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The problem of associating data with targets in a cluttered multi-target environment is discussed and applied to passive sonar tracking. The probabilistic data association (PDA) method, which is based on computing the posterior probability of each candidate measurement found in a validation gate, assumes that only one real target is present and all other measurements are Poisson-distributed clutter. In this paper, a new theoretical result is presented: the joint probabilistic data association (JPDA) algorithm, in which joint posterior association probabilities are computed for multiple targets (or multiple discrete interfering sources) in Poisson clutter. The algorithm is applied to a passive sonar tracking problem with multiple sensors and targets, in which a target is not fully observable from a single sensor. Targets are modeled with four geographic states, tw'o or more acoustic states, and realistic (Le., low) probabilities of detection at each sample time. A simulation result is presented for two heavily interfering targets illustrating the dramatic tracking improvements obtained by estimating the targets' states using joint association probabilities.

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Cell migration depends on the generation of structural asymmetry and on different steps: protrusion and adhesion at the front and traction and detachment at the rear part of the cell. The activity of Ca 2+ channels coordinate these steps by arranging intracellular Ca 2+ signals along the axis of movement. Here, we investigated the role of the putative mechanosensitive canonical transient receptor potential channel 1 (TRPC1) in cell migration. We analyzed its function in transformed renal epithelial (Madin-Darby canine kidney-focus) cells with variation of TRPC1 expression. As shown by time lapse video microscopy, TRPC1 knockdown cells have partially lost their polarity and the ability to persistently migrate into a given direction. This failure is linked to the suppression of a local Ca 2+ gradient at the front of migrating TRPC1 knockdown cells, whereas TRPC1 overexpression leads to steeper Ca 2+ gradients. We propose that the Ca 2+ signaling events regulated by TRPC1 within the lamellipodium determine polarity and directed cell migration.

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