In this paper, a centrifugal force model is developed for pedestrian dynamics. The effects of both the headway and the relative velocity among pedestrians are taken into account, which can be expressed by a "centrifugal force" term in dynamic equation. The jamming probability due to the arching at exits for crowd flows is provided. A quantitative analysis of the crowd flowing out of a hall shows that the average leaving time T is a function of the exit width W in negative power. The related simulation indicates that the proposed model is able to reproduce the self-organization phenomena of lane formation for sparse flows.
An extended car following model is proposed by incorporating an intelligent transportation system in traffic. The stability condition of this model is obtained by using the linear stability theory. The results show that anticipating the behavior of more vehicles ahead leads to the stabilization of traffic systems. The modified Korteweg-de Vries equation (the mKdV equation, for short) near the critical point is derived by applying the reductive perturbation method. The traffic jam could be thus described by the kink-antikink soliton solution for the mKdV equation. From the simulation of space-time evolution of the vehicle headway, it is shown that the traffic jam is suppressed efficiently with taking into account the information about the motion of more vehicles in front, and the analytical result is consonant with the simulation one.
Two lattice traffic models are proposed by incorporating a cooperative driving system. The lattice versions of the hydrodynamic model of traffic flow are described by the differential-difference equation and difference-difference equation, respectively. The stability conditions for the two models are obtained using the linear stability theory. The results show that considering more than one site ahead in vehicle motion leads to the stabilization of the system. The modified Korteweg-de Vries equation (the mKdV equation, for short) near the critical point is derived by using the reductive perturbation method to show the traffic jam which is proved to be described by kink-anti-kink soliton solutions obtained from the mKdV equations.
This paper studies many fundamental aspects of a newly proposed multi-class traffic flow model. For the first time it presents a complete discussion on the hyperbolicity of the system; and based upon this, the admissible waves of the Riemann problem are deeply investigated. Many important conclusions are made in discussions, and the related physical meanings are interpreted. For the confirmation of main conclusions, numerical examples are given at the end.
Dishevelled (Dvl) family proteins are overexpressed in nonsmall cell lung cancer (NSCLC), but the correlation between Dvl overexpression and patient prognosis is not clear. The underlying mechanisms of Dvl-1 and Dvl-3 promoting lung cancer cell invasion require further research. We used immunohistochemistry to assess the presence of Dvl-1, Dvl-3, beta-catenin, and p120ctn, and compared their expression to the prognosis in 102 specimens from NSCLC patients. We also examined the effect of Dvl-1 and Dvl-3 on Tcf-dependent transcriptional activity, as well as on the invasiveness in A549 and LTEP-alpha-2 lung cancer cells. The results showed that Dvl-1 correlated to the abnormal expression of beta-catenin, while Dvl-3 correlated to p120ctn. Both Dvl-1 and Dvl-3 were related to the poor prognosis of patient. Dvl-1 overexpression enhanced the Tcf-dependent transcriptional activity and beta-catenin expression significantly. However, Dvl-3 had little effect on the Tcf-dependent transcriptional activity and beta-catenin expression, which was accompanied by p38 and JNK phosphorylation. Furthermore, the invasiveness of Dvl-3-enhanced cells was inhibited by p38 and JNK inhibitors. Exogenous expression of both Dvl-1 and Dvl-3 increased the p120ctn protein expression, while only Dvl-3 upregulated p120ctn mRNA. We conclude that both protein and mRNA of Dvl-1 and Dvl-3 are overexpressed in NSCLC in a manner related to poor prognosis. Dvl-1 may affect the biological behavior of lung cancer cells mainly through beta-catenin (canonical Wnt pathway), while Dvl-3 mainly through p38 and JNK pathway (noncanonical Wnt pathway).
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