Identifying and predicting social lifestyles in people’s trajectories by neural networks

Abstract In this research, we exploit repeated parts in daily trajectories in people’s movements, which we refer to as mobility patterns, to train models to identify and predict a person’s lifestyles. We use cellular data of a group (“society”) of people and represent a person’s daily trajectory using semantic labels (e.g., “home”, “work”, and “gym”) given to the main places of interest (POI) he has visited during the day, as determined collectively based on interviewing all people of the group. First, in an unsupervised manner using a neural network (NN), we embed POI-based daily trajectories that always appear together with others in consecutive weeks and identify the result of this embedding with social lifestyles. Second, using these lifestyles as labels for lifestyle prediction, user POI-based daily trajectories are used to train a convolutional NN to extract mobility patterns in the trajectories and a dynamic NN with flexible memory to assemble these patterns to predict a lifestyle for a trajectory never-seen-before. The two-stage algorithm shows model accuracy and generalizability in lifestyle identification and prediction (both for a novel trajectory and a novel user) that are superior to those shown by state-of-the-art algorithms. The code for the algorithm and data sets used in our experiments are available online

Localization and magnetic moment

estimation of a ferromagnetic target by simulated annealin

The SCAR and WASp nucleation-promoting factors act sequentially to mediate Drosophila myoblast fusion

The actin nucleation-promoting factors SCAR/WAVE and WASp, together with associated elements, mediate the formation of muscle fibres through myoblast fusion during Drosophila embryogenesis. Our phenotypic analysis, following the disruption of these two pathways, suggests that they function in a sequential manner. Suppressor of cyclic AMP receptor (SCAR) activity is required before the formation of pores in the membranes of fusing cells, whereas Wiskott–Aldrich syndrome protein (WASp) promotes the expansion of nascent pores and completion of the fusion process. Genetic epistasis experiments are consistent with this step-wise temporal progression. Our observations further imply a separate, Rac-dependent role for the SCAR complex in promoting myoblast migration. In keeping with the sequential utilization of the two systems, we observe abnormal accumulations of filamentous actin at the fusion sites when both pathways are disrupted, resembling those present when only SCAR-complex function is impaired. This observation further suggests that actin-filament accumulation at the fusion sites might not depend on Arp2/3 activity altogether