Improving the Reliability of Computer Communication Networks

For networks that are directed or can be represented by a directed network,reversing one or more of the uni-directional links may provide the ability to reconnect a network that has been disconnected by link failure.In this paper,a new approach to reconfigure such networks is proposed.We develop a linear time algorithm which,when reachability has been destroyed by the removal of a single link,optimally restores reachability through the reversal of selected links.Multi-link failure reconnectability is discussed and an algorithm with polynomial complexity is given which provides a nearly optimum solution to reconnect the network.We show that the reliability of a network that allows reversals is at least twice more than that in which reversals are not permitted.Unfortunately,the reconnection of some networks cannot be established.Therefore,we discuss the maximization of reachability of such networks so that each node can reach maximum number of the other nodes.     

Analyzing the Reliability of Degradable Networks

The reachability of a strongly connected network may be destroyed after link damage,Since many networds have directed links with the potential for reversal,the reachability may be restored by reversing the direction of links.In this paper,the reliability of a network that allows reversal of links in discussed.     

Persistently exaggerated startle responses in rats treated with pyridostigmine bromide

Troops in the Persian Gulf War have registered complaints consistent with CNS dysfunction that emerged after returning from the Gulf. A common experience among Persian Gulf War veterans was exposure to pyridostigmine bromide (PB) for prophylaxis against nerve gas exposure. To determine whether PB causes emergent CNS dysfunction, Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats were given PB for 7 consecutive days in their drinking water. The WKY, but not the SD, rats exhibited a delayed-onset, persistently exaggerated startle response. The WKY rats exhibited exaggerated startle responses that appeared 15 days after the end of PB treatment and were still evident 22 days after the end of treatment. Both the duration and the magnitude of the exaggerated startle responses were related to the dosage of PB. The PB-treated rats exhibited normal short-term and long-term habituation. However, exaggerated startle responses were related to the development of enhanced short-term sensitization. Treating the rats for a second time, 7 weeks after the end of the first PB treatment, induced an exaggerated startle response that appeared sooner and dissipated faster than was evident after the first PB treatment. Inasmuch as the WKY rat has inherently low butyrylcholinesterase activity, a scavenger for PB, these results suggest that prophylactic PB may influence CNS function in individuals with low butyrylcholinesterase activity. Elaboration of the factors that mediate enhanced sensitization in the WKY rat may provide insight into some of the complaints registered by veterans of the Persian Gulf War.     

Effect of life in a constant light environment on the course of hypertension in Dahl rats

An important goal for biobehavioral scientists is to evaluate treatments that might extend life in the presence and absence of disease. The prototypic example of such a treatment is food restriction. Importantly, we have shown that exposure to a life-long environment of constant light extends life in hamsters with severe, life-threatening heart disease. The purpose of this experiment was to determine whether constant light would also extend the life of rats with an inherited form of hypertension. Constant light neither delayed the progression of hypertension nor extended life in this model. These data suggest that constant light may have a more limited use as an experimental therapeutic modality to extend life as compared to food restriction.     

Exposure to inescapable stress persistently facilitates associative and nonassociative learning in rats.

The present study examined the proactive effects of inescapable stress on aversive Pavlovian conditioning. Stressed rats were restrained and exposed to 90 1-mA tailshocks. Twenty-four hours later, all rats were exposed to 10 conditioned stimuli (CS; 350 ms of white noise at 85 dB). Rats then received either paired training in which the CS coterminated with a 100-ms, 0.7-mA periorbital shock or the same stimuli presented in an explicitly unpaired fashion. After the unpaired exposures, these rats were also exposed to paired training. Previously stressed rats exhibited persistent sensitization to the white-noise stimulus. Stressed rats exposed to unpaired stimuli, and no longer exhibiting a sensitized response, acquired the eyeblink conditioned response at a facilitated rate when these stimuli were presented in a paired fashion. These results also demonstrate that the effect of stress on classical conditioning is long-lasting, in excess of 48 hr. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Early acquisition, but not retention, of the classically conditioned eyeblink response is N-methyl-D-aspartate (NMDA) receptor dependent

N-methyl-D-aspartate (NMDA) antagonists impair performance in some tasks, but whether they impair learning directly or through effects on sensorimotor performance remains controversial. Rats administered a competitive NMDA antagonist, CGP-39551, 24 hr before training could not acquire a classically conditioned eyeblink response. The associative deficit remained evident during training with a high-intensity conditioned stimulus, even though sensory reactivity was unaffected. The antagonist did not alter retention and thus did not affect motor performance of the task. These results extend and confirm studies that implicate NMDA-receptor activation in the acquisition of classically conditioned associations and specifically in tasks not dependent on the hippocampus for learning itself. Moreover, they substantiate recent claims that NMDA receptor activation (and by association, long-term potentiation) may be involved in early processes of procedural memory formation.