Agent-based distributed software verification

Despite decades of research, the takeup of formal methods for developing provably correct software in industry remains slow. One reason for this is the high cost of proof construction, an activity that, due to the complexity of the required proofs, is typically carried out using interactive theorem provers. In this paper we propose an agent-oriented architecture for interactive theorem proving with the aim of reducing the user interactions (and thus the cost) of constructing software verification proofs. We describe a prototype implementation of our architecture and discuss its application to a small, but non-trivial case study.

A Reactive Agent-based Neural Network Car Following Model

This paper presented a novel approach to develop car following models using reactive agent techniques for mapping perceptions to actions. The results showed that the model outperformed the Gipps and Psychophysical family of car following models. The standing of this work is highlighted by its acceptance and publication in the proceedings of the International IEEE Conference on Intelligent Transportation Systems (ITS), which is now recognised as the premier international conference on ITS. The paper acceptance rate to this conference was 67 percent. The standing of this paper is also evidenced by its listing in international databases like Ei Inspec and IEEE Xplore. The paper is also listed in Google Scholar. Dr Dia co-authored this paper with his PhD student Sakda Panwai.

Changes in inositol lipids and phosphates after stimulation of the MAS-transfected NG115-401L-C3 cell line by mitogenic and non-mitogenic stimuli

A neuronal cell line (NG115-401L-C3) was stimulated by mitogenic (angiotensin) and non-mitogenic (bradykinin) peptides and examined for the time course of changes in the levels of radiolabelled inositol phosphates and phospholipids. Both peptides stimulated the time-dependent production of Ins(1,4,5)P3 and related metabolites. Bradykinin caused a much larger increase in Ins(1,4,5)P3 than did angiotensin. However, both peptides stimulated similar rises in the levels of Ins(1,3,4)P3 and InsP4. Bradykinin but not angiotensin, caused a rapid (within 2 s) fall in the levels of PtdIns(4,5)P2 and PtdIns(4)P. Serum pretreatment of the cells caused a 2-3-fold potentiation of both the responses to bradykinin and angiotensin. Although significant levels of PtdIns(3)P were detected in resting cells neither mitogenic (angiotensin, insulin-like growth factor I, transforming growth factor beta) nor non-mitogenic (bradykinin, nerve growth factor interleukin-1) receptor activation changed its levels, arguing against regulation of either PtdIns 3-kinase or PtdIns(3)P phosphatase. We conclude that, as judged by the levels of its product. PtdIns(3)P, the enzyme PtdIns 3-kinase is not activated. This questions the significance of this activity in the receptor-mediated initiation of DNA synthesis.