No description available.

In Multi-Agenten-Systemen (MAS) kooperieren und konkurrieren Agenten um ihre jeweiligen Ziele zu erreichen. Für optimierte Agenten-Interaktionen sind Kenntnisse über die aktuellen und zukünftigen Handlungen anderer Agenten (Interaktionsparter, IP) hilfreich. Bei der Ermittlung und Nutzung solcher Kenntnisse kommt dem automatischen Erkennen und Verstehen sowie der Vorhersage von Verhalten der IP auf Basis von Beobachtungen besondere Bedeutung zu. Die Dissertation beschäftigt sich mit der automatischen Bestimmung und Vorhersage von Verhalten der IP durch einen Modellierenden Agenten (MA). Der MA generiert fallbasierte, adaptive Verhaltens-Modelle seiner IP und verwendet diese zur Vorhersage ihrer Verhalten. Als Anwendungsszenario wird mit dem virtuellen Fußballspiel des RoboCup ein komplexes und populäres MAS betrachtet. Der Hauptbeitrag dieser Arbeit besteht in der Ausarbeitung, Realisierung und Evaluierung eines Ansatzes zur automatischen Verhaltens-Modellierung für ein komplexes Multi-Agenten-System. / In multi-agent-systems agents cooperate and compete to reach their personal goals. For optimized agent interactions it is helpful for an agent to have knowledge about the current and future behavior of other agents. Ideally the recognition and prediction of behavior should be done automatically. This work addresses a way of automatically classifying and an attempt at predicting the behavior of a team of agents, based on external observation only. A set of conditions is used to distinguish behaviors and to partition the resulting behavior space. From observed behavior, team specific behavior models are then generated using Case Based Reasoning. These models, which are derived from a number of virtual soccer games (RoboCup), are used to predict the behavior of a team during a new game. The main contribution of this work is the design, realization and evaluation of an automatic behavior modeling approach for complex multi-agent systems.

It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production.

It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production.