Dragan Djuric

Model Driven Engineering and Ontology Development

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Ontology Modeling and MDA.

The paper presents Ontology Definition Metamodel (ODM) that enables using Model Driven Architecture (MDA) standards in ontological engineering. Other similar metamodels are based on ontology representation languages, such as RDF(S), DAML+OIL, etc. However, none of these other solutions uses the recent W3C effort – The Web Ontology Language (OWL). In our approach, we firstly define the ODM place in the context of the MDA four-layer architecture and identify the main OWL concepts. Then, we define ODM using Meta-Object Facility (MOF). The relations between similar MOF and OWL concepts are discussed in order to show their differences (e.g. MOF or UML Class and OWL Class). The proposed ODM is a good starting point for defining an OWL-based UML profile that will enable using the well-known UML notation in ontological engineering more extensively.

Converting UML to OWL ontologies

This paper presents automatic generation of the Web Ontology Language (OWL) from an UML model. The solution is based on an MDA-defined architecture for ontology development and the Ontology UML Profile (OUP). A conversion, that we present here, transforms an ontology from its OUP definition (i.e. XML Metadata Interchange -- XMI) into OWL description. Accordingly, we illustrate how an OUP-developed ontology can be shared with ontological engineering tools (i.e. Protégé).

MDA-based Automatic OWL Ontology Development

This paper presents an eXtensible Stylesheet Language Transformation (XSLT)-based approach for automatic generation of the Web Ontology Language (OWL) from a UML model. Similar solutions that treat this problem are mostly partial since they do not use full metamodeling potentials. Although they emphasize the notion of the use UML for ontology development and propose necessary transformations into Semantic Web languages (e.g., RDF Schema, DAML, DAML+OIL), their UML models must be further refined using ontology-specialized tool. None of these approaches enables instance modeling and generation of OWL ontologies. In our efforts to make ontological and software engineering techniques closer, we have firstly defined ontology metamodeling architecture using Model Driven Architecture (MDA) concepts. This architecture consists of the Ontology Definition Metamodel defined using Meta Object Facility (MOF) and based on the OWL, as well as the related Ontology UML Profile (OUP). A transformation, that we present here, extends this metamodeling architecture and transforms an ontology from its OUP definition (i.e., XML Metadata Interchange – XMI) into the OWL description. Accordingly, we illustrate how an OUP-developed ontology can be shared with ontological engineering tools (i.e., Protégé).

The Tao of Modeling Spaces.

The paper introduces modeling spaces in order to help software practitioner to understand modeling. Usually software engineers often think of a specific kind of models – UML models, but there are many open questions such as: Should we assume that the code we write is a model or not; What are models and metamodels, and why do we need them; What does it mean to transform a model into a programming language. Unlike current research efforts that answer to those questions in rather partial ways, we define a formal encompassing framework (i.e. Modeling spaces) for studying many modeling problems in a more comprehensive way. We illustrate the benefits of that framework for explaining present dilemmas practitioners have regarding models, metamodels, and model transformations.

The activity of erythrocyte and brain Na+/K+ and Mg2+-ATPases in rats subjected to acute homocysteine and homocysteine thiolactone administration

Hyperhomocysteinemia is associated with various pathologies including cardiovascular disease, stroke, and cognitive dysfunctions. Systemic administration of homocysteine can trigger seizures in animals, and patients with homocystinuria suffer from epileptic seizures. Available data suggest that homocysteine can be harmful to human cells because of its metabolic conversion to homocysteine thiolactone, a reactive thioester. A number of reports have demonstrated a reduction of Na+/K+-ATPase activity in cerebral ischemia, epilepsy and neurodegeneration possibly associated with excitotoxic mechanisms. The aim of this study was to examine the in vivo effects of d,l-homocysteine and d,l-homocysteine thiolactone on Na+/K+- and Mg2+-ATPase activities in erythrocyte (RBC), brain cortex, hippocampus, and brain stem of adult male rats. Our results demonstrate a moderate inhibition of rat hippocampal Na+/K+-ATPase activity by d,l-homocysteine, which however expressed no effect on the activity of this enzyme in the cortex and brain stem. In contrast,d,l-homocysteine thiolactone strongly inhibited Na+/K+-ATPase activity in cortex, hippocampus and brain stem of rats. RBC Na+/K+-ATPase and Mg2+-ATPase activities were not affected by d,l-homocysteine, while d,l-homocysteine thiolactone inhibited only Na+/K+-ATPase activity. This study results show that homocysteine thiolactone significantly inhibits Na+/K+-ATPase activity in the cortex, hippocampus, and brain stem, which may contribute at least in part to the understanding of excitotoxic and convulsive properties of this substance.

