We explore a dynamic approach to the problems of call admission and resource allocation for communication networks with connections that are differentiated by their quality of service requirements. In a dynamic approach, the amount of spare resources is estimated on-line based on feedbacks from the network's quality of service monitoring mechanism. The schemes we propose remove the dependence on accurate traffic models and thus simplify the tasks of supplying traffic statistics required of network users. In this paper we present two dynamic algorithms. The objective of these algorithms is to find the minimum bandwidth necessary to satisfy a cell loss probability constraint at an asynchronous transfer mode (ATM) switch. We show that in both schemes the bandwidth chosen by the algorithm approaches the optimal value almost surely. Furthermore, in the second scheme, which determines the point closest to the optimal bandwidth from a finite number of choices, the expected learning time is finite.
We explore a dynamic approach to the problems of call admission and resource allocation for communication networks with connections that are differentiated by their quality of service requirements. In a dynamic approach, the amount of spare resources is estimated on-line based on feedbacks from the network's quality of service monitoring mechanism. The schemes we propose remove the dependence on accurate traffic models and thus simplify the tasks of supplying traffic statistics required of network users. In this paper we present two dynamic algorithms. The objective of these algorithms is to find the minimum bandwidth necessary to satisfy a cell loss probability constraint at an asynchronous transfer mode (ATM) switch. We show that in both schemes the bandwidth chosen by the algorithm approaches the optimal value almost surely. Furthermore, in the second scheme, which determines the point closest to the optimal bandwidth from a finite number of choices, the expected learning time is finite.
One model for cancer initiation by 4-aminobiphenyl (ABP) involves N-oxidation by cytochrome P450 CYP1A2 followed by O-conjugation by Nacetyltransferase(s) NAT1 and/or NAT2 and decomposition to a DNA-binding nitrenium ion. We recently observed that neonatal ABP exposure produced liver tumors in male but not in female mice, and that NAT deficiency reduced liver tumor incidence. However, ABP-induced liver tumor incidence did not correlate with liver levels of N-(deoxyguanosin-8-yl)-ABP adducts 24 hr after exposure. In this study, we compared in vivo ABPinduced DNA mutant frequencies and spectra between male and female wild-type and NATdeficient Muta TM Mouse using both the tumorinducing neonatal exposure protocol and a 28-day repetitive dosing adult exposure protocol. ABP produced an increase in liver DNA mutant frequencies in both neonates and adults. However, we observed no sex or strain differences in mutant frequencies in neonatally exposed mice, and higher frequencies in adult females than males. Neonatal ABP exposure of wild-type mice increased the proportion of G-T transversions in both males and females, while exposure of Nat1/2(-/-) mice produced increased G-T transversions in males and a decrease in females, even though females had higher levels of N-(deoxyguanosin-8-yl)-4-ABP adducts. There was no correlation of mutant frequencies or spectra between mice dosed as neonates or as adults. These results suggest that observed sex-and NATdependent differences in ABP-induced liver tumor incidence in mice are not due to differences in either mutation rates or mutational spectra, and that mechanisms independent of carcinogen bioactivation, covalent DNA binding and mutation may be responsible for these differences. Environ. Mol. Mutagen. 53:350-357, 2012. V V C 2012 Wiley Periodicals, Inc.
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