Defeasible Reasoning in SROEL: from Rational Entailment to Rational Closure

In this work we study a rational extension $SROEL^R T$ of the low complexity description logic SROEL, which underlies the OWL EL ontology language. The extension involves a typicality operator T, whose semantics is based on Lehmann and Magidor's ranked models and allows for the definition of defeasible inclusions. We consider both rational entailment and minimal entailment. We show that deciding instance checking under minimal entailment is in general $\Pi^P_2$-hard, while, under rational entailment, instance checking can be computed in polynomial time. We develop a Datalog calculus for instance checking under rational entailment and exploit it, with stratified negation, for computing the rational closure of simple KBs in polynomial time.Comment: Accepted for publication on Fundamenta Informatica

Characterized subgroups of topological abelian groups

A subgroup $H$ of a topological abelian group $X$ is said to be characterized by a sequence $\mathbf v =(v_n)$ of characters of $X$ if $H=\{x\in X:v_n(x)\to 0\ \text{in}\ \mathbb T\}$. We study the basic properties of characterized subgroups in the general setting, extending results known in the compact case. For a better description, we isolate various types of characterized subgroups. Moreover, we introduce the relevant class of autochacaracterized groups (namely, the groups that are characterized subgroups of themselves by means of a sequence of non-null characters); in the case of locally compact abelian groups, these are proved to be exactly the non-compact ones. As a by-product of our results, we find a complete description of the characterized subgroups of discrete abelian groups.Comment: 22 page

Novel perspectives in redox biology and pathophysiology of failing myocytes: modulation of the intramyocardial redox milieu for therapeutic interventions - A review article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology

The prevalence of heart failure (HF) is still increasing worldwide, with enormous human, social, and economic costs, in spite of huge efforts in understanding pathogeneticmechanisms and in developing effective therapies that have transformed this syndrome into a chronic disease. Myocardial redox imbalance is a hallmark of this syndrome, since excessive reactive oxygen and nitrogen species can behave as signaling molecules in the pathogenesis of hypertrophy and heart failure, leading to dysregulation of cellular calcium handling, of the contractile machinery, of myocardial energetics and metabolism, and of extracellular matrix deposition. Recently, following new interesting advances in understanding myocardial ROS and RNS signaling pathways, new promising therapeutical approaches with antioxidant properties are being developed, keeping in mind that scavenging ROS and RNS tout court is detrimental as well, since these molecules also play a role in physiological myocardial homeostasis