Preemptive and delay-based mechanisms to provide preference to emergency traffic

Preemptive and delay-based policies are derived here to provide preferential treatment to emergency users as motivated by the need to respond to natural or man-made disasters. These are applied in circuit switched networks or IP-based networks in conjunction with reservation mechanisms at single links or routers where congestion occurs. A unique optimization formulation is provided where policies are constrained by blocking requirements for emergency traffic, then optimized to provide lowest preemption probabilities. An iterative optimization approach is derived for a multi-dimensional Markov chain to provide an approximate solution for a non-linear integer program. Markov state space concerns are mitigated by introducing and analyzing algorithmic simplifications. Polices are found for hard preemption where sessions are interrupted or soft preemption where session quality is reduced. In addition, delay-based approaches are also examined where emergency users are allowed to wait for network resources if they are first blocked. All of the above approaches are compared with each other and with traditional approaches that hold back resources for emergency traffic. The results demonstrate that in general no approach is superior based on network performance characteristics alone. Qualitative factors must also be considered, most notably the nuisance to non-emergency users from preemption.     

Bim: a novel member of the Bcl-2 family that promotes apoptosis

Certain members of the Bcl-2 family inhibit apoptosis while others facilitate this physiological process of cell death. An expression screen for proteins that bind to Bcl-2 yielded a small novel protein, denoted Bim, whose only similarity to any known protein is the short (nine amino acid) BH3 motif shared by most Bcl-2 homologues. Bim provokes apoptosis, and the BH3 region is required for Bcl-2 binding and for most of its cytotoxicity. Like Bcl-2, Bim possesses a hydrophobic C-terminus and localizes to intracytoplasmic membranes. Three Bim isoforms, probably generated by alternative splicing, all induce apoptosis, the shortest being the most potent. Wild-type Bcl-2 associates with Bim in vivo and modulates its death function, whereas Bcl-2 mutants that lack survival function do neither. Significantly, Bcl-xL and Bcl-w, the two closest homologues of Bcl-2, also bind to Bim and inhibit its activity, but more distant viral homologues, adenovirus E1B19K and Epstein-Barr virus BHRF-1, can do neither. Hence, Bim appears to act as a 'death ligand' which can only neutralize certain members of the pro-survival Bcl-2 sub-family.     

Rigorous and approximate solutions for the three-conductor lossy transmission lines problem

The coupled first-order linear differential equations governing the voltage and the current on three-conductor lossy (identical) transmission lines are solved by two methods. One method is rigorous, and the other one is approximate and applies in the low- and high-frequency ranges. Although the rigorous solution is a numerical one, the approximate solution consists of explicit expressions that are easy to calculate and give physical insight into the coupling process. Experimental results that are available for two parallel identical lossy wires of finite length situated above a perfectly conducting ground (when only one of the wires is driven by a source) and previously published theoretical results compare satisfactorily with the results obtained by the two methods.<>     

The anti-apoptosis function of Bcl-2 can be genetically separated from its inhibitory effect on cell cycle entry

The Bcl-2 family of proteins regulate apoptosis, some antagonizing cell death and others facilitating it. It has recently been demonstrated that Bcl-2 not only inhibits apoptosis but also restrains cell cycle entry. We show here that these two functions can be genetically dissociated. Mutation of a tyrosine residue within the conserved N-terminal BH4 region had no effect on the ability of Bcl-2 or its closest homologs to enhance cell survival and did not prevent heterodimerization with death-enhancing family members Bax, Bak, Bad and Bik. Neither did this mutation override the growth-inhibitory effect of p53. However, on stimulation with cytokine or serum, starved quiescent cells expressing the mutant proteins re-entered the cell cycle much faster than those expressing comparable levels of wild-type proteins. When wild-type and Y28 mutant Bcl-2 were co-expressed, the mutant was dominant. Although R-Ras p23 has been reported to bind to Bcl-2, no interaction was detectable in transfected cells and R-Ras p23 did not interfere with the ability of Bcl-2 to inhibit apoptosis or cell cycle entry. These observations provide evidence that the anti-apoptotic function of Bcl-2 is mechanistically distinct from its inhibitory influence on cell cycle entry.     

