Games on graphs: A minor modification of payoff scheme makes a big difference

Various social dilemma games that follow different strategy updating rules have been studied on many networks.The reported results span the entire spectrum, from significantly boosting,to marginally affecting,to seriously decreasing the level of cooperation.Experimental results that are qualitatively different from theoretical prediction have also been reported.It is widely believed that the results are largely determined by three elements,including payoff matrices of the underlying 2*2 games,the way that the strategic states of the players are updated and the structure of the networks.Here we discuss the impact of a seemly non-essential mechanism -- what we refer to as a "payoff scheme". Specifically, in each round after the states of all of the players are determined,the payoff scheme is how each player's payoff is calculated.In addition to the two conventions in which either the accumulated or the averaged payoff is calculated from playing with all of the neighboring players,we here study the effects of calculating the payoff from pairing up with one random player from among the neighboring players. Based on probability theory, in a situation of uncorrelated events, the average payoff that involves all of the neighbors should,in principal,be equivalent to the payoff from pairing up with one neighbor.However,our simulation of games on graphs shows that, in many cases,the two payoff schemes lead to qualitatively different levels of cooperation.This finding appears to provide a possible explanation for a wide spectrum of observed behaviors in the literature.We have also observed that results from the randomly-pairing-one mechanism are more robust than the involving-all-neighbours mechanism because,in the former case, neither the other three main elements nor the initial states of the players have a large impact on the final level of cooperation compared with in the latter case.Comment: 23 pages,171 figure

Cigarette Smoke (CS) and Nicotine Delay Neutrophil Spontaneous Death via Suppressing Production of Diphosphoinositol Pentakisphosphate

Diphosphoinositol pentakisphosphate (InsP7), a higher inositol phosphate containing energetic pyrophosphate bonds, is beginning to emerge as a key cellular signaling molecule. However, the various physiological and pathological processes that involve InsP7 are not completely understood. Here we report that cigarette smoke (CS) extract and nicotine reduce InsP7 levels in aging neutrophils. This subsequently leads to suppression of Akt deactivation, a causal mediator of neutrophil spontaneous death, and delayed neutrophil death. The effect of CS extract and nicotine on neutrophil death can be suppressed by either directly inhibiting the PtdIns(3,4,5)P3/Akt pathway, or increasing InsP7 levels via overexpression of InsP6K1, an inositol hexakisphosphate (InsP6) kinase responsible for InsP7 production in neutrophils. Delayed neutrophil death contributes to the pathogenesis of CS-induced chronic obstructive pulmonary disease. Therefore, disruption of InsP6K1 augments CS-induced neutrophil accumulation and lung damage. Taken together, these results suggest that CS and nicotine delay neutrophil spontaneous death by suppressing InsP7 production and consequently blocking Akt deactivation in aging neutrophils. Modifying neutrophil death via this pathway provides a strategy and therapeutic target for the treatment of tobacco-induced chronic obstructive pulmonary disease

RFID-Based Vehicle Positioning and Its Applications in Connected Vehicles

This paper proposed an RFID-based vehicle positioning approach to facilitate connected vehicles applications. When a vehicle passes over an RFID tag, the vehicle position is given by the accurate position stored in the tag. At locations without RFID coverage, the vehicle position is estimated from the most recent tag location using a kinematics integration algorithm till updates from the next tag. The accuracy of RFID positioning is verified empirically in two independent ways with one using radar and the other a photoelectric switch. The former is designed to verify whether the dynamic position obtained from RFID tags matches the position measured by radar that is regarded as accurate. The latter aims to verify whether the position estimated from the kinematics integration matches the position obtained from RFID tags. Both means supports the accuracy of RFID-based positioning. As a supplement to GPS which suffers from issues such as inaccuracy and loss of signal, RFID positioning is promising in facilitating connected vehicles applications. Two conceptual applications are provided here with one in vehicle operational control and the other in Level IV intersection control

Deactivation of Akt by a Small Molecule Inhibitor Targeting Pleckstrin Homology Domain and Facilitating Akt Ubiquitination

The phosphatidylinositol-3,4,5-triphosphate (PIP3) binding function of pleckstrin homology (PH) domain is essential for the activation of oncogenic Akt/PKB kinase. Following the PIP3-mediated activation at the membrane, the activated Akt is subjected to other regulatory events, including ubiquitination-mediated deactivation. Here, by identifying and characterizing an allosteric inhibitor, SC66, we show that the facilitated ubiquitination effectively terminates Akt signaling. Mechanistically, SC66 manifests a dual inhibitory activity that directly interferes with the PH domain binding to PIP3 and facilitates Akt ubiquitination. A known PH domain-dependent allosteric inhibitor, which stabilizes Akt, prevents the SC66-induced Akt ubiquitination. A cancer-relevant Akt1 (e17k) mutant is unstable, making it intrinsically sensitive to functional inhibition by SC66 in cellular contexts in which the PI3K inhibition has little inhibitory effect. As a result of its dual inhibitory activity, SC66 manifests a more effective growth suppression of transformed cells that contain a high level of Akt signaling, compared with other inhibitors of PIP3/Akt pathway. Finally, we show the anticancer activity of SC66 by using a soft agar assay as well as a mouse xenograft tumor model. In conclusion, in this study, we not only identify a dual-function Akt inhibitor, but also demonstrate that Akt ubiquitination could be chemically exploited to effectively facilitate its deactivation, thus identifying an avenue for pharmacological intervention in Akt signaling