Modeling and Prediction of Driving Behaviors Using a Nonparametric Bayesian Method with AR Models

To develop a new generation advanced driver assistance system that avoids a dangerous condition in advance, we need to predict driving behaviors. Since a nonparametric Bayesian method with a two-level structure successfully predicted the symbolized behaviors only, we applied a nonparametric Bayesian method with linear dynamical systems to predicting the driving behavior. The method called the beta process autoregressive hidden Markov model (BP-AR-HMM) segments driving behaviors into states each of which corresponds to an AR model and it predicts future behaviors using the estimated future state sequence and the dynamical systems therein. Here, the segmentation as well as the parameters of the dynamical systems are determined using given training data in an unsupervised way. We carried out experiments with real driving data and found that the BP-AR-HMM predicted driving behaviors better than other methods

Shootin1-cortactin interaction mediates signal-force transduction for axon outgrowth

Motile cells transduce environmental chemical signals into mechanical forces to achieve properly controlled migration. This signal-force transduction is thought to require regulated mechanical coupling between actin filaments (F-actins), which undergo retrograde flow at the cellular leading edge, and cell adhesions via linker "clutch" molecules. However, the molecular machinery mediating this regulatory coupling remains unclear. Here we show that the F-actin binding molecule cortactin directly interacts with a clutch molecule, shootin1, in axonal growth cones, thereby mediating the linkage between F-actin retrograde flow and cell adhesions through L1-CAM. Shootin1-cortactin interaction was enhanced by shootin1 phosphorylation by Pak1, which is activated by the axonal chemoattractant netrin-1. We provide evidence that shootin1-cortactin interaction participates in netrin-1-induced F-actin adhesion coupling and in the promotion of traction forces for axon outgrowth. Under cell signaling, this regulatory F-actin adhesion coupling in growth cones cooperates with actin polymerization for efficient cellular motility