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The problem of electrothermal stability due to different cooling conditions has been investigated by computing the thermal transients in a nonplanar GTO-thyristor. In the first simulation, a steady state occurs with a heat sink removing all the dissipated power. In the second simulation severe thermal runaway is induced due to bad cooling conditions, allowing the analysis of destructive electrothermal interaction. The simulations are based on an advanced model for self-heating effects in silicon devices derived from first principles of irreversible thermodynamics. Self-consistently incorporating a phenomenological model of band gap narrowing in order to take account of heavy doping effects. The system of governing equations is valid in both the steady state and the transient regimes. Four characteristic effects contributing to the heat generation can be identified: Joule heating, recombination heating, Thomson heating, and carrier source heating. Thermal runaway is significantly accelerated in the simulations based on the thermodynamic model of thermoelectric transport compared to a conventional heuristic theory of thermoelectricity. The importance of the entropy balance equation is emphasized in order to derive the mathematical form of the heat flux and the current relations for electrons and holes. Limitations of underlying assumptions are discussed. It is shown that the heat generation implies the Thomson relations.

With the fast improvements of broadband technologies, more and more demanding services can be accessed. Broadband access is supported by a range of wireless and wireline technologies. Well known representatives are WLAN and UMTS for wireless and xDSL for wireline access. However, the highly varying nature of wireless channels and the crosstalk behavior of the DSL channel are typical traits, and most challenging to combat. Moreover, the stringent requirements of real-time applications require enhancements in service delivery. The tremendous interest in communication has driven the deployment of new access systems. Hence, for the End-to-End point of view, the service delivery multifarious due to the heterogeneity of the underlying transport network. Therefore, to enable a transport independent path set-up, application and network properties that may influence the user-perceived quality need to be unified. Thereby, media scalability plays a key role. Recently, cross-layer communication is getting acceptance as a method that efficiently increases the system performance. Unlike previous works that mainly addressed the issue of application based feedback, we focus on the information that the application can provide to guide the network for local stream management. We present the necessary set of Application Layer information for scalable audiovisual streams to offer individual QoS, at lowermost packet overhead. Finally, we show the sustainable gain in system performance based on a DSL use-case.

1. In order to elucidate the mechanism underlying the interactions between glucose and alloxan when competing for the sugar binding site of glucokinase from pancreatic B-cells or liver, the structural requirements of the enzyme for inhibition by alloxan and for protection by glucose were determined. 2. With a half-maximal inhibitory concentration of 5 microM, alloxan was the most potent pyrimidine derivative inhibitor of glucokinase. Uramil was a less potent enzyme inhibitor. A variety of other pyrimidine derivatives and related substances were ineffective. 3. Ninhydrin also inhibited glucokinase with a half-maximal inhibitory concentration of 5 microM. Isatin was a slightly less potent enzyme inhibitor. Several other indoline derivatives were ineffective. 4. Only glucose derivatives with a sufficiently bulky substituent in position C-2, such as the glucokinase substrates glucose and mannose and the inhibitors mannoheptulose, glucosamine, and N-acetylglucosamine, protected glucokinase against inhibition by alloxan by binding to the active site of the enzyme. Glucose epimers which differed in other positions did not protect the enzyme against alloxan inhibition. 5. DTT (dithiothreitol) protected glucokinase against inhibition by alloxan and reversed the inhibition of the enzyme induced by alloxan. Thus the mechanism of glucokinase inhibition by alloxan and other inhibitors, such as uramil and ninhydrin, is an oxidation of functionally essential SH groups of the enzyme, where the most reactive keto group of the inhibitor acts as the hydrogen acceptor. The protective action of glucose and several C-2 epimers demonstrates that these functionally essential SH groups are situated in the sugar binding site of the glucokinase. 6. The present results support our contention, that the pancreatic B-cell glucokinase is the major target mediating the inhibition of insulin secretion by alloxan.