Penetrating the Omerta of Predatory Publishing: The Romanian Connection

AbstractNot so long ago, a well institutionalized predatory journal exposed itself by publishing a hoax article that blew the whistle for its devastating influence on the academic affairs of a small country. This paper puts that experiment in context, gives all the important details and analyzes the results. The experiment was inspired by well-known cases of scientific activism and is in line with recent efforts against predatory publishers. The paper presents the evidence in detail and uses it to analyze the publishing practices of the offending journal, using established criteria for assessing predatory publications. That journal somehow acquired an impact factor and charged money to publish thousands of “scientific” papers without any peer review. Since the impact factor is the major official evaluation criteria for scientists in Serbia, these papers disturbed the whole academic evaluation process. Credentials acquired by those publications form a strong obstacle to institutionalized reasoned efforts against such practices. This case warns the whole community of the long lasting damage when journals with low publishing ethics are taken seriously.

Inhibition of the Neuronal Nitric Oxide Synthase Potentiates Homocysteine Thiolactone- Induced Seizures in Adult Rats

Nitric oxide (NO), one of the gaseous neurotransmitters, is produced in reaction catalyzed by family of NO synthases (NOS). The involvement of neuronal NOS (nNOS) in seizures induced by homocysteine thiolactone has not been studied. Therefore, the aim of this study was to determine the effects of 7-nitroindazole, a selective nNOS inhibitor, on behavioral manifestations of homocysteine - induced seizures in adult rats. Adult male Wistar albino rats were treated with 7-nitroindazole (25, 50 and 75 mg/kg, i.p.) 30 min before injection of subconvulsive dose of homocysteine (D,L homocysteine thiolactone 5.5 mmol/kg, i.p.). Convulsive behavior was assessed during 90 min upon homocysteine administration by the following parameters: seizure incidence, duration of latency, number of seizure episodes per rat and their severity. Severity of seizures was evaluated using a descriptive scale graded from 0 to 4. It was shown that 7-nitroindazole increased seizure incidence, shortened latency time to first seizure, increased number of seizure episodes per rat and increased severity of seizures induced by homocysteine in rats. 7- nitroindazole in dose of 25 mg/kg led to a statistically significant increase in the seizure incidence and number of seizure episodes per rat, while doses of 50 and 75 mg/kg significantly increased severity of homocysteine-induced seizures. It could be concluded that inhibition of nNOS by 7-nitroindazole potentiates seizures induced by homocysteine in rats.

The role of nitric oxide in convulsions induced by lindane in rats.

Lindane is an organochloride pesticide and scabicide. It evokes convulsions mainly trough the blockage of GABA(A) receptors. Nitric oxide (NO), gaseous neurotransmitter, has contradictor role in epileptogenesis due to opposite effects of L-arginine, precursor of NO syntheses (NOS), and L-NAME (NOS inhibitor) observed in different epilepsy models. The aim of the current study was to determine the effects of NO on the behavioral and EEG characteristics of lindane-induced epilepsy in male Wistar albino rats. The administration of L-arginine (600, 800 and 1000 mg/kg, i.p.) in dose-dependent manner significantly increased convulsion incidence and severity and shortened latency time to first convulsion elicited by lower lindane dose (4 mg/kg, i.p.). On the contrary, pretreatment with L-NAME (500, 700 and 900 mg/kg, i.p.) decreased convulsion incidence and severity and prolonged latency time to convulsion following injection with a convulsive dose of lindane (8 mg/kg, i.p.). EEG analyses showed increase of number and duration of ictal periods in EEG of rats receiving l-arginine prior to lindane and decrease of this number in rats pretreated with L-NAME. These results support the conclusion that NO plays a role of endogenous convulsant in rat model of lindane seizures.

Coordination Between Nitric Oxide and Superoxide Anion Radical During Progressive Exercise in Elite Soccer Players

Background: Exercise increases production of reactive oxygen and nitrogen species (RONS) via several mechanisms. Inter alia, increased blood flow during exercise exposes endothelial cells to shear stress, resulting in increased nitric oxide (NO) production. Increased oxygen consumption or hypoxia during exercise induces increased production of superoxide anion radical (O2-). Objective: This study investigates the effects of maximal progressive treadmill exercise test on time-course of peripheral blood NO and O2- production, as well as the effect of long-term training on NO bioavailability. Methods: Blood samples of 19 elite soccer players were gathered immediately before the test, during last 10 sec of every test stage, and during active recovery phases. Results: Significant increase (p<0.05) in NO production (estimated through nitrites (NO2-)), found between stage I (5.69 ± 1.32 nmol/ml) and basal values (5.36 ± 1.25 nmol/ml), was followed by the decrease in stage II (4.21 ± 0.42 nmol/ml) and production lower than basal to the end of the test. Significant increase (p<0.05) in O2- values was found between stage I (4.18 ± 0.77 nmol/ml) and resting values (4.01 ± 0.69 nmol/ml), and at stages V (4.24 ± 0.85 nmol/ml) and 1st phase of recovery (4.39 ± 0.92 nmol/ml). Conclusion: The regression lines of NO2- and O2- crossed at the level of anaerobic threshold, suggesting that anaerobic threshold could be of a crucial importance not only in the anaerobic and aerobic metabolism but in mechanisms of signal transductions as well. Long-term exercise increases NO bioavailability, and there is positive correlation between NO bioavailability and maximal oxygen uptake (VO2max).