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Researchers and practitioners in the field of expert systems all generally agree that to be useful, any fielded intelligent system must be adequately verified and validated. But what does this mean in concrete terms? What exactly is verification? What exactly is validation? How are they different? Many authors have attempted to define these terms and, as a result, several interpretations have surfaced. It is our opinion that there is great confusion as to what these terms mean, how they are different, and how they are implemented. This paper, therefore, has two aims-to clarify the meaning of the terms validation and verification as they apply to intelligent systems, and to describe how several researchers are implementing these. The second part of the paper, therefore, details some techniques that can be used to perform the verification and validation of systems. Also discussed is the role of testing as part of the above-mentioned processes. [ABSTRACT FROM AUTHOR]

Antigen recognition triggers the recruitment of the critical adaptor protein SLP-76 to small macromolecular clusters nucleated by the T-cell receptor (TCR). These structures develop rapidly, in parallel with TCR-induced increases in tyrosine phosphorylation and cytosolic calcium, and are likely to contribute to TCR-proximal signaling. Previously, we demonstrated that these SLP-76-containing clusters segregate from the TCR and move towards the center of the contact interface. Neither the function of these clusters nor the structural requirements governing their persistence have been examined extensively. Here we demonstrate that defects in cluster assembly and persistence are associated with defects in T-cell activation in the absence of Lck, ZAP-70, or LAT. Clusters persist normally in the absence of phospholipase C-γ 1, indicating that in the absence of a critical effector, these structures are insufficient to drive T-cell activation. Furthermore, we show that the critical adaptors LAT and Gads localize with SLP-76 in persistent clusters. Mutational analyses of LAT, Gads, and SLP-76 indicated that multiple domains within each of these proteins contribute to cluster persistence. These data indicate that multivalent cooperative interactions stabilize these persistent signaling clusters, which may correspond to the functional complexes predicted by kinetic proofreading models of T-cell activation. [ABSTRACT FROM AUTHOR]