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No abstract received. [ABSTRACT FROM AUTHOR]

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]

In this paper we discuss ways in which coverage analysis, obtained during execution of test cases over a rule-base, can be used to highlight problems in both the test suite and the rule-base, thereby pointing to areas in which we cannot guarantee or predict the system's performance. In particular, we present a series of heuristics which use coverage information and meta-knowledge about the larger population to select additional test cases from the population, in the event that the initial test set is incomplete. This forms the basis of an incremental approach to rule-base testing which allows us to both increase completeness of the test set and improve coverage of the rule-base, thereby increasing the kinds of cases for which the rule-base has been executed during testing. We demonstrate this heuristic approach to test data selection using information generated by TRUBAC, a tool which implements the coverage analysis methods, applied to analyze a prototype system for diagnosis of rheumatological diseases. [ABSTRACT FROM AUTHOR]

The biotic resistance hypothesis predicts that diverse native communities are more resistant to invasion. However, past studies vary in their support for this hypothesis due to an apparent contradiction between experimental studies, which support biotic resistance, and observational studies, which find that native and non‐native species richness are positively related at broad scales (small‐scale studies are more variable). Here, we present a novel analysis of the biotic resistance hypothesis using 24 456 observations of plant richness spanning four community types and seven ecoregions of the United States. Non‐native plant occurrence was negatively related to native plant richness across all community types and ecoregions, although the strength of biotic resistance varied across different ecological, anthropogenic and climatic contexts. Our results strongly support the biotic resistance hypothesis, thus reconciling differences between experimental and observational studies and providing evidence for the shared benefits between invasive species management and native biodiversity conservation. [ABSTRACT FROM AUTHOR]

Evaluates several computer software. Design of Headroom software; Features of Visible Computer software by Software Masters; Capabilities of Paradox by Borland International.

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]