The location of hydrogen in the kinetics of oxidation of ferrous alloys by superheated steam

The rate of emission of hydrogen from the metal surface and from the oxide surface has been determined during the oxidation of ferrous alloys at 501°C. The kinetics were in accordance with the assumption of a parabolic rate law, and the rate constants were in agreement with those calculated from the thickness of the oxide layer at the end of the reaction. The proportion of hydrogen emitted from the metal to that from the oxide surface showed a dependence on the partial pressure of steam for the 9%Cr-1%Mo alloy at 501°C. The ratio was dependent on the alloy composition, and also on temperature, as shown by results for the 9%Cr-1%Mo alloy at 450 and 552°C. For this alloy, the activation energy and rate constants are consistent with a rate-determining step dependent on cation diffusion. The oxide film is almost impermeable to hydrogen gas. A possible oxidation mechanism is suggested.     

Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis

Activation of the cell surface receptor Fas/APO-1 (CD95) induces apoptosis in lymphocytes and regulates immune responses. The cytoplasmic membrane protein Bcl-2 inhibits lymphocyte killing by diverse cytotoxic agents, but we found it provided little protection against Fas/APO-1-transduced apoptosis in B lymphoid cell lines, thymocytes and activated T cells. In contrast, the cowpox virus protease inhibitor CrmA blocked Fas/APO-1-transduced apoptosis, but did not affect cell death induced by gamma-radiation or serum deprivation. Signalling through Fas/APO-1 did not down-regulate Bcl-2 or induce its antagonists Bax and Bcl-xS. In Fas/APO-1-deficient lpr mice, Bcl-2 transgenes markedly augmented the survival of antigen-activated T cells and the abnormal accumulation of lymphocytes (although they did not interfere with deletion of auto-reactive cells in the thymus). These data raise the possibility that Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis.     

The importance of losses in the coupling of transmission lines

A simple model for weakly coupled lossy transmission lines of finite length has recently been proposed by Olsen (1984). He derived a simple formula for the coupling voltage on a load situated at one extremity of the undriven wire. The importance of the coupling due to losses on this voltage with respect to the coupling due to capacitance and inductance is investigated in this paper. It is found that only in a special case, called the resonance matching case, is the role of the losses dominant in the coupling process. This case is characterized by the condition that the characteristic impedance of the wires squared by equal to the product of two loads Z_LG and Z _0R situated at opposite ends of the driven and the undriven wire     

Reflection coefficient at the feed of a radome-covered reflector antenna

The reflection coefficient at the feed of a paraboloidal reflector antenna covered with a paraboloidal radome is evaluated by means of the power-coupling theorem. An asymptotic value of the subsequent expression leads to a simple physical interpretation of the result. A comparison between theoretical and experimental results shows that there is a satisfactory measure of agreement between the two.     

The ability to manipulate behavior and to understand manipulation of beliefs: A comparison of individuals with autism, mental retardation, and normal development.

This study investigated the ability to deceive in participants with autism, mental retardation ( MR ), and normal development. The authors used S. Hala, M. Chandler, and A. S. Fritz's (see record, 78:20899) procedures, in which children deceive by creating false trails or by erasing all trails and lying about the true location of a hidden object. Participants with autism and those with MR did not differ in their ability to use a deceptive method to manipulate the behavior of another person. Participants with autism were significantly less able than participants with MR to understand that they manipulated the beliefs of another person by predicting the outcome of their deceptive act. The normal group outperformed the group with autism but not the group with MR on both parts of the task. Different possible interpretations of the results are discussed, including a deficit in theory of mind and a deficit in executive control functions. (PsycINFO Database Record (c) 2010 APA, all rights reserved)