of markers or therapeutic targets of many diseases. In cancer research, a number of gene expression screens have been carried out to identify genes differentially expressed in cancerous tissue such as Pancreatic Ductal Adenocarcinoma (PDAC). PDAC carries very poor prognosis, it eludes early detection and is characterised by its aggressiveness and resistance to currently available therapies. To identify molecular markers and suitable targets, there exist a research effort that maps differentially expressed genes to protein interactions to gain an understanding at systems level. Such interaction networks have a complex interconnected structure, whose the understanding of which is not a trivial task. Several formal approaches use simulation to support the investigation of such networks. These approaches suffer from the missing knowledge concerning biological systems. Reasoning in the other hand has the advantage of dealing with incomplete and partial information of the network knowledge. The initial approach adopted was to provide an algorithm that utilises a network-centric approach to pancreatic cancer, by re-constructing networks from known interactions and predicting novel protein interactions from structural templates. This method was applied to a data set of co-expressed PDAC genes. To this end, structural domains for the gene products are identified by using threading which is a 3D structure prediction technique. Next, the Protein Structure Interaction Database (SCOPPI), a database that classifies and annotates domain interactions derived from all known protein structures, is used to find templates of structurally interacting domains. Moreover, a network of related biological pathways for the PDAC data was constructed. In order to reason over molecular networks that are affected by dysregulation of gene expression, BioRevise was implemented. It is a belief revision system where the inhibition behaviour of reactions is modelled using extended logic programming. The system computes a minimal set of enzymes whose malfunction explains the abnormal expression levels of observed metabolites or enzymes. As a result of this research, two complementary approaches for the analysis of pancreatic cancer gene expression data are presented. Using the first approach, the pathways found to be largely affected in pancreatic cancer are signal transduction, actin cytoskeleton regulation, cell growth and cell communication. The analysis indicates that the alteration of the calcium pathway plays an important role in pancreas specific tumorigenesis. Furthermore, the structural prediction method reveals ~ 700 potential protein-protein interactions from the PDAC microarray data, among them, 81 novel interactions such as: serine/threonine kinase CDC2L1 interacting with cyclin-dependent kinase inhibitor CDKN3 and the tissue factor pathway inhibitor 2 (TFPI2) interacting with the transmembrane protease serine 4 (TMPRSS4). These resulting genes were further investigated and some were found to be potential therapeutic markers for PDAC. Since TMPRSS4 is involved in metastasis formation, it is hypothesised that the upregulation of TMPRSS4 and the downregulation of its predicted inhibitor TFPI2 plays an important role in this process. The predicted protein-protein network inspired the analysis of the data from two other perspectives. The resulting protein-protein interaction network highlighted the importance of the co-expression of KLK6 and KLK10 as prognostic factors for survival in PDAC as well as the construction of a PDAC specific apoptosis pathway to study different effects of multiple gene silencing in order to reactivate apoptosis in PDAC. Using the second approach, the behaviour of biological interaction networks using computational logic formalism was modelled, reasoning over the networks is enabled and the abnormal behaviour of its components is explained. The usability of the BioRevise system is demonstrated through two examples, a metabolic disorder disease and a deficiency in a pancreatic cancer associated pathway. The system successfully identified the inhibition of the enzyme glucose-6-phosphatase as responsible for the Glycogen storage disease type I, which according to literature is known to be the main reason for this disease. Furthermore, BioRevise was used to model reaction inhibition in the Glycolysis pathway which is known to be affected by Pancreatic cancer