Specifying agent interaction protocols with UML activity diagrams

In this paper, we will demonstrate how the Unified Modeling Language (UML) can be used to describe agent interaction protocols. The approach that is presented in this paper does not propose major enhancements or completely new diagrams but instead it relies on existing UML elements that are part of the standard. This conformity with the base UML is a major advantage of the idea as it prevents a diversification of the UML into different potentially incompatible dialects. The practical use of the method is demonstrated in the specification of a realistic agent interaction protocol

A process model for the design of multi-agent systems

In this paper, we propose a pragmatic process model for the development of multi-agent system based on the combination of standard software engineering techniques with a special focus on multi-agent systems. The resulting process model is the attempt to make our experience in the design of multi-agent systems available to other system designers. The approach presented in this paper has evolved over several years and it has been successfully applied and refined in different types of multi-agent systems. A short case study of our latest project is included in the paper

The EMS model

The interface which connects the agent to its environment is usually based on the particular architecture of the agent. This makes it difficult for agents of different architectures to interact with each other within the same virtual environment. In this paper, we present a model to describe the agent/world interface in a generic, architecture independent way. The usefulness of the model is demonstrated in a generic testbed library which facilitates rapid prototyping for experimental multi-agent systems. Also, a network protocol derived from the basic model which allows for the development of distributed testbeds is presented

Ein System zur Definition und Ausführung von Protokollen für Multi-Agentsysteme

Mit der hier entwickelten Protokollsprache können Multiagenten-Protokolle klar und eindeutig spezifiziert werden. Durch die automatische Code-Generierung aus einer Protokoll-Spezifikation entfällt der fehleranfällige Arbeitsschritt der Implementierung des festgelegten Protokoll-Ablaufs. Das Protokoll-Ausführungs-Systems übernimmt die Steuerung des Ablaufs, erkennt Fehler (z.B. falsche Nachrichten) und überwacht Timeout-Fristen. Ein Programmierer muss nach der Festlegung eines Protokolls lediglich den Code für die anwendungsabhängigen Abläufe (Anwendungs-Prozeduren) und die Agentenumgebung (Zugriff auf andere Agenten, Zustellen der Nachrichten) zu Verfügung stellen. Durch die Trennung von Protokoll und Anwendung können so einmal entworfene Protokolle für unterschiedliche Anwendungen verwendet werden, ohne den eigentlichen Protokoll-code zu verändern. Durch dieses System ergibt sich für das Deutsche Forschungszentrum für Künstliche Intelligenz die Möglichkeit, neue Protokolle schneller zu entwickeln und einzusetzen

Symbolic dynamics and synchronization of coupled map networks with multiple delays

We use symbolic dynamics to study discrete-time dynamical systems with multiple time delays. We exploit the concept of avoiding sets, which arise from specific non-generating partitions of the phase space and restrict the occurrence of certain symbol sequences related to the characteristics of the dynamics. In particular, we show that the resulting forbidden sequences are closely related to the time delays in the system. We present two applications to coupled map lattices, namely (1) detecting synchronization and (2) determining unknown values of the transmission delays in networks with possibly directed and weighted connections and measurement noise. The method is applicable to multi-dimensional as well as set-valued maps, and to networks with time-varying delays and connection structure.Comment: 13 pages, 4 figure

Noncompaction of the Ventricular Myocardium Is Associated with a De Novo Mutation in the β-Myosin Heavy Chain Gene

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the α- and β-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium

Genome-wide interaction study of a proxy for stress-sensitivity and its prediction of major depressive disorder

Individual response to stress is correlated with neuroticism and is an important predictor of both neuroticism and the onset of major depressive disorder (MDD). Identification of the genetics underpinning individual differences in response to negative events (stress-sensitivity) may improve our understanding of the molecular pathways involved, and its association with stress-related illnesses. We sought to generate a proxy for stress-sensitivity through modelling the interaction between SNP allele and MDD status on neuroticism score in order to identify genetic variants that contribute to the higher neuroticism seen in individuals with a lifetime diagnosis of depression compared to unaffected individuals. Meta-analysis of genome-wide interaction studies (GWIS) in UK Biobank (N = 23,092) and Generation Scotland: Scottish Family Health Study (N = 7,155) identified no genome-wide significance SNP interactions. However, gene-based tests identified a genome-wide significant gene, ZNF366, a negative regulator of glucocorticoid receptor function implicated in alcohol dependence (p = 1.48x10-7; Bonferroni-corrected significance threshold p < 2.79x10-6). Using summary statistics from the stress-sensitivity term of the GWIS, SNP heritability for stress-sensitivity was estimated at 5.0%. In models fitting polygenic risk scores of both MDD and neuroticism derived from independent GWAS, we show that polygenic risk scores derived from the UK Biobank stress-sensitivity GWIS significantly improved the prediction of MDD in Generation Scotland. This study may improve interpretation of larger genome-wide association studies of MDD and other stress-related illnesses, and the understanding of the etiological mechanisms underpinning stress-sensitivity

Fifth European Dirofilaria and Angiostrongylus Days (FiEDAD) 2016

Peer reviewe

Hair Cortisol in Twins : Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes

A. Palotie on työryhmän jäsen.Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables.Peer reviewe

The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals

To dissect the genetic architecture of blood pressure and assess effects on target-organ damage, we analyzed 128,272 SNPs from targeted and genome-wide arrays in 201,529 individuals of European ancestry and genotypes from an additional 140,886 individuals were used for validation. We identified 66 blood pressure loci, of which 17 were novel and 15 harbored multiple distinct association signals. The 66 index SNPs were enriched for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary role in blood pressure control through modulation of vascular tone across multiple tissues. The 66 index SNPs combined in a risk score showed comparable effects in 64,421 individuals of non-European descent. The 66-SNP blood pressure risk score was significantly associated with target-organ damage in multiple tissues, with minor effects in the kidney. Our findings expand current knowledge of blood pressure pathways and highlight tissues beyond the classic renal system in blood pressure regulation